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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)
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2
Q

AAA management

A

Ruptured: urgent emergency repair via laparotomy + blood transfusion

Small (5.5cm) or expanding: laparoscopic surgical repair + EVAR

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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
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4
Q

Aortic aneurysm definition

A

An abnormal dilatation of the aortic lumen 1.5x the normal diameter

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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
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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)
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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

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8
Q

Aortic dissections most commonly occur in:

A

Men, aged 60-65yo

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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)

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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

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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

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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

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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

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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

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15
Q

Management of aortic dissection (initial, type A, type B, long-term)

A

Initial: analgesia, IV β blocker (↓ sBP

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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
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17
Q

Most common site of abdominal aortic aneurysms

A

Below the renal arteries

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18
Q

Pathophysiology of carotid stenosis

A

Inflammation of the arterial wall → deposition of lipids and calcification → plaque development → stenosis → embolization + thrombosis → TIA/stroke

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19
Q

Population with a high prevalence of AAA

A

Elderly, hypertensive males (>75yo)

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20
Q

Risk factors for aortic dissection

A

HTN, CTDs, smoking, FHX, age, pregnancy, surgical/catheter manipulation, atherosclerotic aneurysmal disease, arteritis, heavy lifting

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21
Q

Risk factors for carotid stenosis

A

HTN, smoking, diabetes, CAD/PVD, dyslipidaemia, CKD, obesity, FHx

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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)
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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
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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

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25
Q

Types of broad complex tachycardia

A

VT (including torsades de pointes)

VF

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26
Q

Aetiology of SVT

- cardiac + non-cardiac

A

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

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27
Q

Clinical presentation of SVT

A

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

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28
Q

Investigations for SVT

A

BLOODS: FBE, UEC, BSL, CMP, TFTs
ECG/Holter monitor
IMAGING: echo

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29
Q

Management of paroxysmal SVT

A

ACUTE: Valsalva manoeuvre, carotid sinus massage → adenosine (not asthma/COPD) → verapamil → amiodarone, DC cardioversion, pacing

PROPHYLAXIS: β-blockers → flecainide/ verapamil → amiodarone

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30
Q

Characteristics of AF

A

Narrow complex tachycardia Absent P waves

Irregularly irregular rhythm

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31
Q

Classification of AF

A

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

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32
Q

Aetiology of AF

A

Valvular heart disease (MR, MS, AR), AMI, alcohol, hyperthyroidism, idiopathic, postoperative, HTN, cardiomyopathy, PE, COPD

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33
Q

Pathophysiology of AF

A

Single circuit re-entry, ectopic foci → atrial tachycardia → irregular conduction → remodelling → ↑ AF → ↓ CO + ↑ risk of thrombus formation

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34
Q

Clinical presentation of AF

A

Palpitations, fatigue, syncope, precipitating/worsening HF, single flicker on JVP (no a wave = absent atrial contraction), irregularly irregular pulse

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35
Q

Management of AF

A

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)

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36
Q

Characteristics of atrial flutter

A

Sawtooth flutter waves (most common type of flutter) in inferior leads (II/III/aCF), narrow QRS, commonly see HR of 150

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37
Q

Aetiology of atrial flutter

A

CAD, thyrotoxicosis, mitral valve disease, cardiac surgery, COPD, PE, pericarditis

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38
Q

Pathophysiology + Classification of atrial flutter

A

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

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39
Q

Management of atrial flutter

A

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)

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40
Q

Characteristics of sinus tachycardia

A

Heart rate >100bpm; normal PR interval; P wave precedes each QRS complex

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41
Q

Aetiology of sinus tachycardia

A

Pain, fever, stress, caffeine, hypoxaemia, exercise, hypovolaemia, HF

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42
Q

Pathophysiology of sinus tachycardia

A

↑ SA node firing

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43
Q

Management of sinus tachycardia

A

Directed at treatment of cause

May require metoprolol/atenolol if uncontrolled.

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44
Q

Aetiology of VT

A

Myocardial scarring, ischaemia (AMI), myocarditis, electrolyte disturbances, cocaine, idiopathic

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45
Q

Management of VT

A

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)

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46
Q

Characteristics of torsades de pointes

A

Subset of VT; height of QRS complexes vary

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47
Q

Aetiology of torsades de pointes

A

Long QT syndrome, electrolyte disturbances , antiarrhythmics, erythromycin, TCAs, fluoroquinolones, antihistamines

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48
Q

Characteristics of VF

A

Irregular uncoordinated ventricular fibrillatory waves; no clear morphology; initially course VF (big fibrillation waves) which progressed to fine VF (smaller waves).

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49
Q

Management of VF

A

Course/unstable: DC cardioversion

Fine VF: IV adrenaline → DCCV

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50
Q

ECG characteristics of hyperkalaemia

A

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

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51
Q

ECG characteristics of hypokalaemia

A

ST depression
T wave flattening
Appearance of U waves
Prolonged QT interval

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52
Q

Characteristics of Wolff-Parkinson White Syndrome

A

PR interval

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53
Q

Aetiology of Wolff-Parkinson White Syndrome

A

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

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54
Q

Definition of bundle branch blocks

A

Conduction defects which cause broad QRS complexes (0.12sec)

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55
Q

How to distinguish between L + R bundle branch blocks on ECG

A

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

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56
Q

Digoxin ECG changes

A

Reverse ‘nike tick’

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57
Q

Types of bradyarrythmias

A

Sinus bradycardia
AV nodal block (1st degree, 2nd degree (I/II), 3rd degree)
Cushing’s reflex

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58
Q

Characteristics of sinus bradycardia

A

Normal P axis

Rate

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59
Q

Aetiology of sinus bradycardia

A

↑ vagal tone/stim, vomiting, inferior MI, sick sinus syndrome, ↑ICP, hypothyroidism, hypothermia, drugs (β, CCBs)

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60
Q

Treatment of sinus bradycardia

A

Atropine (acute episodes)
Pacing (SSS)
Reduction/withdrawal of drugs

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61
Q

Characteristics of 1st degree AV block

A

PR interval >0.2sec; normal QRS

Common, no Tx required

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62
Q

Characteristics + classification of 2nd degree AV block

A

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)

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63
Q

Characteristics of 3rd degree AV block

A

Complete heart block
Complete dissociation of P and QRS waves
Treatment with pacing (PPM/temp)

64
Q

Cushing’s reflex presentation + significance

A

Seen in conditions causing ↑ ICP, and is a sign of impending brain herniation

Bradycardia + irregular breathing + HTN

65
Q

Epidemiology of sudden cardiac arrest

A

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
Q

Reversible causes of cardiac arrest

A

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
Q

Pathophysiology of sudden cardiac arrest

A

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
Q

Cardiac rhythm disturbances that comprise sudden cardiac arrest

A

VF
Pulseless VT
Pulseless electrical activity (PEA)
Asystole

69
Q

Risk factors for cardiac arrest

A

CAD, LV dysfunction, LCH, ARVD, LQTS, acute medical/surgical emergency

70
Q

Clinical presentation of cardiac arrest

A

The patient is responsive; assessment of airway, breathing, and circulation shows absence of normal breathing and no signs of circulation.

71
Q

Investigation of cardiac arrest

A

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
Q

Clinical assessment of cause of cardiac arrest

A
  • 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
Q

Management of cardiac arrest

A

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
Q

Complications of cardiac arrest

A

Death, rib/sternal fractures, anoxic brain injury, ischaemic liver injury (shock liver), renal acute tubular necrosis (ATN), recurrent cardiac arrest

75
Q

Definition of cardiac failure

A

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
Q

Precipitants of decompensation of cardiac failure

A

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
Q
  1. Neuro-hormonal mechanism of cardiac failure
A

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
Q

Pro-inflammatory mechanism of cardiac failure

A

↑ cytokine + TNFα release

79
Q

Pathophysiology + aetiology of LHF

A

Backlog of blood in pulmonary vasculature → pulmonary congestion/APO; renal ischaemia; hypoxic encephalopathy → LV hypertrophy

AETIOLOGY: HTN, aortic/mitral valve disease

80
Q

Pathophysiology + aetiology of RHF

A

Backlog of blood in peripheral vasculature → peripheral venous congestion + oedema → RV hypertrophy

AETIOLOGY: LHF, lung disease/cor pulmonale, pulmonary stenosis

81
Q

Definition of CCF

A

LHF + RHF

82
Q

Definition + pathophysiology + aetiology of acute HF

A

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
Q

Pathophysiology + aetiology of chronic HF

A

Slowly developing/progressing HF with venous congestion; arterial pressure maintained until advanced

84
Q

Pathophysiology + aetiology of systolic HF (HFREF)

A

↓ myocardial contractility → ↓V contraction → ↓CO/SV (LVEF

85
Q

Pathophysiology + aetiology of diastolic HF (HFPEF)

A

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
Q

Pathophysiology + characteristics + aetiology of low output HF

A

↓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
Q

Pathophysiology + aetiology of high output HF

A

No intrinsic cardiac disease; demand for ↑CO (systemic needs ↑); uncommon; RHF → LHF

AETIOLOGY: Anaemia, pregnancy, hyperthyroidism, Paget’s, beri beri

88
Q

Clinical presentation of LHF

A

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
Q

Clinical presentation of RHF

A

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
Q

Grading of cardiac failure symptoms

A

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
Q

Signs of APO on CXR

A

ABCDE

o	Alveolar oedema 
o	Kerley B lines
o	Cardiomegaly 
o	Upper lobe Diversion
o	Pleural Effusion
92
Q

Investigations for cardiac failure

A

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
Q

Management of APO

A 
o	Lasix (frusemide) IV
o	Morphine
o	Nitrates
o	Oxygen
o	Positioning (upright), Pressure (CPAP)
94
Q

Principles of management of HF

A 
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
Q

Fluid management in HF

A

o Fluid restriction (1kg for 2d)

o Fluid balance chart, patient diary

96
Q

Pharmacological management in HF

A 
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
Q

Procedural interventions for HF

A

o Cardiac resynchronisation therapy (CRT) (LVEF 1 year)
o Ventricular assist devices (LVAD, RVAD): destination/bridging therapy
o Cardiac transplantation, valve repair

98
Q

Complications of HF

A
  • 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
Q

S1 heart sound

A

AV valve closure

100
Q

S2 heart sound

A

Semilunar valve closure

101
Q

A systolic murmur is between …

A

S1 & S2

102
Q

A diastolic murmur is between …

A

S2 & S1

103
Q

Characteristics of aortic stenosis murmur

A

Ejection systolic (crescendo-decrescendo) murmur radiating to the carotids; louder on expiration/ squatting; softer on Valsalva

104
Q

Aetiology of aortic stenosis

A

o Progressive valvular calcification (age)
o Congenital bicuspid valve
o Rheumatic heart disease

105
Q

Pathophysiology of aortic stenosis

A

Narrowing of aortic valve → LV outflow obstruction

106
Q

Clinical presentation of aortic stenosis

A

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
Q

Investigations for aortic stenosis

A 
o	ECG: LVH, LV strain (ST ↓, T wave inversion in leads I, aVL and V4-V6)
o	Echo (degree of stenosis)
108
Q

Management of aortic stenosis

A

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
Q

Characteristics of aortic sclerosis murmur

A 
Ejection systolic (crescendo-decrescendo) murmur with NO radiation. 
Asymptomatic, though can progress to aortic stenosis
110
Q

Pathophysiology of aortic sclerosis

A

Aortic valve leaflet thickening w/o impairment of valvular function (no obstructive or regurgitant defect).

111
Q

Characteristics of aortic regurgitation murmur

A

Early diastolic murmur best heard over the tricuspid area; louder on expiration

112
Q

Aetiology of aortic regurgitation

A 
Usually aortic root dilatation:
	Idiopathic
	Rheumatic heart disease
	Marfan’s syndrome, CTDs
	Infective endocarditis
113
Q

Pathophysiology of aortic regurgitation

A

Incompetent aortic valve → blood leaks backwards into the LV from the aorta during diastole

114
Q

Clinical presentation of aortic regurgitation

A

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
Q

Investigation for aortic regurgitation

A 
o	ECG (LVH + signs of ventricular strain)
o	Echo (level of regurgitation)
116
Q

Management of aortic regurgitation

A

o Management of heart failure

o Surgery

117
Q

Characteristics of mitral valve prolapse murmur

A

Late systolic murmur with mid-systolic click; louder on Valsalva

118
Q

Associations + pathophysiology of mitral valve prolapse

A

Associated with Marfan’s syndrome, osteogenesis imperfecta and PKD.

Prolapse of a thickened mitral valve leaflet into the LA during ventricular systole.

119
Q

Characteristics of mitral stenosis murmur

A

Mid-diastolic murmur that is louder on expiration; opening snap

120
Q

Epidemiology of mitral stenosis

A

Common in Indigenous Australians (strep throat → RF)

121
Q

Aetiology + pathophysiology of mitral stenosis

A

Narrowing of the mitral valve, usually due to rheumatic heart disease.

122
Q

Clinical presentation of mitral stenosis

A

o Mitral facies (malar flash)
o Tapping apex beat
o → AF (due to LA enlargement)

123
Q

Investigation of mitral stenosis

A

ECG – LA hypertrophy (bifid P wave)

124
Q

Management of mitral stenosis

A

o Angina: β-blockers, CCBs, nitrates
o Management of HF
o Balloon mitral valvoplasty (transcatheter)
o Mitral valve replacement

125
Q

Characteristics of mitral regurgitation murmur

A

Pansystolic murmur radiating to the axilla; louder on expiration/squatting

126
Q

Aetiology of mitral regurgitation

A

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
Q

Pathophysiology of mitral regurgitation

A

Backflow of blood into the LA during ventricular systole due to an incompetent mitral valve.

128
Q

Clinical presentation of mitral regurgitation

A 
o	Volume-loaded apex beat (from LVH)
o	AF (due to L atrial dilation)
129
Q

Investigation of mitral regurgitation

A

Echocardiogram

130
Q

Management of mitral regurgitation

A

Mitral valve replacement/ repair + medical treatment of associated HF

131
Q

Characteristics of tricuspid regurgitation

A

Pansystolic murmur; louder on inspiration.

132
Q

Aetiology of tricuspid regurgitation

A

Usually due to RV dilatation or tricuspid annulus dilatation (e.g. post-inferior MI, pulmonary HTN)

133
Q

Pathophysiology of tricuspid regurgitation

A

Incompetent tricuspid valve → regurgitant jet of blood back into the RA during ventricular systole.

134
Q

Clinical presentation of tricuspid regurgitation

A

o ↑ JVP with giant v waves and sharp y descent

o Pulsatile hepatomegaly

135
Q

Management of tricuspid regurgitation

A 
o	Diuretics (as may cause RHF = peripheral oedema and ascites)
o	Tricuspid valve replacement or repair
136
Q

Characteristics of HOCM murmur

A

Ejection systolic murmur that is louder on Valsalva (distinguish from AS)

137
Q

Characteristics of patent ductus arteriosus murmur

A

Continuous machinery murmur heard over left infraclavicular region

138
Q

Characteristics of atrial septal defect murmur

A

Ejection systolic murmur at the left upper sternal border with a widely split S2

139
Q

Characteristics of ventricular septal defect murmur

A

Harsh pansystolic murmur at the lower left sternal border

140
Q

Characteristics + associations of flow murmur

A

Benign mid-systolic murmur.

Associated with hyperdynamic circulation = ↑CO (anaemia, pregnancy)

141
Q

Clinical presentation of carotid stenosis

A
  • 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
Q

Investigation of carotid stenosis

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
143
Q

Management of asymptomatic carotid stenosis

A

o Aggressive medical management: antiplatelets + anti-HTN + statin + appropriate glycaemic control
o Smoking cessation

144
Q

Management of symptomatic carotid stneosis

A

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
Q

What is deep vein thrombosis?

A

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
Q

Describe how Virchow’s triad leads to DVT, and what factors predispose to each component

A
  • 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
Q

Pathophysiology of DVT

A
  • 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
Q

What increases the risk of thrombosis in the groin or iliac veins?

A

Pregnancy

Total hip arthroplasty

149
Q

Risk factors for DVT

A
  • 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
Q

Clinical presentation of DVT

A
  • 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
Q

Investigation of DVT

A
  • 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
Q

Management of acute DVT

A

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
Q

Management of ongoing DVT

A
  • Postnatal → breastfeed: LMWH/SC heparin

- Postnatal → no breastfeed: LMWH/SC heparin + gradient stockings + physical activity

154
Q

Ongoing monitoring for DVT

A

aPTT (heparin), INR (warfarin)

155
Q

Complications of DVT

A

PE, acute/delayed bleeding, HIT, heparin resistance, post-phlebitic syndrome, OP (due to heparin)

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