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Phase 2a Conditions > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the definition of stable angina pectoris?

A

Mismatch of myocardial oxygen supply and demand results in recurrent transient episodes of chest pain due to myocardial ischaemia

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2
Q

What is the aetiology of stable angina pectoris?

A

Atheromatous plaque, coronary artery vasospasm (Prinzmetals)

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3
Q

What is the clinical presentation of stable angina pectoris?

A

Chest pain (heavy or tight, central pain which can radiate up the neck and down the arm, occurs upon exertion, and is relieved by rest or medication), breathlessness

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4
Q

What are the investigations of stable angina pectoris?

A

o ECG: Normal

o Coronary angiography: luminal narrowing

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5
Q

What is the treatment of stable angina pectoris?

A

Lifestyle modifications, beta blockers, calcium channel blockers, aspirin, statins, ACE inhibitors, sublingual GTN spray, PCI, and CABG

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6
Q

What is the definition of unstable angina pectoris?

A

Prolonged angina at rest, new onset of severe angina, angina that is increasing in frequency, longer in duration, or lower in threshold

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7
Q

What is the aetiology of unstable angina pectoris?

A

Non-occlusive thrombus formation on an atheromatous plaque

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8
Q

What is the clinical presentation of unstable angina pectoris?

A

Heavy or tight, central chest pain with a crescendo pattern, which increases in frequency and severity, retrosternal chest pain which radiates to the jaw, arm or neck, dyspnoea, fourth heart sound (S4)

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9
Q

What are the investigations of unstable angina pectoris?

A

o ECG: Normal or transient ST-segment depression
o Cardiac biomarkers: normal
o Coronary angiography: luminal narrowing

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10
Q

What is the treatment of unstable angina pectoris?

A

o Hospital: Oxygen, nitrates, morphine, beta blockers, aspirin
o Confirmed unstable angina: lifestyle modifications, aspirin, heparin, beta blockers, calcium channel blockers, statins, ACE inhibitors, sublingual GTN spray

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11
Q

What is the definition of non-ST elevation myocardial infarction (NSTEMI)?

A

Necrosis of cardiac tissue due to prolonged myocardial ischaemia

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12
Q

What is the aetiology of non-ST elevation myocardial infarction (NSTEMI)?

A

Rupture of an atherosclerotic with subsequent arterial thrombosis which results in transient occlusion of a major coronary artery or near complete occlusion of a minor coronary artery

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13
Q

What is the clinical presentation of non-ST elevation myocardial infarction (NSTEMI)?

A

o Males: Chest pain (tightness, heaviness, aching, burning, pressure, or squeezing which is most often retrosternal and can radiate to the left arm but may also radiate to the lower jaw, neck, both arms, back, and epigastrium, where it may mimic heartburn)
o Females: Middle/upper back pain or dyspnoea

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14
Q

What are the investigations of non-ST elevation myocardial infarction (NSTEMI)?

A

o ECG: non-specific ST-T wave or ischemic changes
o Cardiac biomarkers: elevated troponin and creatine kinase
o Coronary angiogram: occlusion or near occlusion of the artery

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15
Q

What is the treatment of non-ST elevation myocardial infarction (NSTEMI)?

A

o Initial: 300mg Aspirin
o Hospital: morphine, oxygen, nitrates, aspirin and ticagrelor, PCI
o Long-term: lifestyle modifications, aspirin, clopidogrel, anti-coagulation (fondaparinux or heparin), ACE inhibitor, beta blocker

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16
Q

What is the definition of ST elevation myocardial infarction (STEMI)?

A

Necrosis of cardiac tissue due to prolonged myocardial ischaemia

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17
Q

What is the aetiology of ST elevation myocardial infarction (STEMI)?

A

Rupture of an atherosclerotic plaque and subsequent arterial thrombosis in a major coronary artery

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18
Q

What is the clinical presentation of ST elevation myocardial infarction (STEMI)?

A

Chest pain (diffuse, severe chest pain that can occur at rest or with exertion, is heavy in nature, located centrally with radiation to the left arm or jaw, and lasts for at least 20 minutes), dyspnoea, pallor, diaphoresis, cardiogenic shock

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19
Q

What are the investigations of ST elevation myocardial infarction (STEMI)?

A

o ECG: ST elevation in two or more leads and tall T waves
o Cardiac biomarkers: elevated troponin and creatine kinase
o Plasma glucose: elevated
o Coronary angiogram: thrombus with occlusion of the artery

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20
Q

What is the treatment of ST elevation myocardial infarction (STEMI)?

A

o Initial: 300mg Aspirin
o Hospital: morphine, oxygen, nitrates, aspirin and ticagrelor, PCI, thrombolysis (streptokinase)
o Long-term: lifestyle modifications, aspirin, clopidogrel and an anti-coagulant (fondaparinux or heparin), ACE inhibitor, beta blocker

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21
Q

What is the definition of heart failure?

A

Cardiac output is inadequate to deliver blood and oxygen at the rate the body needs to meet metabolic demands

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22
Q

What is the aetiology of heart failure?

A

o Left ventricular heart failure: systolic failure (IHD, myocardial infarction, dilated cardiomyopathy), diastolic failure (ventricular hypertrophy, aortic stenosis, constrictive pericarditis, tamponade, restrictive cardiomyopathy, and obesity)
o Right ventricular failure: pulmonary stenosis, pulmonary hypertension (cor pulmonale), pulmonary embolism, COPD

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23
Q

What is the pathophysiology of heart failure?

A

Myocardial failure leads to a reduction in blood ejected which increases the ventricular load and causes hypertrophy. Hypertrophy increases the myocardial demand and leads to ischemia, patchy fibrosis, stiffness, and reduced contractibility. The ventricles stretch and dilate, increasing the force required to maintain the cardiac output. The myocytes become damaged and weakened, reducing the cardiac output. The decreased cardiac output activates the RAAS and leads to sodium and water retention and thus fluid build-up.

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24
Q

What is the clinical presentation of heart failure?

A

Shortness of breath, fatigue, peripheral oedema

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25
Q

What are the investigations of heart failure?

A

o BNP: elevated
o Echocardiogram: structural and functional abnormalities
o Chest X-ray: alveolar oedema (bat wing shadowing), Kerley B lines, cardiomegaly, dilated upper lobe vessels, effusions

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26
Q

What is the treatment of heart failure?

A

o Acute: ventilation, IV diuretics, IV inotropes and vasopressors, IV nitrates
o Chronic: lifestyle modifications, diuretics, ACE inhibitors, beta blockers, aldosterone antagonists, ARB, hydralazine and nitrate, digoxin

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27
Q

What is the definition of hypertension?

A

An elevated blood pressure, ≥140/90 mmHg

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28
Q

What is the aetiology of hypertension?

A

o Primary: no identifiable cause

o Secondary: primary aldosteronism, phaeochromocytoma, Cushing’s syndrome, acromegaly

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29
Q

What is the clinical presentation of hypertension?

A

Asymptomatic, headache

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30
Q

What are the investigations of hypertension?

A

o Blood pressure: ≥140/90 mmHg

o 24-hour ambulatory blood pressure monitoring (ABPM): ≥135/85 mmHg

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31
Q

What is the treatment of hypertension?

A

o <55, not of Afro-Caribbean origin, type II diabetes: ACEi or ARB -> CCB -> thiazide-like diuretic
o >55, Afro-Caribbean origin: CCB -> ACEi or ARB -> thiazide-like diuretic
o Resistant hypertension: Spironolactone, alpha blocker, beta blocker

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32
Q

What is the definition of sinus bradycardia?

A

Heart rhythm slower than 60 bpm

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33
Q

What is the aetiology of sinus bradycardia?

A

Drugs, infection, hypothyroidism, hypothermia

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34
Q

What is the clinical presentation of sinus bradycardia?

A

Asymptomatic, dizziness, syncope, fatigue, exercise intolerance, shortness of breath, jugular venous distention

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35
Q

What are the investigations of sinus bradycardia?

A

ECG: regular rhythm, narrow QRS, rate < 60 bpm

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36
Q

What is the treatment of sinus bradycardia?

A

o < 40 bpm and acutely symptomatic: IV atropine

o < 40 and persistently symptomatic: pacemaker

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37
Q

What is the definition of sinus tachycardia?

A

Heart rhythm faster than 100 bpm

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38
Q

What is the aetiology of sinus tachycardia?

A

Physiological (exercise, excitement, anxiety), pathological (hyperthyroidism, pulmonary embolism, fever, pain, anaemia, hypovolaemia, drugs)

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39
Q

What is the clinical presentation of sinus tachycardia?

A

Asymptomatic, palpitations, dizziness

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40
Q

What are the investigations of sinus tachycardia?

A

ECG: regular rhythm, narrow QRS, rate > 100 bpm

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41
Q

What is the treatment of sinus tachycardia?

A

o Acute: adenosine, digoxin, atenolol, verapamil, amiodarone, carotid massage (if haemodynamically stable)
o Long-term: Beta blockers, non-dihydropyridine calcium channel blockers (diltiazem, verapamil)

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42
Q

What is the definition of atrial flutter?

A

Macro re-entrant atrial tachycardia with atrial rates usually above 250 bpm, but up to 320 bpm

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43
Q

What is the aetiology of atrial flutter?

A

Structural or functional conduction abnormalities

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44
Q

What is the clinical presentation of atrial flutter?

A

Worsening heart failure or pulmonary symptoms, jugular venous pulsations with rapid flutter waves

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45
Q

What are the investigations of atrial flutter?

A

ECG: P waves at around 300 bpm in a saw-tooth pattern, more P waves than QRS complexes

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46
Q

What is the treatment of atrial flutter?

A

Beta blockers, cardioversion, catheter ablation of the re-entrant circuit

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47
Q

What is the definition of atrial fibrillation?

A

Supraventricular tachyarrhythmia which is characterised by uncoordinated atrial activity

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48
Q

What is the aetiology of atrial fibrillation?

A

Ischaemic heart disease, hypertension, heart failure, valvular disease, diabetes, thyroid disorders COPD, obstructive sleep apnoea

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49
Q

What is the pathophysiology of atrial fibrillation?

A

Dilation of the atria with fibrosis and inflammation causes a difference in refractory periods within the atrial tissue and promotes electrical re-entry that results in atrial fibrillation

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50
Q

What is the clinical presentation of atrial fibrillation?

A

Asymptomatic, palpitations, chest pain, shortness of breath, dizziness, syncope

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51
Q

What are the investigations of atrial fibrillation?

A

ECG: irregularly irregular rhythm, absent P waves, absence of isoelectric baseline, fibrillatory waves

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52
Q

What is the treatment of atrial fibrillation?

A

Rhythm control (beta blockers, digoxin), rate control (amiodarone, flecainide)

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53
Q

What score assess the risk of thrombosis in atrial fibrillation?

A

CHA2DS2-VASc

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54
Q

What is the definition of Wolff-Parkinson-White syndrome?

A

Congenital myocardial fibres capable of conducting electrical impulses connect the atrium to the ipsilateral ventricle

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55
Q

What is the clinical presentation of Wolff-Parkinson-White syndrome?

A

Atrial fibrillation, atrial flutter, palpitations, dizziness, shortness of breath, chest pain

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56
Q

What are the investigations of Wolff-Parkinson-White syndrome?

A

ECG: short PR interval, wide QRS complex, delta wave (slurring of the QRS upstroke)

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57
Q

What is the treatment of Wolff-Parkinson-White syndrome?

A

Vagal manoeuvre, adenosine, radiofrequency ablation of accessory pathway

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58
Q

What is the definition of ventricular tachycardia?

A

Wide complex tachycardia that originates from one of the ventricles, at a rate of 100 bpm or greater

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59
Q

What is the pathophysiology of ventricular tachycardia?

A

An ectopic focus in the ventricle depolarises with high frequency and spreads excitation through the abnormal pathway which leads to a wide QRS complex as the pathway is a less organised system

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60
Q

What is the clinical presentation of ventricular tachycardia?

A

Asymptomatic, tachycardia, hypotension

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61
Q

What are the investigations of ventricular tachycardia?

A

ECG: no visible P or T waves (hidden in the QRS complex), wide abnormal QRS complexes, QRS complexes are at a rapid rate, but are regular

62
Q

What is the treatment of ventricular tachycardia?

A

o Haemodynamically unstable: cardioversion
o Haemodynamically stable: amiodarone
o Long-term: anti-arrhythmic drugs, catheter ablation, or an intracardiac device

63
Q

What is the definition of ventricular fibrillation?

A

Ventricular tachyarrhythmia which is characterised by uncoordinated ventricular activity

64
Q

What is the pathophysiology of ventricular fibrillation?

A

Chaotic excitation of the ventricles due to simultaneous contractions at multiple ectopic foci

65
Q

What is the clinical presentation of ventricular fibrillation?

A

Chest pain, palpitations, shortness of breath, dizziness, syncope

66
Q

What are the investigations of ventricular fibrillation?

A

ECG: no P or T waves, wide, irregular waves at a rapid rate

67
Q

What is the treatment of ventricular fibrillation?

A

Immediate defibrillation and advanced cardiac life support

68
Q

What is the definition of atrioventricular block?

A

Cardiac electrical disorder defined as impaired (delayed or absent) conduction from the atria to the ventricles

69
Q

What is the aetiology of atrioventricular block?

A

Fibrosis and calcification of the conduction system, ischaemic heart disease, drugs

70
Q

What is the pathophysiology of atrioventricular block?

A

o First degree: Delayed condition of the atrial impulse at the AV node
o Second degree: Not every atrial impulse is conducted to the ventricles
o Third degree: No atrial impulse pass through the AV node to the ventricles

71
Q

What is the clinical presentation of atrioventricular block?

A

Syncope, bradycardia, cerebral hypoperfusion (third degree atrioventricular block)

72
Q

What are the investigations of atrioventricular block?

A

ECG:
o First degree: PR interval longer than 0.2 seconds
o Mobitz Type I: progressive lengthening of the PR interval and then a P wave which is not followed by a QRS complex
o Mobitz Type II: constantly long PR interval and then a P wave which is not followed by a QRS complex
o Third degree: P waves at an independent regular rate, QRS complexes at an independent regular rate, no relationship between P waves and QRS complexes

73
Q

What is the treatment of atrioventricular block?

A

o Mobitz Type II: pacemaker if symptomatic

o Third degree: IV atropine, pacemaker

74
Q

What is the definition of left bundle branch block?

A

Impaired conduction down the left bundle branch

75
Q

What is the pathophysiology of left bundle branch block?

A

The left bundle branch does not conduct an impulse and the two ventricles do not receive an impulse simultaneously, the right ventricle receives an impulse first. This causes the right ventricle to contract before the left ventricle

76
Q

What is the clinical presentation of left bundle branch block?

A

Asymptomatic, syncope

77
Q

What are the investigations of left bundle branch block?

A

ECG: there is a deep, slurred S wave in V1, creating a W shaped wave morphology, and a second R wave (R’) in V6, creating an M shaped wave morphology (WiLLiaM)

78
Q

What is the treatment of left bundle branch block?

A

Evaluated for underlying cardiac disease, pacemaker

79
Q

What is the definition of right bundle branch block?

A

Impaired conduction down the right bundle branch

80
Q

What is the pathophysiology of right bundle branch block?

A

The right bundle branch does not conduct an impulse and the two ventricles do not receive an impulse simultaneously, the left ventricle receives an impulse first. This causes the left ventricle to contract before the right ventricle

81
Q

What is the clinical presentation of right bundle branch block?

A

Asymptomatic, syncope

82
Q

What are the investigations of right bundle branch block?

A

ECG: there is a second R wave (R’) in V1, creating an M shaped wave morphology, and a deep, slurred S wave in V6, creating a W shaped wave morphology (MaRRoW)

83
Q

What is the treatment of right bundle branch block?

A

No treatment

84
Q

What is the aetiology of prolonged QT syndrome?

A

Congenital, hypokalaemia, hypocalcaemia, drugs, bradycardia, acute myocardial infarction, diabetes

85
Q

What is the clinical presentation of prolonged QT syndrome?

A

Syncope, palpitations, may progress to ventricular fibrillation

86
Q

What are the investigations of prolonged QT syndrome?

A

ECG: prolonged QT interval, > 0.48 seconds

87
Q

What is the treatment of prolonged QT syndrome?

A

o Acute: treat the underlying cause, IV isoprenaline

o Long-term: lifestyle modifications, beta-blockers

88
Q

What is the definition of an aortic aneurysm?

A

Permanent pathologic dilation of the aorta with a diameter >1.5 times the expected anteroposterior diameter

89
Q

What is the aetiology of an aortic aneurysm?

A

Atheromatous plaque

90
Q

What is the pathophysiology of an aortic aneurysm?

A

Obliteration of collagen and elastin from proteolytic degradation of connective tissue, smooth muscle cell loss, infiltration of lymphocytes and macrophages, and neovascularisation

91
Q

What is the clinical presentation of an aortic aneurysm?

A

o Unruptured: Asymptomatic
o Ruptured: Sudden, severe, tearing abdominal pain with radiation to the back, flank and groin, syncope, hypovolaemic shock, nausea and vomiting

92
Q

What are the investigations of an aortic aneurysm?

A

o Thoracic and abdominal ultrasound: dilation ≥ 3 cm

o CT angiography: dilation ≥ 3 cm

93
Q

What is the treatment of an aortic aneurysm?

A

Surgical repair, observation (small aneurysms)

94
Q

What is the definition of an aortic dissection?

A

Separation in the aortic wall intima causes blood to flow into a new false channel composed of the inner and outer layers of the media

95
Q

What is the aetiology of an aortic dissection?

A

Intimal tear

96
Q

What is the clinical presentation of an aortic dissection?

A

Acute severe, tearing chest pain, interscapular and lower pain, asymmetrical blood pressure differential, pulse deficit, diastolic murmur, syncope, pallor, heavy sweating

97
Q

What are the investigations of an aortic dissection?

A

o ECG: ST segment depression

o CT angiography: intimal flap

98
Q

What is the treatment of an aortic dissection?

A

o Initial: fluid resuscitation, inotropes, noradrenaline

o Long-term: endovascular stent-graft repair and anti-hypertensives

99
Q

What is the definition of peripheral vascular disease?

A

Narrowing or occlusion of peripheral arteries leading to compromise of blood supply to the lower limbs

100
Q

What is the aetiology of peripheral vascular disease?

A

Atherosclerosis, thrombus, embolus

101
Q

What is the clinical presentation of peripheral vascular disease?

A

o Acute Limb Ischaemia: Pain, pulselessness, pallor, paralysis, paraesthesia, perishingly cold
o Chronic Limb Ischaemia: Intermittent claudication, diminished or absent foot pulses, loss of hair on the lower limbs, erectile dysfunction

102
Q

What are the investigations of peripheral vascular disease?

A

o Ankle brachial pressure index: < 0.9 – indicative of lower extremity artery disease
o MR angiography: narrowing or occlusion

103
Q

What is the treatment of peripheral vascular disease?

A

o Acute Limb Ischaemia: analgesia and heparin, revascularisation (catheter-directed thrombolysis, embolectomy, bypass), amputation of dead, non-viable tissue
o Chronic Limb Ischaemia: lifestyle modifications, statins, anti-platelet therapy (aspirin or clopidogrel), revascularisation (angioplasty, endarterectomy, bypass)

104
Q

What is the definition of pericarditis?

A

Inflammation of the pericardium

105
Q

What is the aetiology of pericarditis?

A

Idiopathic, viral, bacterial, autoimmune, neoplastic, metabolic, traumatic, iatrogenic, myocardial infarction (Dressler’s syndrome)

106
Q

What is the clinical presentation of pericarditis?

A

Chest pain (severe, sharp, pleuritic pain relieved by sitting forward, exacerbated by lying down and inspiration), pericardial rub, dyspnoea, cough, hiccups

107
Q

What are the investigations of pericarditis?

A

o ECG: diffuse, saddle shaped ST segment elevation, no reciprocal ST depression, PR depression
o ESR and CRP: may be elevated
o Serum troponin: mildly elevated

108
Q

What is the treatment of pericarditis?

A

Treat underlying cause, NSAIDs or aspirin, colchicine, sedentary activity until resolution of symptoms, pericardiocentesis (if cardiac tamponade is present)

109
Q

What is the definition of infectious endocarditis?

A

Infection involving the endocardial surface of the heart

110
Q

What is the aetiology of infectious endocarditis?

A

Bacterial infections (staphylococcal aureus)

111
Q

What is the clinical presentation of infectious endocarditis?

A

Fever, chills, night sweats, malaise, fatigue, anorexia, weight loss, myalgias, weakness, arthralgias, headache, shortness of breath

112
Q

What are the investigations of infectious endocarditis?

A

o Blood cultures: bacteraemia, fungaemia
o Transthoracic echocardiography: valvular, mobile vegetations
o Transoesophageal echocardiography: valvular, mobile vegetations

113
Q

What is the treatment of infectious endocarditis?

A

IV antibiotics (6 weeks), surgery

114
Q

What is the definition of aortic stenosis?

A

Narrowing of the aortic valve to a quarter of the normal value, restricting blood flow

115
Q

What is the aetiology of aortic stenosis?

A

Degenerative calcification, congenital aortic stenosis, bicuspid aortic valve, rheumatic heart disease

116
Q

What is the pathophysiology of aortic stenosis?

A

Valve narrowing creates a pressure gradient between the left ventricle and the aorta, resulting in an increased afterload. The left ventricular function is initially maintained by compensatory pressure hypertrophy but when the compensatory mechanisms are exhausted, the left ventricular function decreases

117
Q

What is the clinical presentation of aortic stenosis?

A

o Dyspnoea, anginal chest pain, syncope upon exertion,
o Slow rising carotid pulse (pulsus tardus) with deceased amplitude (pulsus parvus), systolic ejection murmur (crescendo-decrescendo), soft or absent second heart sound, S4 gallop

118
Q

What are the investigations of aortic stenosis?

A

Transthoracic echocardiogram: left ventricular hypertrophy and dilation, elevated aortic pressure gradient, decreased valve area, decreased ejection fraction, thickened, calcified and immobile valve cusps

119
Q

What is the treatment of aortic stenosis?

A

Valve replacement, valvotomy

120
Q

What is the definition of mitral regurgitation?

A

Backflow of blood from the left ventricle to the left atrium during systole due to mitral valve incompetence

121
Q

What is the aetiology of mitral regurgitation?

A

Myxomatous degeneration, ischemic mitral regurgitation, rheumatic heart disease, infective endocarditis, Marfan’s syndrome

122
Q

What is the pathophysiology of mitral regurgitation?

A

Volume overload of the left ventricle causes compensatory left atrial enlargement, left ventricular hypertrophy and increased contractility. There will be progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension and progressive left ventricular volume overload will lead to dilation and progressive heart failure

123
Q

What is the clinical presentation of mitral regurgitation?

A

o Exertional dyspnoea, fatigue, palpitations, lower extremity oedema
o Blowing pansystolic murmur at the apex, radiating to the axilla, a prominent third heart sound, S3, displaced hyperdynamic apex beat

124
Q

What are the investigations of mitral regurgitation?

A

o ECG: may show left atrial enlargement, atrial fibrillation and left ventricular hypertrophy
o Chest X-ray: left atrial enlargement and central pulmonary artery enlargement
o Transoesophageal echocardiogram

125
Q

What is the treatment of mitral regurgitation?

A

Vasodilators to reduce afterload (ACE inhibitors and hydralazine), rate control and anticoagulation for atrial fibrillation and flutter (beta blockers, calcium channel blockers, digoxin), diuretics for fluid overload (furosemide), surgery (low ejection fraction, dilated left ventricle, new onset atrial fibrillation)

126
Q

What is the definition of aortic regurgitation?

A

Backflow of blood from the aorta to the left ventricle during diastole due to ineffective coaptation of the aortic cusps

127
Q

What is the aetiology of aortic regurgitation?

A

Bicuspid aortic valve, aortic root dilation, rheumatic heart disease, infective endocarditis

128
Q

What is the pathophysiology of aortic regurgitation?

A

Combined pressure and volume overload leads to dilation and hypertrophy of the left ventricle. Progressive dilation of the ventricle can lead to heart failure

129
Q

What is the clinical presentation of aortic regurgitation?

A

o Dyspnoea, palpitations
o Jugular vein distention, wide pulse pressure, diastolic blowing decrescendo murmur, systolic ejection murmur, collapsing water hammer pulse

130
Q

What are the investigations of aortic regurgitation?

A

o Chest X-ray: enlarged cardiac silhouette and aortic root enlargement
o Echocardiogram: evaluation of the aortic valve and aortic root with measurements of the left ventricular dimensions and function

131
Q

What is the treatment of aortic regurgitation?

A

Vasodilators to improve stroke volume and reduce regurgitation (ACE inhibitors), surgery (symptomatic, low ejection fraction, dilated left ventricle)

132
Q

What is the definition of mitral stenosis?

A

Narrowing of the mitral valve, restricting blood flow

133
Q

What is the aetiology of mitral stenosis?

A

Rheumatic heart disease, infective endocarditis, mitral annular calcification

134
Q

What is the pathophysiology of mitral stenosis?

A

Pressure across the mitral valve increases and leads to atrial enlargement and atrial fibrillation. The reduced atrial emptying can cause increased pulmonary pressure and congestion

135
Q

What is the clinical presentation of mitral stenosis?

A

o Right heart failure, dyspnoea, haemoptysis, mitral facies (vasoconstriction due to decreased cardiac output results in pinkish-purple patches on the cheek)
o Prominent a wave in jugular venous pulsation, low-pitched mid-diastolic rumble most prominent at the apex (heard best with the patient lying on their left side in held expiration)

136
Q

What are the investigations of mitral stenosis?

A

o ECG: may show atrial fibrillation and left atrium enlargement
o Chest x-ray: left atrium enlargement, pulmonary congestion and occasionally a calcified mitral valve
o Echocardiogram: assesses mitral valve mobility and gradient and mitral valve area

137
Q

What is the treatment of mitral stenosis?

A

Rate control to prolong diastole (beta blockers, digoxin), diuretics for fluid overload (furosemide), anticoagulation if there is atrial fibrillation, percutaneous mitral balloon valvotomy

138
Q

What is the definition of hypertrophic cardiomyopathy?

A

Left ventricular hypertrophy obstructs the left ventricular outflow tract

139
Q

What is the aetiology of hypertrophic cardiomyopathy?

A

Sarcomeric protein gene mutation

140
Q

What is the pathophysiology of hypertrophic cardiomyopathy?

A

Systole is normal, but diastole is affected; the heart is unable to relax due to the thickening of the ventricular walls

141
Q

What is the clinical presentation of hypertrophic cardiomyopathy?

A

Angina, dyspnoea, syncope

142
Q

What are the investigations of hypertrophic cardiomyopathy?

A

ECG: large QRS complexes, large, inverted T waves

143
Q

What is the treatment of hypertrophic cardiomyopathy?

A

Amiodarone, beta blockers and calcium channel blockers, implantable cardioverter defibrillator, septal myomectomy

144
Q

What is the pathophysiology of dilated cardiomyopathy?

A

Ventricular dilation and hypertrophy results in reduced contractility capability of the heart

145
Q

What is the clinical presentation of dilated cardiomyopathy?

A

Breathlessness, tiredness, oedema

146
Q

What are the investigations of dilated cardiomyopathy?

A

o Chest X-ray: cardiomegaly, pulmonary oedema
o ECG: tachycardia
o Echocardiogram: marked dilation

147
Q

What is the treatment of dilated cardiomyopathy?

A

Diuretics for fluid overload, ACE inhibitors, beta blockers, transplantation

148
Q

What is the aetiology of restrictive cardiomyopathy?

A

Idiopathic, amyloidosis, endomyocardial fibrosis

149
Q

What is the pathophysiology of restrictive cardiomyopathy?

A

Restrictive filling of the ventricles which results in poor dilation of the heart

150
Q

What is the clinical presentation of restrictive cardiomyopathy?

A

Dyspnoea, elevated JVP, hepatomegaly, ascites, 3rd and 4th heart sounds

151
Q

What are the investigations of restrictive cardiomyopathy?

A

Echocardiography: thickened ventricular walls, valves, and atrial septum

152
Q

What is the treatment of restrictive cardiomyopathy?

A

Treat underlying cause, heart transplant

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