1
Q
what is angina caused by
A
atherosclerosis affecting the coronary arteries narrowing the lumen and reducing blood flow to the myocardium. During times of high demand there is insufficient supply to meet the demand causing symptoms
2
Q
when is angina labeled as stable
A
when it only comes on with exertion and is always relieved by rest or with GTN
3
Q
what investigations should be done for someone with stable angina
A
physical examination
ECG
FBC, U+E, LFT, lipid profile, TFT
HbA1c and fasting glucose
cardiac stress testing
CT coronary angiography
invasive coronary angiography
4
Q
what is CT coronary angiography
A
it involves injecting contrast and taking CT images times with the heart contractions to give a detailed view of the coronary arteries, highlighting the specific locations of any narrowing
5
Q
what is invasive coronary angiography
A
involves an invasive procedure performed in a catheter lab. A catheter is inserted into the patients brachial or femoral artery directed through the arterial system to the aorta and the coronary arteries under X ray guidance, where contrast is injected to visualise the coronary arteries and identify areas of stenosis
- Gold standard
6
Q
what are the five principles of management for someone with angina
A
RAMPS
Refer to cardio
Advise them about diagnosis, management and when to call the ambulance
Medical treatment
Procedural or surgical interventions
Secondary prevention
7
Q
what are the three aims of medical management of angina
A
immediate symptomatic relief during episodes
long term symptomatic relief
secondary prevention
8
Q
what can be given for immediate relief of stable angina
A
sublingual glyceryl trinitrate (GTN) in the form of spray or tablets
9
Q
how should patients be advised to take GTN spray
A
take the GTN when symptoms start
take a second dose after 5 minutes if symptoms remain
call an ambulance if symptoms remain five minutes after the second dose
10
Q
what are the side effects of GTN spray
A
headaches and dizziness
11
Q
for long term symptomatic relief what is given for stable angina
A
beta blocker - bisoprolol
calcium channel blocker - verapamil
a specialist may also consider long acting nitrates, ivabradine, nicorandil, ranolazine
12
Q
what medications should be avoided in heart failure with reduced ejection fraction
A
calcium channel blockers diltiazem and verapamil
13
Q
what medications are used for secondary prevention of heart disease in stable angina
A
the four As
- Aspirin 75mg
- Atorvastatin 80mg
- ACE inhibitor (if diabetes, htn, CKD or HF also present)
- Already on BB for symptomatic relief
13
Q
what is percutaneous coronary intervention
A
it involved inserting a catheter into the patients brachial or femoral artery
this is fed up to the coronary arteries
contrast is then injected to visualise the arteries and identify stenosis
areas of stenosis can then be treated by dilating a balloon to widen the limen and inserting a stent
13
Q
what surgical interventions are offered for acute angina
A
given in more severe disease
- percutaneous coronary intervention
- coronary artery bypass graft
13
Q
what is coronary artery bypass grafting
A
it involves opening the chest and a graft vessel is attached to the affected coronary artery bypassing the stenotic area
14
Q
what are the three main options for graft vessels in a CABG procedure
A
saphenous vein
internal thoracic artery
radial artery
15
Q
what are the advantages of a PCI over CABG
A
faster recovery
lower rate of stroke as complication
16
Q
what are the benefits of CABG over PCI
A
lower rates of requiring repeat revascularisation
17
Q
what is cardiac X syndrome
A
causes angina like pain without the presence of coronary artery disease when investigated with angiograms
18
Q
who does cardiac syndrome X most commonly effect
A
women in the perimenopausal or postmenopausal period
19
Q
what is the pathophysiology of cardiac syndrome X
A
not fully understood
may involve microvascular dysfunction causing reduced blood flow
it may also be due to increased sensitivity of the heart muscle lowering the pain threshold
20
Q
what conditions make up acute coronary syndrome
A
it encompasses STEMI, NSTEMI and unstable angina
21
Q
what is unstable angina
A
it is an acute coronary syndrome that is defined by the absence of biochemical evidence of myocardial damage
22
what is the definition of unstable angina
prolonged (over 20 mins) angina at rest
new onset of severe angina
angina that is increasing in frequency, longer duration or lower in threshold
angina that occurs after a recent episode of MI
23
how is unstable angina diagnosed
clinical assessment
troponins - normal
ECG - may be normal
24
what is the management of unstable angina
Beta blockade (or other rate limiting agent if contraindicated)
ACE inhibitor
Atorvastatin 80mg
25
what is acute coronary syndrome
term used to describe sudden reduction in blood flow to the heart which may result in irreversible damage to the myocardium
26
what is the aetiology of an NSTEM
there is partial coronary artery obstruction from a ruptured plaque, partial occlusion from a stable plaque, coronary artery vasospasm or coronary arteritis
27
what are non modifiable risk factors for NSTEMI
male sex
older age
previous history of ACS/ischaemic heart disease
family history of ACS/ischaemic heart disease
renal insufficiency
diabetes
28
what are modifiable risk factors for NSTEMI
tobacco smoking
longstanding hypertension
hyperlipidaemia
29
what are typical symptoms of ACS/NSTEMI
sudden onset central crushing chest pain radiating to the left arm and/or jaw lasting longer than 20 mins
diaphoresis
nausea
SOB
30
what are clinical findings of ACS/NSTEMI
signs of respiratory distress, pallor, diaphoresis
tachycardia
high or low blood pressure
s4 heart sound; reduced ATP impairing left ventricular relaxation
signs of papillary muscle dysfunction (mitral regurg)
pulmonary oedema
31
what investigations should be done on someone with suspected NSTEMI
serial 12 lead ECG
troponins - will be raised
U+E, glucose, FBC
coronary angio
echo
CXR
32
what will be seen on ECG for NSTEMI
regional ST depression
T wave inversion or flattening
any dynamic or new Q or T wave changes
33
what is traponin
it is a structural protein found solely in cardiac myocytes. Presence in blood indicates necrosis
- to indicate myocardial damage, troponin levels need to be about three standard deviations from the normal range
34
what is the pattern of troponins in NSTEMI
troponin is expected to rise two to three hours after the onset of chest pain, peaking 12-48 hours post incident and then declining
35
how is NSTEMI diagnosed
clinical history + abnormal troponins + absence of ST elevation
36
what is the immediate management of ACS
antiplatelet therapy: 300mg aspirin
analgesia: GTN/IV opioids
initial anti-thrombin therapy: fondaparinux if low bleeding risk and patient isnt undergoing immediate angiography. Unfractionated heparin in patients with renal impairment
supplemental 02 if Sp02 under 94
37
what is management of NSTEMI after acute treatment
coronary angiography with PCI
- coronary angiography is required for all clinically unstable adult patients asap and at least within 24 hours of becoming instable
38
what is a clinically unstable patient - NSTEMI
ongoing or recurring pain despite treatment
haemodynamically unstable
dynamic ECG changes
left ventricular failure
39
after NSTEMI has been confirmed what risk stratification is performed ?
look at 6 month mortality of patients diagnosed with unstable angina or NSTEMI to help with treatment - done using the GRACE scale
40
what patients are determined low risk by the GRACE score
those with a predicted 6 month mortality of less than 3%
41
what is the long term treatment for those who have a low risk GRACE score post NSTEMI
conservative management
- duel antiplatelet therapy: ticagrelor if bleeding risk not high, clopidogrel/aspirin of bleeding risk is high
left ventricular function tests
42
what is long term treatment for those who have a high risk GRACE score after NSTEMI
coronary angiography
duel antiplatelet therapy - prasugrel or ticagrelor
if undergoing PCI patients should be offered unfractionated heparin
assess left ventricular function
43
what is the drug regime recommended for all patients post NSTEMI to prevent future MI
ACE inhibitor/ARB
dual antiplatelet therapy (aspirin plus second agent): up to 12 months
beta blocker for at least 12 months
statin
44
what lifestyle advice can be given to someone after NSTEMI
eating healthy diet (Mediterranean diet)
regular physical activity
low risk drinking
smoking cessation
maintaining healthy body weight
45
what cardiac rehabilitation should be offered to all patients with NSTEMI
advice on lifestyle, driving, flying, sex
tailored physical activity
stress management
health and lifestyle education
46
what are mechanical complications of NSTEMI
papillary muscle rupture
ventricular aneurysm
free wall rupture
47
what are non mechanical complications of NSTEMI
arrythmias
thromboembolic complications
heart failure
pericarditis
depression
48
what is a STEMI
it is a clinical event characterised by transmural myocardial ischaemia resulting un injury or necrosis
49
what is the aetiology of STEMI
caused predominantly by complete occlusion of one or more corocary arteries that supply the heart usually due to thrombosisc
- can involve full thickness of myocardium
50
what are non modifiable risk factors for STEMI
Male sex
Older age
Previous history of ACS/ischaemic heart disease
Family history of ACS/ischaemia heart disease
Renal insufficiency
Diabetes
51
what are modifiable risk factors for STEMI
Smoking
Longstanding hypertension
Hyperlipidaemia
Obesity & sedentary lifestyle
52
what are typical features of cardiac chest pain
Site: central or left-sided chest pain (usually lasting > 15 minutes)
Onset: “crescendo pain” with increasing severity over several minutes
Character: described as substernal pressure, heaviness, squeezing, and aching
Radiation: left arm, shoulders, neck, or jaw
Severity: variable, can range from 1 to 10 out of 10
sweating, nausea, vomiting, dyspnoea, fatigue
53
what may be found on examination of someone with STEMI
Hypotension or hypertension may occur depending on the extent of the myocardial infarction
Low-grade fever
Pale, cool and/or clammy skin
Signs of acute heart failure: tachycardia, gallop rhythm, third and fourth heart sounds, bibasal crackles, peripheral oedema, elevated jugular venous pressure and/or tender hepatomegaly
Systolic murmur due to acute mitral regurgitation or ventricular septal rupture and/or pericardial rub
54
what investigations should be done on someone with suspected STEMI
12 lead ECG - ASAP
troponins
FBC, U+E, LFT, Lipids, TFTs, HBa1C and glucose
CXR
55
what are the cut off points for ST elevation on ECG
≥2.5 mm in men <40
≥2 mm in men >40
≥ 1.5 mm in women regardless of age
56
what leads does occlusion of
a. left anterior descending
b. right coronary artery
c. left circumflex artery
produce ST changes in
a. V1-3 (precordial leads)
b. II - III - AVF (inferior leads)
c. I, AVL, V5-6 (lateral leads)
57
what are other causes of raised troponins that isnt ACS
Tachy/bradyarrhythmias
Aortic dissection
Heart failure
Myocarditis
Chronic kidney disease
Sepsis
58
what is the immediate management of suspected STEMI
ACBDE approach
continuous monitoring - ECG, BP, pulse, o2 sats
analgesia - morphine
loading dose of aspirin - 300mg
oxygen if spo2 under 94
nitrates
59
when should patients presenting with STEMI get reperfusion therapy
NICE advise that patients presenting with STEMI within 12 hours of onset should be discussed urgently for either
- PCI (if less than 2 hours of presentation)
- thrombolysis (if PCI not possible within 2 hours)
60
what thrombolytic agents are used for reperfusion therapy in STEMI
streptokinase
alteplase
tenecteplase
61
what medications are recommended to reduce the risk of future events and improve myocardial function post STEMI
ACE inhibitor or ARB: continued indefinitely
Dual antiplatelet therapy (aspirin plus a second agent): for up to 12 months
Beta-blocker for at least 12 months: continued indefinitely in the presence of reduced left ventricular ejection fraction
Statin: continued indefinitely
62
what complications can occur after STEMI
tachyarrhythmias
bradyarrhythmias
re-infarction or infarct extension
ventricular free-wall/septal rupture
acute mitral regurgitation
left ventricular aneurysm
stent thrombosis following PCI
bleeding following thrombolysis
pericarditis (dressler syndrome)
depression
63
what features are associated with a worse prognosis in STEMI
greater severity of myocardial necrosis
site of the infarction: anterior myocardial infarction generally has less favourable
delayed reperfusion
comorbidities
older age
64
what are symptoms of ACS
Chest pain
Referred pain: chest pain can radiate to the epigastrium, arm, neck and jaw
Shortness of breath
Palpitations
Nausea and vomiting
Sweating
Fatigue
Pre-syncope and syncope
65
what are clinical signs of ACS
Tachycardia
Tachypnoea
Pallor
Evidence of impaired myocardial function: hypotension, raised jugular venous pressure (JVP), coarse crackles on chest auscultation, and additional heart sounds (e.g. pan-systolic murmur)
66
what is a myocardial infarction
detection of a rise and/or fall in cardiac biomarker values (troponin) with at least one value above the 99th percentile and at least one of the following:
symptoms of ischaemia
new or presumed new ECG changes
pathological Q waves on ECG
imaging evidence of loss of myocardium
identification of intracoronary thrombus on angiography
67
what are pathological Q waves on ECG
the Q wave reflects septal depolarisation. This is normally hidden behind the ventricular wall depolarisation. If the ventricular wall is dead a window is created which allows the septal depolarisation to show up on the ECH
68
what is the ischaemic cascade which occurs in MI
flow disruption - hypoperfusion - diastolic dysfunction with impaired relaxation of the ventricle - systolic dysfunction where areas of the ventricular wall stop moving - ECG changes - angina
69
what is a type 1 MI
spontaneous MI - atherosclerosis and thrombus formation causing partial or total occlusion of the artery
70
what is a type 2 MI
myocardial infarction secondary to ischaemia
patients with stable coronary artery disease +/- previous coronary intervention are unwell and put additional stress on their heart
if there is sufficient imbalance between blood supply and demand the myocardium will become ischaemic without a plaque rupture event
71
what is a type 3 MI
post mortem diagnosis of MI
72
what is a type 4a MI
PCI related - caused by angioplasty procedure blocking a side branch or damaging the main coronary artery causing ischaemia
73
what is a type 4b MI
stent thrombosis = if patients stop anti-platelets early post angioplasty or continue to smoke stents can occlude
74
what is a type 5 MI
bypass - related to CABG operation
75
what leads are affected in anterior STEMI
V1-4
76
what leads are affected in posterior STEMI
dominant R wave in V1-3 with ST depression in V1-3 (mirror image of anterior MI)
77
what is prinzmetal angina
it is a clinical condition characterised by chest pain at rest with transient ECG changes in the ST segment and prompt response to nitrates, which occurs due to coronary artery spasm
78
what causes printzmetal angina
diffuse or segmental spasm in the coronary arteries causing a decrease in blood supply to the myocardium generating sx such as chest pain
79
what can cause coronary artery spasm in printzmetal angina
cold weather
exercise
substances that promote vasoconstriction such as alpha agonists
recreational drug use especially when used in combination with cigarettes
80
what is acute heart failure
rapid onset/worsening of heart failure symptoms: life threatening
81
what is the pathophysiology of acute heart failure
acute failure to pump blood around the body causing:
1. Congestion in the pulmonary or systemic circulation. Pulmonary oedema develops when the left ventricle cant empty properly
2. hypoperfusion of vital organs
82
what percentage of patients show
1. congestion
2. hypoperfusion
3. both
in acute heart failure
50% will show signs of congestion without hypoperfusion
45% of patients will show signs of congestion with hypoperfusion
5% of patients will show no signs of congestion
83
what are causes of new onset acute heart failure
Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
Acute valve dysfunction
Arrhythmias
84
what are causes of acute decompensation of chronic heart failure
infection
acute myocardial dysfunction
uncontrolled hypertension
arrhythmias
worsening chronic valve disease
non adherence to medications
change in drug regime - withdrawal/reduction in medication, initiation/increase of rate control medications, other medications such as steroids/NSAIDS
85
what are typical symptoms of acute heart failure
Dyspnoea
Reduced exercise tolerance (classify using the New York Heart Association classification)3
Ankle swelling (clarify how high and whether this is progressing)
Fatigue
Pink frothy sputum
Orthopnoea (ask about the number of pillows used)
Paroxysmal nocturnal dyspnoea
86
what are signs of pulmonary or systemic congestion
Fine basal crackles (bilateral)
Peripheral oedema (bilateral)
Dull percussion at the lung bases
Raised jugular venous pressure (JVP)
Hepatomegaly
Gallop rhythm (S3 or S4 heart sounds)
Murmur
87
what are signs of hypoperfusion
Hypoxia
Tachypnoea and accessory muscle use
Tachycardia
Cyanosis
Cold, pale, and sweaty peripheries
Oliguria
Confusion/agitation
Syncope/pre-syncope
Narrow pulse pressure
88
what are differential diagnosis for acute heart failure
asthma
COPD
pneumonia
pulmonary oedema due to acute heart failure
MI
89
what investigations should be done in suspected acute heart failure
SpO2 (often under90)
HR, RR
BP
EGC
B type natriuretic peptide (BNP)
ABG
Baseline bloods
TSH
D Dimer
CXR
Echo
lung uss
90
what should be assessed on transthoracic echo in suspected AHF
Biventricular systolic and diastolic function for ventricular dilation, reduced ejection fraction, ventricular hypertrophy and poor contractility
Valve disease
Ventricular wall rupture
Pericardial effusion
Intracardiac shunts: the presence of a dilated inferior vena cava with reduced respiratory variation is indicative of high venous pressure
91
what are the chest x ray findings in acute heart failure
ABCDE
Alveolar oedema
kerley B lines
Cardiomegaly
Dilated upper lobe vessels
Effusions
92
what conditions should you look out for that may have precipitated acute heart failure
CHAMP
acute Coronary syndrome
Hypertensive crisis
Arrhythmias
Mechanical problems
Pulmonary embolism
93
what is the medical management of acute heart failure
Oxygen - between 94-98 15l/M with non rebreath
loop diuretics - 40mg furosemide IV
nitrates
Non invasive ventilation
Cardiogenic shock - dobutamine and adrenaline
94
who should you not use nitrates in during treatment of acute heart failure
those with a systolic pressure of under 90mmhg
those with aortic stenosis as they rely on sufficient preload to overcome their pressure gradient
95
what is the long term management of acute heart failure
diuretics - loop to increase sodium excretion
ACE i/ARB
beta blockers
aldosterone agonists
96
what are the use of ACEi/ARBs contraindicated in
Contraindications include a history of angioedema, bilateral renal artery stenosis, hyperkalaemia (>5 mmol/L), severe renal impairment (serum creatinine >220 μmol/L) and severe aortic stenosis.
97
what are the use of beta blockers contraindicated in
Contraindications include asthma, 2nd or 3rd-degree atrioventricular block, sick sinus syndrome and sinus bradycardia
98
what other specialist drugs can be used in acute heart failure long term
Ivabradine: if they cant have BB/on max dose
Sacubitril valsartan: patients who decompensate on ACEi/ARB
hydralazine and nitrate: if they cant tolerate ARB/ACEi or on max dose
Digoxin: in AF and uncontrolled tachycardia despite BB
99
what are complications of acute heart failure
40% of people admitted to hospital die or are readmitted within 1 yr
AHF may cause arrhythmias, AF
increased risk of stroke and other thromboembolic diseases
100
what is chronic heart failure
it is a clinical syndrome involving reduced cardiac output because of impaired cardiac contraction
101
what does stroke volume require to be normal
adequate pre load
optimal myocardial contractility
decreased afterload
102
what factors can reduce cardiac output which can potentially cause chronic heart failure
decreased heart rate
decreased preload
decreased contractility
increased afterload
103
what is the equation for working out cardiac output
cardiac output is equal to stroke volume times heart rate
104
what are causes of heart failure
coronary heart disease (MI)
atrial fibrillation
valvular heart disease
hypertension
endocrine diseases
medications
infection
genetic conditions
ischaemic heart disease
infiltration: sarcoidosis, amyloidosis
septal defects
105
what infectious/immune conditions can cause chronic heart failure
viral - HIV
bacterial - sepsis
autoimmune - lupus, RA
106
what genetic conditions can cause chronic heart failure
hypertrophic obstructive cardiomyopathy
dilated cardiomyopathy
107
what endocrine diseases can cause chronic heart failure
hypothyroidism
hyperthyroidism
diabetes
adrenal insufficiency
cushings
108
what medications can cause chronic heart failure
calcium antagonists
anti-arrhythmias
cytotoxic medications
beta blockers
109
what is the clinical history of someone with chronic heart failure
breathlessness - on exertion, rest, lying flat
nocturnal cough
fluid retention - swelling and oedema
fatigue, decreased exercise tolerance
lightheadedness
syncope
paroxysmal nocturnal dyspnoea
110
what clinical findings might be seen in someone with chronic heart failure
tachycardia
arrhythmia
third and fourth heart sounds
narrow pulse pressure
displaced apex beat
right ventricular heave
hypertension
raised JVP
enlarged liver
tachypnoea, basal crepitations, pleural effusions
oedema
obesity
111
what investigations should be done for someone with suspected chronic heart failure
ECH
urinalysis
lab investigations - bloods + N-terminal pro B type natriuretic peptide
cardiomyopathy screen
echocardiogram
chest X ray
cardiac MRI
112
what is involved in a cardiomyopathy screen
serum iron and copper studies
rheumatoid factor, ANCA/ANA, ENA, dsDNA
serum ACE- sarcoidosis
Serum free light chains
113
what levels of NT-proBNP indicate heart failure
under 400 - HF unlikely
400-2000 - refer routinely for assessment and transthoracic echo in 6 weeks
over 2000 - urgent referral and echo within 2 weeks
114
what other conditions, other than heart failure, can cause an increase in NT-proBNP
left ventricular hypertrophy
tachycardia
liver cirrhosis
diabetes
acute or chronic renal disease
115
what chest X ray findings will be seen in someone with chronic heart failure
Alveolar oedema (perihilar/bat-wing opacification)
Kerley B lines (interstitial oedema)
Cardiomegaly (cardiothoracic ratio >50%)
Dilated upper lobe vessels
Effusions (e.g. pleural effusions – blunted costophrenic angles)
116
what is the structural classification of chronic heart failure
based on left ventricular ejection fraction
- look at whether it is reduced or not
117
what is the symptomatic/functional classification of chronic heart failure
Class I: no symptoms during ordinary physical activity
Class II: slight limitation of physical activity by symptoms
Class III: less than ordinary activity leads to symptoms
Class IV: inability to carry out any activity without symptoms
118
what is the general management for someone with chronic heart failure
lifestyle management
vaccinations (influenza and pneumococcal)
medication review
monitoring
119
what medications can be harmful in the context of heart failure
Calcium channel blockers (e.g. verapamil, diltiazem)
Tricyclic antidepressants
Lithium
NSAIDs and COX-2 inhibitors
Corticosteroids
QT-prolonging medications
120
what monitoring needs to happen in patients with chronic heart failure
Functional capacity, fluid status, cardiac rhythm, cognitive status and nutritional status
Renal function
121
what can be prescribed if the heart failure is caused by coronary artery disease
statins
aspirin
122
what should be prescribed if the heart failure is caused by a.fib
oral anticoagulation
123
what pharmacological management can be offered to patients with chronic heart failure
diuretics - relieve fluid overload
ACE inhibitors - with a reduced EF: proven to improve ventricular function and reduce mortality
beta blockers - with reduced EF: decrease HR, o2 demand and RAAS activation
ARBs - cant tolerate ACEi
mineralocorticoid - spironolactone: if continued sx
SGLT2 inhibitors - reduced EF: shown to reduce cardiovascular events and hospital admission
124
what are the contraindications to ACE inhibitors
history of angioedema, bilateral renal artery stenosis, hyperkalaemia (>5 mmol/L), severe renal impairment (serum creatinine >220 μmol/L) and severe aortic stenosis.
125
what needs to be checked before starting ACE inhibitors
U&Es should be checked prior to starting treatment and then after 1-2 weeks of treatment.
126
what are the contraindications to beta blockers
asthma, 2nd or 3rd degree AV block, sick sinus syndrome and sinus bradycardia.
127
what must patients have in order to be started on an ARB
normal serum potassium and adequate renal function to commence an ARB.
128
what specialist pharmacological treatments are there for heart failure
Ivabradine - inhibits SAN
ARNI - increases BNP levels by inhibiting the enzyme that breaks it down. Higher BNP causes natriuresis/diuresis decreasing afterload
129
what are surgical management options for heart failure
revascularization
valve surgery
implantable cardiac defib.
cardiac resynchronization therapy and defibrillator
cardiac transplantation
130
what are complications of chronic heart failure
Arrhythmias: atrial fibrillation and ventricular arrhythmias
Depression and impaired quality of life
Loss of muscle mass
Sudden cardiac death
131
what is the most common cause of right sided heart failure
left ventricular failure leading to increased pressure in pulmonary vessels and volume overload
132
what are symptoms of right sided heart failure
chest discomfort
breathlessness
palpitations
raised JVP
enlarged liver
133
what conditions can cause right sided heart failure
pneumonia
acute pulmonary embolism
mechanical ventilation
acute respiratory distress syndrome
primary pulmonary arterial hypertension
secondary pulmonary hypertension
congenital heart disease
right tricuspid valve insufficiency
shunts - ASD
right ventricular ischaemia
amyloidosis/sarcoidosis
genetics
pericarditis
tricuspid stenosis
cardiac tamponade
hypovolaemia
134
what is atherosclerosis
chronic inflammation and activation of immune cells in medium to large artery walls leading to deposition of lipids in the wall, followed by the development of fibrous atheromatous plaques
135
what do atheromatous plaques lead to the walls of arteries becoming
stiff
stenosed
and can cause plaque rupture
136
what does stiffening of the artery walls lead to
hypertension and strain on the heart as it tries to pump the blood against the extra resistance
137
what does stenosis of blood vessels lead to
reduced blood flow = angina
138
what does plaque rupture lead to
creation of a thrombus that can block distal vessels and cause ischaemia
139
what are non modifiable risk factors for cardiovascular disease
older age
family history
male
140
what are modifiable risk factors for cardiovascular disease
Raised cholesterol
Smoking
Alcohol consumption
Poor diet
Lack of exercise
Obesity
Poor sleep
Stress
141
what are co-morbidities that can increase the risk of atherosclerosis
Diabetes
Hypertension
Chronic kidney disease (CKD)
Inflammatory conditions, such as rheumatoid arthritis
Atypical antipsychotic medications
142
what are the end results of atheroma formation
Angina
Myocardial infarction
Transient ischaemic attacks
Strokes
Peripheral arterial disease
Chronic mesenteric ischaemia
143
how can we optomise the modifiable risk factors in cardiovascular disease
Address diet, exercise and obesity
Stop smoking
Reducing alcohol consumption
Optimise treatment of co-morbidities (such as diabetes)
144
what are the NICE guidelines recommendations for dietary changes in cardiovascular disease
Total fat is less than 30% of total calories (primarily monounsaturated and polyunsaturated fats)
Saturated fat is less than 7% of total calories
Reduced sugar intake
Wholegrain options
At least 5 a day of fruit and vegetables
At least 2 a week of fish (one being oily)
At least 4 a week of legumes, seeds and nuts
145
what exercise is recommended by NICE for reduction in cardiovascular disease risk
Aerobic activity for a total of at least 150 minutes at moderate intensity or 75 minutes at vigorous intensity per week
Strength training activities at least 2 days a week
146
what risk score determines medications prescribed for the primary prevention of cardiovascular disease
the QRISK3 score
147
what is the QRISK3 score
it is a score which estimates the percentage risk that a patient will have a stroke or MI in the next 10 years
148
when should you offer someone medication based on their QRISK3 score
The NICE guidelines (updated February 2023) recommend when the result is above 10%, they should be offered a statin, initially atorvastatin 20mg at night.
149
what diseases is atorvastatin offered to as primary prevention for all patients with the condition
chronic kidney disease (eGFR less than 60ml/min/1.73m2)
type 1 diabetes (for more than 10 years or who are over 40)
150
how do statins help reduce cholesterol
inhibits HMG CoA reductase in the liver
151
how often should lipids be checked after starting a statin
NICE recommend checking lipids 3 months after starting statins and increasing the dose to aim for a greater than 40% reduction in non-HDL cholesterol
NICE also recommend checking LFTs within 3 months of starting a statin and again at 12 months.
152
what are rare and significant side effects of statins
Myopathy (causing muscle weakness and pain)
Rhabdomyolysis (muscle damage – check the creatine kinase in patients with muscle pain)
Type 2 diabetes
Haemorrhagic strokes (very rarely)
153
what is a key medication that interacts with statins
macrolide antibiotics - clarithromycin/erythromycin
154
what other cholesterol lowering drugs are there
Ezetimibe - inhibits absorption of cholesterol in the intestine
PCSK9 inhibitors - monoclonal antibodies that lower cholesterol
155
what medications are given for secondary prevention of cardiovascular disease
A – Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
A – Atorvastatin 80mg
A – Atenolol (or an alternative beta blocker – commonly bisoprolol) titrated to the maximum tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to the maximum tolerated dose
156
after a MI what medications are offered to patients initially
dual antiplatelet treatment initially, with:
Aspirin 75mg daily (continued indefinitely)
Clopidogrel or ticagrelor (generally for 12 months before stopping)
157
what is familial hypercholesterolaemia
an autosomal dominant genetic condition causing very high cholesterol levels. Several genes have the potential to cause the disorder.
158
what is the criteria used to make a clinical diagnosis of familial hypercholesterolaemia
The Simon Broome criteria or the Dutch Lipid Clinic Network Criteria
159
what are the important features used to make a clinical diagnosis of familial hypercholesterolaemia
Family history of premature cardiovascular disease (e.g., myocardial infarction under 60 in a first-degree relative)
Very high cholesterol (e.g., above 7.5 mmol/L in an adult)
Tendon xanthomata (hard nodules in the tendons containing cholesterol, often on the back of the hand and Achilles)
160
how do you manage familial hypercholesterolaemia
Specialist referral for genetic testing and testing of family members
Statins
161
what is coronary heart disease/ischaemic heart disease
a type of heart disease involving the reduction of blood flow to the cardiac muscle due to build up of atheromatous plaque in the arteries of the heart
162
what is a common symptom of coronary heart disease
angina
shortness of breath
163
what are risk factors for coronary heart disease
Risk factors include high blood pressure, smoking, diabetes mellitus, lack of exercise, obesity, high blood cholesterol, poor diet, depression, and excessive alcohol consumption
164
what is hypertrophic cardiomyopathy
it is the presence of an asymmetrical increase in the left ventricular wall thickness, not solely explained by abnormal loading conditions
165
what is the inheritance pattern of hypertrophic cardiomyopathy
autosomal dominant with mutations in cardiac sarcomere protein genes
166
what is the role of sarcomere proteins in the heart
These proteins, namely beta-myosin heavy chain, myosin-binding protein C and cardiac troponin C, are structurally important in cardiac muscle
167
what are the characteristics of hypertrophic cardiomyopathy
the primary feature is asymmetrical left ventricular wall thickening (typically the septum, but can be seen in any part of the ventricle)
myocardial fobrosis/disarray
systolic anterior motion of the mitral valve
abnormal microcirculatory function
168
what are risk factors for hypertrophic cardiomyopathy
The only risk factor for hypertrophic cardiomyopathy (given it is a mostly inherited condition) is family history.
169
what are typical symptoms of hypertrophic cardiomyopathy
dyspnoea (90%)
syncope and presyncope - patients with this are at high risk of sudden cardiac death
chest pain
palpitations
170
what clinical findings are seen in hypertrophic cardiomyopathy
Systolic ejection murmur loudest between the apex and left sternal border: indicative of left ventricular outflow tract obstruction (accentuated with Valsalva manoeuvre).
Fourth heart sound (S4) of atrial systole against a non-compliant ventricle.
Holosystolic murmur loudest at the apex or axilla: indicative of mitral regurgitation.
Double apical beat of ventricular contraction and left atrial contraction against hypertrophic ventricle.
Lateral displacement of the apical pulse.
Splitting of the second heart sound.
Prominent a wave: indicative of reduced right ventricular compliance with massive left ventricular hypertrophy.
171
what are differential diagnosis foe hypertrophic cardiomyopathy
need to distinguish it from hypertension, aortic stenosis, athletic heart, cardiac amyloidosis
metabolic disorders (e.g. Anderson-Fabry disease, Pompe disease)
Primary mitochondrial disease
Neuromuscular disease (e.g. Friedreich’s ataxia)
Malformation syndromes (e.g. Noonan syndrome, LEOPARD syndrome)
172
what investigations are done for hypertrophic cardiomyopathy
blood pressure
ECG
ambulatory ECG
Lab investigations - bloods
echo - transthoracic, exercise stress, and transoesophageal
cMRI
cCT
cardiopulmonary exercise testing
electrophysiological testing
173
what would be seen on ECG in hypertrophic cardiomyopathy
left ventricular hypertrophy manifests as increased voltages in precordial leads and non-specific ST-segment and T-wave abnormalities. Deep, narrow Q-waves are common. P-mitrale reflects left atrial dilatation.
174
what would be seen on ambulatory ECG in hypertrophic cardiomyopathy
Primary findings of interest include asymptomatic non-sustained ventricular tachycardia (NSVT) and paroxysmal supraventricular arrhythmias (SVT).
175
what is cardiopulmonary exercise testing
provides functional information about the patient’s cardiac function. Useful in differentiation between athletic hypertrophy and hypertrophic cardiomyopathy.
176
what general lifestyle advice can be given to someone with hypertrophic cardiomyopathy
avoid dehydration and alcohol
encourage weight loss
safety net for symptoms of deterioration
177
what can be given to patients with hypertrophic cardiomyopathy for angina
beta blockers
calcium channel blockers
oral nitrites if below is excluded - use with caution
- in the absence of significant left ventricular outflow obstruction and coronary artery disease
178
how many patients with hypertrophic cardiomyopathy will have Afib
22.5%
179
how often should patients with hypertrophic cardiomyopathy be monitored for Afib
If left atrial diameter is ≥45mm, the patient should undergo 6 to 12 monthly, 48-hour ambulatory electrocardiogram monitoring to exclude atrial fibrillation
180
what is the management of Afib in someone with hypertrophic cardiomyopathy
Haemodynamically unstable: emergency direct current cardioversion
Haemodynamically stable: beta-blockers or verapamil/diltiazem
181
what is the anticoagulant of choice given to people with hypertrophic cardiomyopathy if they suffer from Afib
warfarin
182
how do you manage a patient with hypertrophic cardiomyopathy who has heart failure with preserved ejection fraction
beta blockers or
verapamil/diltiazem
if indicated loop diuretics
183
how do you manage a patient with hypertrophic cardiomyopathy who has heart failure with reduced ejection fraction
diuretics, beta blockers, ACEi/ARBs and MRAs recommended in keeping with heart failure guidelines
cardiac transplantation can be considered in patients with functional class three or four symptoms, not responding to medical management and without left ventricular outflow tract obstruction
184
when is an implantable cardioverter-defibrillator indicated in someone with hypertrophic cardiomyopathy
secondary prevention after a cardiac arrest due to ventricular tachycardia/ventricular fibrillation, and in patients with sustained ventricular tachycardia causing syncope/haemodynamic instability
185
what is left ventricular outflow tract obstruction
Left ventricular outflow tract obstruction (LVOTO) is a blockage restricting blood flow from the heart's main pumping chamber (left ventricle) into the aorta, often due to thickened heart muscle (hypertrophy), narrowed valves, or other structural issues.
It is defined by tract pressure gradients ≥30mmHg.
186
what investigations are done for LVOTO
2D and doppler echocardiogram at rest, valsalva and on standing
stress test echocardiography
187
what treatments are recommended based on the exercise stress echocardiography om LVOTO
f on exercise stress echocardiography the outflow tract gradient is >50mmHg then septal reduction therapy is indicated. If <50mmHg, medical therapy is the mainstay of treatment.
188
what medications are used for LVOTO
vasodilating beta blockers
disopyramide if QTc normal or verapamil if BB are ineffective or contraindicated
189
what surgical management is offered for LVOTO
If symptoms of left ventricular outflow tract obstruction remain despite best medical therapy, septal reduction therapy can be considered. The two main procedures are ventricular septal myomectomy or septal alcohol ablation.
190
what are the indicators for septal reduction therapy in LVOTO
Left ventricular outflow tract gradient ≥50mmHg
New York Heart Association (NYHA) grade III or IV
Recurrent exertional syncope despite medical treatment
191
what are complications of hypertrophic cardiomyopathy
Sudden cardiac death
Arrhythmias: supraventricular (especially atrial fibrillation) and ventricular in origin
Heart failure
Infective endocarditis
192
what increases the risk of sudden death in someone with hypertrophic cardiomyopathy
Maximal left ventricular wall thickness
Left atrial diameter
Maximal left ventricular outflow tract gradient
Family history of sudden cardiac death
Non-sustained ventricular tachycardia
Unexplained syncope
Age
193
what is dilated cardiomyopathy
disease of the myocardium in which the muscle wall stretched and dilates, making it harder for the heart to pump blood around the body
194
what can cause dilated cardiomyopathy
genetics
heart valve issue
viral infection causing inflammation
MI
congenital heart disease
high alcohol intake
recreational drug use
cancer treatment
pregnancy if it causes peripartum cardiomyopathy
195
what are symptoms of dilated cardiomyopathy
tiredness
chest pain
shortness of breath
swelling of feet, ankles, stomach and lower back
palpitations
new murmur
196
what investigations are done for dilated cardiomyopathy
ECG
exercise ECG
Echo
angio
MRI
Bloods
genetic testing
197
how is dilated cardiomyopathy treated
advise patient to stop drinking
ACEi and beta blockers
diuretics for sx of congestion
may need antiarrhythmic drugs = amiodarone
anticoagulation - mandatory if they have aFIB
cardiac transplantation and cardiomyoplasty
198
what is cor pulmonale
it is right sided heart failure caused by respiratory disease
199
what is the pathophysiology of cor pulmonale
the increased pressure and resistance in the pulmonary arteries limits the right ventricle pumping blood into the pulmonary arteries. This causes back pressure into the right atrium, vena cava and systemic venous system
200
what are causes of cor pulmonale
COPD - most common
pulmonary embolism
interstitial lung disease
cystic fibrosis
primary pulmonary hypertension
201
what are symptoms of cor pulmonale
Often patients with early cor pulmonale are asymptomatic. Symptoms of cor pulmonale include:
Shortness of breath
Peripheral oedema
Breathlessness of exertion
Syncope (dizziness and fainting)
Chest pain
202
what are signs of cor pulmonale
Hypoxia
Cyanosis
Raised JVP (due to a back-log of blood in the jugular veins)
Peripheral oedema
Parasternal heave
Loud second heart sound
Murmurs (e.g., pan-systolic in tricuspid regurgitation)
Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
203
what is the management of cor pulmonale
involves treating the symptoms - i.e diuretics for oedema and treating the underlying cause
long term oxygen therapy
prognosis is poor unless there is a reversible underlying cause
204
what is an abdominal aortic aneurysm
condition where an area of the abdominal aorta bulges out
205
what is thought to be the cause of AAA
largely believed to be due to atherosclerosis which compresses the aortic media, leading to ischaemia and weakening
206
what is the abdominal aorta a continuation of and what does it supply
it is a continuation of the descending aortic tracts
it supplies all abdominal organs and its terminal branches supply the pelvis and legs. It also supplies the undersurface of the diaphragm and parts of the abdominal wall
207
which spinal levels does the abdominal aorta begin and end at
begins at T12
ends at L4
208
what does the abdominal aorta divide into
the left and right common iliac arteries
209
what is the normal diameter of the abdominal aorta
less than 2cm
210
how does atherosclerosis cause dilation of the aortic wall
Atherosclerosis causes inflammation, which leads to infiltration by macrophages and deposition of immune complexes in the aortic wall.1 There is then elastin depletion, collagen degradation and smooth muscle loss.2 This results in dilatation in all layers of the aortic wall.
211
where can AAAs be located
Juxta-renal - located within 1cm of renal arteries
infra-renal - below the renal arteries
supra-renal - starting above the renal arteries
212
what are the types of AAAs
saccular (a spherical outpouching) or, more commonly, fusiform (diffuse and circumferential dilation).
213
what are risk factors for AAA
smoking
family history
increased age
hyperlipidaemia
hx of atherosclerosis
hx of other aneurysms
hypertension
CODP - elastin degradation due to smoking
Hx of connective tissue disorders i.e marfans
european ancestry
males - 4-6X higher prevalence
214
what appears to be a protective factor against AAA
diabetes
215
how does someone present with a ruptured AAA
rapid onset abdominal, flank or back pain
shock
rapid loss of consciousness usually with cardiac arrest
216
what is the typical history of someone with AAA
usually asymptomatic and clinically well. most patients are diagnosed via screening programs or when it ruptures
217
what are signs of an AAA
expansile pulsatile central abdominal mass superior to the umbilicus
signs of hyperlipidaemia
abdominal scars
features of marfans syndrome
renal bruits on auscultation
abdominal distension
grey turners sign - haemorrhage post rupture
signs of hypovolaemic shock
218
how is AAA usually diagnosed
screening ultrasound
219
what is the criteria for diagnosing an AAA
abdominal aortic dilation of >1.5 times the expected anterior-posterior diameter, this is usually >3cm.1
220
who is invited for AAA screening
all men over 65
221
when should someone be seen by a vascular specialist if they have an AAA
If the AAA is ≥5.5 cm, they should be seen by a vascular specialist within 2 weeks
If the AAA is <5.5cm, they should continue surveillance by the screening programme
222
what other investigations can be done for AAA
ultrasound for surveillance of asymptomatic AAA and following surgery
contrast enhanced CT angio (can confirm rupture)
pre-operative blood tests
pre-operative ECG
223
what is the conservative management for AAA
if the aneurysm is < 5.5cm, conservative management and surveillance is indicated:1
Lifestyle advice: including referral to stop smoking services
Antiplatelet therapy: aspirin 75mg OD
Statins
Appropriate anti-hypertensives if BP >140mmHg
224
when are people with AAA called in for surveillance
Annually for AAA 3.0-4.4cm.
Every 3 months for aneurysms 4.5-5.4cm.
225
when are AAAs surgically managed
if the aneurysm is over 5.5cm in diameter or over 4cm and rapidly growing (over 1cm per year) the patient will need an elective surgical repair
226
what are the general principals of the surgical management of AAA
Antibiotic prophylaxis
VTE prophylaxis: LMWH the evening following surgery.
Open aortic repair or endovascular aortic repair (EVAR).
Open repairs have an arterial line, central venous line, epidural, and urinary catheter, and most have an NG tube inserted in the anaesthetic room
patients require 2 units of RBC cross matched and cell salvage
227
what is EVAR
Endovascular Aneurysm Repair (EVAR) is a minimally invasive surgical procedure used to repair an abdominal aortic aneurysm (AAA). It involves inserting a graft into the aorta via small incisions in the groin, using X-ray guidance to position it correctly and exclude the aneurysm
228
when is EVAR considered for AAA repair
for patients with more co-morbidities, women, men over 70
229
is EVAR or open repair of AAA more prone to long term complications
EVAR
- 48% risk of graft related complications
230
after EVAR how often is the patient required to have imaging for AAA
one, six and twelve months to check the graft and any endoleaks (where blood flows outside the stend graft and around it in the aneurysm sac)
annual ultrasound is recommended after this
231
what are the different types of endoleak
1. blood flow into aneurysm sac due to incomplete seal. puts pressure and increases rupture risk
2. blood back bleeding into aneurysm sac from branched arteries (less dangerous)
3. blood flows into sac due to defects in graft material/seal between graft components. Dangerous
4. blood flows into sac via stent graft fabric pores
5. AAA expansion with no radiographic sign of leak
232
when is an open aortic repair done in AAA
if the patient is healthier or in men under 70
233
what is the management of a ruptured AAA
ABCDE
bedside USS
blood tests, cross match, coag. profile, FBC
CT angiography
IV access, analgesia, antibiotic prophylaxis, major haemorrhage protocol, blood transfusion in HB is under 100
urgent surgical repair
234
what can occur following an AAA rupture
abdominal compartment syndrome- This is where the intra-aortic pressure exceeds 20mmHg, leading to organ failure.22 This requires a laparostomy and delayed -
235
what are early postoperative complications of AAA
postoperative ileus
AKI
bowel ischaemia
spinal cord ischaemia
pseudoaneurysms
distal embolisation
retrograde ejaculations
risks of open surgery
236
what are late postoperative complications of AAA repair
aortic neck dilation
graft infection
graft occlusion
endoleak
incisional hernia
abdominal adhesions
237
what is aortic dissection
a tear in the intimal layer of the aortic wall allowing blood to flow between the intima and media, creating a false lumen
238
what is the anatomy of the aorta
the aortic wall consists of 3 layers: intima, media, adventitia
between the intima and media you have the internal elastic membrane
and between the media and externa you have the external elastic membrane
239
where is the most common place in the aorta for dissection to occur
ascending aorta
240
what is the pathophysiology of aortic dissection
the true lumen will often become smaller due to compression by blood flowing into the false lumen
the aortic dissection can propagate longitudinally along the aorta either anterograde or retrograde.
propagation can cause branch occlusion and ischemia of the affected artery territory
241
what can proximal aortic dissections cause
can progress to the aortic valve root and cause cardiac tamponade, acute aortic regurgitation and aortic rupture
242
what are risk factors of aortic dissection
male
age 50-70
hypertension
connective tissue disorders
abrupt, transient severe increase in BP
atherosclerotic disease
pre existing aortic aneurysm
bicuspid aortic valve
coarctation of the aorta
iatrogenic
cocaine
243
what is the typical presentation of aortic dissection
sudden severe onset chest pain or inter scapular back pain
described as a sharp ripping or tearing pain
pain often settles spontaneously giving the false impression nothing is wrong
around 10% present with no pain
abdominal or flank pain
cardiovascular collapse
244
what are atypical presentations of acute aortic dissection
neurological deficits: syncope, seizure, limb paraesthesia, paraplegia
limb pain and/or pallor
flank pain and/or reduced urine output
abdominal pain: mesenteric ischaemia
245
what are clinical findings in AAD
pulse deficit or asymmetrical blood pressure readings - difference of over 20mmhg
hypertension
hypotension
tachycardia
diastolic murmur
pulsus paradoxus
decreased breath sounds
246
what investigations are done for aortic dissection
ECG - myocardial ischaemia
bloods - FBC, U+E, LFT, coag screen
ABG
group and save
troponin
D-dimer
biomarkers
urgent CT angiogram - GS
247
what chest X ray findings will there be on aortic dissection
widened mediastinum
double or irregular aortic contour
inward displacement or atherosclerotic calcification
pleural effusion or haemothorax: indicative or dissection rupture
248
what imaging confirms the diagnosis of aortic dissection
CT angiogram of the whole aorta
249
what are the CT angiogram findings in aortic dissection
Double lumen (true and false lumens) thus confirming the diagnosis of AAD
The entry tear (where the dissection begins)
Any evidence of aortic dilatation (aneurysmal change)
Evidence of end-organ malperfusion (for example non-enhancing kidney)
Features of acute rupture (including extravasation of contrast or haemothorax)
250
what is the stanford classification of aortic dissection
Type A: dissection involves the ascending aorta with or without involvement of the arch and descending aorta. Accounts for 60-70% of cases.
Type B (TBAD): Involves only the descending aorta (distal to the left subclavian artery) and/or abdominal aorta. Accounts for 30-40% of cases
251
what is the DeBakey classification for aortic dissection
type 1: intimal tear originates in the ascending aorta and involved the ascending aorta, arch and descending
type 2: only ascending
type 3: intimal tear at the descending, distal to left subclavian
252
what are the further classifications of type 3 aortic dissections
Type IIIa (affected region is confined above the diaphragm) or Type IIIb (affected region extends below the level of the diaphragm)
253
what is the initial management for aortic dissection
ABCDE
- high flow oxygen
- IV access, continuous obs
- senior support
- on call vascular/cardiothoracic team
analgesia
254
why is BP control important in aortic dissection
they need rapid lowering of BP, pulse pressure and pulse rate to minimise stress of the dissection
- target HR is 60-80
- target BP is 100-120
IV beta blockers - 1st
IV calcium channel blockers - nicardipine
IV nitrate infusion or vasodilators
arterial line
255
what is the management of a type A aortic dissection
open surgery - to prevent aortic rupture
removal or ascending aorta and replacement with a synthetic graft. if the dissection has damaged the aortic valve this will also require replacement
256
what is the management for a type B aortic dissection
usually medically managed with endovascular intervention for complicated dissections
257
what is a complicated type B aortic dissection
presence of: aortic rupture, impending rupture or rapidly expanding aortic diameter, malperfusion due to branch vessel occlusion or aortic lumen compression, ongoing pain, and refractory hypertension
258
what is the management of complicated type B dissections
endovascular stent graft placement - thoracic endovascular aortic repair
- stent and occlude the proximal entry tear
- branch vessel occlusion can be managed by covering the proximal entry tear and restoring the true lumen flow
259
what are the different classifications of a type B aortic dissection
hyperacute (<24 hours), acute (24 hours – 14 days), subacute (2 weeks to 3 months) and chronic (>3 months)
260
what is the management of an uncomplicated type B dissection
medical management - BP control and analgesia
long term management is debated: more evidence for endovascular intervention (done in the subacute phase)
if they arent suitable for intervention then follow up with CT surveillance
261
when should CT surveillance be done post aortic dissection
1. for TBAD medically managed: CT at 2-3d/1w/1m (/6m/12m)
2. TBAD surgically managed: CT at 4w followed by annual scans
262
what are complications of aortic dissection
aortic rupture
site and propagation of dissection
Acute aortic regurgitation
Myocardial ischaemia
Cardiac tamponade
Aneurysmal dilatation
Ischaemic stroke or paraplegia
Acute limb ischaemia
Renal failure
Bowel ischaemia
263
what are symptoms of aortic rupture
hypotension, syncope, haemothorax, cardiac tamponade, mediastinal haematoma, or retroperitoneal haemorrhage
264
what is the prognosis for aortic dissection
10-35%
265
what is a supraventricular tachycardia
not a diagnosis: a rapid heart rate that originates from above or within the atrioventricular (AV) node
266
what is a focal tachycardia
he tachycardia originates from a single point (or points) in the atrium or AV node. Also knows as ‘enhanced automaticity’ – the sinus node is meant to be the most autonomic part of the heart and as such takes charge. If another part of the heart becomes MORE autonomic (or the sinus node becomes LESS autonomic), it takes over and a focal tachycardia results.
267
what arrhythmias are focal tachycardias
sinus tachycardia
atrial tachycardia
multifocal atrial tachycardia
junctional rhythms
268
what arrhythmias are re-entry tachycardias
atrial flutter
atrial fibrillation
AVNRT
AVRT
269
what is atrial tachycardia
a different focus in the atrium takes over from the SAN resulting in abnormal P waved preceding the QRS complex
270
what is multifocal atrial tachycardia
there are multiple foci meaning that P waves will have different morphologies as the atrial foci changes from beat to beat
271
what are junctional rhythms
this is where the AV node takes over from the SAN if its non functional
the impulse originates from the AVN and propagates to the atrium and ventricles simultaneously
P waves are often hidden on the QRS complex
272
what is the management of inappropriate sinus tachycardias
can be slowed using beta blockers or ivabradine (selective sinus node blocker) however can be left
atrial tachycardias can usually be rate controlled with beta blockers or calcium channel blockers
273
what is atrial flutter
it is a macro-re-entrant tachycardia meaning that there is a single large re-entry circuit around the atrium which stimulates the AVN every time it passes
- typical runs anticlockwise around tight atrium and across the cavotricuspid valve isthmus
- atypical can be clockwise in the right atrium, the left atrium or around sites of previous surgeries
274
which leads on an ECG can atrial flutter be best seen in
inferior leads and is caused by the circuit alternately heading towards the inferior leads and away as it speeds round the atrium
275
what is the normal rate in atrial flutter
The ventricular rate then depends on the degree of AV block:
2:1 = 150bpm
3: 1 = 100bpm
276
what causes atrial fibrillation
not entirely clear: Micro-re-entrant tachycardia with multiple circuits contributing to the chaotic and random fibrillation of the atrium
277
what is atrio-ventricular node re-entrant tachycardia
often labelled as SVT
issue within the node resulting in a circuit that activates both the ventricles and atria almost simultaneously. The two anatomical pathways next to the AVN form a circuit with very rapid conduction that produces a rapid regular tachycardia
278
how does a AVNRT look like on an ECG
seen as a pseudo R wave which is actually the retrograde P wave superimposed on the QRS complex
279
what is atrio-ventricular re-entrant tachycardia
two pathways - the normal AV conduction and an accessory pathway.
accessory pathways can conduct antegrade (atria to ventricles) or retrograde (ventricle to atria)
280
what are the different types of AVRTs
orthodromic
antidromic
281
what is an orthodromic AVRT
conduction goes down the AV node and up the accessory pathway
- as the impulse goes down QRS is narrow
- the movement up the accessory pathway results in a long PR interval
282
what is an antidromic AVRT
conduction goes down the accessory pathway and up the normal AV conduction
- as the impulse goes down the AP the ECG will have a broad QRS complex with delta waves
283
what should you not use in antidromic AVRT arrhythmias
AV nodal blocking agents - promotes transmission down the accessory pathway and if there is AF, the fibrillation waves can be transmitted to the ventricles……….causing VF
284
if someone has a re-entrant SVT and is haemodynamically unstable what is the treatment
CARDIOVERSION
285
what are the treatment strategies for atrial fibrillation and atrial flutter
Rate control: B-blockers, CCBs, Digoxin
Rhythm control: chemical cardioversion (amiodarone flecainide), electrical cardioversion
Ablation
anticoagulation
286
which patients in AF should be considered for cardioversion
New-onset AF
Symptomatic AF
LV dysfunction secondary to AF
Patients with a reversible cause of AF (e.g. post-surgical, post-infection)
Patients who have a reasonable chance of maintaining sinus rhythm
Previous successful cardioversion
Minimal dilatation of the left atrium
No significant mitral valve disease
287
how do you treat AVNRT
induce AV node blockade and the tachycardia is terminated
- mechanical: vasovagal maneuvers, carotid sinus massage
- chemical: adenosine, beta blockers, verapamil
288
how do you treat AVRT
AVOID AV node block
electrical cardioversion
flecainide can be used to chemically cardiovert
ablation of the pathway is a curative option
289
what does adenosine do to the heart
when it is administered IV it causes transient complete AV node blockade
- safe in pregnancy
- safe in asthma unless they have brittle severe asthma
290
how do you administer adenosine
large cannula in antecubital fossa
ensure patient has ECG attached
draw up adenosine in smallest syringe possible
draw up 20ml normal saline flush
connect adenosine syringe to the top port of the cannula and flush into the backport
warn patient about sense of impending doom
give adrenaline as fast as possible, then immediately by the flush as fast as possible
291
what are the effects of adenosine
total AV block - complete pause in ventricular contraction
if you terminate the tachycardia the rhythm is an AVNRT or orthodromic AVNRT
if you pause the tachycardia but it returns you have demonstrated its a supraventricular tachycardia, where the re-entry circuit doesnt involve the AVN
292
if you dont see a AV block after delivering amiodarone what could have occurred
1. you havent delivered it correctly
2. the rhythm doesnt involve the AV node - a ventricular tachycardia
293
what is paroxysmal AF
episodes last over 30 seconds and terminate spontaneously or with intervention within 7 days of onset
294
what is persistent AF
episodes lasting longer than 7 days, including episodes terminated by cardioversion
295
what is permanent AF
AF that is accepted by the patient and clinician and no further attempts to restore or maintain sinus rhythm are planned
296
what is the pathophysiology of atrial fibrillation
- arrhythmia often from left atrial myocytes
- leads to micro re-entry circuits
- resulting activity is intermittently conduced through the AVN
- the ventricular rate is very variable and depends on the speed of AVN conduction
- leads to ineffective atrial contraction which can cause blood stasis and increase risk of thrombosis
297
what are cardiac causes of AF
Hypertension – most common risk factor
Ischaemic heart disease
Heart failure with reduced ejection fraction
Structural pathology (e.g. valve stenosis or valve regurgitation)
Congenital heart disease
Atrial or ventricular dilation/hypertrophy
Pre-excitation syndromes (e.g. Wolff-Parkinson-White syndrome)
Sick sinus syndrome
Inflammatory conditions (e.g. pericarditis or myocarditis)
Infiltrative conditions (e.g. amyloidosis)
298
what are non cardiac causes of AF
Acute infection
Electrolyte imbalances (e.g. hypokalaemia or hyponatraemia)
Pulmonary embolism
Thyrotoxicosis or hypothyroidism
Diabetes mellitus
299
what are risk factors for developing AF
Male sex
Caucasian ethnicity
Increasing age
Alcohol
Cigarette smoking
Obesity
Co-morbidities (e.g. chronic kidney disease and obstructive sleep apnoea)
300
what are typical symptoms of AF
Breathlessness
Chest discomfort
Palpitations
Light-headedness
Reduced exercise tolerance
Syncope: due to bradycardia, particularly in paroxysmal AF when sinus rhythm is restored as the SAN re-establishes normal conduction
301
what are clinical findings seen in AF
Irregularly irregular pulse
Radial-apical deficit: each ventricular contraction may not be sufficiently strong enough to transmit a pulse to the radial artery, and palpating only the radial artery can miss tachycardia
302
what is the criteria set out by the European Society of Cardiology for diagnosis of AF
1. A standard 12-lead ECG recording or a single-lead ECG recording of ≥30 seconds showing a heart rhythm of no discernible repeating P-waves AND
2. Irregular RR intervals
303
what is the immediate management for someone in AF
ABCDE - signs of haemodynamic instability
304
what is used for rhythm control in AF
electrical or chemical cardioversion
- for patients presenting with new onset AF lasting less than 48hrs
305
what are the two options for chemical cardioversion
flecainide - blocks sodium channels in the heart
Amiodarone - blocks potassium channels in the heart
306
what are side effects of amiodarone
ling fibrosis
liver failure
photosensitivity
hyper/hypothyroidism
neuropathy
visual defects
307
when is anticoagulation required for cardioversion
it is required for 4-6 weeks before and 4 weeks after electrical/chemical cardioversion unless the onset of AF is within 48 hours and is a single isolated episode
308
which groups is rate control and appropriate treatment strategy in AF
Patients presenting with AF onset <48 hours
Patients whose AF does not have a reversible cause
Patients who do not have heart failure thought to be caused primarily by AF
Patients for whom rhythm control would not be more suitable based on clinical judgment
309
what are pharmacological options for rate control in AF
beta blockers - bisoprolol
rate limiting calcium blockers - verapamil/diltiazem
digoxin
310
when is anticoagulation required in AF
considered life long for those opting for rate control
reviewed at the end of 4 week period after rhythm control
need to use the CHA2DS2VASc tool
311
what are the options for anticoagulation in AF
DOAC - apixaban, rivaroxaban
Warfarin - acts on CF 10, 9, 7, 2
312
what are invasive managements of AF
left atrial ablation
pace and ablate strategy - pacemaker insertion followed by ablation of the AVN
313
what are complications of AF
Thromboembolic events: TIA and ischaemic stroke/systemic embolism
Tachycardia-induced cardiomyopathy
Decompensation of pre-existing cardiac disease, i.e. heart failure, valvular disease
Cardiac ischaemia can be associated with poorly controlled AF with the high ventricular rate leading to angina and type 2 myocardial infarction
314
what is wolff-parkinson-white (WPW) syndrome
condition that predisposes to supraventricular tachycardia due to an accessory pathway in the heart
315
what is the aetiology of WPW
an accessory pathway leads to stimulation of the ventricles. This allows the electrical conduction to bypass the AVN and stimulate the proximal ventricles prematurely. this leads to double excitation of the ventricles
- can move anterograde or retrograde
316
what are risk factors for WPW syndrome
most common in males 30-40
most cases sporadic however a small percentage are due to mutation in the PRKAG2 gene
associated with congenital heart disease such as Ebsteins anomaly
317
what are clinical features of WPW
tachyarrhythmias
some asymptomatic
Palpitations
Feeling lightheaded
chest pain
SOB
Sweating
Presyncope
Syncope
Cardiac arrest
318
what are key characteristic features of WPW on an ECG
short PR intervals <120ms
delta wave: slurred upstroke of QRS
Widened QRS >11oms
incongruous st segment and t wave changes
prominent R waves in V1-3
319
what is a type A vs type B WPW syndrome
type A is left sided and type B is right sided
Type A: positive delta wave in V1-6
Type B: negative delta wave in V1-2
320
what is the management of WPW syndrome
vagal maneuvers 1st line
IV adenosine
cardioversion
catheter ablation long term
321
what are complications of WPW syndrome
periods of tachycardia: palpitations, dizziness, syncope, sudden cardiac death
322
are ventricular tachycardia and ventricular fibrillation shockable rhythms
Yes
323
what is a broad complex tachycardia
fast heart rate with a QRS complex duration of more than 0.12 seconds or 3 small squares on an ECG.
324
what are the different causes of broad complex tachycardia
Ventricular tachycardia or unclear cause
Polymorphic ventricular tachycardia, such as torsades de pointes
Atrial fibrillation with bundle branch block
Supraventricular tachycardia with bundle branch block
325
what medication can you use to treat ventricular tachycardia
IV amiodarone
326
what medication can you use to treat polymorphic ventricular tachycardia like torsades de pointes
IV magnesium
327
what causes torsades de pointes
when there are after depolarisations within a ventricle. Caused by prolonged QT. there is a prolonged repolarisation period. Waiting a long time can cause spontaneous depolarisation in some muscle cells, which can spread throughout the ventricles and cause contraction before proper repolarisation. This leads to recurrent contractions without repolarisation
328
what is the outcome of torsades de pointes
it will either terminate spontaneously and revert to sinus rhythm or it will progress to ventricular tachycardia which can lead to cardiac arrest
329
what are causes of prolonged QT
Long QT syndrome
Medications
Electrolyte imbalances
330
what medications can cause a prolonged QT
antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
331
what electrolyte imbalances can cause prolonged QT
hypokalaemia, hypomagnesaemia and hypocalcaemia
332
what is the acute management of torsades de pointes
correct underlying cause
magnesium infusion
defibrillation
333
what is the management of a prolonged QT
stopping and avoiding medications
correcting electrolyte imbalances
beta blockers
pacemakers or implantable cardioverter defibrillators
334
what are ventricular ectopics
premature ventricular beats caused by random electrical discharges outside the atria
335
how do ventricular ectopics appear on an ECG
isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG
336
what does the term Bigeminy refer to
when every other beat is a ventricular ectopic. The ECG shows a normal beat (with a P wave, QRS complex and T wave), followed immediately by an ectopic beat, then a normal beat, then an ectopic, and so on
337
what is the management of ventricular ectopics
Reassurance and no treatment in otherwise healthy people with infrequent ectopics
Seeking specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g., chest pain or syncope), or a family history of heart disease or sudden death
Beta blockers are sometimes used to manage symptoms
338
what is atrioventricular block
the partial or complete interruption of impulse transmission from the atria to the ventricles.
339
what is the most common cause of AV block
idiopathic fibrosis and sclerosis
340
what is first degree heart block
consistent prolongation of the PR interval (defined as >0.20 seconds) due to delayed conduction via the atrioventricular node
- every P wave is followed by a QRS
341
what are causes of first degree heart block
Enhanced vagal tone: often seen in athletes (non-pathological)
Post myocardial infarction
Lyme disease
Systemic lupus erythematosus
Congenital
Myocarditis
Electrolyte derangements
Drugs: particularly AV blocking drugs such as beta-blockers, rate-limiting calcium-channel blockers, digoxin and magnesium1
Thyroid dysfunction
342
what are the ECG findings seen in first degree heart block
Rhythm: regular
P wave: every P wave is present and followed by a QRS complex
PR interval: prolonged >0.2 seconds (5 small squares)
QRS complex: normal morphology and duration (<0.12 seconds)
343
what is the management of first degree heart block
any AV blocking drugs should be stopped
no intervention unless the patient is symptomatic (pacemaker may be needed )
344
what are complications of first degree heart block
may be at an increased risk of atrial fibrillation
345
what is Second-degree AV block (type 1)
where there is a progressive prolongation of the RR interval until eventually the atrial impulse is not conduced and the QRS is dropped
346
what are causes of Second-degree AV block (type 1)
increased vagal tone: in athletes
drugs: beta blockers, ccbs, digoxin, amiodarone
inferior myocardial infarction
myocarditis
cardiac surgery (mitral valve repair, tetralogy of fallot repair)
347
what is seen on ECG in Second-degree AV block (type 1)
Rhythm: irregular
P wave: every p wave is present
PR interval: progressively lengthens before a QRS is dropped
QRS: normal morphology and duration but occasionally dropped
348
what are clinical features of Second-degree AV block (type 1)
Patients normally asymptomatic but some can develop symptomatic bradycardia and present with symptoms such as pre-syncope and syncope
349
what will be seen on clinical examination in someone with Second-degree AV block (type 1)
irregular pulse
bradycardia
350
what is the management of Second-degree AV block (type 1)
AV blocking drugs stopped
usually no intervention required
if symptomatic pacemaker can be considered
351
what is Second-degree AV block (type 2)
It is when there is a consistent PR interval duration with intermittently dropped QRS complexes due to failure of conduction
- follows a repeated cycle of every 3rd or every 4th wave
352
what is the cause behind Second-degree AV block (type 2)
it is always pathological with the block either being in the bundle of his or the bundle branches:
MI
idiopathic fibrosis
cardiac surgery
inflammatory conditions
autoimmune (SLE)
infiltrative myocardial disease
hyperkalaemia
drugs
thyroid dysfunction
353
what inflammatory conditions can cause Second-degree AV block (type 2)
rheumatic fever
myocarditis
lyme disease
354
what infiltrative myocardial disease can cause Second-degree AV block (type 2)
amyloidosis
haemochromatosis
sarcoidosis
355
what drugs can cause Second-degree AV block (type 2)
beta blockers
calcium channel blockers
digoxin
amiodarone
356
what are the ECG findings in Second-degree AV block (type 2)
Rhythm: irregular (may be regularly irregular in 3:1 or 4:1 block)
P wave: present but there are more P waves than QRS complexes
PR interval: consistent normal PR interval duration with intermittently dropped QRS complexes
QRS complex: normal (<0.12 seconds) or broad (>0.12 seconds)
The QRS complex will be broad if the conduction failure is located distal to the bundle of His
357
what are the symptoms of Second-degree AV block (type 2)
palpitations
pre-syncope
syncope
358
what is the management of Second-degree AV block (type 2)
patients should be placed on a cardiac monitor
underlying block investigated
temporary pacing or isoprenaline may be required if they are haemodynamically compromised
permanent pacemaker
359
what are complications of Second-degree AV block (type 2)
may progress to symptomatic complete heart block
risk of developing asystole
360
what is third degree heart block
when there is no electrical communication between the atria and ventricles due to a complete failure of conduction.
361
what are causes of third degree heart block
structural heart defects
autoimmune
idiopathic fibrosis
ischaemic heart disease
non ischaemic heart disease (stenosis, cardiomyopathy)
iatrogenic: ablation therapy
drug induced
infections
thyroid
362
what are the ECG findings seen in third degree heart block
Rhythm: variable
P wave: present but not associated with QRS complexes
PR interval: absent (as there is atrioventricular dissociation)
QRS complex: narrow (<0.12 seconds) or broad (>0.12 seconds) depending on the site of the escape rhythm
363
why can you have either a narrow or broad escape rhythm in type 3 heart block
narrow complex: rhythms originate above the bifurcation of the bundle of his
Broad complex: rhythms originate below the bifurcation of the bundle of his. These rhythms produce slower, less reliable heart rates
364
what is the typical history of someone with type three heart block
Palpitations
Pre-syncope/syncope
Confusion
Shortness of breath (due to heart failure)
Chest pain
Sudden cardiac death
365
what are clinical findings of someone with type three heart block
Irregular pulse
Profound bradycardia
Haemodynamic compromise (e.g. prolonged capillary refill time and hypotension)
366
what is the management of someone with type three heart block
cardiac monitoring
Transcutaneous pacing/temporary pacing wire or isoprenaline infusion may be required. Some rhythms (particularly narrow-complex escape rhythms) may respond to atropine.
A permanent pacemaker is usually required.
367
what are complications of type three heart block
The main complication is sudden cardiac death due to ventricular arrhythmia
368
what is the diagnostic criteria for a right bundle branch block
Broad QRS complex: >120 ms (3 small squares)
RSR’ pattern in V1-V3: an initial small upward deflection (R wave), a larger downward deflection (S wave), then another large upward deflection (a second R wave, which is indicated as R’)
Wide, slurred S wave in lateral leads: I, aVL, V5-V6
369
what is the pathophysiology of a right bundle branch block
The sino-atrial node acts as the initial pacemaker
Depolarisation reaches the atrioventricular node
Depolarisation through the bundle of His occurs only via the left bundle branch. The left branch still depolarises the septum as normal.
The left ventricular wall depolarises as normal.
The right ventricular walls are eventually depolarised by the left bundle branch, this occurs by a slower, less efficient pathway.
370
what is the clinical relevance of a right bundle branch block
can either be physiological or the result of damage to the right bundle branch
damage can be caused by: COPD, pulmonary emboli, cor pumonale, primary heart muscle disease, congenital heart disease, ischaemic heart disease and primary degeneration of the right bundle
371
what is the diagnostic criteria for a left bundle branch block
Broad QRS complex: >120 ms (3 small squares)
Dominant S wave in V1
Broad, monophasic R wave in lateral leads: I, aVL, V5-V6
Absence of Q waves in lateral leads
Prolonged R wave >60ms in leads V5-V6
372
what is the WiLLiaM MaRRoW mnemonic used for in bundle branch block
it can be used to recognise left and right bundle branch block by looking at V1 and V6
373
What part of the WiLLiaM MaRRoW mnemonic can be used to identify a left bundle branch block
We use the name William
W: complexes in V1 resemble the letter W: deep downward deflection (dominant S wave), which may be notched
M: complexes in V6 resemble the letter M: broad, notched or ‘M’ shaped R wave in V6
374
what part of the WiLLiaM MaRRoW mnemonic can we use to recognise a right bundle branch block
use the name MaRRoW
M: complexes in V1 resemble the letter M: initial small upward deflection (r wave), a larger downward deflection (S wave), then another large upward deflection (second R wave)
W: complexes in V6 resemble a W: initial small downward deflection (Q wave), then a larger upward deflection (R wave), and then a wide downward deflection (S wave)
375
what is the pathophysiology of a left bundle branch block
The sino-atrial node acts as the initial pacemaker
Depolarisation reaches the atrioventricular node
Depolarisation down the bundle of His occurs only via the right bundle branch. The septum is abnormally depolarised from right to left.
The right ventricular wall is depolarised as normal.
The left ventricular walls are eventually depolarised by the right bundle branch, this occurs by a slower, less efficient pathway.
376
what is the clinical relevance of a left bundle branch block
it is always pathological
may be due to conduction system degeneration, ischaemic heart disease, cardiomyopathy, valvular disease
may occur after cardiac procedures
377
why can a left bundle branch block lead to axis deviation
Due to the relatively greater mass of the left ventricle, disruptions in the depolarisation of the left ventricular muscle can cause cardiac axis changes.
378
what does the left bundle branch split into
the anterior and posterior fascicles - a left bundle branch block is block of both of these
379
what deviation does damage to the
a. anterior fascicle block
b. posterior fascicle block
cause
a. left axis deviation - mc
b. right axis deviation
380
what are other types of heart block that can occur
Bifascicular block involves both right bundle branch block and the blockade of one of the fascicles of the left bundle branch.
Trifascicular block is present when a 3rd-degree heart block exists alongside bifascicular block.
381
what is sick sinus syndrome
sinus node dysfunction - occurs when SAN dysfunction causes bradyarrhythmias or tachyarrhythmias
382
what are the two types of cells found in the SAN
Pacemaker cells - initiate APs
Transitional cells - facilitate propagation of impulse across atria
383
what are intrinsic causes of sick sinus syndrome
idiopathic fibrosis - age related
ischaemic heart disease
myocarditis
pericarditis
rheumatic heart disease
infiltrative disease - sarcoidosis, amyloidosis, haemochromotosis
congenital abnormalities
iatrogenic - damage
384
what are extrinsic causes of sick sinus syndrome
drugs
hypos: hypothermia, hypothyroidism, hypoxia
Hypers: Hyperkalaemia, hyperthyroidism
autonomic dysfunction
385
what drugs can cause sick sinus syndrome
digoxin
beta blockers
calcium channel blockers
anti-arrhythmics
386
what is tachycardia-bradycardia syndrome (sick sinus syndrome)
it is identified by periods of bradycardia or sinus arrest interspersed with periods of tachycardia, most commonly AF
387
what causes tachy-brady syndrome
abnormal conduction within the atrial tissue
- most common manifestation of sick sinus syndrome
388
what are the features of sinus bradycardia/sinus arrest in relation to sick sinus syndrome
severe inappropriate sinus brady is often a feature
a pause of three seconds or more without any atrial activity is sinus arrest
389
how might the heart rescue a severe sinus bradycardia in sick sinus syndrome
utilising pacemaker tissue that is outside of the SAN to generate a new action potential and allow systole to occur. This is called an escape rhythm and it acts to preserve cardiac output.
Escape rhythms may arise from atrial tissue (atrial escape rhythm) the AVN (junctional escape rhythm) or the ventricular myocytes (ventricular escape rhythm) and give characteristic appearances on the ECG
390
what is sinoatrial exit block
it is similar to atrioventricular heart blocks but instead of affecting the atrioventricular node, here the cause is a failure of the SAN transitional cells to propagate the impulses across the atria
391
what are risk factors for developing sick sinus syndrome
advancing age
cardiac disease: ischaemic, inflammatory, structural, congenital
electrolyte derangement
thyroid disease
medication
392
what are symptoms of sick sinus syndrome
Fatigue
Dizziness
Palpitations during periods of arrhythmia
Pre-syncope or syncope due to cerebral hypoperfusion
Angina: often caused by rate-related myocardial ischaemia
393
what investigations should be done for sick sinus syndrome
ECG
U&Es, TFTs, drug levels
24 hour ECG
implantable loop recorder
394
what is the management of sick sinus syndrome
removal of extrinsic causes
definitive management is implanting a pacemaker - dual chamber with both atrial and ventricular leads is preferred
if patients have tachy-brady syndrome they will require BB
395
what are complications of sick sinus syndrome
Syncope and pre-syncope (sometimes with injury)
During periods of profound tachycardia (e.g. fast AF) patients may experience rate-related myocardial ischaemia, which can cause a troponin rise.
Tachyarrhythmias may also precipitate acute heart failure
Heart block due to AVN fibrosis
Patients with tachy-brady syndrome (paroxysmal atrial fibrillation) are at risk of thromboembolic events, such as stroke.
Sudden cardiac death (rare, more common in AVN disease/heart block)
396
what is Brugada syndrome
it is a rare autosomal dominant inherited cardiac sodium channelopathy characterised by ST segment elevation in at least one of the anterior precordial leads (v1-3) in the context of a normally structured heart
397
what are patients with brugada syndrome at risk of
sudden cardiac death secondary to polymorphic ventricular tachycardia or ventricular fibrillation
398
what gene mutations have been implicated in Brugada syndrome
multiple however only variants in the SCV5A gene are considered pathogenic - encodes the alpha unit of the cardiac voltage gated sodium channels
399
what is the pathophysiology of Brugada syndrome
mutations in the scn5A gene result in defective sodium channels in the cardiac cell membrane which play a crucial role in the initial depolarisation phase of the cardiac action potential. This loss of function leads to delayed depolarisation causing slower condition in the heart and increasing the risk of ventricular arrhythmias
400
what are risk factors for Brugada syndrome
Male (~8-10 times more prevalent than female)
Middle age (30-50 y/o)
Asian ancestry, especially Southeast Asia (leading cause of death in male <40 in Southeast Asia)
Positive family history
401
what are clinical features of brugada syndrome
2/3 of patients are asymptomatic
cardiogenic syncope
unexplained cardiac arrest
documented polymorphic VT/VF
atrial fibrillation/flutter
nocturnal agonal respirations
402
what things can trigger symptoms of brugada syndrome
febrile illness
use of medications which affect sodium channels - antiarrhythmics, anaesthetics, antipsychotics
excessive alcohol intake
use of illicit drugs like cannabis and cocaine
403
what is a type one brugada ECG pattern
ST-T configuration – coved-type ST elevation
J wave amplitude ≥ 2mm
Negative T wave
404
what is a type 2 brugada ECG pattern
ST-T configuration – saddle-back ST elevation (rSr’ pattern)
J wave amplitude ≥ 2mm
Positive or biphasic T wave
405
what is a type 3 brugada ECG pattern
Right precordial ST-segment elevation
Coved type, saddle-back type, or both
Not meeting the above criteria
406
what is drug provocation testing
when sodium channel blockers are given to help unmask brugada syndrome - in patients with baseline type2/3 on ECG or if suspected due to Hx/fhx
not recommended if type 1 is suspected
407
what is the drug of choice used for drug provocation testing in brugada syndrome
ajmaline or flecainide
408
what other tests can be done to help diagnose brugada syndrome
genetic testing
baseline echocardiogram
cardiac CT/MRI
electrophysiological study with programmed electrical stimulation
409
how is brugada syndrome diagnosed
using the shanghai score system/europrean society of cardiology - can be diagnosed in presence of type 1 ECG pattern.
if this isnt the case then consider the clinical history, family history, ECG findings and genetic testing
410
what is the management of brugada syndrome
no cure - current management is to prevent sudden cardiac death with ICD implantation
- lifestyle advice: avoid medications, prompt fever treatment, avoid illicit drugs
- family screening
- pharmacological tx: quinidine
411
what is quinidine
it is a class 1a antiarrhythmic that inhibits voltage gated sodium channels to decrease phase zero of rapid depolarisation - it prolongs the effective refractory period
412
when should quinidine be considered
ICD indicated but not implanted due to contraindications or patient preferences
ICD implanted but experiencing recurrent shocks
Asymptomatic spontaneous type 1 Brugada ECG
History of electrical storm (>2 episodes of VT or VF within 24 hours)
History of asymptomatic ventricular arrhythmia
413
what are complications of brugada syndrome
Polymorphic VT
VF
Sudden cardiac death
Cardiogenic syncope
Atrial arrhythmias (e.g., new-onset atrial fibrillation)
414
what are complications of having an ICD device inserted
Procedure-related complications – pneumothorax, haematoma
Physiological and physical impact
Lead malfunction
Infection
Inappropriate shocks
415
what are the two shockable rhythms in cardiac arrest
pulseless ventricular tachycardia and ventricular tachycardia
416
what are the two non shockable rhythms in cardiac arrest
pulseless electrical activity
asystole
417
what can be done in those with non shockable rhythms
high quality CPR and 1mg of IV/IO adrenaline
418
what is pulseless electrical activity
Pulseless electrical activity is defined as the absence of a pulse in a patient with electrical activity that would normally be expected to produce a cardiac output (except VT)
419
what can cause pulseless electrical activity
severe fluid depletion or blood loss, cardiac tamponade, massive pulmonary embolism and tension pneumothorax.
420
what are inotropes
medications that affect the hearts contractility
- positive inotropes increase the contractility increasing CO and MAP
- the majority of positive inotropes are catecholamines which stimulate the sympathetic nervous system
421
what are examples of positive inotropic catecholamines
Adrenaline
Noradrenaline
Dobutamine
Dopamine
422
what are vasopressors
vasopressors cause vasoconstriction which increases systemic vascular resistance and subsequently the MAP
423
what are examples of vasopressors
Adrenaline
Noradrenaline
Vasopressin
Metaraminol
Ephedrine
424
when are the indications for use of adrenaline
initial drug of choice in anaphylactic shock and in cardiac arrest as per the Advanced Life Support algorithm.
425
what is the mechanism of action of adrenaline
adrenaline is a non selective alpha and beta adrenergic receptor agonist.
alpha receptor agonism mediates peripheral vasoconstriction and reduce tissue oedema
beta receptor agonism mediates bronchodilation, positive inotropic effects and suppresses inflammatory marker release
426
what dose of adrenaline is given in cardiac arrest
give 1mg IV adrenaline, administered as 10mL of 1:10,000
427
what are side effects of adrenaline
tachyarrhythmia
ischaemia
elevates lactate
risk of tissue necrosis and hypoperfusion
428
what medical conditions should you be careful of when using adrenaline
closed angle glaucoma
429
when is use of noradrenaline indicated
septic shock
430
what is the mechanism of noradrenaline
Noradrenaline is a predominant vasopressor which causes vasoconstriction, increasing systemic vascular resistance and blood pressure. It primarily acts as an alpha-1 agonist, but it also has some beta-1 agonist activity.
431
when is use of dobutamine indicated
used in those with reduced cardiac output causing cardiac shock
432
what is the mechanism of action of dobutamine
Dobutamine is an inotrope that acts by selectively stimulating beta-1 receptors, resulting in increased inotropy and subsequently increased cardiac output and blood pressure
433
what is the dose of dobutamine given in cardiogenic shock
The initial dose of dobutamine is 0.5 – 1 micrograms/kg/min via IV infusion, increasing to a maximum of 40 micrograms/kg/min
434
what are side effects of dobutamine
hypertension
tachycardia
chest pain
arrhythmia
bronchospasm
435
when is use of dobutamine contraindicated
acute cardiovascular conditions such as acute MI, arrhythmias, acute myocarditis or pericarditis and severe hypertension
436
what is hypertension
it is persistently elevated arterial blood pressure
437
what is the single biggest risk factor for cardiovascular disease
hypertension
438
what are the different types of hypertension
primary
secondary
accelerated or malignant
white coat
masked hypertension
439
what is malignant hypertension
it is severe increase in blood pressure of over 180/120mmhg and often associated with signs of retinal haemorrhage and/or papilloedema
440
what is masked hypertension
Clinic blood pressure measurements are <140/90mmHg but ambulatory or home blood pressure measurements are >140/90mmHg
441
what are causes of secondary hypertension
kidney disease - most common
renal artery stenosis
coarctation of the aorta
hyperaldosteronism
phaeochromicytoma
cushings/acromegaly
hypo/hyperthyroidism
COCP
steroids
NSAIDS
alcohol/illicit drugs
obstructive sleep apnoea
gestational hypertension
connective tissue disorders
442
what are risk factors for developing hypertension
sex: under 65 men more likely, between 65-75 women more likely
Black African and Black Caribbean
Increased age
lifestyle factors: smoking, alcohol, increased salt, obesity, lack of exercise
443
what are important red flags to look out for with hypertension
Headache
Visual disturbances
Seizures
Nausea and vomiting
Chest pain
444
what are symptoms suggestive of kidney disease causing secondary hypertension
Haematuria
‘Frothy’ urine suggestive of proteinuria
Dyspnoea (pulmonary oedema)
Lower limb swelling (peripheral oedema)
Flank tenderness and pain
Weight loss is suggestive of renal cell carcinoma
445
what are symptoms suggestive of coarctation of the aorta causing secondary hypertension
Headache
Epistaxis
Intermittent claudication
Lower limb weakness
Cold legs and feet
446
what should all patients with hypertension undergo
fundoscopy looking for hypertensive retinopathy
447
what investigations are done for hypertension
blood pressure - clinic, ambulatory, home blood pressure readings
- need to measure in both arms
Urinalysis, urine albumin creatinine ratio
ECG
U+E, diabetes screen, lipid profile
QRISK3
448
what is stage 1 hypertension
over 140/80 in clinic
over 135/85 at home
449
what is stage two hypertension
over 160/100 in clinic
over 150/95 at home
450
what is stage three hypertension
over 180/120
451
what are common errors made when taking blood pressure readings
Incorrect patient positioning
Poor understanding of measuring technique
Incorrect cuff size: the bladder should encircle at least 80% of the arm
Incorrect cuff position: the cuff should be placed 2cm above the brachial artery and the ‘artery mark’ on the cuff should be aligned with the brachial artery
452
what are the blood pressure targets for someone with hypertension
under 80 = under 140/90 in clinic
over 80 = under 150/90 in clinic
453
what is conservative management for hypertension
Advising patients to follow a healthy diet and exercise regularly.
Encouraging patients to reduce dietary salt intake.
Encouraging patients to reduce caffeine consumption.
Advising patients to stop smoking.
Advising patients to reduce their alcohol consumption.
454
what is the management of stage 1 hypertension
discuss antihypertensive therapy in those under 80 who have one of the following: cardiovascular disease, kidney disease, or increased QRISK3
consider antihypertensives in those over 80 with systolic of over 150
consider antihypertensives in patients under 60 with a QRISK3 over 10%
455
what is the management of stage two/three hypertension
offer antihypertensives to all patients
456
what is the first stage of prescribing antihypertensives
those under 55 who are not black african or caribbean and diabetics offer ACEi
those over 55 and patients of black african/caribbean descent offer calcium channel blockers
457
what is step two of prescribing antihypertensives
patients already on an ACEi offer a CCB or a thiazide like diuretic like indapamide
visa versa for those already on a CCB
if an ACEi isnt tolerated offer an ARB such as losartan
458
what is step three of prescribing antihypertensives
Offer a combination of an ACE inhibitor or angiotensin-II receptor blocker plus a calcium channel blocker and thiazide-type diuretic
459
what is step four of prescribing antihypertensives
those not controlled after step three said to have resistant hypertension
management depends on the serum potassium
460
how does step 4 antihypertensive prescribing depend upon the patients potassium concentration
Serum potassium ≤4.5mmol/l: offer low-dose spironolactone.
Serum potassium of >4.5mmol/L: offer an alpha-blocker such as doxazosin or a beta-blocker such as atenolol.
461
how do you manage malignant hypertension
admission to hospital for same day referral if there is signs of retinal haemorrhage/papilloedema or lifre threatening symptoms such as new onset confusion, chest pain, signs of heart failure, or signs of AKI
if none of the above are present investigate for signs of complications associated with hypertension
462
what is the aim of medical management of malignant hypertension
to reduce the blood pressure over a 24-48 hour period (dont reduce too quickly or it can cause organ hypoperfusion)
463
how is malignant hypertension medically managed
Intravenous anti-hypertensive agents such as nitroprusside, labetalol and nicardipine can be used to control blood pressure in accelerated or malignant HTN
464
what are complications of hypertension
Brain: stroke (both ischaemic and haemorrhagic) and vascular dementia
Eye: hypertensive retinopathy
Heart: coronary artery disease, peripheral vascular disease, cardiac arrhythmias and heart failure
Kidneys: chronic kidney disease
465
what is a pulmonary embolism
it is a luminal obstruction of one or more pulmonary arteries by an embolised venous thrombus but can also be due to an embolised solid, liquid or gas
466
what is a thrombus
it is a blood clot that is formed within a blood vessel and remains in its place of origin
467
what is an embolism
it is the process where the bloodstream carries a detached intravascular solid, liquid or gaseous mass from its origin to a distant site
468
what are causes of PE
deep vein thrombosis
fat embolism
air embolism
amniotic fluid embolism
septic emboli
de novo thrombosis (rare)
469
what are the pathological consequences of pulmonary embolism
- ventilation/perfusion mismatch causing impaired gas exchange
- pulmonary arterial hypertension leading to right ventricular overload
- pleural and lung inflammation and infarction
470
what are risk factors for developing a PE
diagnosis of DVT
increasing age
previous DVT
venous state - prolonged immobilisation, venous insufficiency of lower limb
hypercoagulable state - active malignancy, pregnancy, postnatal period, thrombophilia, COCP
endothelial injury - trauma, surgery, cigarette smoking, obesity
471
what is considered as prolonged immobilisation when thinking about PE risk factors
bed rest >5 days, major surgery within the last 2 months, recent trauma or fracture, paralysis of the lower limb, long-haul flights
472
what are symptoms of a PE
Dyspnoea: the most common feature
Tachypnoea (~20-40% cases)
Pleuritic chest pain (~40% of cases)
Features of concurrent DVT (typically unilateral red, painful swollen leg)
Haemoptysis
Retrosternal chest pain (due to right ventricular ischaemia)
Cough
473
what are clinical features of a pulmonary embolism
Tachycardia
Tachypnoea
Hypoxia
Low-grade fever
Pleural rub
Gallop rhythm, a wide split-second heart sound and tricuspid regurgitant murmur.
474
what are the features of a massive PE
Haemodynamic instability: hypotension and cardiogenic shock
Presyncope/syncope
Elevated jugular venous pressure (JVP)
475
what investigations should be done for someone with suspected PE
12 lead ECG
D dimer
FBC, U&E, LFT, cardiac biomarkers, coagulation studies
chest X ray
CT pulmonary angiogram
Echo
476
what is seen on ECG in a PE
Sinus tachycardia: the most common finding
Right ventricular strain pattern: T wave inversion in anterior leads (V1-V4) +/- inferior leads (II, III, aVF)
Right bundle branch block (RBBB)
Right axis deviation (RAD)
The classic ‘S1Q3T3’ ECG change is only seen in <20% patients – large S wave in lead I, large Q wave in lead III, and inverted T wave in lead III
477
what things can cause a rise in D dimer
Pregnancy
Malignancy
Liver disease
Severe infection or inflammatory disease
Disseminated intravascular coagulation (DIC)
Recent trauma/surgery/hospitalised patients
478
what are possible chest X ray findings in PE
Wedge-shaped pulmonary infarction: wedge-shaped opacification without air bronchograms
Atelectasis
Pleural effusion
Raised hemidiaphragm
479
what is the general management of PE
ABCDE
- if PE suspicion low use the pulmonary embolism rule out criteria
- if not then use the Wells score
480
what is included in the pulmonary embolism rule out criteria
if all the following criteria are absent it reduces the possibility of a PE to under 2%:
Age ≥ 50 y/o
HR ≥ 100 bpm
SpO2 < 95% on room air
Unilateral leg swelling
Haemoptysis
Recent surgery/trauma ≤4 weeks ago requiring general anaesthesia
Previous DVT / PE
Hormone use (oral contraceptives/hormone replacement/estrogenic hormones)
481
what is included in the wells score
clinical signs and symptoms of a DVT: 3
an alternative diagnosis is less likely than PE: 3
HR >100bmp: 1.5
immobilisation for more than three days/surgery in the last 4 weeks: 1.5
previous DVT/PE: 1.5
haemoptosis: 1
malignancy: 1
482
if a PE is likely what do you do next
offer immediate CTPA
if it cant be done immediately then offer interim therapeutic anticoagulation
if CTPA is positive then start anticoagulation
if CTPA is negative consider proximal leg vein ultrasound
483
if a PE is unlikely on the wells score what is done next
offer a D dimer test within 4hrs
if it cant be done in 4 hours do interim therapeutic anticoagulation
if D-dimer positive = CTPA
if its negative then PE unlikely
484
what is the management of a confirmed PE with haemodynamic instability
Offer continuous UFH (unfractionated heparin) infusion, and consider thrombolytic therapy
IV tissue plasminogen activator (tPA) (e.g. alteplase) is often used
Catheter-directed thrombolysis
Open pulmonary embolectomy
485
what is the management of PE with haemodynamic stability
anticoagulation
First line: apixaban or rivaroxaban, both direct oral anticoagulants (DOACs)
Second line: low molecular weight heparin (LMWH) followed by dabigatran/edoxaban OR LMWH followed by warfarin
486
what is the treatment of PE in pregnancy
low molecular weight heparin only
487
what is the treatment of PE in severe renal impairment
unfractionated heparin or dose adjusted low molecular weight heparin
488
how long do you anticoagulate for in PE
If VTE was provoked → 3 months of anticoagulation
If VTE was unprovoked → 6 months of anticoagulation
If there is active cancer → 3-6 months of anticoagulation
489
what is a provoked PE
recent (within three months) and transient major risk factor
490
what are short term complications of PE
sudden cardiac arrest or death
pulmonary infarction
right ventricular infarction
atelectasis
exudative pleural effusion
491
what are long term complications of PE
increased risk of recurrence
chronic thromboembolic pulmonary hypertension - fibrotic tissue replaces residual emboli causing chronic obstruction
492
what is a deep vein thrombosis
formation of a thrombus within the deep venous system, most often occurring in the veins of the leg but also in the pelvis and arm
493
what are risk factors for developing a DVT
inherited thrombophilia
pregnancy and oestrogen therapy
malignancy
infection and inflammation
dehydration
nephrotic syndrome
immobility
varicose veins
obesity
physical trauma
foreign devices
hypertension
bacterial infection
494
what are clinical features of a DVT
Unilateral:
Oedema
Pain (often cramping, may progress over several days)
Erythema & warmth
Peripheral venous distention
495
what is the wells score for DVT
active cancer
paralysis, paresis or recent immobility
recently bedridden (>3 days) or major surgery in the last 3 months
localised tenderness along leg
entire leg swollen
calf swelling at least 3cm than other
pitting oedema in sx leg
collateral superficial veins
previous DVT
an alternative diagnosis is at least as likely as DVT = - 2 points
496
if a DVT is likely then what is the management
proximal leg vein doppler ultrasound within 4 hours
if positive then anticoagulate
if it cant be done in 4 hours then D dimer and interim anticoagulation
if ultrasound is negative check d dimer
497
if a DVT is unlikely then what is the management
offer a D dimer within 4 hours
if positive then do proximal leg vein doppler ultrasound and anticoagulate
if negative then another diagnosis is considered
498
what are differential diagnosis for a DVT
acute limb ischaemia
compartment syndrome
cellulitis
ruptured bakers cyst
499
what is peripheral arterial disease
refers to the narrowing of the arteries supplying the limbs and periphery, reducing the blood supply to these areas. It usually refers to the lower limbs, resulting in symptoms of claudication
500
what is intermittent claudication
symptom of ischaemia in a limb, occurring during exertion and relieved by rest. It is typically a crampy, achy pain in the calf, thigh or buttock muscles associated with muscle fatigue when walking beyond a certain intensity
501
what is chronic limb threatening ischaemia
end-stage of peripheral arterial disease, where there is an inadequate supply of blood to a limb to allow it to function normally at rest. There is a significant risk of losing the limb
502
what are features of chronic limb threatening ischaemia
burning pain thats worse at night when the leg is raised
503
what is acute limb ischaemia
rapid onset ischaemia in a limb - this is typically due to a thrombus blocking the arterial supply of a distal limb
504
what are non modifiable risk factors for atherosclerosis
Older age
Family history
Male
505
what are modifiable risk factors of atherosclerosis
Smoking
Alcohol consumption
Poor diet (high in sugar and trans-fat and low in fruit, vegetables and omega 3s)
Low exercise / sedentary lifestyle
Obesity
Poor sleep
Stress
506
what medical comorbidities increase the risk of atherosclerosis
Diabetes
Hypertension
Chronic kidney disease
Inflammatory conditions such as rheumatoid arthritis
Atypical antipsychotic medications
507
what is intermittent claudication
a symptom of peripheral arterial disease - patients describe a crampy pain that occurs after walking a certain distance
508
what are features of acute limb ischaemia
pain
pallor
pulselessness
paralysis
paraesthesia
perishingly cold
509
what is Leriche syndrome
Leriche syndrome occurs with occlusion in the distal aorta or proximal common iliac artery. There is a clinical triad of:
Thigh/buttock claudication
Absent femoral pulses
Male impotence
510
what are signs of arterial disease on examination
Skin pallor
Cyanosis
Dependent rubor (a deep red colour when the limb is lower than the rest of the body)
Muscle wasting
Hair loss
Ulcers
Poor wound healing
Gangrene (breakdown of skin and a dark red/black change in colouration)
reduced skin temperature
reduced sensation
prolonged capillary refill
511
what test can be done to assess for peripheral arterial disease in the leg
the Buerger's test
- in patients with arterial disease the limbs will initially be blue as the ischaemic tissue deoxygenates the blood, and then dark red after a short time
512
what are features of arterial ulcers
Are smaller than venous ulcers
Are deeper than venous ulcers
Have well defined borders
Have a “punched-out” appearance
Occur peripherally (e.g., on the toes)
Have reduced bleeding
Are painful
513
what are features of venous ulcers
Occur after a minor injury to the leg
Are larger than arterial ulcers
Are more superficial than arterial ulcers
Have irregular, gently sloping borders
Affect the gaiter area of the leg (from the mid-calf down to the ankle)
Are less painful than arterial ulcers
Occur with other signs of chronic venous insufficiency (e.g., haemosiderin staining and venous eczema)
514
what investigations can be done in suspected arterial disease
Ankle-brachial pressure index (ABPI)
Duplex ultrasound – ultrasound that shows the speed and volume of blood flow
Angiography (CT or MRI) – using contrast to highlight the arterial circulation
515
what is the management of intermittent claudication
lifestyle changes
exercise training
medicine - statin 80mg, clopidogrel, naftidrofuryl oxalate
surgery - stenting, endarterectomy, bypass surgery
516
what is the management of critical limb ischaemia
urgent referral to the vascular team:
Endovascular angioplasty and stenting
Endarterectomy
Bypass surgery
Amputation of the limb if it is not possible to restore the blood supply
517
what is the management of acute limb ischaemia
urgent referral to the on call vascular team:
endovascular thrombolysis
endovascular thrombectomy
surgical thrombectomy
endarterectomy
bypass surgery
amputation
518
what is pericarditis
it is inflammation of the pericardium - the fibrous sac surrounding the heart
519
what is the anatomy of the pericardium
the pericardium is the outer lining of the heart and comprises of two parts - outer fibrous and inner serous part
the serous pericardium consists of an outer parietal layer and an inner visceral layer which attaches to the heart and forms the outer epicardium layer
there is a small space between the parietal and visceral pericardium which is called the pericardial cavity
520
what are causes of pericarditis
most cases are idiopathic
infections: coxsackievirus, HIV, staphylococcus, mycobacterium and fungi
acute MI
dressler syndrome
cancer
autoimmune: RA, SLE
drug induced: hydralazine
uraemic: accumulation of toxic metabolites
521
what are risk factors of pericarditis
age: 40-60
males
idiopathic more common in spring and fall
steroids
522
what are risk factors for bacterial pericarditis
Diabetes
Extensive burn injuries
Systemic infections
Immunosuppression
Heart surgery
Chest trauma
Pre-existing pericardial effusion
523
what are the typical symptoms of pericarditis
chest pain - retrosternal, left sided, radiating to neck, arms, trapezius ridge. Exacerbated by lying down, relieved by sitting up/forward
dyspnoea
524
what are clinical findings of pericarditis
pericardial rub
evidence of pericardial effusion
becks triad indicative of cardiac tamponade: hypotension, muffled heart sounds, raised JVP
525
what are typical symptoms of cardiac tamponade
signs of decreased cardiac output and shock: hypotension, tachycardia, tachypnoea, cool peripheries, diaphoresis, peripheral cyanosis
526
what investigations should be done for suspected pericarditis
12 lead EGC
lab investigations: FBC, ESR/CRP, troponin, U&E, LFT
CXR, Echo, cardiac CT/MRI
527
what is the general lifestyle management of pericarditis
treatment is usually directed at alleviation of symptoms
- restrict physical activity
- safety net for symptoms of deterioration
528
what is symptomatic management of pericarditis
NSAIDs - ibuprofen/aspirin dependent on patients mhx
colchicine is recommended for three months
corticosteroids are second line
529
what are predictors of poor prognosis in pericarditis
Fever >38oC
Subacute onset
Large pericardial effusion
Cardiac tamponade
Failure of response to NSAIDs after a week of therapy
530
what are complications of pericarditis
pericardial effusion
cardiac tamponade
recurrent or chronic pericarditis
constrictive pericarditis
531
why does pericarditis lead to pericardial effusion and cardiac tamponade
pericardial fluid can accumulate due to reduced reabsorption
as an effusion accumulated the pericardial pressure builds up and impedes right heart filling
this can lead to reduced cardiac output
this leads to haemodynamic compromise
532
what is the treatment of cardiac tamponade
pericardiocentesis using echo/fluoroscopic guidance
533
how many patients develop recurrence of symptoms in pericarditis
15-30%
may rise to 50% in patients not given colchicine
534
what is constrictive pericarditis
inflammation in pericardium can lead to fibrosis and calcification with adhesions of the parietal and visceral pericardium. This can lead to the pericardium becoming inelastic and hindering diastolic filling of the chambers.
535
what is myocarditis
it is inflammation of the myocardium - muscular layer of the heart
536
what are the three layers of the heart wall
endocardium - inner layer which lines cavities and valves
myocardium - middle layer formed by cardiac myocytes
epicardium - formed by the visceral layer of the pericardium
537
what are causes of myocarditis
50% of cases no cause is identified
viral infection - coxsackie, parvovirus B19, HHV6, EBV
Bacteria - staph, strep, mycobacterium
fungal - aspergillus, candida
parasites
immune mediated - allergens, alloimmune, autoimmune
toxins - amphetamines, lithium, clozapine, radiation
538
what are risk factors for myocarditis
age - younger
male
immunocompromised patients
history of autoimmune disease
alcohol and drugs
539
what are typical symptoms of myocarditis
chest pain
shortness of breath/breathlessness
palpitations
dizziness
syncope
fatigue
540
what are typical clinical findings in myocarditis
Tachypnoea
Gallop rhythm
Raised jugular venous pressure (JVP)
Peripheral pitting oedema
Inspiratory crackles
Arrhythmias: palpation of a pulse may reveal a fast or slow heart rate
Rash
Ocular inflammation
Lymphadenopathy
pericardial rub, muffled heart sounds, hypotension, raised jvp = cardiac tamponade
541
what investigations are done for myocarditis
12 lead ECG
labs - FBC, CRP/ESR, troponin, BNP, U&E, LFT
autoimmune screen
CXR, transthoracic echo, cardiac MRI
endomyocardial biopsy
542
what is typically seen on a 12 lead EGC in myocarditis
sinus tachycardia
st segment/t wave changes: ST segment concave
may find AV block, QTc prolongation and PR segment depression
543
what are the typical ECG findings in pericarditis
widespread concave/saddle shaped ST elevation (except aVR/V1)
PR segment depression
low voltage QRS - pericardial effusion
544
what is the gold standard testing for myocarditis
endomyocardial biopsy - reveals inflammatory infiltrate with necrosis
545
when should endomyocardial biopsy be performed
when there are high risk features due to the risk:
Cardiogenic shock
Acute heart failure requiring inotropic or mechanical support
Ventricular arrhythmias
Mobitz type II atrioventricular block or higher
546
what is the diagnostic criteria for clinically suspected myocarditis
acute chest pain - ECG changes
new/worsening SOB - elevated troponin
palpitations/syncope - evidence of functional abnormalities on cardiac imaging
cardiogenic shock - cardiac MRI
history of recent viral infection
547
what is the initial management of myocarditis
treatment is supportive
if there is evidence of pleural involvement = NSAIDS and colchicine
if there is evidence of acute HF = oxygen, non invasive ventilation, IV diuretic therapy
cardiogenic shock = inotropes, vasopressors, mechanical support
arrhythmias = temporary pacing, cardioversion, antiarrhythmics
cardiac tamponade = drain
548
what is the long term management of myocarditis
once the patient is stable if they have developed HF then they need:
Diuretics
ACE-inhibitors/angiotensin receptor blockers
Beta-blockers
Sodium-glucose transport 2 inhibitors
Aldosterone receptor antagonists
avoid exercise for 3-6 months
549
what are complications of myocarditis
Dilated cardiomyopathy
Heart failure
Arrhythmias
Pericardial effusion/tamponade
Sudden cardiac death
550
what are factors that predict poor prognosis in myocarditis
Cardiogenic shock
Reduced ejection fraction on imaging
Ventricular arrhythmias
Heart block
551
what is the first heart sound (s1) made by
the closing of the atrioventricular valves (tricuspid and mitral) at the start of the systolic contraction of the ventricles
552
what is the second heart sound (s2) made by
closing of the semilunar valves (pulmonary and aortic) once the systolic contraction is complete
553
what is a 3rd heart sound made by
the rapid ventricular filling causing the chordae tendineae to pull their full length and twang
it can be normal in young healthy people, however in small people it can indicate heart failure
554
what causes a fourth heart sound
normally heard directly before s1
this is always abnormal and indicates a stiff or hypertrophic ventricle and is caused by turbulent flow from the atria contracting against a non compliant ventricle
555
which valvular heart diseases cause hypertrophy
mitral stenosis - left atrial
aortic stenosis - left ventricular
556
which valvular heart diseases causes dilation
mitral regurgitation = left atrial
aortic regurgitation = left ventricle
557
which is the most common valvular heart disease
aortic stenosis
558
what are causes of aortic stenosis
Idiopathic age-related calcification (by far the most common cause)
Bicuspid aortic valve
Rheumatic heart disease
559
what murmur is associated with aortic stenosis
ejection systolic high pitched murmur due to the high blood flow velocity through the aortic valve
- crescendo decrescendo
- radiates to carotids
560
what are signs of aortic stenosis
murmur - ejection systolic
Thrill in the aortic area on palpation
Slow rising pulse
Narrow pulse pressure (the difference between systolic and diastolic blood pressure)
Exertional syncope (lightheadedness and fainting when exercising) due to difficulty maintaining a good flow of blood to the brain
561
what murmur is associated with aortic regurgitation
early diastolic soft murmur
can also cause austin flint murmur - heard at the apex as a diastolic rumbling murmur
562
what are signs of aortic regurgitation
murmur - early diastolic
Thrill in the aortic area on palpation
Collapsing pulse
Wide pulse pressure
Heart failure and pulmonary oedema
563
what is a collapsing pulse
a forcefully appearing and rapidly disappearing pulse. This is typically felt in the radial artery with the patient’s arm held straight upwards. It occurs as blood is forcefully pumped out of the left ventricle, then immediately flows backwards through the incompetent aortic valve.
564
what are causes of aortic regurgitation
Idiopathic age-related weakness
Bicuspid aortic valve
Connective tissue disorders, such as Ehlers-Danlos syndrome and Marfan syndrome
565
what murmur is caused by mitral stenosis
mid-diastolic, low-pitched “rumbling”
will be a loud s1 due to thick valves shutting
566
what are signs of mitral stenosis
murmur - mid diastolic
Tapping apex beat, which is a palpable, prominent S1
Malar flush
Atrial fibrillation (irregularly irregular pulse)
567
what is malar flush
red discolouration of the skin over the upper cheeks and nose. It is due to the back pressure of blood into the pulmonary system, causing a rise in CO2 and vasodilation.
568
what are causes of mitral stenosis
rheumatic heart disease
infective endocarditis
569
what murmur does mitral regurgitation cause
pan systolic high pitched whistling murmur
radiates to the left axilla
may hear third heart sound
570
what can be the outcome of mitral regurgitation
The leaking valve causes a reduced ejection fraction and a backlog of blood waiting to be pumped through the left side of the heart, resulting in congestive cardiac failure
571
what are signs of mitral regurgitation
murmur - pan systolic
Thrill in the mitral area on palpation
Signs of heart failure and pulmonary oedema
Atrial fibrillation (irregularly irregular pulse)
572
what are causes of mitral regurgitation
Idiopathic weakening of the valve with age
Ischaemic heart disease
Infective endocarditis
Rheumatic heart disease
Connective tissue disorders, such as Ehlers-Danlos syndrome or Marfan syndrome
573
what murmur is caused by tricuspid regurgitation
pan-systolic murmur. There is a split second heart sound due to the pulmonary valve closing earlier than the aortic valve, as the right ventricle empties faster than the left ventricle.
574
what are signs of tricuspid regurgitation
Thrill in the tricuspid area on palpation
Raised JVP with giant C-V waves (Lancisi’s sign)
Pulsatile liver (due to regurgitation into the venous system)
Peripheral oedema
Ascites
575
what are causes of tricuspid regurgitation
Pressure due to left-sided heart failure or pulmonary hypertension (“functional”)
Infective endocarditis
Rheumatic heart disease
Carcinoid syndrome
Ebstein’s anomaly
Connective tissue disorders, such as Marfan syndrome
576
what murmur is caused by pulmonary stenosis
ejection systolic murmur loudest in the pulmonary area with deep inspiration. There is a widely split second heart sound, as the left ventricle empties much faster than the right ventricle.
577
what are signs of pulmonary stenosis
Thrill in the pulmonary area on palpation
Raised JVP with giant A waves (due to the right atrium contracting against a hypertrophic right ventricle)
Peripheral oedema
Ascites
578
what congenital causes are there for pulmonary stenosis
noonan syndrome
tetralogy of fallot
579
what are the four co-existing pathologies in tetralogy of fallot
Ventricular septal defect (VSD)
Overriding aorta
Pulmonary valve stenosis
Right ventricular hypertrophy
580
what is infective endocarditis
when the heart’s inner lining (the endocardium) becomes inflamed secondary to an infection.
581
what are the different classifications of endocarditis
depending on the valve affected it can be left (MC) or right sided
this can be divided into native valve or prosthetic valve endocarditis
early PVE is seen within 12 months of valve surgery
late PVE is over 12 months after valve surgery
582
what is the pathophysiology of infective endocarditis
Endocarditis usually occurs in patients with damaged or prosthetic valves as the endothelium is exposed leading to aggregation of platelets and fibrin. pathogens enter the bloodstream and bind to the platelet fibrin matrix and proliferates. the pathogen is buried in this complex leading to vegetation
these vegetations can embolise and cause further complications such as stroke, abscess, pulmonary infarcts or abscesses
583
what is the most common cause of endocarditis
bacteria
- staphylococcus is the most common
584
what gram +VE bacteria can cause infective endocarditis
gram +ve = staphylococcus aureus, streptococci (viridans, intermedius, A, B, C, D, G), enterococci
585
what gram -ve bacteria causes infective endocarditis
HACEK organisms = Haemophilus ssp. aggregatibacter actinomycetemcomitans, cardiobacterium ssp. eikenella corrodens, kingella kingae
pseudomonas aeruginosa
neisseria elongata
586
what fungi can cause infective endocarditis
candida
aspergillus
587
what is blood culture negative infective endocarditis
this is when no causative organism is identified from standard blood culture methods
may be caused by:
HACEK organisms
Coxiella burnetti (Q fever)
Chlamydia spp
Bartonella spp (trench fever and cat-scratch disease)
Legionella
588
what are intrinsic risk factors for getting infective endocarditis
Valvular stenosis or regurgitation: congenital or acquired
Hypertrophic cardiomyopathy
Structural heart disease with turbulent flow (e.g. VSD, PDA): but NOT isolated ASD or fully repaired VSD or PDA
Prosthetic heart valves: these will require replacement if infected
Previous infection (infective endocarditis/rheumatic fever) causing structural damage
589
what are extrinsic risk factors for developing infective endocarditis
Intravenous drug use (right-sided endocarditis)
Invasive vascular procedures (e.g. central lines)
Poor oral hygiene/dental infections
590
what is a typical history of someone with infective endocarditis
fever
malaise
night sweats
weight loss
anorexia
fatigue
breathlessness
591
what are clinical findings in infective endocarditis
Fever
Tachycardia
New or changing heart murmur
Splinter haemorrhages: nailbed petechial haemorrhages
Osler’s nodes (tender subcutaneous nodules in the fingers) and Janeway lesions (painless erythematous macules on the palms): see Table 2
Roth spots (boat-shaped retinal haemorrhages, pale in the centre)
Clubbing: typically a late sign
Mild splenomegaly
Bi-basal lung crepitations: heart failure in severe cases
592
what investigations are done in someone with suspected infective endocarditis
12 lead ECG: exclude 1st degree AV block
urine dipstick
bloods - blood cultures taken before antibiotics are given: three sets, 30 minutes apart, three separate peripheral sites
FBC, CRP/ESR, U+E
transthoracic echo
transoesophageal echo
CXR, CT chest
593
what are the major criteria of the Duke criteria
Positive blood cultures: for typical organisms, persistently positive or a single positive culture for coxiella burnetti or high ab titre
Evidence of endocardial involvement: vegetation, abscess, new valvular regurgitation, new partial dehiscence of prosthetic valve
594
what are the minor criteria of the Dukes criteria
Risk factors for infective endocarditis (see risk factors section)
Fever > 38oC
Vascular phenomena: septic emboli, Janeway lesions, conjunctival haemorrhage, intracranial haemorrhage
Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots, positive rheumatoid factor
Microbiological evidence: positive blood cultures which do not meet the major criteria
595
what is required to make a definite diagnosis of endocarditis with the Dukes criteria
Direct evidence of infective endocarditis by histology or culture of organisms (e.g. from a vegetation)
TWO major criteria
ONE major + THREE minor criteria
FIVE minor criteria
596
what is required to make a possible diagnosis of endocarditis with the Dukes criteria
one major and one minor criteria
three minor criteria
597
what is required to make a rejected diagnosis of endocarditis with the Dukes criteria
firm alternative diagnosis or
sustained symptoms resolution after less than 4 days on antibiotics
598
what is the medical management of infective endocarditis
prolonged antibiotics - IV for at least 2 weeks before switching to oral
- tx is at least 6 weeks in prosthetic valves and 2-6 weeks for native valve
choice of antibiotic depends on multiple factors - previous antibiotic use, type of valve affected, microorganism involved and sensitivities
599
what is the surgical management of infective endocarditis
surgery to repair or replace the valve - indicated in heart failure, uncontrolled infection and to prevent embolism in large vegetations
600
what are complications of infective endocarditis
localised = valve destruction, heart failure, arrhythmia, AV block, MI, pericarditis, aortic root abscess
systemic = emboli, immune complex deposition, septicaemia, death
601
what is rheumatic fever
it is a systemic inflammatory disorder which arises after group A strep infection
602
what is the pathophysiology of rheumatic fever
rheumatic fever develops 1-5 weeks after an initial group A strep infection (strep. pyogenes)
rheumatic fever develops in susceptible hosts due to a hypersensitivity reaction against the bacteria (type 2)
similarities in the cell wall of the bacteria and the human heart valve may result in the bodies antibodies attacking the host instead of the pathogen and damaging the valves
603
what biological factors increase the risk of rheumatic fever
Age: rare in children under 4 years.
Sex: more common in females.
Ethnicity: for example, there is a higher prevalence of rheumatic fever among indigenous groups in Australia and New Zealand.
Immune status: immunocompetent vs immunocompromised.
Genetic susceptibility: as indicated by findings from twin studies.
Prior or untreated infection with Group A Streptococcus.
Virulence of the infective organism.
604
what are social risk factors for developing rheumatic fever
Low socioeconomic status: due to poor access to healthcare and antibiotics.
Overcrowding and poor housing: associated with poor hygiene and sanitation.
Climate: higher incidence over the winter months. In hot countries, streptococcal infection is more likely to present as a skin infection versus pharyngitis.
605
what is the jones criteria
it is used to establish a diagnosis of rheumatic fever using evidence of recent infection (positive throat swab, antigen test, antibody titre, or recent scarlet fever) plus two major criteria or one major and two minor criteria
606
what are the positive Jones criteria for rheumatic fever
polyarthritis: multiple joints affected which can migrate
Carditis: pancarditis, which commonly affects the mitral valve
Sydenhams chorea: late presenting, leads to involuntary semi-purposeful movements
Erythema marginatum: pink macular rash affecting the trunk and limbs
Subcutaneous nodules: extensor surfaces
607
what are the minor jones criteria when diagnosing rheumatic fever
polyarthralgia: pain in joints
prolonged PR on ECG
history of rheumatic fever
fever: over 39
raised inflammatory markers
608
what investigations are done in rheumatic fever
ECG: prolonged PR
vital signs
throat swabs
rapid streptococcal antigen test
anti-streptococcal antibodies (ASO and antiDNAse B
bloods: FBC, ESR/CRP, troponins, rheumatoid factor, anti-ccp
chest xray
doppler echo
609
what is the conservative management in the acute management of rheumatic fever
bed rest - until CRP has returned to normal
limitation of exercise
610
what is the medical management in the acute management of rheumatic fever
penicillin - single stat dose of benzylpenicillin followed by oral penicillin V for at least 10 days
- erythromycin/azithromycin 2nd
high dose aspirin (careful in children)
corticosteroids in moderate to severe carditis
in acute HF use ACEi and diuretics
diazepam/haloperidol can be used in chorea
611
what is given for rheumatic fever prophylaxis
used to reduce the chance of further attacks
- benzathine penicillin G given every 4 weeks as an IM injection
- can also take oral penicillin daily
612
how long is prophylaxis given for rheumatic fever
If carditis is not a feature of the acute episode, and there is no evidence of valvular disease, then prophylaxis may be given for only 5 years, or until age 21 (whichever is sooner).
If carditis is present during the acute episode but there is no valvular disease, then prophylaxis should be given for 10 years.
Where there is both carditis and persistent valvular disease, prophylaxis should be continued for life, or at least up to the age of 40.
613
what are complications of rheumatic fever
chronic rheumatic heart disease
Carditis (e.g. infective endocarditis)
Heart failure
Pericardial effusions
Valvular disease (especially the mitral valve)
Atrial fibrillation (from severe untreated mitral stenosis)
Pulmonary hypertension
Thromboembolic events, such as strokes (a consequence of atrial fibrillation)
Valvular disease
614
what can cause relapse of rheumatic fever
Further relapses can be triggered by re-infection with streptococcal bacteria, as well as the use of the oral contraceptive pill and pregnancy
615
what is chronic venous insufficiency
failure of the venous valves (usually in the legs) causing blood reflux and venous hypertension
616
what are the main causes of chronic venous insufficiency
primary valve incompetence
post thrombotic syndrome post DVT
obstruction (pelvic mass, previous surgery)
617
what are the typical symptoms of chronic venous insufficiency
Leg heaviness, aching, itching, worse on standing
Oedema (ankle swelling)
Varicose veins
Skin changes: hyperpigmentation, eczema, lipodermatosclerosis
Venous ulceration (usually gaiter area, medial malleolus)
618
what are the CEAP clinical stages (0-6) used to describe chronic venous disease
C0: No visible signs
C1: Telangiectasia / reticular veins
C2: Varicose veins
C3: Oedema
C4: Skin changes (pigmentation, eczema, lipodermatosclerosis)
C5: Healed venous ulcer
C6: Active venous ulcer
619
what is the first line investigation for chronic venous insufficiency
Duplex ultrasound of the leg veins to assess reflux and obstruction.
ABPI (ankle-brachial pressure index) to exclude arterial disease before compression therapy.
620
what is conservative management for chronic venous insufficiency
Graduated compression hosiery (if ABPI ≥ 0.8)
Leg elevation when resting
Exercise and weight reduction
Avoid prolonged standing
Skin care with emollients and topical steroids for eczema
621
when should patients with varicose veins or venous symptoms be referred to vascular
Symptomatic primary or recurrent varicose veins
Skin changes suggesting chronic venous disease
Bleeding from a varicosity
Venous ulcer (active or healed)
622
what interventions can be offered for venous reflux
Endothermal ablation (radiofrequency or laser) — first-line
Ultrasound-guided foam sclerotherapy — second line
Surgical ligation and stripping — if others unsuitable
623
what complications can arise from untreated chronic venous insufficiency
Venous ulceration
Recurrent cellulitis
Lipodermatosclerosis
Atrophie blanche (white scarring from microvascular thrombosis)
624
what are contraindications to compression therapy in chronic venous insufficiency
Severe peripheral arterial disease (ABPI < 0.8)
Acute DVT
Severe heart failure (relative)
625
what is lipodermatosclerosis
chronic inflammatory fibrosis of subcutaneous fat due to venous hypertension
626
what is a typical sign of lipodermatosclerosis
inverted champagne bottle lower leg appearance
627
what is gangrene
it is a condition typified by localised skin necrosis
628
what is the primary classification of gangrene
wet and dry
629
what is dry gangrene
results from chronic ischaemia without infection characterised by the mummification of the affected tissue without bacterial infection
630
what is the primary underlying cause of dry gangrene
arterial occlusion which may arise from:
peripheral arterial disease
diabetes mellitus
vasculitis
631
what is wet gangrene
infectious process along with tissue necrosis. It develops rapidly due to blockage in venous or arterial blood flow coupled with bacterial infection
632
what are key risk factors for wet gangrene
critical limb ischaemia
surgical wounds or trauma
immunosuppression
severe burns or frostbite
633
what is gas gangrene
specific type of wet gangrene caused by infection with gas producing bacteria, most commonly clostridium perfringens
634
what conditions promote gas gangrene
contaminated wounds: traumatic injuries contaminated with soil
surgical procedures
635
what is the pathophysiology of gangrene
* ischaemia and hypoxia leading to cell dysfunction and death
* anaerobic metabolism causing intracellular acidosis
* hypoxia and intracellular acidosis leads to irreversible cell damage and death
* necrotic tissue allows for bacterial growth, which produce toxins which can further damage surrounding tissue
* if left untreated gangrene can lead to sepsis
636
what are the clinical features of gangrene
pain in the affected area
skin changes: initially red which darkens into brown and then black
area may be swollen
sensory changes: cold or numbness
tissue loss
fever and malaise
hypotension if shock occurs
multisystem involvement
637
what investigations are done for gangrene
labs: blood cultures, tissue cultures, FBC, U+E, LFT, CRP, ESR
imaging: X-rays, CT, MRI, duplex ultrasound
638
what might be seen on imaging in gangrene
xray: gas bubbles in the tissues
639
what is the management of gangrene
surgical debridement of necrotic tissue
broad spectrum antibiotics
hyperbaric oxygen therapy (used on case-by-case basis)
treatment of nay underlying conditions
640
what are complications of gangrene
sepsis
gas gangrene
necrotising fasciitis
long term pain
limb loss
fistulas
641
what are investigations for tricuspid regurgitation
Echocardiography — diagnostic and quantifies severity
ECG: AF, RV hypertrophy
CXR: cardiomegaly, pleural effusion
642
what is the management of tricuspid regurgitation
Treat underlying cause (pulmonary hypertension, left heart failure)
Diuretics for congestio
Surgical repair or replacement if severe or symptomatic despite optimal therapy (often alongside left-sided surgery)
643
what are causes of tricuspid stenosis
rheumatic heart disease
carcinoid syndrome
congenital causes
pacemaker lead fibrosis
644
what are features of tricuspid stenosis
fatigue
hepatomegaly
ascites
diastolic murmur at the lower left sternal edge which increases with inspiration
645
what is the management of tricuspid stenosis
diuretics for symptoms
surgical repair
646
what are causes of pulmonary stenosis
Congenital (isolated or part of Tetralogy of Fallot)
Rheumatic (rare in UK)
Carcinoid syndrome
647
what investigations are done for pulmonary stenosis
Echocardiography (diagnostic)
ECG: right axis deviation, RV hypertrophy
CXR: post-stenotic dilatation of pulmonary artery
648
what is the management of pulmonary stenosis
Balloon valvuloplasty (preferred in most cases)
Surgical valvotomy if unsuitable for balloon
Endocarditis prophylaxis only for high-risk
649
what are causes of pulmonary regurgitation
Post-surgical (after pulmonary valvotomy for congenital PS)
Pulmonary hypertension
Infective endocarditis
Congenital absence of pulmonary valve
650
what are features of pulmonary regurgitation
Usually asymptomatic
Early diastolic murmur at upper left sternal edge (Graham Steell murmur if due to pulmonary hypertension)
651
what is the management of pulmonary regurgitation
treat the underlying pulmonary hypertension
valve repair or replacement if severe
652
