1
Q
What is atherosclerosis?
A
The build up of plaque (made up of fats, cholesterol, cellular waste products, calcium and fibrin) in and on the artery walls which results in thickening or hardening of the arteries.
2
Q
What are 7 major risk factors for atherosclerosis?
A
- Age
- Tobacco smoking
- High serum cholesterol
- Obesity
- Diabetes
- Hypertension
- Family history
3
Q
What is acute coronary syndrome?
A
A spectrum of acute myocardial ischaemia and/or infarction (unstable angina, STEMI, NSTEMI)
It occurs usually as a result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
4
Q
What are the symptoms of ACS?
A
Pain radiating to the jaw or arms
Nausea and vomiting
Sweating and clammisness
A feeling of impending doom
Shortness of breath
Palpitations
5
Q
Define unstable angina
A
Myocardial ischaemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis.
6
Q
What are 5 risk factors for acute coronary syndrome?
A
- Diabetes mellitus
- Hyperlipidaemia
- Hypertension
- Metabolic syndrome (abdominal obesity, hypertension, impaired fasting glucose, high triglyceride levels, and low HDL cholesterol levels)
- Renal impairment
7
Q
What are 5 key symptoms of unstable angina?
A
- chest pain
- excessive sweating
- epigastric pain
- dyspnoea
- syncope (fainting)
8
Q
What is the first line investigation for acute coronary syndrome?
A
ECG
9
Q
What is the first line treatment for ACS?
A
Aspirin 300mg
10
Q
What is the key presentation for STEMI?
A
New or increased and persistent ST-segment elevation in at least 2 contiguous leads (leads connecting to adjoining areas of tissue)
11
Q
What is the initial management for ACS?
A
CPAIN
Call an ambulance
Perform an ECG
Aspirin 300mg
Intravenious morphine for pain
Nitrate (GTN)
12
Q
What is the key presentation for NSTEMI?
A
elevated troponin levels
13
Q
What is the management for an NSTEMI?
A
Base angiography/PCI decision on the GRACE score
Aspirin 300mg stat
Ticagrelor 180mg stat
Morphine
Antithrombin therapy with fondaparinux
Nitrate (GTN)
Give oxygen only if their sats drop <95% and not in patients with COPD
14
Q
What is the GRACE score and when is it relevant?
A
Unstable patients are considered for immediate angiography using the GRACE score
The GRACE score gives a 6-month porbability od death post-NSTEMI
3% or less is considered low risk
Above 3% is considered medium-high risk
Patients at medium or high risk are considered for early angiography with PCI (within 72hrs)
15
Q
What are myocardial infarction complications?
A
Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm
Dressler syndrome (autoimmune pericarditis)
Embolism
Recurrence regurgitation
16
Q
What is troponin?
A
A protein complex which regulates actin-myosin contraction and acts as a highly sensitive marker for myocardial ischaemia.
17
Q
What does elevated troponin indicate?
A
Higher risk of mortality in patients with suspected ACS
18
Q
What are some other potential causes of a raised troponin?
A
Chronic kidney disease
Sepsis
Myocarditis
Aortic dissection
Pulmonary embolism
19
Q
What is the effect of aspirin?
A
Irreversibly binds to and inactivates cyclo-oxygenase 1 (COX-1), which normally produces prostaglandins and thromboxanes which promote inflammation and clotting. This produces an inhibitory effect on platelet aggregation and so helps to reduce risk of blood clots and myocardial infarction.
20
Q
What is the effect of P2Y12 inhibitors?
A
They bind antagonistically to the platelet P2Y12 receptor and prevent the binding of ADP which attenuates platelet aggregation and reaction of platelets to thrombus stimuli such as thrombin.
21
Q
Give 3 examples of P2Y12 inhibitors
A
Clopidogrel, Prasugrel, Ticagrelor
22
Q
What is the effect of GPIIb/IIIa antagonists?
A
They bind to GPIIb/IIIA receptors on the platelet plasma membrane preventing the binding fibrinogen and von Willebrand factor. This inhibits the aggregation of platelets and formation of thrombi.
23
Q
Give 3 examples of GPIIb/IIIa antagonists
A
Abciximab, Eptifibatide, Tirofiban
24
Q
What is PCI? When is it indicated?
A
Percutaneous coronary intervention describes the combination of coronary angioplasty with stenting.
25
What is CABG?
Coronary artery bypass graft. A piece of a vein from the leg or artery from the chest is used to create an alternative route for blood flow between the aorta and coronary artery's when the normal route is blocked.
26
What is the cause of angina?
Mismatch of oxygen demand and supply.
27
What are the risk factors of IHD?
- age
- smoking
- family history
- diabetes mellitus
- hyperlipidaemia
- hypertension
- kidney disease
- physical inactivity
- male
- stress
- obesity
28
What factors exacerbate IHD?
Affecting supply:
- anaemia
- hypoxaemia
- polycythemia
- hypothermia
- hypovolaemia
- hypervolaemia
Affecting demand:
- tachyarrthythmia
- valvular heart disease
- hypertension
- hypertrophic cardiomyopathy
29
What 4 environmental factors exacerbate IHD?
- cold
- emotional stress
- exercise
- heavy meals
30
What are differential diagnoses for chest pain?
- myocardial ischaemia
- pericarditis/myocarditis
- pulmonary embolism/pleurisy
- chest infection/pleurisy
- gastro-oesophageal
- musculoskeletal pain
- psychological
- dissection of the aorta
31
What is pericarditis?
Inflammation of the pericardium
32
What are the 6 categories for causes of pericarditis?
Viral (coxsackie virus is most common)
Bacterial (TB)
Autoimmune (SLE, Sjorgens Syndrome, RA)
Neoplastic (metastatic lung, breast)
Metabolic
Traumatic and iatrogenic
33
What are the risk factors for pericarditis?
- male
- age 20-50
- transmural myocardial infarction
- cardiac surgery
- neoplasm
- viral and bacterial infection
34
What are the key presentations of pericarditis?
- severe, pleuritic, rapid onset chest pain
- low-grade fever
- pericardial rub on auscultation
35
What is the first investigation for pericarditis? What does it show?
ECG - saddle-shaped ST-elevation and PR depression
36
What is the management of pericarditis?
- sedentary activity until resolution of symptoms and ECG/CRP
- High dose NSAID or Aspirin
- Colchicine (to prevent constrictive pericarditis)
- Steroids may be used 2nd line in recurrent cases or associated with inflammatory conditions
- pericardiocentesis may be required to removed fluid from around the heart if there is a significant pericardial effusion or tamponade
37
What is pericardial/cardiac tamponade
where the pericardial effusion is large enought to raise the intra-pericardial pressure.
This increased pressure squeezes the heart and affects its ability to function.
It is an EMERGENCY and requires prompt drainage to relieve pressure.
38
What is myocarditis?
inflammation of the myocardium
often seen in young people
39
What are some of the causes of myocarditis?
viral - coxsackie B, HIV
bacteria - diptheria, clostridia
spirochaetes - Lyme's disease
protozoa - Chagas' disease, toxoplasmosis
autoimmune
drugs - doxorubicin
40
What are the investigations for myocarditis? And what is shown?
Bloods - increased inflamm markers, increased cardiac enzymes, increased BNP
ECG - tachycardia, arrhythmias, ST/T wave changes including ST_segment elevation and T wave inversion
40
What are the presenting symptoms of myocarditis>
chest pain
dyspnoea
arrthymias
usually young patient with acute history
41
What pathology can be identified using ECG?
- arrhythmias
- myocardial ischaemia and infarction
- pericarditis
- chamber hypertrophy
- electrolyte disturbances (i.e. hyperkalaemia, hypokalaemia)
- drug toxicity (i.e. digoxin and drugs which prolong the QT interval)
42
What is the passage of electrical conduction through the heart?
Sinoatrial node --> AV node --> Bundle of His --> Bundle branches --> Purkinje fibres
43
What are the significances of the letters in the PQRST sequence?
P wave = Atrial depolarisation
PR interval – time taken for electrical activity to move between the atria and the ventricles (120-200ms)
QRS sequence = Atrial repolarisation (not visible) and Ventricular depolarisation
ST segment – time between depolarisation and repolarisation of the ventricles (ventricular contraction)
T wave = Ventricular repolarisation
44
What are unipolar and bipolar leads?
unipolar leads = one point on the body and a virtual reference point with zero electrical potential, located in the centre of the heart
- Measures the potential difference (voltage) between an electrode (positive) and a combined reference electrode (negative)
- Sometimes known as augmented leads
bipolar leads = two different points on the body
- Measure the potential difference (voltage) between two electrodes
- One positive and one negative electrode
45
What is the normal length of the PR interval?
120-200 ms (3-5 little squares)
46
What is the normal width of the QRS complex?
No more than 110ms (<3 little squares)
47
In which leads should the QRS interval be dominantly upright?
Leads I and II
48
In which leads must the P and T waves be upright?
Leads I, II, V2-V6
49
What psychosocial factors affect CHD?
1. behaviour patterns
2. depression/anxiety
3. social support
4. work
50
Which ECG leads produce an inferior view of the heart?
Leads II, III, aVF
51
Which leads produce a lateral view of the heart?
I, aVL, aVR, V5, V6
52
Which leads produce an anterior view of the heart?
V3, V4
53
What is the most common congenital heart problem?
ventricular septal defect
54
Which leads produce a septal view of the heart?
V1, V2
55
What is Prinzmetal's angina?
Mismatch in blood supply and demand to heart muscle due to coronary vasospasm (atherogenesis) --> seen in cocaine users
* ECG shows ST elevation
56
What is Eisenmenger's syndrome?
High pressure pulmonary flow with a VSD so that pressure in the RV is greater and deoxygenated blood enters LV so patient becomes cyanotic (blue) and has clubbing of fingers.
57
What are the clinical signs for VSD?
Large defect: small breathless skinny baby, increased resp rate, tachycardia, big heart
Small defect: loud systolic murmur, thrill (buzzing sensation), well grown, normal heart rate and size
58
What are the clinical signs of ASD?
- pulmonary flow murmur
- fixed split second heart sound (delayed closure of PV because more blood has to get out)
- big pulmonary arteries on CXR
- big heart on CXR
59
What is AVSD?
Atrio-ventricular septal defects - strong association with Down's syndrome
= hole at the centre of the heart which involves the ventricular septum, the atrial septum, the mitral and tricuspid valves
60
What is the tetralogy of Fallot?
A combination of 4 congenital heart defects which usually result in a lack of oxygen-rich blood reaching the body.
- pulmonary stenosis
- ventricular septal defect
- dextroposition (heart on the right, apex to the left)
- right ventricular hypertrophy
61
What is the key issue in tetralogy of Fallot?
Anterior dislocation of the septum below the pulmonary outflow - this results in the other issues.
62
What is a 'Fallot spell'
Stenosis of the RV outflow leads to higher pressure in the RV than the LV this causes deoyxgenated blood to enter the right ventricle and makes patient look blue.
63
What is complete transition of the great arteries (TGA)?
When the aorta comes off the right ventricle and the pulmonary trunk off the left ventricle.
64
What is coarctation of the aorta?
Narrowing of the aorta just after the arch with excessive blood flow being diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body. This occurs as a result of an excessive sclerosing /obliterating process that normally closes the ductus arteriosus, extending into the aortic wall.
65
What is endocardial fibroelastosis?
Secondary endocardial fibroelastosis is a frequent complication of congenital aortic stenosis and coarctation. Profound dense collagen and elastic tissues deposited on the endocardial aspect of the left ventricle produces progressive stiffening of the heart and cardiac failure.
66
What is cor pulmonale?
Right ventricular hypertrophy and dilatation due to pulmonary hypertension.
67
What are the symptoms of a patent ductus arteriosus?
Blood is shunted from aorta to pulmonary trunk which creates risk of pulmonary overload and Eisenmenger's.
Symptoms: dyspnoea, failure to thrive, machine-like murmur
68
What is the definition of heart failure?
The inability of the heart to deliver oxygenated blood to tissues at sufficient rate for the tissue's metabolic requirements.
69
What are the causes of heart failure?
Most common: Ischaemic heart disease
- cardiomyopathy
- vascular disease
- cor pulmonale
- anything which increases cardiac strain (obesity, pregnancy, arrhythmias, hypertension, hyperthyroidism)
70
What are the risk factors for heart failure?
Age (65+ yrs)
Smoking
Obesity
Previous MI
Male
african descent
71
What is the pathophysiology of heart failure?
1. Weakened cardiac muscles result in decreased cardiac output
2. This activates the compensatory mechanisms of RAAS and SNS which temporarily increase BP as a result of increased aldosterone, ADH and adrenaline/NAd
3. Soon compensation fails and heart undergoes cardiac remodelling in response to compensation and cardiac output decreases causing multi-systemic effects.
72
What are the key manifestations of heart failure?
Shortness of breath, ankle swelling, fatigue
73
What is the key blood marker in heart failure diagnosis?
Brain natriuretic peptide (BNP) (released from ventricles in response to increased mechanical stress) - the higher the BNP, the more severe the HF
74
What are the XR findings in heart failure?
Alveolar oedema
Kerley *B* Lines
Cardiomegaly
Dilation of UPPER lobe vessels
Effusions
75
What is the most common cause of heart failure
Ischaemia
76
What is the management for heart failure?
- lifestyle changes
- ACE-i + B-blocker
+ spironolactone + furosemide
77
What is the definition of hypertension?
Blood pressure ≥140/90mmHg
78
What are the initiating factors for hypertension? (8)
DRIED ICE
- Disturbance of autoregulation
- Renal sodium retention
- Insulin resistance/hyperinsulinaemia
- Excess sodium intake
- Dysregulation of RAAS with elevated plasma renin activity
- Increased sympathetic drive
- Cell membrane transporter changes
- Endothelial dysfunction
79
Which medications increase blood pressure?
- NSAIDs
- SNRIs (serotonin and norepinephrine reuptake inhibitors)
- Corticosteroids
- Oral contraceptives (oestrogen containing)
- Stimulants
- Anti-anxiety drugs
- Anti-TNFs
80
What are the risk factors for hypertension?
- age >65yrs
- moderate/high alcohol intake
- sedentary lifestyle
- FH of hypertension of CAD
- obesity
- metabolic syndrome
- diabetes mellitus
- black ancestry
- hyperuricemia
- obstructive sleep apnoea
** Smoking is NOT a risk factor
81
what is the equation for BP?
BP = CO x TPR
82
What factors affect blood pressure?
- Preload
- Contractility
- Vessel hypertrophy
- Peripheral constriction
83
What are the common symptoms of hypertension?
Most often symptomless.
- headache
- visual changes
- dyspnoea
- chest pain
- sensory of motor deficit
84
What is the gold standard screening for hypertension?
ECG
85
What is the management for hypertension?
- Lifestyle modification and monitoring (increase exercise, reduce sodium intake, lose weight)
Medical treatment thresholds: low CDV risk = 160/100mmHg, high CDV risk = 140/90mmHg
- calcium channel blockers, ACEis, ARBs, diuretics, B-blockers
86
What is aortic stenosis?
Narrowing of the aortic valve.
87
What are the causes of aortic stenosis?
Congenital: can occur with unicuspid, bicuspid, tricuspid valve and is commonly associated aortic coarctation, dissection or aneurysm
Acquired: degenerative calcification, rheumatic heart disease, rare causes (infectious vegetations, Paget disease, Rheumatoid arthritis)
88
What is the pathophysiology of aortic stenosis?
Development of a pressure gradient between the left ventricle and aorta (increased afterload).
LV function intially maintained by compensatory pressure hypertrophy but when compensatory mechanism exhausted, LV function declines.
89
What are the key presentations of aortic stenosis?
- Dyspnoea (50%) - on exertion due to heart failure
- Angina (35%) - increased myocardial oxygen demand, demand/supply mismatch
- Syncope (15%) - exertional
- Sudden death (<2%)
90
What are the physical signs of aortic stenosis?
- slow rising carotid pulse + decreased pulse amplitude
- Heart sounds- soft or absent second heart sound, S4 gallop due to LVH.
- Ejection systolic murmur- crescendo-decrescendo character.
91
What is the first line investigation for aortic stenosis?
Echocardiography (LV size and function most important)
92
How is aortic stenosis managed/treated?
- good dental hygiene/care
- medicines have limited role as problem is mechanical
- aortic valve replacement surgery
- transcatheter aortic valve implantation (TAVI)
93
What are the indications for intervention for aortic stenosis?
Any symptomatic patient with severe AS.
Any patient with decreasing EF (ejection fraction).
Any patient undergoing CABG with moderate or severe AS
Consider intervention if adverse features on exercise testing in asymptomatic patients with severe AS
94
What are the risk factors for aortic stenosis?
- age >60yrs
- congenitally bicuspid aortic valve
- rheumatic heart disease
- chronic kidney disease (up to 55% of patients on dialysis have aortic valve calcification)
95
What is mitral regurgitation?
Backflow of blood from the LV to the LA during systole.
Mild MR is seen in 80% of normal individuals.
96
What are the causes of mitral regurgitation?
- Myxomatous degeneration
- Ischaemic MR
- Rheumatic heart disease
- Infective endocarditis
- Cardiac trauma
97
What is the pathophysiology of MR?
Symptoms are caused by pure volume overload of the heart.
- compensatory mechanisms: left atrial enlargement, lVH and increased contractility
- progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension
- progressive left ventricular volume overload leads to dilatation and progressive heart failure
98
What are the clinical manifestations of MR?
- pansystolic murmur at the apex radiating to the axilla
- Exertion dyspnoea
- heart failure
99
How is mitral regurgitation diagnosed?
ECG (LA enlargement , AF, LVH with severe MR)
also: CXR, echocardiogram
100
What is the management for MR?
- rate control medication for AF (B-blockers, CCBs, digoxin)
- anti-COAGs in AF and flutter
- nitrates/diuretics in acute MR
- chronic HF Rx if chronic MR with CCF
- reparative surgery is indicated with any symptoms at rest or on exercise
101
What is normally the length of the compensatory phase in mitral regurgitation?
10-15 years
102
What is aortic regurgitation?
Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps.
103
What are the causes of aortic regurgitation?
Bicuspid aortic valves, rheumatic heart disease, infective endocarditis
104
What is the pathophysiology of aortic regurgitation?
Asymptomatic until the 4th or 5th decade with gradual progression.
Combined pressure and volume overload.
Compensatory mechanisms (LV dilation, LVH, progressive dilation leads to heart failure)
105
What are the clinical manifestations of AR?
- Wide pulse pressure
- palpitations
- Hyperdynamic and displaced apical impulse
On auscultation:
- Diastolic blowing murmur at the left sternal border
- Austin flint murmur (apex): regurgitant jet impinges on anterior MVL (mitral valve leaflet) causing it to vibrate
- Systolic ejection murmur (due to increased flow across the aortic valve)
106
What is the gold standard investigation for AR?
Echocardiogram (evaluation of AV and aortic root with measurements of LV dimensions and function)
107
What is the management for aortic regurgitation?
- consider IE prophylaxis
- medical: vasodilators (ACEIs indicated in CCF or HTN)
- surgical treatment if any symptoms at rest or on exercise
108
Define mitral stenosis
The obstruction of inflow that prevents proper filling during diastole
109
What are the causes of MS?
Rheumatic heart disease (77-99%)
Infective endocarditis
Mitral annular calcification
110
What is the pathophysiology of MS?
LA dilation leading to pulmonary congestion (reduced emptying).
increased transmitral pressures lead to left atrial enlargement and atrial fibrillation.
111
What are the clinical manifestations of MS?
- progressive dyspnoea
- prominant "a" wave in jugular venous pulsation
- signs of right-sided heart failure (advanced disease)
- mitral facies
- diastolic murmur on auscultation
112
What are the investigations for mitral stenosis?
1st line: ECG
Gold standard: Echo (assesses mitral valve mobility, gradient and mitral valve area)
other : CXR (LA enlargement and pulmonary congestion)
113
What is the management for mitral stenosis?
- Medicine cannot prevent progression but BBs, CCBs and digoxin are used to control HR and prolong diastole for improved diastolic filling.
- Diuretics are also used to treat fluid overload
- Percutaneous mitral balloon valvotomy, if not possible MV replacement considered (any symptomatic patient with symptoms at rest, or on daily activity-level exertion)
- IE prophylaxis
114
What is infective endocarditis?
- Infection of the heart valve/s or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc.)
- Alongside the infection it causes infectious emboli to travel through the bloodstream.
115
What are the types of infective endocarditis?
- Left-sided native IE (mitral or aortic)
- Left-sided prosthetic IE
- Right-sided IE
- Device related IE (pacemakers, defibrillators..)
- Prosthetic
116
What are the causes of infective endocarditis?
- Abnormal valves; regurgitant or prosthetic valves are most likely to get infected
- Infectious material introduced to bloodstream or directly onto the heart during surgery
- Previous infective endocarditis
117
What are the risk factors for IE?
- age
- IV drug abuse
- congenital heart disease
- prosthetic heart valves
118
What is the pathophysiology of IE?
IE typically develops on the valvular surfaces of the heart which are subject to turbulent blood flow causing endothelial damage. This results in the adherence of platelets and fibrin to the collagen surface creating a pro-thrombotic environment.
Bacteraemia leads to colonisation of the thrombus and perpetuates further fibrin deposition and platelet aggregation, so a mature infected vegetation develops.
119
What are the key presentation for IE?
dependent on site, organism, etc.
- signs of systemic infection (fever, sweating)
- embolisation (stroke, PE, bone infections, kidney dysfunction, MI)
- valve dysfunction (heart failure, arrhythmia)
120
Signs of IE?
- Petechiae, splinter haemorrhages, Osler's nodes, Janeway lesions, Roth spots
121
What is the 1st line investigation for IE?
Trans-thoracic echocardiogram (TTE)
122
What is the treatment for IE?
- Antibiotics/antimicrobials
- Cardiac surgery to remove infectious material and /or repair the damage (if the infection is not cured with antibiotics)
- Treatment of other complications
123
What is defined as tachycardia?
heart rate >100 bpm
124
What are 5 examples of tachycardia?
- Atrial fibrillation
- Atrial flutter
- Supraventricular tachycardia
- Ventricular tachycardia
- Ventricular fibrillation
125
What is the definition of bradycardia?
Heart rate <60 bpm
126
What is Mobitz type I?
PR interval gradually increases until AV node fails completely and no QRS wave is seen.
Then starts all over again and PR gradually lengthens.
127
What is Mobitz type II?
Sudden unpredictable loss of AV conduction and loss of QRS. Due to loss of conduction in Bundle of His and Purkinje fibres.
128
How does hyperkalaemia present on ECG?
Tall T waves, flattening of P waves, broadening of QRS...eventually 'sine wave pattern'
129
How does hypokalaemia present on ECG?
Flattening of T wave, QT prolongation
130
How does Hypercalcaemia present on ECG?
QT shortening
131
How does hypocalcaemia present on ECG?
QT prolongation
132
How does first degree AV block present on ECG?
PR interval > 0.2s
Can be a sign of CAD, acute rheumatic carditis, digoxin toxicity or electrolyte disturbance but does not usually require treatment
133
How does second degree heart block present on ECG?
Intermittent absence of QRS complexes - indication that there is a blockage somewhere between the AV node and the ventricles.
3 types:
- Mobitz type 2
- Mobitz type 1 (Wenckebach)
- 2:1 and 3:1 conduction
134
How does 3rd degree (complete) heart block present on ECG?
Atrial contraction is normal but no beats are conducted to the ventricles. The ventricles are still excited by their own internal 'ectopic pacemaker' system so both P waves and QRS complexes are seen on ECG but with no relationship between them. QRS is generally broad (160ms)
135
What is 2:1 and 3:1 conduction?
One normal cycle followed by one cycle with an absent QRS (2:1) or one normal cycle, then 2 cycles without a QRS (3:1)
136
What are ectopic beats?
Non-sustained beats arising from ectopic regions of atria or ventricles.
137
What is heart failure?
Inability of the heart to deliver oxygenated blood to tissues at sufficient rate for the tissue's metabolic requirements, despite normal or increased cardiac filling pressures.
138
What is the most common cause of heart failure?
Ischaemic heart disease
139
What are other causes of HF?
- hypertension
- alcohol excess
- cardiomyopathy (primary disease of the heart muscle)
- valvular
- endocardial
- pericardial causes
140
What are the risk factors for HF?
- age >65 yrs
- smoking
- obesity
- previous MI
- male
- alcohol excess
141
What are the categories of the NY Heart Association Classification?
1 - No limitation (asymptomatic)
2 - Slight limitation (mild HF)
3 - Marked limitation (symptomatically moderate HF)
4 - Inability to carry out any physical activity without discomfort (symptomatically severe HF)
142
What is the treatment for HF?
- lifestyle modification (↓BMI, exercise, stop smoking and reduce alcohol)
- ACE-i + B blocker for all patients
+ Spironolactone + furosemide
+ Consider cardiac resynchronisation therapy (improves AV coordination)
- Surgery = consider revascularisation, valve surgery, heart transplant (last resort)
143
What is the gold standard investigation for heart failure?
abnormal ECG (e.g. evidence of LVH)
144
What are the key presentations of heart failure?
Non-specific signs of cardiac disease: SOB, ankle swelling, fatigue
Also: orthopnoea, oedema, 3rd + 4th heart sounds, bibasal crackles, hypotensive, tachycardia
145
What causes 3rd degree (complete) heart block?
MI - can be transient
Chronic - often due to fibrosis around the bundle of His or BBB of both branches
Always indicates underlying disease - more often fibrosis than ischaemia.
146
What is a BBB?
A complete or partial interruption of the electrical pathways inside the wall of the heart between the ventricles.
147
What are the causes of BBB?
- blood clots in the lungs
- chronic lung disease e.g. COPD
- cardiomyopathy
- heart wall defects
148
What happens in RBBB?
The R bundle is not working so the electric signals to the right ventricle are blocked and so the left ventricle contracts just before the right ventricle.
149
What is the presentation of RBBB on ECG?
Wide QRS complexes (>120ms)
RSR 'M' pattern in leads V1-V3
Slurred S waves in leads I, aVL and often V5 and V6
*MaRRoW*
150
What is the presentation of LBBB on ECG?
Wide QRS complexes (>120ms)
Absence of Q wave in leads I, V5 and V6
Monomorphic R wave in I, V5 and V6
ST and T wave displacement opposite to the major deflection of the QRS complex
*WiLLiaM*
151
How can you quickly diagnose RBBB from LBBB on ECG?
LBBB: QRS widened and downwardly deflected in V1
RBBB: QRS widened and upwardly deflected in lead V1
152
What is peripheral vascular disease?
A range of symptoms caused by atherosclerotic obstruction of the lower extremity arteries.
153
What is the most common cause of PVD?
Atherosclerosis
154
What are the risk factors for PVD?
- Smoking
- diabetes mellitus
- hypertension
- hyperlipidaemia
- age >40yrs
- history of CAD, CVD, sedentary lifestyle, CKD, T2DM
155
What are the key presentations of PVD?
Most often asymptomatic, intermittent claudication, diminished/absent pulse
156
What is the 1st line investigation for PVD?
Ankle-brachial index
157
What is the management for PVD?
Intermittent claudication: RF management
Chronic limb ischaemia: revascularization surgery (PCI if small, bypass if larger)
Acute limb threatening ischaemia: surgical emergency - revascularization within 4-6 hours other very high amputation risk
158
What are the 3 presentations of PVD?
Intermittent claudication (least severe)
Chronic critical limb ischaemia
Acute limb ischaemia
159
What are the 6 Ps that indicate limb-threatening ischaemia?
Pulselessness, Pallor, Pain, Persisting cold, Paralysis, Paraesthesia (the more that are present, the more limb threatening)
160
What is atrial fibrillation?
irregularly irregular atrial firing rhythm
161
What are the causes of AF?
Heart failure, hypertension, secondary to mitral stenosis, sometimes idiopathic
162
What are the risk factors for atrial fibrillation?
Age 60+, T2DM, hypertension, valve defects, history of MI
163
What is the pathophysiology of AF?
Rapidly firing ectopic foci (300-600bpm firing rate) cause atrial spasm, this causes atrial blood to pool instead of pumping effectively to ventricles --> decreased CO and increased risk of thromboembolic events
164
What are the key presentations of AF?
Palpitations, irregularly irregular pulse, thromboemboli, chest pain, syncope, hypotension
165
What is the gold standard investigation for AF?
ECG (irregularly irregular pulse with normal QRS and no P waves)
166
What is the management of acutely unstable AF?
DC synchronised cardioversion
167
What is the management for stable, long-term AF?
Rate: BB/CCB + oral anticoag.
Rhythm: cardioversion (DC or pharmacological) + warfarin
Surgical: radiofrequency ablation
168
What is hypertrophic cardiomyopathy?
Genetic disease of the cardiac sarcomere, caused by mutations in genes that encode for different components of the contractile apparatus.
169
How can aortic stenosis lead to heart failure?
The narrowing of the aortic valve means increases the load on the left ventricle and means that it has to work harder to pump blood out of the heart. This results in left ventricular hypertrophy so the muscle is enlarged and weakened which leads to heart failure if not resolved.
170
What is pulmonary embolism?
A life-threatening condition which occurs when a blood clot gets stuck in an artery in the lung, blocking blood flow to part of the lung. This can result in right heart failure and cardiac arrest if not treated.
171
What are the risk factors for PE?
Increasing age
DVT
Obesity
Surgery within last 2 months
Bed rest >5 days
Previous venous thromboembolic event
FHx
Malignancy
172
What is the pathophysiology of PE?
Most often caused as a result of DVT where the clot moves from the legs and travels up through the right side of the heat and passes into the lungs where it sticks and prevents blood flow. This obstruction increases pulmonary vascular resistance, increasing the work of the right ventricle. The right ventricle compensates by increasing the heart rate (Frank-starling mechanism) which leads to over distension of the right ventricle, increased RV end-diastolic pressure and decreased RV cardiac output. Decreased RV output leads to decreased left ventricular preload. As LV filling and cardiac output decrease, low mean arterial pressure progressed to hypotension and shock.
173
What are the key presentations of PE?
Breathlessness
Pleuritic chest pain
sign/symptoms of DVT
tachycardia
tachypnoea
pleural rub
174
What investigations are used for PE?
ECG (sinus tachycardia)
Blood gases (type 1 resp failure, ↓O2 and CO2)
CXR, D-dimer, CT pulmonary angiogram (CTPA) spiral CT with contrast
175
What is the management for PE?
Supportive treatment
LMW Heparin s/c
Oral warfarin INR 2-3
DOAC (direct oral anticoag) e.g. rivaroxaban, apixaban
Treat underlying cause
In emergency scenario: catheter mechanico-chemical thrombectomy or surgical thrombo-embolectomy
176
What is the Wells score?
A number reflecting a patient's risk of developing DVT which is calculated by a points system according to the risk factors and symptoms the patient has.
1< likely DVT
4< likely PE
177
What is rheumatic fever?
An autoimmune condition triggered by strep. bacteria and caused by antibodies created against the bacteria which also target tissues in the body.
It is a multisystem disorder affecting the joints, heart, skin and nervous system.
178
What are the risk factors for RF?
Poverty
Overcrowded living conditions
FHx rheumatic fever
HLA association
Genetic susceptibility
179
What is the pathophysiology of RF?
Caused by group A beta-haemolytic streptococci, typically S. pyogenes causing tonsillitis. The immune system creates antibodies to fight the infection and these antibodies not only target the bacteria but also match antigens on the cells of the person’s body. This results in a type 2 hypersensitivity reaction where the immune system begins attacking cells throughout the body
180
What are the key presentations of RF?
Fever
Joint pain (migratory arthritis affecting the large joints)
Rash (erythema marginatum = pink rings on torso and proximal limbs)
SOB
Chorea (sudden, uncontrollable jerking of limbs and facial muscles)
Nodules (on surfaces of joints)
Carditis (inflammation of the heart) → tachycardia/bradycardia, murmurs, pericardial rub, heart failure
181
What is the Jones criteria for RF diagnosis?
Jones criteria for diagnosis:
Evidence of recent strep. Infection +
Two major criteria (Joint arthritis, Organ inflammation (carditis), Nodules, Erythema marginatum rash, Sydenham chorea)
OR
One major criteria plus two minor criteria (Fever, ECG changes without carditis, Arthralgia without arthritis, Raised inflammatory markers)
182
What are the investigations for RF?
Throat swab
ASO antibody titres (Anti-strep)
Echo, ECG + CXR
183
What is the management for RF?
Antibiotics (penicillin V)
NSAIDs for joint pain
Aspirin and steroid for carditis
Prophylactic antibiotics
Haloperidol for chorea
Monitoring and management of complications
184
What is shock?
life-threatening, generalised form of acute circulatory failure with inadequate oxygen delivery to, and consequently oxygen utilisation by, the tissues and creates risk of organ dysfunction.
185
What are the key presentations of shock?
Weak, rapid pulse
Confusion
Reduced GCS (glasgow coma scale)
Decreased urine output
Pale, clammy skin
Increased capillary refill time
Prolonged hypotension
186
What are the 5 types of shock?
Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic
187
What causes hypovolemic shock?
Blood or fluid loss.
Usually result of trauma, GI bleed, dehydration
188
What is the treatment for hypovolemic shock?
ABCDE, give O2 and IV fluids
189
What are the key symptoms of hypovolemic shock?
hypotension, tachycardia, pale, clammy skin, confusion
190
What causes septic shock?
Uncontrolled bacterial infection
191
What are the symptoms of septic shock?
pyrexic, warm peripheries, bounding pulse, tachycardia
192
What is the treatment for septic shock?
ABCDE, broad spectrum antibiotics (broad spec e.g. piperacillin/tazobactam, ceftriaxone)
193
What causes cardiogenic shock?
Heart pump failure usually as a result of MI, cardiac tamponade, PE
194
What are the key symptoms of cardiogenic shock?
Signs of heart failure (oedema), ↑JVP, S4
195
What is the treatment for cardiogenic shock?
ABCDE + treat underlying cause
196
What causes anaphylactic shock?
IgE mediated Type 1 hypersensitivity reaction to allergen, histamine release → causes excess vasodilation and bronchoconstriction
197
What are the key symptoms of anaphylactic shock?
hypotension, tachycardia, urticaria, puffy face, flushed cheek
198
What is the treatment for anaphylactic shock?
ABCDE + IM adrenaline
199
What causes neurogenic shock?
spinal cord trauma e.g. RTA, disrupted SNS but intact PSNS
200
What are the key symptoms of neurogenic shock?
hypotension
bradycardia
confusion
hypothermia
201
What is the treatment for neurogenic shock?
ABCDE + IV atropine (blocks vagal tone, allows more PSNS inhibition, more chance for SNS to work)
202
What is cardiomyopathy?
disease of the myocardium
203
What are the 3 types of cardiomyopathy?
Hypertrophic, Dilated, Restrictive
204
What causes hypertrophic cardiomyopathy?
Autosomal dominant mutation of sarcomere protein (troponin T, myosin B) (+exercise +aortic stenosis) results in a thick non-compliant heart --> impaired diastolic filling --> ↓CO
205
What are the symptoms of hypertrophic cardiomyopathy?
can present as sudden death, otherwise chest pain, palpitations, SOB, syncope
206
What are the investigations for hypertrophic cardiomyopathy?
confirm w/ abnormal ECG, ECHO (GS) + genetic testing
207
What are the treatments for hypertrophic cardiomyopathy?
BBs, CCBs, amiodarone (anti-arrhythmic)
208
What causes dilated cardiomyopathy?
Autosomal dominant mutation of cytoskeleton gene (+IHD +alcohol) leads to thin cardiac walls which contract poorly -->↓CO
209
What are the symptoms of dilated cardiomyopathy?
SOB, heart failure, atrial fibrillation, thromboemboli
210
What is used to diagnose dilated cardiomyopathy?
ECG, ECHO
211
What is the treatment for dilated cardiomyopathy?
treat underlying conditions e.g. AF, heart failure
212
What causes restrictive cardiomyopathy?
Granulomatous disease (sarcoidosis, amyloidosis), idiopathic, post-MI fibrosis
- Leads to rigid fibrotic myocardium, fills and contracts poorly → ↓CO
213
What are the symptoms of restrictive cardiomyopathy?
severe; dyspnoea, S3 +S4 sounds, oedema, congestive HF, narrow PP
214
What are the diagnostic tests for restrictive cardiomyopathy?
ECG, ECHO, cardiac catheterisation (definitive)
215
What is the treatment for restrictive cardiomyopathy?
none, consider transplant (Px typically die within 1yr)
216
Where is BNP secreted from?
B-type natriuretic peptide is mainly secreted by the ventricular myocardium in response to strain
217
What is raised BNP an indicator of?
Heart failure most commonly
Can also indicated myocardial ischemia or valvular disease
218
What are teh effects of BNP?
Vasodilation
Diuretic and natriuretic
Suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
219
What creates the first heart sound (S1)?
Closing of the atrioventricular valves (tricuspid + mitral) at the start of the systolic contraction of the ventricles
220
What creates the second heart sound (S2)?
Closing of the semilunar valves (pulmonary and aortic) once the systolic contraction is complete.
221
What creates the third heart sound (S3)?
rapid ventricular filling which causes the chordae tendinae to pull their full length and twang like a guitar string (can be normal in young people due to good heart function but in older patients can indicates heart failure)
222
What causes the 4th heart sound (S4)?
Heard directly before S1 and is always abnormal - indicates a stiff or hypertrophic ventricle and is caused by turbulent flow from an atria contracting against a non-compliant ventricle.
223
Where is the stethoscope placed to listen for pulmonary murmurs?
2nd intercostal space left sternal border
224
Where is the stethoscope placed to listen for aortic murmurs?
2nd intercostal right sternal border
225
Where is the stethoscope placed to listen for tricuspid murmurs?
5th intercostal space left sternal border
226
Where is the stethoscope placed to listen for mitral mumurs?
5th intercostal space mid clavilcular line (apex area)
227
What is Erb's point?
The best place to listen for S1/S2, located in the third intercostal space on the left sternal border.
228
What are the heart sounds?
S1 = mitral + tricuspid close
S2 = aortic + pulmonary close
S3 = shows rapid ventricular filling in early diastole (normal in young/pregnant, abnormal in mitral regurg + heart failure)
S4 = pathological "gallop" - due to blood forced into stiff hypertrophic ventricle (LVH + aortic stenosis)
229
What is the CHA2-DS2-VASc scoring system?
Tool used to assess starting anticoagulation in patients with stroke risk due to atrial fibrillation
230
What is the ABCD2 screening tool used for?
Estimation of stroke risk after a suspected TIA
231
What is the HAS-BLED screening tool used for?
Estimates risk of bleeding in patients on anticoagulation
232
What is Well's criteria used for?
estimates risk of pulmonary embolism in clinical presentation
233
What is the treatment for myocarditis?
treat underlying cause e.g. antibiotics if bacterial cause
supportive treatment e.g. of heart failure or arrhythmias
234
What are some potential complications of myocarditis?
heart failure
arrhythmia, possibly leading to sudden death
dilated cardiomyopathy - usually a late complication
235
Phase 2A
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