1
Q
How are atherosclerotic plaques distributed?
A
- found in peripheral and coronary arteries
- focal distribution (small area) along artery length
- change in flow alters endothelial cell function
- wall thickness changed leading to neointima (scar tissue)
- altered gene expression in key cell types
2
Q
What are fatty streaks and when do they appear?
A
- earliest type of lesion < 10 years
- aggregations of lipid laden macrophages and T lymphocytes in the intimal layer of the vessel wall
3
Q
What is an intermediate lesion?
A
- no symptoms and walled off
- foam cells and T lymphocytes
- vascular smooth muscle cell proliferation from media > intima
- adhesion and aggregation of platelets to vessel wall
4
Q
What is a fibrous plaque?
A
- impedes blood flow
- prone to rupture
- covered by dense fibrous cap made of ECM proteins inc collagen, elastin overlying lipid core and necrotic debris
- may experience symptoms e.g. angina
5
Q
Describe plaque rupture
A
- Plaques grow and recede
- fibrous cap is resorbed and redeposited in order to be maintained
- if balance shifts in favour of inflammatory conditions, cap becomes weak and plaque ruptures
6
Q
What is the difference between red and white thrombus?
A
- Red: contains red blood cells and fibrins
- White: platelets and fibrinogen
7
Q
What drugs are commonly used in treatment of atherosclerosis?
A
- aspirin
- clopidogrel/ticagrelor - inhibits P2Y12 ADP receptor on platelets
- statins: reduce cholesterol synthesis by inhibiting HMG CoA reductase
8
Q
How is acute MI diagnosed?
A
- ST elevation MI can be diagnosed on ECG
- Non ST elevation MI is diagnosed retrospectively made after troponin results
9
Q
What are the 3 acute coronary syndromes?
A
- STEMI: ST elevation MI
- NSTEMI: Non-ST elevation MI
- Unstable angina: prolonged, severe angina, usually at rest possibly with ECG changes
10
Q
Describe unstable angina:
- occlusion
- infarction
- ECG
- troponin
A
- partial occlusion of minor coronary artery
- no infarction: ischaemia only
- normal ECG, may show ST depression or T wave inversion
- normal troponin
11
Q
Describe NSTEMI:
- occlusion
- infarction
- ECG
- troponin
A
- partial occlusion of major coronary artery/total occlusion of minor coronary artery
- sub endothelial infarction so area distal to occlusion dies
- ST depression, T wave inversion, new LBBB
- elevated troponin
12
Q
Describe STEMI:
- occlusion
- infarction
- ECG
- troponin
A
- total occlusion of major c.a.
- transmural infarction (full thickness of myocardium)
- ST elevation in local leads,
- elevated troponin
13
Q
What are the causes of ACS?
A
- most common: rupture of an atherosclerotic plaque + consequent arterial thrombosis
14
Q
What are the risk factors for ACS/IHD?
A
- age
- smoking
- family history
- diabetes
- hyperlipidaemia + htn
- obesity
- stress
- male 1.5:1
15
Q
What are the symptoms of MI?
A
- unremitting cardiac chest pain radiating to left arm, neck, jaw (crushing/squeezing)
- usually severe but may be mild or absent
- associated with sweating, breathlessness, nausea/vomiting
- dyspnoea
16
Q
What are the symptoms of unstable angina and how can it be diagnosed?
A
- cardiac chest pain at rest, with crescendo pattern
- new onset angina
- diagnosed by history, ECG and troponin
17
Q
What is the first line investigation for ACS?
A
12 lead ECG
18
Q
What is seen on an ECG after an MI?
A
- hyperactive T waves
- pathologically steep Q waves
- LBBB (left bundle branch block - electrical impulse disrupted) (prolonged QRS complex)
19
Q
What is the gold standard investigation for ACS?
A
CT coronary angiogram
20
Q
How is ACS managed?
A
- MONAC if acute
- coronary reperfusion: PCI (<12h) or thrombolysis w alteplase (>12h)
- patient should be given aspirin, β blocker
- 2nd antiplatelet agent e.g. clopidogrel
- atorvastatin + ACEi
21
Q
What should patients be offered for secondary prevention of ACS/stable angina?
A
- lifestyle advice firstly
- ACE inhibitor/ARB
- β blocker
- dual anti platelet therapy
- statin
22
Q
How are MIs managed?
A
- oxygen therapy if hypoxic
- pain relief (opiates/nitrates)
- Aspirin (and maybe P2Y12 inhibitor)
- potentially β blocker, antianginal therapy, angoigraphy
23
Q
What is troponin?
A
- protein complex regulating actin:myosin contraction
- highly sensitive marker of cardiac muscle injury
- may not represent permanent muscle damage
24
Q
What is the pathophysiology of stable angina?
A
- oxygen supply ≠ demand
- most commonly attributed to IHD
- impairment of blood flow by proximal arterial stenosis
- increased distal resistance
- reduced oxygen carrying capacity of the blood
25
What are the criteria for stable angina?
- central crushing chest pain radiating to neck/jaw
- brought on with exertion e.g. walking up hill, cold weather, heavy meal
- relieved with 5 mins rest/ GTN spray
26
What are the symptoms of stable angina?
- central crushing chest pain radiating to neck/jaw (worsens with time)
- nausea
- sweating
- fatigue
- dyspnoea
27
What is the gold standard investigation for stable angina?
CT coronary angiography to highlight any narrowing
28
What is the management strategy for immediate symptomatic relief of angina?
- GTN spray used as required to cause vasodilation and ease symptoms
- a second dose is taken after 5 mins if pain hasn't subsided
- call an ambulance after another 5 mins if pain hasn't gone
29
What medications are used for long term symptomatic relief of angina?
- β blockers (contraindicated by asthma)
- calcium channel blockers (CCB)
- lifestyle changes
30
How do calcium channel blockers work and in which disease are they contraindicated?
- reduce afterload
- relax smooth muscle cells in arterial walls
- contraindicated by heart failure
31
What is a CABG?
- coronary artery bypass graft
- for multi vessel disease
- a graft vein is taken from the leg (usually great saphenous vein) or internal mammary artery and sewn on to bypass the stenosis
32
What is PCI?
- Percutaneous coronary intervention with coronary angioplasty
- putting a catheter into the brachial or femoral artery
- contrast injected so stenosis is evident
- balloon stent can be inserted
33
Describe the anatomy of the pericardium
- great vessels lie within pericardium
- 2 layers are continous
- LA is mainly outside pericardium
- parietal layer uses fibrous attachments to fix heart in thorax
34
What is acute pericarditis?
- an inflammatory pericardial syndrome with or without effusion
35
What factors are used in diagnosis of acute pericarditis and how many factors are needed?
- diagnosis made with 2 of 4 factors:
- chest pain
- friction rub
- ECG changes
- pericardial effusion
36
What is the epidemiology of pericarditis?
- 80-90% is idiopathic + seasonal with viral trends
- higher in young, previously healthy patients
37
What are the infectious causes of pericarditis?
- MAINLY viral: enteroviruses, herpesviruses (EBV, CMV, HHV-6), adenoviruses
- bacterial: mycobacterium tuberculosis
38
What are the non-infectious causes of pericarditis?
- autoimmune: Sjogren, rheumatoid arthritis, scleroderma
- neoplastic (most common): secondary metastatic tumours
- trauma (most common): PCI, pacemaker insertion
- other (rare): amyloidosis, aortic dissection
39
How does pericarditis present?
- severe chest pain, sharp and pleuritic (not constricting + crushing like IHD)
- KEY: **relieved by sitting forward and exacerbated by lying down**
- rapid onset
- left ant chest/epigastrium
- breathlessness, coughing, hiccups
40
How can pericarditis be investigated?
- pericardial rub: heard around 2nd heart sound, sounds like crunching snow
- ECG, bloods, CXR, Echo
41
What is seen on the ECG in pericarditis?
- PR depression
- concave (saddle shaped) ST elevation
- similar ECG to acute STEMI
42
Describe the management of pericarditis
- restricting physical activiity
- NSAIDs + PPIs
- colchicine
- 2nd line: corticosteroids if NSAIDs or colchicine fail
43
What is cardiomyopathy and what is hypertrophic cardiomyopathy the cause of?
- disease of the heart muscle
- caused by autosomal dominant mutation of sarcomeric protein genes
- HCM = most common cause of sudden cardiac death in young people
44
What is the pathology behind HCM?
- thickening of the cardiac muscle leads to impaired filling of the ventricles (esp LV)
- this leads to decreased cardiac output
- can lead to diastolic heart failure
- may be white areas of fibrosis/scarring of the heart muscle + septum becomes asymmetrically thickened
- patients with troponin T mutation at greatest risk
45
What are the risk factors for HCM?
- young + asymptomatic
- family history of sudden cardiac death
- history of arrhythmia
- playing competitive sport
46
How does HCM present?
- exertion chest pain, dyspnoea
- palpitations
- fatigue
- exertion syncope: suggests LV outflow tract obstruction
47
What is seen on ECG for HCM?
- diagnosed by ECG: sharp, deep Q waves > 40ms
- wide P waves
- T wave inversion
48
How is HCM managed?
- control arrhythmias with amiodarone
- control LV function: β blockers and verapamil
49
What is the cause of dilated cardiomyopathy?
- cytoskeletal gene mutations
- enlarged ventricular size and systolic dysfunction
- thin cardiac muscle walls contract poorly > dec CO
50
How does DCM present?
- dyspnoea
- fatigue
- peripheral oedema
- loud 3rd and 4th heart sounds
51
How is DCM diagnosed?
- ECG: sinus tachycardia, T wave inversion, ST depression, LBBB
- CXR: enlarged heart, pleural effusion
52
How is DCM managed?
- treat reversible causes
- prophylactic anticoagulation
- consider pacemaker
- treat as heart failure
53
What is restrictive cardiomyopathy?
- reduced compliance of ventricular walls during diastolic filling
- Commonly affects the LV, but can often affect both.
- Causes high diastolic filling pressures > pulmonary hypertension
- reduced CO
54
What are the symptoms of RCM?
- dyspnoea
- fatigue
- pulmonary oedema
- loud 3rd heart sound
- AF in 75% of patients
55
How is restrictive cardiomyopathy diagnosed and managed?
- ECG: T wave and ST changes, pathological Q waves
- echocardiogram: may have dilated atria or myocardial hypertrophy
- no treatment, maybe transplant
56
What is tetralogy of fallot and its 4 features ?
- key issue: interior dislocation of the septum which partially obstructs RVOT and PA
1. ventricular septal defect: leading to equal ventricular pressures
2. pulmonary stenosis
3. overriding aorta
4. RV hypertrophy
57
What is the presentation of tetralogy of fallot?
- cyanosis
- dyspnoea on feeding, crying, exertion
- failure to thrive
- murmur
- fallot spells: sudden onset dyspnoea/cyanosis
- inc venous return to RV and severe spells > death
58
How is tetralogy of fallot managed?
- VSD patched
- PV widened or replaced
59
What is a ventricular septal defect?
- most common form of congenital heart disease
- malformation of ventricular septum
- if LV pressure > RV then blood flows LV to RV
- inc blood flow through lungs
60
How does a VSD present?
- loud systolic murmur
- severe: breathlessness, poor feeding, failure to thrive, tachycardia
- mild: small inc in pulmonary blood flow, endocarditis risk, asymptomatic
61
How is a VSD diagnosed and managed?
- gold standard: echocardiogram
- CXR, ECG
- percutaneous/open heart surgery, patch application
62
What is an atrial septal defect?
- congenital heart defect causing a shunting of blood from L to R atria
- inc flow into right heart and lungs
- secundum ASD: patent foramen ovale
- leads to right heart dilation in severe
63
How does an ASD present?
- pulmonary flow murmur
- split S2 heart sound due to delayed closure of PV and inc blood volume
- big pulmonary arteries and heart on CXR
64
What is an atrio-ventricular septal defect (AVSD)?
- Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves
- Can be complete or partial
65
What is a patent ductus arteriosus (PDA)?
- Persistence of the connection between the aorta and pulmonary artery
- normally rise in PaO2 and decline in prostaglandins close the duct
66
How does a patent ductus arteriosus present?
- tachycardia and tachypnoea
- continuous murmur at left sternal edge
- failure to thrive
- poor feeding
- risk of endocarditis
67
How is PDA diagnosed and managed?
- diagnosis: echocardiogram
- management: usually closed via cardiac catheterisation
68
What is coarctation of the aorta and how does this present in severe and mild patients?
- narrowing of the aorta at the site of the ductus arteriosus
- presents with htn and murmur
69
How does coarctation of the aorta present?
- right arm hypertension
- bruits over scapulae and back
- murmur
70
How is coarctation of the aorta managed?
- repaired by surgical or percutaneous intervention - narrow section removed
71
What is an abdominal aortic aneurysm and what is the pathophysiology?
- permanent dilation of the abdominal aorta with a diameter of more than 3cm
- mostly originate below the renal arteries
- smooth muscle, elastic and structural degeneration in all 3 layers of the vascular tunica
72
What are the risk factors for an AAA/TAA?
- men more than women, and at a younger age
- smoking
- hypertension
- family history
- existing CVD
73
What is the aetiology of AAAs?
- coarctation of the aorta
- Marfan's syndrome
- aortic surgery
- 3rd trimester pregnancy
74
How does AAA present?
- mostly asymptomatic and detected on rupture
- non-specific abdominal pain
- Pulsatile and expansile mass in the abdomen when palpated with both hands
- incidental finding on x-ray, ultrasound or CT
75
What is the diagnostic investigation for AAA?
ultrasound then CT angiogram to guide elective surgery
76
How are AAAs managed?
- treating reversible risk factors
- screening yearly/3 monthly
- surgical: artificial graft: open repair or EVAR (endovascular aneurysm repair) stent
77
How do TAAs present?
- dilation of thoracic aorta = asymptomatic
- chest or back pain
- trachea/L bronchus compression > cough, shortness of breath, stridor
- same nerve compressions as pericardial effusion
78
How do ruptured aortic aneurysms present?
- severe chest/back pain (TAA)
- abdo pain radiating to back/groin (AAA)
- haemodynamic instability
- collapse
79
How are ruptured aortic aneurysms treated?
- permissive hypotension to decrease blood loss
- immediate surgery
80
What is pericardial effusion?
- collection of excess fluid in the pericardial sac
- can be acute or chronic
- transudates, exudates, blood, pus, gas
- creates inward pressure on heart making it more difficult to expand during diastole
81
What causes pericardial effusion?
- Transudative: congestive heart failure, pulmonary htn
- Exudative: infection, autoimmune, injury to pericardium
- rupture > tamponade: MI, trauma, aortic dissection
82
How does pericardial effusion present?
- chest pain
- SOB and orthopnoea
- fullness in chest
- quiet heart sounds
- pulsus paradoxus
83
What nerve compressions cause which symptoms in pericardial effusion?
- phrenic nerve compression > hiccups
- oesophageal compression > dysphagia
- recurrent laryngeal > hoarse voice
84
What is cardiac tamponade?
- the pericardial effusion is large enough to raise the intra-cardiac pressure
- inc pressure leads to reduced filling during diastole and decreased CO during systole
85
How is pericardial effusion diagnosed?
- Echo: diagnose and assess size and effect on heart function
- fluid analysis: protein content, bacterial, viral, tumour markers
86
How is pericardial effusion managed?
- treatment of underlying cause: aspirin, NSAIDs, colchicine, steroids
- drainage: needle pericardiocentesis or surgical drainage
87
What is a pulmonary embolism and what causes it?
- formation of a blood clot in pulmonary arteries
- usually results from DVT developed in leg, travelled through venous system and RHS of heart to PAs
- blocks blood flow to lungs and creates strain on RHS of heart
88
What are the risk factors for DVT/PE?
- immobility
- recent surgery
- long haul flights
- pregnancy
89
How does a PE present?
- shortness of breath
- cough ± haemoptysis
- pleuritic chest pain
- hypoxia
- tachycardia
- tachypnoea + breathlessness
- low grade fever
90
What is aortic stenosis and what are the 3 types and causes?
- narrowing of the aortic valve area
- symptoms occur when valve area is 1/4 of normal
- types: supravalvular, subvalvular, valvular
91
What is the pathophysiology of aortic stenosis?
- pressure gradient develops between LV and aorta (inc after load)
- LV function initially maintained by compensatory pressure hypertrophy
- LV function declines when compensatory mechanisms are exhausted
92
What are the symptoms of aortic stenosis?
- syncope
- angina
- dyspnoea
93
What are the signs of aortic stenosis?
- slow rising carotid pulse with decreased amplitude (little difference between systolic and diastolic)
- soft/absent 2nd heart sound, S4 aortic gallop
- crescendo descendo murmur
94
How is aortic stenosis investigated?
- GOLD: Echocardiogram: LV size and function, Doppler derived area and gradient
95
How is atrial stenosis managed?
- vasodilators fairly contraindicated
- aortic valve replacement, prosthetic requires anticoagulants (healthy patient)
- TAVI: trans catheter aortic valve implantation (less invasive)
96
What is mitral regurgitation and what causes it?
- back flow of blood from LV to LA during systole
- LV dilatation
- myxomatous mitral valve (mass of cells makes leaflets heavier
- rheumatic heart disease and infective endocarditis
97
What is the pathophysiology of MR?
- volume overload: need a larger SV to compensate for backflow
- compensatory mechanisms: left atrial enlargement, LV hypertrophy, increased contractility
- progressive LV overload > dilatation > heart failure
98
How does MR present?
- auscultation: apex beat is displaced downwards and laterally
- intensity of murmur correlates with severity
- S3 heart sound
- exertion dyspnoea
- heart failure (may coincide with inc haemodynamic burden)
99
What investigations are done for MR?
- ECG: LA enlargement, atrial fibrillation, LV hypertrophy
- CXR: LA and central PA enlargement
- GOLD: Echo: size estimation and valve structure
100
How is MR managed?
- rate control for AF: β blockers, CCB, digoxin
- anticoagulation for AF and flutter
- nitrates/diuretics
- valve replacement if serious
101
What is aortic regurgitation and what is its aetiology?
- leakage of blood back from aorta into LV during diastole due to ineffective coming together of aortic cusps
- bicuspid aortic valve
- rheumatic fever and infective endocarditis
102
What is the pathophysiology of aortic regurgitation?
- combined pressure and volume overload due to backflow of blood in addition to circulating blood
- leads to LV hypertrophy and dilatation. Progressive dilation > heart failure
103
How does aortic regurgitation present?
- wide pulse pressure
- early diastolic blowing murmur at 2nd intercostal space on R sternal border
- pulmonary oedema, pallor, sweating
104
How is aortic regurgitation investigated?
- GOLD: Echo: evaluate AV and aortic root, measure LV dimension and function
- CXR: enlarged cardiac silhouette
105
How is aortic regurgitation managed?
- IE prophylaxis as differential diagnosis
- ACEIs can improve SV and regurgitation
- surgical valve replacement
106
What is mitral stenosis and what causes it?
- obstruction of LV inflow preventing proper filling during diastole
- rheumatic carditis
107
What causes dyspnoea in mitral stenosis?
- progressive dyspnoea due to LA enlargement leading to pulmonary congestion
- inc transmitral pressures > LA enlargement and AF
108
How does mitral stenosis present?
- mitral facies: vasoconstriction causing pink/purple tinge on face
- low pitched diastolic rumble at apex
- loud S1
- opening snap after S2
109
How is mitral stenosis investigated?
- ECG: AF and LA enlargement
- CXR: LA enlargement and pulmonary congestion
- GOLD: Echo: mitral valve mobility, gradient, area
110
How is mitral stenosis managed?
- serial echocardiography
- β blockers, CCBs, Digoxin, diuretics
- percutaneous mitral balloon valvotomy
111
What is infective endocarditis?
- infection of heart valve(s) or other endocardial lined structures within the heart
- damages the valves + can cause heart failure
112
What are risk factors for infective endocarditis?
- rheumatic heart disease
- valvular degeneration/prosthetic valve
- IV drug use
113
What is the pathophysiology behind infective endocarditis?
- endocardial damage > thrombi formation made of platelets and fibrin
- valve cusps are avascular preventing normal immune response
- high pressure makes infection more likely
- thrombus is colonised by bacteria and these break off and travel round the bloodstream
- tricuspid most commonly affected due to first contact w blood from body
114
How does infective endocarditis present?
- fever and heart murmur
- haematuria (blood in urine)
- splinter haemorrhages
- Osler's nodes (nodules on digits)
- Janeway lesions (haemorrhages and nodules in fingers
- Petechiae (small purple spots)
- Roth spots (retinal haemorrhages)
- malaise
115
What is the Duke criteria?
- major: 2 +ve blood cultures, echo shows vegetation
- minor: immunological signs, septic emboli, 1 +ve culture, fever, IV drug user
- present if: 2 major criteria, 1 major & 3 minor or 5 minor
116
How is infective endocarditis investigated?
- Transthoracic echo for vegetations
- Raised CRP
- ECG: showing new heart block, ischaemia or infarction
- FBC, blood cultures, urinalysis
117
How is infective endocarditis managed?
- S. aureus: vancomycin + rifampicin
- S. viridian: benzylpenicillin + gentamicin
- surgery if valve incompetent
118
What is aortic dissection?
- tear in inner layer of aorta
- blood found between intima and media creating a false lumen
- MC in ascending aorta and aortic arch
119
What are some causes of aortic dissection?
- bicuspid aortic valve
- coarctation of aorta
- CABG
- Ehlers-Danlos/Marfan's syndrome
120
How is aortic dissection classified?
- R lateral area is most common site
- Type A: affects ascending aorta, before brachiocephalic artery
- Type B: descending aorta after L subclavian artery
121
What are the risk factors for aortic dissection?
- hypertension
- age
- male
- smoking
- poor diet
- low physical activity
- raised cholesterol
122
How does aortic dissection present?
- ripping/tearing pain in chest
- pain in anterior chest if ascending aorta affected or back if descending aorta
- hypertension > hypotension
- radial pulse deficit/difference in bp between arms
- diastolic murmur
- focal neurological deficit
123
What is a differential diagnosis for aortic dissection?
- MI
124
How is aortic dissection diagnosed?
- ECG and CXR exclude MI
- widened mediastinum
- 1st: CT/MRI angiogram
- Gold: TOE shows intimal flap and false lumen
125
How is aortic dissection managed?
- analgesia for pain
- β blockers to control BP and HR and reduce stress on walls
- Type A: open surgery replaced with graft
- Type B: thoracic endovascular aortic repair (TEVAR) using catheterisation
126
What are some common complications of aortic dissection?
- MI, stroke
- paraplegia
- cardiac tamponade
- aortic regurgitation
127
What is heart failure?
- An inability of the heart to deliver blood (and oxygen) at a rate that meets the requirements of metabolising tissues despite normal or increased cardiac filling pressure
128
What is the aetiology of heart failure?
- IHD: MI
- hypertension: inc strain
- valvular disease
- pericarditis/pericardial effusion
- cardiomyopathy
- alcohol
129
What is the pathophysiology behind heart failure?
- Heart failure causes a drop in MAP. This is compensated for by inc TPR, RAAS and vasoconstriction.
- The compensatory mechanisms are not sustainable
- causes inc afterload, workload and strain on the heart as well as fluid retention
130
What are the different types of heart failure?
- Systolic: inability to eject adequate volumes of blood
- Diastolic: reduced compliance, filling and ejection
- LHF: LV failure: ejection <40%
- RHF: RV failure > pulmonary hypertension
- Congestive HF: LV and RV failure
- HFpEF: HF in normal/high CO due to inc metabolic demand
131
What are the signs of heart failure?
- tachycardia
- 3rd heart sound (unless <25)
- Raised JVP
- displaced apex beat
- peripheral oedema (R side - venous backlog) or pulmonary oedema (L side)
132
What are some symptoms of heart failure?
- dyspnoea
- fatigue
- paroxysmal nocturnal dyspnoea
- cold peripheries
- cough productive of pink frothy sputum
133
What are the NY heart association classes of heart failure?
I: no limitation (asymptomatic)
II: slight limitation (mild HF)
III: Marked limitation (symptomatically moderate)
IV: inability to carry out physical activity without discomfort
134
What investigations are done for heart failure?
- b-type natriuretic peptide
- ECG
- CXR
- Gold: Echo: checks diastolic volume and ejection fraction for heart failure
135
What is ABCDE for heart failure?
- alveolar oedema (batwing opacification)
- Kerley B lines (interstitial oedema)
- cardiomegaly
- dilated upper lobe vessels
- effusions (pleural)
136
How is heart failure (reduced EF) managed?
- ACEi (ARB if intolerant) and β blockers
- diuretics: furosemide or spironolactone(K sparing)
- neurohumoral blockade
137
What is atrial fibrillation?
- uncoordinated, rapid, irregular contraction of the atria
- An irregularly irregular atrial firing rhythm
- disorganised activity overriding SAN
- can lead to heart failure due to poor filling in diastole
- is a common cause of stroke
138
How does atrial fibrillation present?
- palpitations
- tachycardia
- shortness of breath
- syncope
- symptoms of associated conditions e.g. stroke, sepsis
139
How is atrial fibrillation recognised on ECG?
- Absent P waves
- narrow QRS complex tachycardia
- irregularly irregular ventricular rhythm
140
How is atrial fibrillation managed?
- treat underlying cause
- rate and rhythm control
- restore sinus rhythm: electrical/pharmacological cardioversion
141
What is rate control for atrial fibrillation?
- aims to extend diastole and coordinate filling
- β blocker (1st line), CCB, Digoxin
142
What is rhythm control in atrial fibrillation?
- aims to return patient to a normal sinus rhythm
- flecanide or amiodarone 1st line cardioversion or electrical using defib
- long term: β blockers (1st line), dronedarone, amiodarone
143
What are the causes of AF?
- sepsis
- mitral valve pathology
- IHD
- thyrotoxicosis
- hypertension
144
What is paroxysmal AF and how is it treated?
- comes and goes in episodes <48 hrs
- anticoagulation based on CHADSVASc score
- pill in the pocket approach: flecanide
145
What is the CHA2DS2VASc scoring system?
- calculates stroke risk for AF
- Congestive heart failure/left ventricular dysfunction
- Hypertension
- Age ≥75 (+2)
- Diabetes
- stroke/TIA (+2)
- Vascular disease
- Age 64-74 (+1)
- Sex category (female)
- score of ≥2 or ≥1 in men = anticoagulation offered
146
How can AF lead to stroke?
- uncontrolled and unorganised movement leads to stagnating blood, especially in atrial appendage
- this leads to a thrombus which becomes an embolus
- can lodge in brain
147
What is atrial flutter?
- A re-entrant rhythm where the electrical signal recirculates in a self-perpetuating loop
- stimulates atrial contraction at 300bpm
- signal enters ventricles every 2nd lap due to long refractory period at AV node
- 150 bpm in ventricle
148
How does atrial flutter present and how is its investigated and treated?
- dyspnoea and palpitations
- sawtooth appearance on ECG
- rate/rhythm control
- radiofrequency ablation
- anticoagulation
149
What is 1st degree heart block and how does it present on ECG?
- delayed AV conduction through AV node
- PR interval greater than 0.20 seconds
150
What is 2nd degree heart block?
- some atrial impulses don't make it through the AV node > ventricles so some P waves aren't followed by QRS complexes
- Mobitz T1 and T2
151
What is Mobitz type 1?
- atrial impulses become weaker until they don't pass through AV node.
- fails to stimulate ventricular contraction
- atrial impulse returns to strong and cycle repeats
- shows as increasing PR interval until P wave no longer conducts to ventricles and QRS is missed then returns on next cycle
152
What is Mobitz type 2?
- failure or interruption of AV conduction
- leads to missing QRS complexes
- usually set ratio of P waves:QRS complexes
- e.g. 3:1 block
153
What is 3rd degree heart block?
- complete heart block
- no observable relationship between P waves and QRS complexes
- significant risk of asystole
154
How is heart block treated?
- atropine
- pacemaker
155
What is supraventricular tachycardia?
- caused by electrical signal re-entering atria from ventricles causing self-perpetuating loop
- results in narrow complex tachycardia
- appears on ECG as QRS, T, QRS, T...
156
How is supraventricular tachycardia managed?
- continuous ECG monitoring
- Valsalva
- carotid sinus massage
- adenosine: slows cardiac conduction through AV node
- same medications as AF
157
What is the home and what is the clinical bp threshold for hypertension?
Home: 135/85
Clinic: 140/90
- higher in clinic due to white coat effect
158
What investigations should be done for hypertension?
- urine dip
- ECG
- HbA1c
- renal function
- fundoscopy: hypertensive retinopathy
- lipid profile
- QRISK
159
What are the stages of hypertension?
- 1: 140/90 or 135/85
- 2: 160/100 or 150/95
- 3: 180 and/or 110
160
What medications are used to treat hypertension?
- A: ACE inhibitor (ramipril)
- B: β blocker (bisoprolol)
- C: calcium channel blocker (amlodipine)
- D: thiazide-like diuretic (indapamide)
- ARB: can be used in place of ACEi
161
What are the steps for choosing hypertension medications?
- 1: <55 and non-black use A otherwise use C
- 2: A+C or A+D or C+D. if black use ARB instead of A
- 3: A+C+D
- 4: A+C+D. spironolactone if K below 4.5mmol/l otherwise α/ β blocker
162
What are the types of hypertension and the causes?
- primary: idiopathic: 95% cases
- secondary: renal disease, obesity, pregnancy, endocrine
163
What is a dihydropyridine?
- Calcium channel blocker
- e.g. amlodipine
- affects vascular smooth muscle
- dilates peripheral arteries
164
What is a phenylalkylamine?
- Calcium channel blocker
- e.g. verapamil
- mainly affects heart
- negatively chronotopic and inotropic
165
How is coronary arterial thrombosis treated?
- aspirin/antiplatelet agent (inhibits platelet function)
- low molecular weight heparin
- streptokinase/TPA (generates plasmin, degrades fibrin)
- catheter directed thrombolysis
166
How is cerebral arterial thrombosis treated and which drug should be avoided?
- aspirin
- catheter directed thrombolysis
- reperfusion e.g. stent
- heparin avoided due to inc risk of bleeding
167
How is venous thrombosis treated?
- DOACs (direct acting oral anticoagulants) e.g. apixaban, rivoraxaban
- LMWH
- warfarin
- for DVT: compression stockings
168
What is the presentation of DVT?
- unilateral
- leg pain
- swelling, tenderness
- warmth
- discolouration
- dilated superficial veins
169
How is DVT/PE investigated?
- D-dimer: normal excludes diagnosis but +ve doesn't confirm
- Gold: ultrasound
- PE: CT coronary angiogram/VQ scan
170
What are the causes and signs of cardiogenic shock?
- heart pump failure, MI, cardiac tamponade, PE
- heart failure signs, raised JVP, 4th heart sound
171
What are the causes and treatment of septic shock?
- uncontrolled bacterial infection
- ABCDE and broad spectrum antibiotics
172
What are the signs of septic shock?
- pyrexic
- warm peripheries
- bounding pulse
- tachycardia
173
What are the causes of hypovolemic shock?
- blood loss: trauma, GI bleed
- fluid loss: dehydration
174
What are the symptoms of hypovolaemic shock?
- clammy, pale skin
- confusion
- hypotension
- tachycardia
175
What are the causes of neurogenic shock?
- spinal cord trauma e.g. RTA
- disrupted SNS, intact PSNS
176
What are the symptoms and treatment of neurogenic shock?
- hypotension, bradycardia, confusion, hypothermia
- ABCDE, IV atropine
177
What are the general signs of shock?
- confusion
- skin: pale, cold, sweaty, vasoconstriction
- prolonged hypotension
- inc capillary refill time
- reduced GCS
- weak, rapid pulse
178
Describe anaphylactic shock?
- IgE mediated type 1 hypersensitivity
- hypotension, tachycardia, urticaria, puffy face
- ABCDE, IM adrenaline
179
What is the cause of rheumatic fever?
- systemic response to group A β haemolytic strep
- post strep pyogenes infection
- typically pharyngitis
180
What is the pathophysiology behind rheumatic fever?
- proteins from S. pyogenes
- Abs to bacterial cell wall cross react with heart valve tissue causing Ab mediated destruction/inflammation
181
What are the major criteria of rheumatic fever?
- Joint arthritis
- nOdules (subcutaneous)
- New murmur (esp mitral stenosis)
- Erythema marginatum (rash with raised edges, clear centre)
- Sydenham's chorea (uncoordinated jerky movements)
182
What are the minor criteria of rheumatic fever?
- Fever
- ECG changes (prolonged PR)
- Arthralgia
- Raised ESR/CRP
183
What is the diagnosis of rheumatic fever?
- recent strep infection + (2 major criteria) OR (1 major + 2 minor)
- CXR: cardiomegaly
- Echo
184
How is rheumatic fever treated?
- IV benzylpenicillin then penicillin V
- haloperidol
- bed rest
185
What does right bundle branch block look like on ECG?
- QRS > 0.12s
- M shape in V1-3
- W shape in V5-6
- caused by PE and cor pulmonale
186
What does left bundle branch block look like on ECG?
- QRS > 0.12s
- W shape in V1-3
- M shape in V5-6
- aortic stenosis, IHD, MI
187
What is peripheral arterial disease?
- narrowing of arteries supplying limbs
- reduced blood supply
- leads to claudication
188
How does peripheral arterial disease present?
- intermittent claudication
- crampy pain after walking
- after stopping and resting, pain disappears
- calf, thighs, buttocks
189
What are the investigations of peripheral arterial disease?
- ultrasound
- Ankle brachial pressure index (systolic in leg: arm)
190
What is the management of peripheral arterial disease?
- risk factor modification
- atorvastatin, clopidogrel
- endarterectomy, endovascular angioplasty
191
What is MONAC?
- management of acute ACS or MI
- Morphine
- Oxygen if sats <94%
- fast acting Nitrates
- Aspirin
- Clopidogrel
Osha 2a
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