Cardiovascular Flashcards
1
Q
AAA investigations
A
Ruptured → take to theatre immediately
Bloods
- FBE (anaemia, leucocytosis if infective)
- Blood cultures (infective)
- ESR/CRP (inflam)
- Coags + group and hold (if ruptured).
Imaging
- Abdo U/S (asymptomatic, follow-up)
- CT chest/abdo (preoperative, complications)
- Aortogram (preop EVAR)
- TOE (concurrent dissection)
2
Q
AAA management
A
Ruptured: urgent emergency repair via laparotomy + blood transfusion
Small (5.5cm) or expanding: laparoscopic surgical repair + EVAR
3
Q
Aetiology of AAA
A
- Atherosclerotic aortic disease → saccular
- Infection: syphilis (aortitis → saccular thoracic aneurysms) + other bugs
- CTDs: Marfan’s (weakens aortic media → AR, dilated aneurysm/dissection), Ehlers-Danlos
- Trauma
- Inflammatory vasculitis
4
Q
Aortic aneurysm definition
A
An abnormal dilatation of the aortic lumen 1.5x the normal diameter
5
Q
Aortic dissection classification & prevalence
A
Stanford A
- 70%
- Ascending aorta + arch proximal to LSC
- DeBakey I (to descending aorta)
- DeBakey II (only AA)
Stanford B
- 30%
- DeBakey III
6
Q
Aortic dissection clinical presentation
A
SYMPTOMS
- Acute severe tearing central chest pain radiating to the back and arms which may move
- AA = anterior CP
- DA = intrascapular pain
- Syncope, collapse, nausea, diaphoresis, dyspnoea, weakness
SIGNS
- AR, asymmetrical upper limb/carotid/ femoral pulses and BP, absent peripheral pulses, HTN → hypotension w haemorrhage, ischaemic syndromes
RUPTURE
- Pleura (L pleural effusion, dyspnoea, haemoptysis)
- Peritoneum (haemorrhage, shock)
- Pericardium (tamponade)
7
Q
Aortic dissection investigations
A
ECG: ST depression
BLOODS: FBE (anaemia if haemorrhage), UEC (↑ creatinine if ↓ renal perfusion), troponins, amylase, lactate (gut ischaemia), blood G&H
IMAGING: CXR (wide upper mediastinum, L pleural effusion, distorted aortic knuckle), CT, TOE, CT/MRI aortogram
8
Q
Aortic dissections most commonly occur in:
A
Men, aged 60-65yo
9
Q
Carotid stenosis investigations
A
ECG (AF, prior AMI, myocardial ischaemia, LV dysfunction)
BSL (diabetes)
URINALYSIS (proteinuria due to renal ischaemia)
BLOODS: FBE, UEC (renal function), lipids (hyperlipidaemia), coags (hypercoagulable states)
IMAGING
o Carotid duplex U/S (screening test of choice; evaluates stenosis)
o Carotid angiogram (gold standard but invasive; 1-2% risk of stroke)
o CT/MRI head (presence of intracranial lesions or infarcts)
o Echocardiogram (if suspected aortic stenosis radiating to neck)
10
Q
Classic presentation of AAA
A
Intermittent or continuous severe epigastric pain radiating to the back
Triad of AAA: Hypotension + pain + pulsatile abdominal mass
SYMPTOMS
Intermittent or continuous severe epigastric pain radiating to the back
- Syncope, distal embolization to lower limbs, aortic thrombotic occlusion, back pain, DVT/lower limb oedema (IVC obstruction)
SIGNS
Hypotension, tachycardia, profound anaemia, pulsatile abdominal mass, discolouration of lower limbs due to thromboembolisation
11
Q
Clinical presentation of carotid stenosis
A
Often asymptomatic
SYMPTOMS: TIA, amaurosis fugax (loss of sight in one eye on ipsilateral side), stroke, tinnitus
SIGNS: carotid bruits (do NOT indicate severity), signs of stroke, signs of cardiac/aortic/peripheral atherosclerosis
12
Q
Clinical presentation of TAA
A
SYMPTOMS
- Acute chest pain
- Hoarse voice (RLN palsy)
- Dysphagia (oesophageal compression)
- Haematemesis (aorto-oesophageal fistula)
- Haemoptysis (aorto-bronchial fistula)
SIGNS
AR, differential blood pressures on arms, radio-radial delay, stridor, SVC syndrome, hypotension, tachycardia
13
Q
Difference between true and false/pseudo aneurysm
A
TRUE: involves all arterial layers (intima, media, adventitia)
FALSE: does not involve all arterial layers
14
Q
Extension of dissection sequentially occludes other branches, leading to:
A
SCARS
Subclavians → acute limb ischaemia, unequal arm pulses and BP
Carotids → hemiplegia
Anterior spinal artery → paraplegia
Renal arteries → anuria/AKI
Rupture into the L pleural Space/pericardium → usually fatal
15
Q
Management of aortic dissection (initial, type A, type B, long-term)
A
Initial: analgesia, IV β blocker (↓ sBP
16
Q
Management of carotid stenosis (asymptomatic + symptomatic)
A
Asymptomatic
- Aggressive medical management: antiplatelets + anti-HTN + statin + appropriate glycaemic control
- Smoking cessation
Symptomatic
- Medical management as above
- Carotid endarterectomy (post-stroke or TIA OR if stenosis >70% – if TIA or stroke, within 2 weeks due to high risk of recurrence)
- PCI – less effective and not routinely recommended unless high surgical risk
17
Q
Most common site of abdominal aortic aneurysms
A
Below the renal arteries
18
Q
Pathophysiology of carotid stenosis
A
Inflammation of the arterial wall → deposition of lipids and calcification → plaque development → stenosis → embolization + thrombosis → TIA/stroke
19
Q
Population with a high prevalence of AAA
A
Elderly, hypertensive males (>75yo)
20
Q
Risk factors for aortic dissection
A
HTN, CTDs, smoking, FHX, age, pregnancy, surgical/catheter manipulation, atherosclerotic aneurysmal disease, arteritis, heavy lifting
21
Q
Risk factors for carotid stenosis
A
HTN, smoking, diabetes, CAD/PVD, dyslipidaemia, CKD, obesity, FHx
22
Q
Risk factors for AAA
A
↑ age (>65) Male (prevalence), female (rupture) Hypertension, hyperlipidaemia FHx Hx of vascular disease Smoking Non-diabetic CTDs (Marfan’s, Ehler’s Danlos)
23
Q
Symptoms + signs of TAA
A
Symptoms
- Acute chest pain
- Hoarse voice (RLN palsy)
- Dysphagia (oesophageal compression)
- Haematemesis (aorto-oesophageal fistula)
- Haemoptysis (aorto-bronchial fistula)
Signs
- AR
- Differential blood pressures on arms
- Radio-radial delay
- Stridor
- SVC syndrome
- Hypotension, tachycardia
24
Q
Types + locations of narrow complex tachycardia
A
AKA SVTs
Atrial origin o Sinus tachycardia o Atrial tachycardia o Atrial fibrillation o Atrial flutter o Multifocal atrial tachycardia
Atrioventricular origin:
o AVRT, AVNRT
25
Types of broad complex tachycardia
VT (including torsades de pointes)
| VF
26
Aetiology of SVT
| - cardiac + non-cardiac
CARDIAC
o AMI, CAD, LV aneurysm, mitral S/R, cardiomyopathy, myocarditis, conduction anomalies
NON-CARDIAC:
o Caffeine, alcohol, drugs (TCA, levodopa, digoxin), metabolic derangement (Ca, K, Mg, thyroid disease), phaeochromocytoma
27
Clinical presentation of SVT
o Asymptomatic
o Chest pain, syncope, postural hypotension, palpitations
o HF (peripheral oedema, APO)
o Take a thorough HOPC, symptoms, FHx, PMHx and drug/alcohol Hx
28
Investigations for SVT
BLOODS: FBE, UEC, BSL, CMP, TFTs
ECG/Holter monitor
IMAGING: echo
29
Management of paroxysmal SVT
ACUTE: Valsalva manoeuvre, carotid sinus massage → adenosine (not asthma/COPD) → verapamil → amiodarone, DC cardioversion, pacing
PROPHYLAXIS: β-blockers → flecainide/ verapamil → amiodarone
30
Characteristics of AF
Narrow complex tachycardia Absent P waves
| Irregularly irregular rhythm
31
Classification of AF
PAROXYSMAL: episodes that terminate spontaneously/with Tx within 7 days; may recur; episodes usually 7 days
LONGSTANDING PERSISTENT: continuous
PERMANENT: continuous AF that did not respond to cardioversion
NONVALVULAR: no rheumatic MS, mitral valve repair, replaced heart valve
32
Aetiology of AF
Valvular heart disease (MR, MS, AR), AMI, alcohol, hyperthyroidism, idiopathic, postoperative, HTN, cardiomyopathy, PE, COPD
33
Pathophysiology of AF
Single circuit re-entry, ectopic foci → atrial tachycardia → irregular conduction → remodelling → ↑ AF → ↓ CO + ↑ risk of thrombus formation
34
Clinical presentation of AF
Palpitations, fatigue, syncope, precipitating/worsening HF, single flicker on JVP (no a wave = absent atrial contraction), irregularly irregular pulse
35
Management of AF
RACE
RATE CONTROL (β blockers, diltiazem/ verapamil, HF = digoxin/amiodarone)
ANTICOAGULATION (warfarin/NOAC)
DC CARDIOVERSION
48hr = anticoag for 3w before + 4w after DC (↑ thrombus risk)
Haemodynamically unstable (uncontrolled HF, angina from tachycardia, hypotensive): DC immediately
CHEMICAL CARDIOVERSION (sotalol, amiodaron, flecainide; same criteria)
AETIOLOGY (treat underlying cause)
36
Characteristics of atrial flutter
Sawtooth flutter waves (most common type of flutter) in inferior leads (II/III/aCF), narrow QRS, commonly see HR of 150
37
Aetiology of atrial flutter
CAD, thyrotoxicosis, mitral valve disease, cardiac surgery, COPD, PE, pericarditis
38
Pathophysiology + Classification of atrial flutter
Associated with AV nodal block → atrial contractions > ventricular contractions
Block type determines ventricular rate
o 2:1 block = HR 150 (carotid sinus massage/ Valsalva/adenosine → ↓ AV conduction → flutter
o 3:1 block = HR 100
o Variable
39
Management of atrial flutter
RACE (same as for AF)
RATE CONTROL (β blockers, diltiazem/ verapamil, HF = digoxin/amiodarone)
ANTICOAGULATION (warfarin/NOAC)
DC CARDIOVERSION
48hr = anticoag for 3w before + 4w after DC (↑ thrombus risk)
Haemodynamically unstable (uncontrolled HF, angina from tachycardia, hypotensive): DC immediately
CHEMICAL CARDIOVERSION (sotalol, amiodaron, flecainide; same criteria)
AETIOLOGY (treat underlying cause)
40
Characteristics of sinus tachycardia
Heart rate >100bpm; normal PR interval; P wave precedes each QRS complex
41
Aetiology of sinus tachycardia
Pain, fever, stress, caffeine, hypoxaemia, exercise, hypovolaemia, HF
42
Pathophysiology of sinus tachycardia
↑ SA node firing
43
Management of sinus tachycardia
Directed at treatment of cause
| May require metoprolol/atenolol if uncontrolled.
44
Aetiology of VT
Myocardial scarring, ischaemia (AMI), myocarditis, electrolyte disturbances, cocaine, idiopathic
45
Management of VT
NON-SUSTAINED: only if symptomatic or unstable; correct underlying cause → atenolol/metoprolol (1st) → sotlol/ amiodarone/flecainide (2nd)
SUSTAINED: haemodynamically unstable (DC cardioversion), stable (amiodarone/sotalol/lignocaine)
Consider prophylaxis (ICD, β-blocker, amiodarone/sotalol)
46
Characteristics of torsades de pointes
Subset of VT; height of QRS complexes vary
47
Aetiology of torsades de pointes
Long QT syndrome, electrolyte disturbances , antiarrhythmics, erythromycin, TCAs, fluoroquinolones, antihistamines
48
Characteristics of VF
Irregular uncoordinated ventricular fibrillatory waves; no clear morphology; initially course VF (big fibrillation waves) which progressed to fine VF (smaller waves).
49
Management of VF
Course/unstable: DC cardioversion
Fine VF: IV adrenaline → DCCV
50
ECG characteristics of hyperkalaemia
Tenting (peaked) T waves in all leads
Flattened P waves
Prolonged PR interval (1st degree AV block)
Widened QRS complexes and peaked T waves become almost indistinguishable → sine-wave pattern
51
ECG characteristics of hypokalaemia
ST depression
T wave flattening
Appearance of U waves
Prolonged QT interval
52
Characteristics of Wolff-Parkinson White Syndrome
PR interval
53
Aetiology of Wolff-Parkinson White Syndrome
Accessory conducting bundle (bundle of Kent) connect the atria and ventricles → depolarisation is not delayed by AV node → depolarising reaches ventricles early → pre-excitation of ventricles
54
Definition of bundle branch blocks
Conduction defects which cause broad QRS complexes (0.12sec)
55
How to distinguish between L + R bundle branch blocks on ECG
WiLiam MaRRoW
LBBB: W in QRS of V1; M in QRS of V6; wide positive QRS
RBBB: M in QRS of V1; W in QRS of V6; wide negative QRS
56
Digoxin ECG changes
Reverse 'nike tick'
57
Types of bradyarrythmias
Sinus bradycardia
AV nodal block (1st degree, 2nd degree (I/II), 3rd degree)
Cushing’s reflex
58
Characteristics of sinus bradycardia
Normal P axis
| Rate
59
Aetiology of sinus bradycardia
↑ vagal tone/stim, vomiting, inferior MI, sick sinus syndrome, ↑ICP, hypothyroidism, hypothermia, drugs (β, CCBs)
60
Treatment of sinus bradycardia
Atropine (acute episodes)
Pacing (SSS)
Reduction/withdrawal of drugs
61
Characteristics of 1st degree AV block
PR interval >0.2sec; normal QRS
| Common, no Tx required
62
Characteristics + classification of 2nd degree AV block
Mobitz Type I (Wenkebach): progressive lengthening on PR until a QRS is dropped; no pacing needed
Mobitz Type II: constant normal PR interval; QRS is suddenly dropped, often in a pattern (2:1, 3:1 common).
Treatment with pacing (↑ risk of complete heart block)
63
Characteristics of 3rd degree AV block
Complete heart block
Complete dissociation of P and QRS waves
Treatment with pacing (PPM/temp)
64
Cushing’s reflex presentation + significance
Seen in conditions causing ↑ ICP, and is a sign of impending brain herniation
Bradycardia + irregular breathing + HTN
65
Epidemiology of sudden cardiac arrest
Cases are roughly equal between gender, with 83% occurring over 65y, and highest among black people. Out-of hospital VF has a survival rate of
66
Reversible causes of cardiac arrest
Hs & Ts
H: hypovolaemia, hypoxia, H+ (acidosis), hyperkalaemia/hypokalaemia, hypothermia, hyperglycaemia/hypoglycaemia
T: tablets (TCAs, CCBs, cocaine, digoxin), cardiac tamponade, tension PTX, thrombosis (AMI), thromboembolism (PE), trauma
67
Pathophysiology of sudden cardiac arrest
Ischaemic heart disease → VF/VT
- Non-ischaemic LV dysfunction, premature V beats, meds → prolonged QT interval, electrolyte + familial conduction abnormalities, cardiomyopathies, intoxication (cocaine).
MI, hypovolaemia, hypoxia, PE → PEA
68
Cardiac rhythm disturbances that comprise sudden cardiac arrest
VF
Pulseless VT
Pulseless electrical activity (PEA)
Asystole
69
Risk factors for cardiac arrest
CAD, LV dysfunction, LCH, ARVD, LQTS, acute medical/surgical emergency
70
Clinical presentation of cardiac arrest
The patient is responsive; assessment of airway, breathing, and circulation shows absence of normal breathing and no signs of circulation.
71
Investigation of cardiac arrest
Investigate cause
BEDSIDE: ECG (QT/ST/T ∆, conduction abnormality, ventricular hypertrophy)
BLOODS: FBC (↓ Hb in haemorrhage), electrolytes, ABG (resp/metabolic acidosis, compensation), cardiac markers (+/↑), toxicology screen
IMAGING: CXR (pneumothorax), echo (LV function, valvular abnormalities, scarring, CM, pericardial effusion)
72
Clinical assessment of cause of cardiac arrest
- Family history (long QT, familial CM)
- Pulmonary disease (hypoxia, hypercarbia)
- Chest pain (MI), palpitations (pre-existing arrhythmia), syncope (heart disease, pre-existing arrhythmia)
- HTN, hypercholesterolaemia, DM, kidney disease, CAD FHx
- ↑JVP, bilateral creps→ decompensated HF
- Trauma → cardiac tamponade, valvular disturbance, myocardial puncture, tension pneumothorax
- Tracheal deviation, absent air entry → tension pneumothorax
- Murmur → valvular cause
- Neurological examination → intracranial path
73
Management of cardiac arrest
Unwitnessed: CPR
Shockable rhythms (pVT/VT): CPR + defibrillation + adrenaline (1mg/3-5min) + Mg (torsades de pointes) + amiodarone/lignocaine (after 2-3 attempts at defib)
Non-shockable rhythms (PEA/asystole): CPR + adrenaline (1mg/3-5min)
74
Complications of cardiac arrest
Death, rib/sternal fractures, anoxic brain injury, ischaemic liver injury (shock liver), renal acute tubular necrosis (ATN), recurrent cardiac arrest
75
Definition of cardiac failure
Heart failure is an inability for the heart to maintained sufficient blood flow to meet the metabolic requirements of the body, or to do so only at a raised filling pressure. It is a clinical syndrome characterised by diminished effort capacity and dyspnoea due to cardiac dysfunction.
76
Precipitants of decompensation of cardiac failure
MADHATTER 3P
- Myocardial ischaemia (ACS)
- Arrhythmia
- Drugs (compliance, NSAIDs + ACE-I + diuretics)
- Hypertension
- Anaemia
- Toxic (UTI, respiratory infection)
- Thyroid disease (hyper/hypo)
- Eclampsia
- Rupture of the mitral valve chordae → acute torrential MR
- PE → acute right HF
- Perioperative: illness before surgery, ↑↑ fluid replacement, cessation of diuretics/meds
- Pregnancy: ↑ circulating volume, ↑ CO requirement, peripartum cardiac hypertrophy
77
1. Neuro-hormonal mechanism of cardiac failure
SYMPATHETIC OVERACTIVITY
o ↓CO → ↓BP → ↑ Adr release → ↑HR + β agonism (→ + inotrope) → strains heart → ventricular hypertrophy + arrhythmias
o Catecholamine → α agonism → ↑BP → peripheral vascular constriction → ↑ afterload + ↓ systolic function
o Venous vessel contraction → ↑ preload/VR → maintain SV
Resolved with β blockers
RAAS OVERACTIVITY
o ↑CO → ↓ renal perfusion → RAAS activation
o Angiotensin → peri. vasoconstriction
o Aldosterone + ADH → salt/H2O retention → strains heart + oedema
Resolved with ACE-I/ARB
78
Pro-inflammatory mechanism of cardiac failure
↑ cytokine + TNFα release
79
Pathophysiology + aetiology of LHF
Backlog of blood in pulmonary vasculature → pulmonary congestion/APO; renal ischaemia; hypoxic encephalopathy → LV hypertrophy
AETIOLOGY: HTN, aortic/mitral valve disease
80
Pathophysiology + aetiology of RHF
Backlog of blood in peripheral vasculature → peripheral venous congestion + oedema → RV hypertrophy
AETIOLOGY: LHF, lung disease/cor pulmonale, pulmonary stenosis
81
Definition of CCF
LHF + RHF
82
Definition + pathophysiology + aetiology of acute HF
New onset sudden HF OR acute decompensation of chronic
* Acute-onset pulmonary/peripheral oedema + peripheral hypoperfusion + no active compensation
* Cardiogenic shock (↓BP + oliguria)
AETIOLOGY: AMI, arrhythmia, acute valvular disease
83
Pathophysiology + aetiology of chronic HF
Slowly developing/progressing HF with venous congestion; arterial pressure maintained until advanced
84
Pathophysiology + aetiology of systolic HF (HFREF)
↓ myocardial contractility → ↓V contraction → ↓CO/SV (LVEF
85
Pathophysiology + aetiology of diastolic HF (HFPEF)
Impaired V relaxation/filling → ↓ V filling → ↑V filling P (LVEF >50%) → upstream venous congestion
AETIOLOGY: Constrictive pericarditis, cardiac tamponade, acute ischaemia, restrictive CM, hypertrophy (HTN, AS, HOCM)
86
Pathophysiology + characteristics + aetiology of low output HF
↓CO → fails to ↑ with exertion
Majority of cases; elderly
AETIOLOGY:
- Pump failure (post-MI, β blockers, heart block, antiarrythmic)
- ↑preload (MR, fluid overload)
- Chronic ↑afterload (AS, HTN)
87
Pathophysiology + aetiology of high output HF
No intrinsic cardiac disease; demand for ↑CO (systemic needs ↑); uncommon; RHF → LHF
AETIOLOGY: Anaemia, pregnancy, hyperthyroidism, Paget’s, beri beri
88
Clinical presentation of LHF
LHF → blood not pumped out of LV → pools in LV → back into lung = pulmonary oedema
↓CO: fatigue, syncope, systemic HTN, cool extremities, slow capillary refill, peripheral cyanosis, pulsus alternans, S3
Venous congestion: dyspnoea, orthopnoea, PND, cough, crackles
Presentation: poor exercise tolerance, wheezing, APO (nocturnal cough, pink frothy sputum), nocturia, WL, muscle wasting
89
Clinical presentation of RHF
RHF → blood not pumped out of RV → pools in RV → back into venous system → venous congestion → peripheral oedema + ascites
↓CO: ↓RV output → LV underfilling → LHF Sx
tricuspid regurgitation, S3 (R)
Venous congestion: peripheral oedema, ↑JVP w hepatojugular reflex, Kussmaul’s sign, hepatomegaly, pulsatile liver
Presentation: ascites, hepatomegaly, facial engorgement, nausea, anorexia, epistaxis and pulsation in the neck and face (tricuspid regurgitation)
90
Grading of cardiac failure symptoms
Class I: ordinary physical activity causes no Sx of heart failure
Class II: comfortable at rest; ordinary physical activity → Sx (fatigue, palpitations, SOB)
Class III: marked limitation of ordinary physical activity; mild exertion →Sx
Class IV: inability to carry out any physical activity without Sx; Sx present at rest
91
Signs of APO on CXR
ABCDE
```
o Alveolar oedema
o Kerley B lines
o Cardiomegaly
o Upper lobe Diversion
o Pleural Effusion
```
92
Investigations for cardiac failure
ECG/Holter monitor
Rate, rhythm, ischaemic ∆, hypertrophy, QRS, tachycardia
BLOODS
FBE, UEC, CMP, LFTs, INR (if anticoagulated), troponins, BNP (diff. SOB from HF vs. other causes), TFTs, CRP, cardiomyopathy screen
IMAGING
CXR (cardiomegaly, APO, effusion, devices, signs of surgery), echo (heart size, LV/RVEF, pulmonary pressure, valvular + pericardial pathology.
93
Management of APO
```
o Lasix (frusemide) IV
o Morphine
o Nitrates
o Oxygen
o Positioning (upright), Pressure (CPAP)
```
94
Principles of management of HF
```
APO management
Treat underlying cause
Cardiac rehab
o Education, self-management supervised exercise, meds, group support
Fluid management
Mortality-benefit drugs
Symptomatic treatment
Procedural interventions
```
95
Fluid management in HF
o Fluid restriction (1kg for 2d)
| o Fluid balance chart, patient diary
96
Pharmacological management in HF
```
Mortality-benefit drugs: “Brakes on – ABS (I)”
o For HRERF; ALL PATIENTS
o ACE-I or ARB
o Beta-blockers (metoprolol, bisoprolol)
o Spironolactone (or epleronone)
o Ivabradine
```
Symptomatic treatment
o Diuretics (frusemide, bumetanide, hydrochlorothiazide)
o Nitrates
o Anti-arrhythmic drugs (digoxin for AF, amiodarone, β blockers)
o Anticoags
97
Procedural interventions for HF
o Cardiac resynchronisation therapy (CRT) (LVEF 1 year)
o Ventricular assist devices (LVAD, RVAD): destination/bridging therapy
o Cardiac transplantation, valve repair
98
Complications of HF
- Acute decompensation (APO, periph oedema)
- Arrhythmias: supraventricular (esp. AF), ventricular (esp. VF/VT: ↑ risk with ↓EF)
- Hypoperfusion, meds (esp. ACE-I) → renal impairment
- RHF → hepatic congestion → RUQ pain, anorexia
- LHF/ lung disease → pulmonary HTN
99
S1 heart sound
AV valve closure
100
S2 heart sound
Semilunar valve closure
101
A systolic murmur is between ...
S1 & S2
102
A diastolic murmur is between ...
S2 & S1
103
Characteristics of aortic stenosis murmur
Ejection systolic (crescendo-decrescendo) murmur radiating to the carotids; louder on expiration/ squatting; softer on Valsalva
104
Aetiology of aortic stenosis
o Progressive valvular calcification (age)
o Congenital bicuspid valve
o Rheumatic heart disease
105
Pathophysiology of aortic stenosis
Narrowing of aortic valve → LV outflow obstruction
106
Clinical presentation of aortic stenosis
o Exertional SAD (syncope, angina and dyspnoea); symptoms are a LATE sign.
o Narrow pulse pressure
o Slow-rising, ↓ volume plateau (anacrotic) pulse
o Pressure-loaded apex beat
107
Investigations for aortic stenosis
```
o ECG: LVH, LV strain (ST ↓, T wave inversion in leads I, aVL and V4-V6)
o Echo (degree of stenosis)
```
108
Management of aortic stenosis
o Angina: β-blocker, CCB (second-line)
o Manage associated HF
o Surgery (always required if symptomatic or asymptomatic critical stenosis; open valve replacement or TAVI/TAVR)
109
Characteristics of aortic sclerosis murmur
```
Ejection systolic (crescendo-decrescendo) murmur with NO radiation.
Asymptomatic, though can progress to aortic stenosis
```
110
Pathophysiology of aortic sclerosis
Aortic valve leaflet thickening w/o impairment of valvular function (no obstructive or regurgitant defect).
111
Characteristics of aortic regurgitation murmur
Early diastolic murmur best heard over the tricuspid area; louder on expiration
112
Aetiology of aortic regurgitation
```
Usually aortic root dilatation:
Idiopathic
Rheumatic heart disease
Marfan’s syndrome, CTDs
Infective endocarditis
```
113
Pathophysiology of aortic regurgitation
Incompetent aortic valve → blood leaks backwards into the LV from the aorta during diastole
114
Clinical presentation of aortic regurgitation
o Wide pulse pressure
o Volume-loaded apex beat
o Quincke’s sign (capillary pulsations)
o Collapsing/water-hammer pulse (Corrigan’s carotid pulse)
o De Musset’s sign (head bobbing in synchrony with heart beats)
o Traube’s signs (pistol shot systolic sound over femoral artery)
115
Investigation for aortic regurgitation
```
o ECG (LVH + signs of ventricular strain)
o Echo (level of regurgitation)
```
116
Management of aortic regurgitation
o Management of heart failure
| o Surgery
117
Characteristics of mitral valve prolapse murmur
Late systolic murmur with mid-systolic click; louder on Valsalva
118
Associations + pathophysiology of mitral valve prolapse
Associated with Marfan’s syndrome, osteogenesis imperfecta and PKD.
Prolapse of a thickened mitral valve leaflet into the LA during ventricular systole.
119
Characteristics of mitral stenosis murmur
Mid-diastolic murmur that is louder on expiration; opening snap
120
Epidemiology of mitral stenosis
Common in Indigenous Australians (strep throat → RF)
121
Aetiology + pathophysiology of mitral stenosis
Narrowing of the mitral valve, usually due to rheumatic heart disease.
122
Clinical presentation of mitral stenosis
o Mitral facies (malar flash)
o Tapping apex beat
o → AF (due to LA enlargement)
123
Investigation of mitral stenosis
ECG – LA hypertrophy (bifid P wave)
124
Management of mitral stenosis
o Angina: β-blockers, CCBs, nitrates
o Management of HF
o Balloon mitral valvoplasty (transcatheter)
o Mitral valve replacement
125
Characteristics of mitral regurgitation murmur
Pansystolic murmur radiating to the axilla; louder on expiration/squatting
126
Aetiology of mitral regurgitation
o Usually as a progression of MVP
o Post-MI (rupture of the chordae tendinae → torrential acute MR → acute HF)
o Rheumatic heart disease
o Infective endocarditis
127
Pathophysiology of mitral regurgitation
Backflow of blood into the LA during ventricular systole due to an incompetent mitral valve.
128
Clinical presentation of mitral regurgitation
```
o Volume-loaded apex beat (from LVH)
o AF (due to L atrial dilation)
```
129
Investigation of mitral regurgitation
Echocardiogram
130
Management of mitral regurgitation
Mitral valve replacement/ repair + medical treatment of associated HF
131
Characteristics of tricuspid regurgitation
Pansystolic murmur; louder on inspiration.
132
Aetiology of tricuspid regurgitation
Usually due to RV dilatation or tricuspid annulus dilatation (e.g. post-inferior MI, pulmonary HTN)
133
Pathophysiology of tricuspid regurgitation
Incompetent tricuspid valve → regurgitant jet of blood back into the RA during ventricular systole.
134
Clinical presentation of tricuspid regurgitation
o ↑ JVP with giant v waves and sharp y descent
| o Pulsatile hepatomegaly
135
Management of tricuspid regurgitation
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o Diuretics (as may cause RHF = peripheral oedema and ascites)
o Tricuspid valve replacement or repair
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136
Characteristics of HOCM murmur
Ejection systolic murmur that is louder on Valsalva (distinguish from AS)
137
Characteristics of patent ductus arteriosus murmur
Continuous machinery murmur heard over left infraclavicular region
138
Characteristics of atrial septal defect murmur
Ejection systolic murmur at the left upper sternal border with a widely split S2
139
Characteristics of ventricular septal defect murmur
Harsh pansystolic murmur at the lower left sternal border
140
Characteristics + associations of flow murmur
Benign mid-systolic murmur.
| Associated with hyperdynamic circulation = ↑CO (anaemia, pregnancy)
141
Clinical presentation of carotid stenosis
- Symptoms: TIA, amaurosis fugax (loss of sight in one eye on ipsilateral side), stroke, tinnitus
- Signs: carotid bruits (do NOT indicate severity), signs of stroke, signs of cardiac/aortic/peripheral atherosclerosis
142
Investigation of carotid stenosis
- ECG (AF, prior AMI, myocardial ischaemia, LV dysfunction), BSL (diabetes), urinalysis (proteinuria due to renal ischaemia)
- Bloods: FBE, UEC (renal function), lipids (hyperlipidaemia), coags (hypercoagulable states)
- Imaging
o Carotid duplex U/S (screening test of choice; evaluates stenosis)
o Carotid angiogram (gold standard but invasive; 1-2% risk of stroke)
o CT/MRI head (presence of intracranial lesions or infarcts)
o Echocardiogram – if suspected aortic stenosis radiating to neck
143
Management of asymptomatic carotid stenosis
o Aggressive medical management: antiplatelets + anti-HTN + statin + appropriate glycaemic control
o Smoking cessation
144
Management of symptomatic carotid stneosis
o Aggressive medical management: antiplatelets + anti-HTN + statin + appropriate glycaemic control
o Carotid endarterectomy (post-stroke or TIA OR if stenosis >70% – if TIA or stroke, within 2 weeks due to high risk of recurrence)
o Percutaneous angioplasty + stenting (↓ effective, not routinely recommended unless ↑ surgical risk)
145
What is deep vein thrombosis?
Blood clot development in a major deep vein in the leg, thigh, pelvis, or abdomen, which may result in impaired venous blood flow, leg swelling and pain
146
Describe how Virchow's triad leads to DVT, and what factors predispose to each component
- Trauma, previous DVT, surgery, venous harvest, CV cath → vessel wall damage → thrombus formation (at venous valves)
- Venous stasis + congestion → valvular damage → thrombus formation
o Ass. with age >40 years, immobility, general anaesthesia, paralysis, spinal cord injury, MI, prior CVA, varicose veins, advanced CHF/COPD
- Hypercoagulability: from cancer, ↑ oestrogen states (obesity, pregnancy, HRT), IBD, nephrotic syndrome, sepsis, blood transfusion, inherited thrombophilia.
147
Pathophysiology of DVT
- Most blood clots that develop in the deep venous system of the leg begin to form just above and behind a venous valve.
- The soleal vein has no valves → thrombi form circumferentially attached to wall by thin membrane + prone to pooling/stagnation → ↑ propagation + embolism
148
What increases the risk of thrombosis in the groin or iliac veins?
Pregnancy
| Total hip arthroplasty
149
Risk factors for DVT
- Active malignancy
- Recent major surgery, (esp. orthopaedic knee procedures), hospitalisation, trauma (lower limb)
- Medical illness, prothrombotic condition
- Age, pregnancy, obesity, air travel
- Drugs (OCP, tamoxifen/raloxifen, thalidomide, EPO, antibodies developed to adalimumab)
150
Clinical presentation of DVT
- Majority are asymptomatic
- Unilateral calf/leg swelling, localised pain + tenderness along vein, asymmetric oedema, collateral superficial veins, phlegmasia cerulean dolens (massive DVT).
- Prior history of DVT/PE
151
Investigation of DVT
- Bedside: Wells’ criteria (>2 = 40% risk)
- Bloods: D-dimer, INR, aPTT, UEC, LFT, FBC
- Imaging: DUS (cannot compress lumen, ↓/no spontaneous flow, no respiratory variation, intraluminal echo, colour flow patency abnormalities)
152
Management of acute DVT
Gradient stockings + physical activity
- Low-bleeding: anticoag
- Low-bleeding, pregnant: LMWH/SC heparin
- High bleeding: IV heparin
- Active bleeding: IVC filter
- PE-related CV compromise: individualised
153
Management of ongoing DVT
- Postnatal → breastfeed: LMWH/SC heparin
| - Postnatal → no breastfeed: LMWH/SC heparin + gradient stockings + physical activity
154
Ongoing monitoring for DVT
aPTT (heparin), INR (warfarin)
155
Complications of DVT
PE, acute/delayed bleeding, HIT, heparin resistance, post-phlebitic syndrome, OP (due to heparin)
