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Cardiology Flashcards

1
Q

Define stable angina pectoris

A

A symptom of ischaemic heart disease. Central crushing pain due to decreased coronary artery blood flow causing oxygen supple/demand mismatch in exertion.

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2
Q

Describe the aetiology for stable angina pectoris

A

Narrowing of coronary artery by atherosclerosis. Rare: reduced o2 carrying capacity (anaemia), peripheral resistance (LV hypertrophy), coronary artery spasm (Prinzmetal angina)

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3
Q

What are the risk factors for stable angina pectoris

A

Non-modifiable: age, gender, race.
Modifiable: diabetes, hypertension, obesity high LDL, smoking

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4
Q

Describe the pathophysiology for stable angina pectoris

A

High oxygen demand on exertion. Narrowing of coronary arteries from atherosclerotic plaque reduces blood flow > myocardial ischaemia > angina
Atherogenesis: fatty streak > intermediate lesions > fibrous plaque

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5
Q

What are the key presentations for stable angina pectoris

A

Central crushing chest pain which can radiate to jaw, neck, arms, relieved with GTN spray or 5 min rest, pain brought on by exertion

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6
Q

Describe the symptoms for stable angina pectoris

A

Dyspnoea, nausea, sweating, fainting

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7
Q

What is the gold standard investigation for stable angina pectoris

A

CT angiography (presence of luminal narrowing, plaques)

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8
Q

Describe the first line investigations for stable angina pectoris

A

ECG (normal)

Other: Echocardiogram, exercise tolerance test (induces ischaemia), invasive angiography (shows pressure gradient across stenosis), bloods – lipid profile, HbA1c

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9
Q

What are the differential diagnosis for stable angina pectoris

A

Unstable angina, STEMI, NSTEMI

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10
Q

Describe the management for stable angina pectoris

A

Immediate symptomatic relief – GTN spray
Long term relief: 1st line – education. Beta blockers and/or CCB (amlodipine. Do not combine BB with non-dihydropyridine CCB). + other antianginal (long-acting nitrates, e.g. isosorbide mononitrate)
Procedural intervention: PCI, CABG
Secondary prevention: Aspirin, Atorvastatin, ACE inhibitor

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11
Q

Describe the complications for stable angina pectoris

A

MI, stroke, heart failure

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12
Q

Define unstable angina

A

Acute coronary syndrome includes unstable angina and myocardial infarction (STEMI, NSTEMI). Unstable angina is myocardial ischaemia at rest or on minimal exertion with the absence of myocardial injury. It is not relieved with GTN or rest.

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13
Q

Describe the aetiology for unstable angina

A

Atherosclerotic plaque rupture and subsequent thrombosis and inflammation

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14
Q

What are the risk factors for unstable angina

A

Non-Modifiable: age, gender, race. Modifiable: diabetes, hypertension, obesity, high LDL, smoking

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15
Q

Describe the pathophysiology for unstable angina

A

Atheroslerotic plaque rupture and thrombus forms around the ruptured plaque causing partial occlusion of the minor coronary artery causing reduced blood flow > myocardial ischaemia > angina

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16
Q

Describe the key presentations for unstable angina

A

Central crushing chest pain radiating to arms neck jaw, not relieved by GTN or rest, persists longer than 20 minutes, crescendo chest pain (frequent, easier to provoke)

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17
Q

Describe the clinical manifestations for unstable angina

A

Sweating, dyspnoea, nausea, fainting, palpitations

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18
Q

What is the gold standard investigation for unstable angina

A

ECG (no ST elevation) + biomarkers (no troponin increase)

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19
Q

Describe the first line investigations for unstable angina

A

History, ECG (normal or ST depression and T wave inversion), biomarkers (no increases in troponin)

Other: CT angiography

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20
Q

What are the differential diagnosis for unstable angina

A

Stable angina, pericarditis, myocarditis

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21
Q

Describe the management for unstable angina

A

Immediate management – MONA (morphine, oxygen <92%, nitrates, aspirin)
GRACE score (6 month risk of death or repeat MI after NSTEMI),
Prevention: aspirin, clopidogrel (antiplatelet), statin (atorvastatin), metoprolol (BB or CCB), ACEi, modify risk factors
High risk: angiography and PCI

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22
Q

What are the complications for unstable angina

A

MI, stroke, heart failure

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23
Q

Define a STEMI

A

ST elevated myocardial infarction is part of ACS. Ischaemic event leading to death of heart tissue and troponin release.

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24
Q

Describe the aetiology for a STEMI

A

Rupture and thrombosis of plaque causing complete occlusion of major coronary artery lumen.

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25
Q

Describe the risk factors for a STEMI

A

Non-modifiable: age, gender, race. Modifiable: hypertension, diabetes, obesity, high LDL, smoking

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26
Q

Describe the pathophysiology for a STEMI

A

Atherosclerotic plaque rupture and thrombosis causes complete occlusion of coronary artery leading to transmural injury and infarct to the myocardium.

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27
Q

What are the key presentations for a STEMI

A

Central crushing chest pain radiating down arms jaw neck, not relieved by rest or GTN spray, persists >20 mins, impending doom feeling

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28
Q

Describe the clinical manifestations for a STEMI

A

Signs: Tachycardia, high/low BP, 4th heart sound
Symptoms: Sweating, N+V, dyspnoea, fatigue, palpitations

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29
Q

What is the gold standard investigation for a STEMI

A

ECG (ST elevation) + biomarkers (troponin elevated)

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30
Q

Describe the first line investigations for a STEMI

A

ECG (ST elevation in anterolateral leads. After some time, T wave inversion, deep broad Q waves. Left bundle branch block), biomarkers (troponin elevated).

Other: CT angiography, bloods

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31
Q

What are the differential diagnosis for a STEMI

A

Unstable angina, NSTEMI, pericarditis

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32
Q

Describe the management for a STEMI

A

Acute treatment: MONA (morphine, oxygen <92%, nitrates, aspirin)
Primary PCI if available within 120minutes of first medical contact or within 12hours of symptoms, if unavailable, fibrinolysis to break down clot (e.g., alteplase)
Secondary prevention: aspirin, clopidogrel (antiplatelet), statin (atorvastatin), metoprolol (BB or CCB), ACEi, modify risk factors

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33
Q

What are the complications for a STEMI

A

Heart failure, rupture of infarcted ventricle, rupture of interventricular septum, heart block, arrhythmias, mitral regurgitation, post-MI pericarditis (Dressler’s syndrome)

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34
Q

Define an NSTEMI

A

Non-ST-elevated myocardial infarction is part of ACS. Acute ischaemic event causing myocardial cell necrosis and troponin release.

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35
Q

Describe the aetiology of an NSTEMI

A

Rupture and thrombosis of atherosclerotic plaque causing partial occlusion of major coronary artery or total occlusion of minor coronary artery.

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36
Q

Describe the risk factors for an NSTEMI

A

Non modifiable: age, gender, race. Modifiable: hypertension, diabetes, obesity, high LDL, smoking

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37
Q

Describe the pathophysiology for an NSTEMI

A

Atherosclerotic plaque rupture and thrombosis causes partial occlusion to coronary artery. This causes necrosis of cardiac tissue and infarction to sub endothelium.

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38
Q

What are the key presentations for an NSTEMI

A

Central crushing chest pain radiating down arms jaw neck, not relieved by rest or GTN spray, persists >20 mins, impending doom feeling

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39
Q

Describe the clinical manifestations for an NSTEMI

A

Signs: Tachycardia, high/low BP, 4th heart sound
Symptoms: Sweating, N+V, dyspnoea, fatigue, palpitations

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40
Q

What is the gold standard investigation for an NSTEMI

A

ECG (ST depression) + biomarkers (elevated troponin)

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41
Q

Describe the first line investigations for an NSTEMI

A

1st line: ECG (ST depression, T wave inversion. Also, transient ST elevation, R wave regression and biphasic T waves), biomarkers (troponin elevated)

Other: CT angiography, bloods

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42
Q

What are the differential diagnosis for an NSTEMI

A

STEMI, unstable angina

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43
Q

Describe the management for an NSTEMI

A

Immediate management – MONA (morphine, oxygen <92%, nitrates, aspirin)
Then: invasive coronary angiography and PCI
GRACE score (6-month risk of death or repeat MI after NSTEMI),
Prevention: aspirin, clopidogrel (antiplatelet), statin (atorvastatin), metoprolol (BB or CCB), ACEi, modify risk factors

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44
Q

Describe the complications for an NSTEMI

A

Heart failure, ruptured infarcted ventricle, ruptured interventricular septum, mitral regurgitation, arrhythmias, heart block, post-MI pericarditis (Dressler syndrome)

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45
Q

Describe the types of MI

A

Type 1: Traditional MI due to an acute coronary event
Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with procedures such as PCI, coronary stenting and CABG

ACDC
Type 1: A – ACS-type MI
Type 2: C – Can’t cope MI
Type 3: D – Dead by MI
Type 4: C – Caused by us MI

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46
Q

Define heart failure

A

Heart failure is the inability of the heart to deliver oxygenated blood to tissues at a satisfactory rate for the tissues metabolic requirements.
Systolic heart failure: failure of heart to contract efficiently to eject adequate volumes of blood. Ejection fraction <40%. Heart failure with reduced ejection fraction. HFrEF
Diastolic heart failure: inability of the ventricles to relax and fill normally, causing increased filling pressures. Ejection fraction >50%. Heart failure with preserved ejection fraction. HFpEF
Right heart failure: inability of the right ventricle to pump adequate amount of blood leading to systemic venous congestion.
Left heart failure: inability of left ventricle to pump adequate amount of blood leading to pulmonary circulation congestion and oedema.

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47
Q

Describe the epidemiology for heart failure

A

10% of over 70s, male > women, increases with age, typical effects 1-2% developed world

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48
Q

Describe the aetiology for heart failure

A

Ischaemic heart disease, hypertension, cardiomyopathy, alcohol excess, valve disease
Right heart failure: pulmonary hypertension, pulmonary embolism, COPD, cor pulmonale (right heart enlargement as a result of disease of lungs or blood vessels)
Left heart failure: coronary artery disease, valve defect, myocardial infection, congenital heart defects, arrhythmias

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49
Q

Describe the risk factors for heart failure

A

Older, male, smoking, obesity, previous MI

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50
Q

Describe the pathophysiology for heart failure

A

Stroke volume requires adequate preload, optimal myocardial contractility (Frank-starling mechanism), decreased afterload. Therefore reduced cardiac output (heart failure) can be caused by decreased preload, decreased contractility, increased afterload, decreased heart rate.
Once the heart begins to fail compensatory changes occur to maintain CO: increased SNS (increases HR and contractility), increased RAAS (increased fluid retention = increased preload), natriuretic peptides (diuretic, hypotensive, vasodilators), ventricular dilation, ventricular hypertrophy.
Compensatory mechanisms become exhausted and pathological: SNS and RAAS also cause vasoconstriction which increases afterload and myocardial work. Increased cardiac work damages the myocytes reducing CO = heart failure

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51
Q

What are the key presentations for heart failure

A

SOB, fatigue and oedema

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52
Q

Describe the clinical manifestations for heart failure

A

Signs: Oedema (LHF = pulmonary congestion – pulmonary oedema, RHF = systemic backlog – peripheral oedema)
LHF: bibasal pulmonary crackles, 3rd and 4th heart sounds, cardiomegaly (displaced apex beat), tachycardia
RHF: raised JVP, hepatomegaly, pitting oedema, weight gain (fluid)
Symptoms: LHF: dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, poor exercise tolerance, fatigue, nocturnal cough (pink frothy sputum), wheeze, cold peripheries
RHF: peripheral oedema, ascites, nausea, anorexia, facial engorgement, epistaxis

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53
Q

What is the gold standard investigation for heart failure

A

Echocardiogram (may confirm cause, e.g., MI, valvular heart disease, and can show LV dysfunction)

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54
Q

Describe the first line investigations for heart failure

A

1st line: ECG (abnormal – may indicate cause, e.g., ventricular hypertrophy), BNP (brain natriuretic peptide – elevated. Released from myocardial walls under stress). Chest x-ray (ABCDE – alveolar oedema, Kerley B lines, cardiomegaly, dilated upper lobe vessels, effusions (pleural)

Other: FBC

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55
Q

What are the differential diagnosis for heart failure

A

COPD, pulmonary embolism

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56
Q

Describe the management for heart failure

A

1st line - ABAL. ACE inhibitor (ramipril), beta blocker (bisoprolol), aldosterone antagonist (spironolactone), loop diuretic (furosemide)
Consider cardiac resynchronisation therapy. Surgery: LVAD, cardiac transplantation

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57
Q

What are the complications for heart failure

A

Pleural effusion, acute kidney injury, sudden cardiac death

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58
Q

Describe the prognosis for heart failure

A

50% die within 5 years of diagnosis

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59
Q

Define hypertension

A

Blood pressure >140/90 in clinic, >135/85 with ambulatory or home readings

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60
Q

Describe the epidemiology for hypertension

A

Biggest risk factor for cardiovascular disease

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61
Q

Describe the aetiology for hypertension

A
  1. Essential hypertension (95%) - idiopathic
  2. Known cause (5%) – ROPED renal disease, obesity, pregnancy/pre-eclampsia, endocrine syndrome (Conn’s), Drugs (alcohol, steroids, NSAIDS, oestrogen and liquorice)
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62
Q

Describe the risk factors for hypertension

A

Non-modifiable: age, FHx, ethnicity (Afro-Caribbean). Modifiable: alcohol, sedentary lifestyle, diabetes, smoking, salt intake

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63
Q

Describe the pathophysiology for hypertension

A

Causes of hypertension will increase RAAS and SNS causing increased cardiac output and total peripheral resistance, and therefore increase in blood pressure. BP = CO x TPR

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64
Q

What are the key presentations for hypertension

A

Asymptomatic

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65
Q

Describe the clinical manifestations for hypertension

A

Malignant hypertension (180/120): headache, visual disturbances, chest pain, seizures.
Also look for secondary causes of HTN: renal disease, phaeochromocytoma, Cushing’s coarctation of aorta

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66
Q

What is the gold standard investigation for hypertension

A

Ambulatory BP (worn 24hrs) > 135/85 mmHg

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67
Q

Describe the first line investigations for hypertension

A

Clinic BP >140/90 mmHg

Stage Clinic BP ABPM BP
1 >140/90 >135/85
2 >160/90 150/95
3 >180/120*

Other: Fundoscopy (HTN retinopathy), urine albumin:creatinine (proteinuria) and dipstick (haematuria) for renal failure, bloods (HbA1c, GFR, lipids), ECG (abnormalities)

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68
Q

What are the differential diagnosis for hypertension

A

Chronic kidney disease, Cushing syndrome, phaeochromocytoma

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69
Q

Describe the management for hypertension

A
  1. T2DM or Age <55 = ACEi (or ARB). Age > 55 or Black-African/Afro-Caribbean origin = CCB
  2. ACEi + CCB
  3. ACEi + CCB + thiazide-like diuretic
  4. If potassium <4.5 = 1,2,3 + spironolactone. If potassium >4.5 = 1,2,3 + alpha or beta blocker
    Note: If T2DM + Black/Afro + age >55, diabetes takes precedence so give ACEi
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70
Q

Describe the monitoring for hypertension

A

Treatment targets: Age <80 = <140/90mmHg. Age >80 = <150/90mmHg

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71
Q

Describe the complications for hypertension

A

Ischaemic heart disease, cerebrovascular event (stroke, MI), heart failure, CKD

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72
Q

Define Cor Pulmonale

A

Right sided heart failure caused by respiratory disease

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73
Q

Describe the aetiology for Cor Pulmonale

A

COPD, pulmonary embolism, interstitial lung disease, cystic fibrosis, primary pulmonary hypertension

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74
Q

Describe the risk factors for Cor Pulmonale

A

Respiratory disease

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75
Q

Describe the pathophysiology for Cor Pulmonale

A

Increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries. This leads to back pressure of blood in the right atrium, the vena cava and systemic venous system.

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76
Q

What are the key presentations for Cor Pulmonale

A

SOB, peripheral oedema, chest pain

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77
Q

Describe the clinical manifestations for Cor Pulmonale

A

Signs: Hypoxia, cyanosis, raised JVP, peripheral oedema, 3rd heart sound, murmurs (e.g., pan-systolic in tricuspid regurgitation), hepatomegaly
Symptoms: Shortness of breath, syncope, dizziness,

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78
Q

What is the gold standard investigation for Cor pulmonale

A

Right heart catheterisation

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79
Q

Describe the first line investigations for Cor Pulmonale

A

ABG (hypoxia and hypercapnia), spirometry, chest CT, echocardiogram

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80
Q

What are the differential diagnosis for Cor Pulmonale

A

Primary pulmonary hypertension, pulmonary valve stenosis

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81
Q

Describe the management for Cor Pulmonale

A

Treat symptoms and underlying cause. Long term oxygen therapy. Treat heart failure (ABAL). Consider venesection (reduces RBCs) if haematocrit > 55. Consider heart-lung transplantation in young patients

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82
Q

Describe the complications for Cor Pulmonale

A

Tricuspid regurgitation, hepatic congestion and cardiac cirrhosis, death

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83
Q

Describe the prognosis for Cor Pulmonale

A

50% 5 year survival

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84
Q

Define atrial fibrillation

A

Atrial fibrillation is a supraventricular tachycardia caused by uncoordinated, rapid and irregular atrial activity, resulting in an irregularly irregular ventricular pulse

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85
Q

Describe the epidemiology for AF

A

Most common sustained cardiac arrhythmia, more males than females

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86
Q

Describe the aetiology for AF

A

Heart failure, hypertension, coronary artery disease, valvular disease (especially mitral valve stenosis), cardiac surgery, cardiomyopathy, idiopathic

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87
Q

Describe the risk factors for AF

A

Age 60+, hypertension, T2DM, heart failure, past MI

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88
Q

Describe the pathophysiology for AF

A

Contraction of the atria is uncoordinated, rapid and irregular due to disorganised electrical activity which overrides the sinoatrial node activity. 300-600bpm.

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89
Q

What are the key presentations for AF

A

Irregular pulse, tachycardia, palpitations, ECG: no P waves, irregularly irregular pulse and narrow QRS

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90
Q

Describe the clinical manifestations for AF

A

Signs: Irregularly irregular ventricular contractions, tachycardia, apical pulse > radial rate, thromboembolism. ECG: no P waves, irregularly irregular pulse with narrow QRS
Symptoms: Asymptomatic, chest pain, palpitations, dyspnoea, fainting

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91
Q

What is the gold standard investigation for AF

A

ECG: absent P waves, irregularly irregular pulse (irregular R-R intervals with narrow QRS)

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92
Q

Describe the first line investigations for AF

A

1st line ECG: absent P waves, irregularly irregular pulse (irregular R-R intervals with narrow QRS)

Other: FBC

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93
Q

What are the differential diagnosis for AF

A

Atrial flutter, Wolff-Parkinson-white syndrome, atrial tachycardia

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94
Q

Describe the management for AF

A

1st line haemodynamically unstable – DC direct current cardioversion (shocks AF to sinus rhythm)
1st line haemodynamically stable - rate control beta blockers (bisoprolol/metoprolol) or CCB (verapamil/diltiazem) + digoxin. Also, rhythm control with electrical or pharmacological (flecainide) cardioversion + pre-cardioversion anticoagulant.
Long term: catheter ablation

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95
Q

Describe the monitoring for AF

A

CHA2DS2-VASc score calculates stroke risk for atrial fibrillation patients. It includes: congestive heart failure, hypertension, age >75 x2, diabetes, stroke x2, vascular disease, age 65-74, sex category (female). If the score is <2, anticoagulant is required.

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96
Q

Describe the complications for AF

A

Acute stroke, myocardial infarction, congestive heart failure

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97
Q

Describe the prognosis for AF

A

Double mortality risk and 5x stroke risk

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98
Q

Define atrial flutter

A

Macro re-entrant atrial tachycardia caused by organised electrical activity in the atrium with a rate of 250-350bpm. Less common than AF

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99
Q

Describe the aetiology of atrial flutter

A

Idiopathic, coronary heart disease, obesity, heart failure, hypertension, COPD, pericarditis

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100
Q

Describe the risk factors for atrial flutter

A

AF

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101
Q

Describe the pathophysiology for atrial flutter

A

Originates from a re-entrant circuit around the tricuspid valve annulus. Short circuit causes the atria to fire very rapidly

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102
Q

What are the key presentations for atrial flutter

A

ECG: flutter waves saw-tooth pattern, often 2:1 block (p-wave: QRS complex)

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103
Q

Describe the clinical manifestations for atrial flutter

A

Signs: ECG: saw-tooth pattern (F waves), often 2:1 block (2 P waves for every QRS), tachycardia (above 150bpm)
Symptoms: Palpitations, dyspnoea, chest pain, dizziness, syncope, fatigue

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104
Q

What is the gold standard investigation for atrial flutter

A

ECG: saw-tooth pattern (flutter waves), often 2:1 block (2 P waves for every QRS)

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105
Q

Describe the first line investigations for atrial flutter

A

ECG: saw-tooth pattern (flutter waves), often 2:1 block (2 P waves for every QRS)

Other FBC

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106
Q

What are the differential diagnosis for atrial flutter

A

Atrial fibrillation, atrial tachycardia

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107
Q

Describe the management for atrial flutter

A

Haemodynamically unstable – DC cardioversion
Haemodynamically stable – 1. rate control (beta blocker) + anticoagulant (LMWH), 2. electrical cardioversion, 3. pharmacological cardioversion
Ongoing – catheter ablation (removes faulty electrical pathway)

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108
Q

Describe the monitoring for atrial flutter

A

CHA2SD2-VASc for risk of stroke in atrial fibrillation/flutter

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109
Q

Describe the complications for atrial flutter

A

Acute stroke, medication related bradycardia

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110
Q

Define heart block

A

AV block involves partial or complete interruption of impulse transmission from atria to ventricles. Types: 1st degree, 2nd degree Mobitz type 1, 2nd degree Mobitz type 2, 3rd degree (complete)

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111
Q

Describe the aetiology for heart block

A

Main: Coronary artery disease, cardiomyopathy, fibrosis
1st degree: AV blocking drugs (beta blockers, CCB, digoxin)
2nd degree Mobitz type 1: AV blocking drugs (beta blockers, CCB, digoxin, amiodarone), inferior MI
2nd degree Mobitz type 2: drugs, MI, rheumatic fever
3rd degree (complete): MI, hypertension, structural heart defect

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112
Q

Describe the risk factors for heart block

A

Coronary artery disease, cardiomyopathy, fibrosis

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113
Q

Describe the pathophysiology for heart block

A

1st degree: consistent prolongation of PR interval due to delayed conduction via AV node. Every P wave followed by a QRS
2nd degree Mobitz type 1: progressive prolongation of the PR interval until the atrial impulse is not conducted and a QRS complex is dropped. AVN conduction begins with next beat and sequence repeats. Wenckebach phenomenon.
2nd degree Mobitz type 2: consistent prolonged PR interval duration with intermittently dropped QRS complexes due to failure of conduction. PR interval is constant, but every 3rd/4th QRS is dropped.
3rd degree (complete): no communication between atria and ventricles due to complete failure of conduction. P waves and QRS complexes have no association due to atria and ventricles functioning independently.

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114
Q

What are the key presentations for heart block

A

1st degree: asymptomatic.
2nd degree Mobitz type 1: asymptomatic/ bradycardia, syncope, irregular pulse
2nd degree Mobitz type 2: palpitations, syncope, regular irregular pulse
3rd degree (complete): palpitations, syncope, irregular pulse, bradycardia, chest pain, shortness of breath

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115
Q

Describe the gold standard investigations for heart block

A

1st degree: ECG: every P followed by QRS, prolonged PR(>200ms), regular rhythm
2nd degree Mobitz type 1: ECG: Progressive lengthening of PR interval until a QRS is dropped and cycle repeats with shorter PR interval, irregular rhythm
2nd degree Mobitz type 2: ECG: Constant enlarged PR interval, but every nth QRS complex is missing, irregular rhythm
3rd degree (complete): ECG: P waves and QRS complexes random. PR interval absent due to atria-ventricle dissociation.

Other investigations: troponin (may be elevated)

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116
Q

What are the differential diagnosis for heart block

A

SVT, AF

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117
Q

Describe the management for heart block

A

1st degree: asymptomatic = no treatment, symptomatic = pacemaker
2nd degree Mobitz type 1: asymptomatic = no treatment, symptomatic = pacemaker
2nd degree Mobitz type 2: pacemaker
3rd degree (complete): IV atropine/isoprenaline + permanent pacemaker

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118
Q

Describe the complications for heart block

A

Sudden cardiac death

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119
Q

Define ventricular ectopics

A

Premature ventricular beats caused by random electrical discharges from the ventricles before an electrical impulse can be made by the atrium

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120
Q

What are the key presentations for ventricular ectopics

A

Random, brief palpitations, abnormal beat, syncope

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121
Q

What is the gold standard investigation for ventricular ectopics

A

ECG: individual random, abnormal, broad QRS complexes on a background of a normal ECG

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122
Q

Describe the management for ventricular ectopics

A

Reassurance and self-monitoring. Beta blocker or CCB. Ablation to stop abnormal signals

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123
Q

Describe the complications for ventricular ectopics

A

Bigeminy - ventricular ectopics occur so frequently that they happen after every sinus beat. ECG shows normal sinus beat followed by ectopic, normal, ectopic

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124
Q

Define long QT syndrome

A

Ventricular tachyarrhythmia characterised by prolonged QT interval on ECG >480ms

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125
Q

Describe the aetiology for long QT syndrome

A

Congenital channelopathy: Romano-Ward syndrome, hypokalaemia, hypocalcaemia, bradycardia, drugs (amiodarone, tricyclic antidepressants)

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126
Q

What are the key presentations for long QT syndrome

A

Syncope, palpitations, may progress to V-fib

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127
Q

What is the gold standard investigation for long QT syndrome

A

ECG: prolonged QT interval >480ms

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128
Q

Describe the management for long QT syndrome

A

Correct electrolyte disturbances and remove causative factors, give beta blocker, pacemaker or implantable defib

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129
Q

Describe the complications for long QT syndrome

A

Torsades de pointes

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130
Q

Define Wolff-Parkinson-White syndrome (AVRT)

A

AVRT- atrioventricular re-entry tachycardia. There is an accessory pathway for impulse conduction caused by a congenital connection between the atria and ventricles. Not through the AV node.

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131
Q

Describe the aetiology for Wolff-Parkinson-White syndrome

A

Congential abnormality, Epstein’s anomaly

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132
Q

What are the risk factors for AVRT

A

Congenital heart defects

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133
Q

Describe the pathophysiology for AVRT

A

An accessory pathway between the atria and ventricles allows electrical conduction to bypass the AV node and for the ventricles to be stimulated pre-maturely. Alongside the AV node conduction, this leads to double exciting of the ventricles. The accessory pathway in WPW is called Bundle of Kent. As conduction is not regulated by the AV node, this causes tachycardia.

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134
Q

What are the key presentations for AVRT

A

Palpitations, ECG: short PR interval, wide QRS, slurred upstroke of QRS complex = delta wave

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135
Q

Describe the clinical manifestations for AVRT

A

Signs: Tachycardia, ECG: short PR interval, wide QRS, slurred upstroke of QRS complex = delta wave
Symptoms: Palpitations, dizziness, dyspnoea

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136
Q

What is the gold standard investigation for AVRT

A

ECG: short PR interval, wide QRS, slurred upstroke of QRS complex = delta wave

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137
Q

Describe the first line investigations for AVRT

A

ECG: short PR interval, wide QRS, slurred upstroke of QRS complex = delta wave

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138
Q

What are the differential diagnosis for AVRT

A

AF, atrial flutter, AVNRT

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139
Q

Describe the management for AVRT

A

1st line – Vagal manoeuvre to slow heart: Valsalva manoeuvre (pinch nose, blow out of mouth) or carotid sinus massage
2. If unsuccessful give IV adenosine (slows conduction through heart. 6mg, then 12mg)
3. Cardioversion. Long term - catheter ablation (remove faulty electrical pathway)

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140
Q

Describe the complications for AVRT

A

Sudden cardiac death

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141
Q

Define abdominal aortic aneurysm

A

Dilation of the abdominal aorta >50% with a diameter greater than 3cm (aneurysm typically infrarenal)

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142
Q

Describe the epidemiology for AAA

A

Men affected more often and younger

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143
Q

Describe the aetiology of AAA

A

Mainly idiopathic, atheroma, trauma, infection, connective tissue disorders (Marfan’s and Ehlers-Danlos syndrome)

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144
Q

Describe the risk factors for AAA

A

Smoking, atherosclerosis, obesity, hypertension, increasing age

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145
Q

Describe the pathophysiology for AAA

A

Inflammation and degeneration of smooth muscle cells > loss of structural integrity of the aortic wall > widening of the vessel > mechanical stress (e.g., hypertension) acts on weakened wall tissue > dilation and rupture may occur
Dilation of vessel may disrupt laminar flow and turbulence causing thrombi formation in the aneurysm and thromboembolism

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146
Q

What are the key presentations for AAA

A

Asymptomatic, palpable pulsatile abdominal mass

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147
Q

Describe the clinical manifestations for AAA

A

Signs: Pulsatile mass on abdomen palpitation, bruit, hypotension, tachycardia
Symptoms: Back pain, RUPTURE = severe epigastric pain radiating to back and flank, loss of consciousness, N+V, painful pulsatile mass, hypovolemic shock

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148
Q

What is the gold standard investigation for AAA

A

Computed tomography angiography

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149
Q

Describe the first line investigations for AAA

A

1st line Abdominal Ultrasound (>3cm. ruptured = immediate management)

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150
Q

What are the differential diagnosis for AAA

A

Acute pancreatitis, diverticulitis, appendicitis

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151
Q

Describe the management for AAA

A

Ruptured = emergency. Urgent surgical repair EVAR (endovascular aneurysm repair, stent inserted through femoral arteries) or open surgical repair. + resuscitation measures (oxygen, fluids, catheter, permissive hypotension – aiming for lower-than-normal BP during fluid resuscitation as higher BP may increase blood loss)
Unruptured: symptomatic = urgent surgical repair. Asymptomatic = surveillance and risk management (smoking, diet, exercise, HTN). If asymptomatic but aneurysm > 5.5cm or rapidly growing = elective surgical repair. EVAR or open surgery

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152
Q

What are the complications for AAA

A

Ruptured aneurysm, thrombosis, embolism, abdominal compartment syndrome

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153
Q

Describe the prognosis for AAA

A

80% mortality if ruptured

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154
Q

Define aortic dissection

A

Tear in the intima of the aorta allowing blood to flow dissect the media, forming a false lumen between the inner and outer layers of the media.

Stanford classification: Type A – affects ascending aorta before brachiocephalic artery. Type B – affects descending aorta after the left subclavian. Most common location: sinotubular junction where aortic roots becomes tubular aorta (type A)

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155
Q

Describe the epidemiology of aortic dissection

A

Men aged 50-70

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156
Q

Describe the aetiology for aortic dissection

A

Mechanical wall stress due to risk factors. Also, connective tissue disorders (Marfan’s and Ehlers-Danlos syndrome), and aorta conditions (bicuspid aortic valve, coarctation of the aorta, CABG)

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157
Q

Describe the risk factors for aortic dissection

A

Hypertension, smoking, trauma, raised LDL, obesity, sedentary lifestyle, male, increasing age.

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158
Q

Describe the pathophysiology for aortic dissection

A

Tear in the intima causes blood to pass through the media creating a false lumen. As the dissection spreads, flow through the false lumen can occlude flow through branches of the aorta including coronary, brachiocephalic, carotid, intercostal, renal and visceral > ischemia of supplied regions.

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159
Q

What are the key presentations for aortic dissection

A

Sudden and severe ripping/tearing pain in chest

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160
Q

Describe the clinical manifestations for aortic dissection

A

Signs: Asymmetrical blood pressure in arms (>20mmHg), hypotension, radial pulse deficit (radial pulse in one arm is decreased/absent and doesn’t match apex beat), diastolic murmur, focal neurological deficit (e.g., muscle weakness/paralysis – carotid and spinal arteries), interscapular and lower pain
Symptoms: Syncope, chest, and abdominal pain, muscle weakness

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161
Q

What is the gold standard investigation for aortic dissection

A

CT angiogram or transoesophageal echocardiogram (intimal flap and false lumen)

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162
Q

Describe the first line investigations for aortic dissection

A

1st line ECG (ST depression may occur), chest x-ray (widened mediastinum), TTE echocardiogram (intimal flap in acute, two lumens in chronic)

Other: MRI

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163
Q

What are the differential diagnosis for aortic dissection

A

Myocardial infarction, cardiac arrest, pericarditis

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164
Q

Describe the management for aortic dissection

A

1st line – immediate surgery. Type A (open surgery to replace aortic defect with stent), Type B (TEVAR thoracic endovascular aortic repair). Maintain haemodynamic stability (fluids, adrenaline, transfusion)
Medical: 1. Beta blocker (labetalol), or, 2. Non-dihydropyridine CCB (diltiazem/verapamil). Also, vasodilator sodium nitroprusside

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165
Q

Describe the complications for aortic dissection

A

Cardiac tamponade, aortic regurgitation, pre-renal AKI

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166
Q

Describe the prognosis for aortic dissection

A

High mortality from rupture

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167
Q

Define peripheral vascular disease

A

Range of syndromes that are caused by atherosclerotic obstruction of lower-extremity arteries.

168
Q

Describe the epidemiology for peripheral vascular disease

A

Very common, increases with age, more men

169
Q

Describe the aetiology for peripheral vascular disease

A

Atherosclerosis

170
Q

Describe the risk factors for peripheral vascular disease

A

Non-modifiable: age, gender, race. Modifiable: obesity, diabetes, hypertension, high LDL, smoking

171
Q

Describe the pathophysiology for peripheral vascular disease

A

Atherosclerotic plaques cause narrowing of arteries, reducing blood supply to limbs.
Intermittent claudication: ischaemia in a limb during exertion, relieved by rest
Acute limb ischemia: rapid onset of ischaemia in limb due to thrombus blocking blood supply
Critical limb ischaemia: blood supply barely adequate to meet metabolic demands of tissue. End stage of PVD, can cause gangrene and complete limb loss

172
Q

What are the key presentations for peripheral vascular disease

A

Intermittent claudication (exercise cramp in calf, thigh, buttock relieved with rest), 6 PS (pain, pale, pulseless, perishing cold, paraesthesia, paralysis), ankle brachial pressure index <0.9 (ratio of SBP in ankle to arm)

173
Q

Describe the clinical manifestations for peripheral vascular disease

A

Signs: Gangrene, non-healing ulcer, weak foot pulses, erectile dysfunction, bruits, Buerger’s test (raise foot = pale, but foot down = blue (deoxy blood returns to foot), and then dark red (reactive hyperaemia)
Symptoms: Severe unremitting pain in foot (worse at night as gravity doesn’t pull blood into foot), skin changes

174
Q

What is the gold standard investigation for peripheral vascular disease

A

CT angiogram (shows occlusions)

175
Q

Describe the first line investigations for peripheral vascular disease

A

Ankle brachial pressure index (0.5-0.9 = mild PAD, <0.5 = severe PAD).
Fontaine classification: 1. Asymptomatic, 2. Intermittent Claudication, 3. Ischaemic rest pain, 4. Ischaemic ulcers, e.g., gangrene

Other: Duplex ultrasound (shows speed and volume of blood flow)

176
Q

Describe the management for peripheral vascular disease

A

Intermittent claudication: risk factor management (smoking, exercise, weight loss, statins, antiplatelet – aspirin, clopidogrel)
Chronic limb ischaemia: risk factor management, revascularisation surgery (stenting and angioplasty, vein bypassing), amputation if severe
Acute limb ischaemia: urgent surgery (endovascular thrombolysis, endarterectomy, bypass surgery) or amputation

177
Q

Describe the complications for peripheral vascular disease

A

Amputation, permanent limb weakness, gangrene

178
Q

Define acute pericarditis

A

Inflammation of the pericardium with or without pericardial effusion

179
Q

Describe the epidemiology for acute pericarditis

A

80-90% idiopathic, higher in young patients

180
Q

Describe the aetiology for acute pericarditis

A

Viral (enteroviruses), bacterial (TB), autoimmune (rheumatoid arthritis, Sjogren syndrome), neoplastic, metabolic (uraemia), traumatic and iatrogenic, idiopathic, Dressler’s syndrome (post MI)

181
Q

Describe the risk factors for acute pericarditis

A

Bacterial/viral infections, past MI, autoimmune disease, trauma

182
Q

Describe the pathophysiology for acute pericarditis

A

Inflamed pericardial layers rub against each other due to narrowed pericardial space from inflammation, which exacerbates current inflammation. This may remain fibrinous – dry, or can become effusive as extra fluid needs to compensate for friction (purulent serous exudate or haemorrhagic exudate)

183
Q

What are the key presentations for acute pericarditis

A

Severe, sharp, and pleuritic chest pain of rapid onset that can radiate to the left arm jaw neck. Relieved by sitting forward, exacerbated by lying down.

184
Q

Describe the clinical manifestations for acute pericarditis

A

Signs: Pericardial friction rub on auscultation (patient leans forward, squeaky leather to and fro sound), raised JVP, ECG changes (saddle-shaped concave ST elevation, PR depression)
Symptoms: Dyspnoea, hiccups (irritation of phrenic nerve), cough, skin rash

185
Q

What is the gold standard investigation for acute pericarditis

A

ECG changes (ST saddle shaped concave elevation, PR depression). Clinical diagnosis needs at least 2 of: chest pain, friction rub, ECG changes, pericardial effusion

186
Q

Describe the first line investigations for acute pericarditis

A

Clinical exam (pericardial rub, sinus tachycardia, fever, signs of effusion – pulsus paradoxus drop in BP). ECG, bloods (WCC + ESR increase), chest x ray, echocardiogram

Other: Serum troponin (elevation indicates myopericarditis or ACS), blood cultures

187
Q

What are the differential diagnosis for acute pericarditis

A

MYOCARDIAL INFARCTION!!! Pneumonia, pulmonary embolus

188
Q

Describe the management for acute pericarditis

A

Sedentary activity until symptoms resolve and ECG/CRP. 1 - NSAID or aspirin. + Colchicine (anti-inflammatory)

189
Q

What are the complications for acute pericarditis

A

Pericardial effusion, cardiac tamponade, chronic constrictive pericarditis

190
Q

Describe the prognosis for acute pericarditis

A

Pretty good with acute

191
Q

Define infective endocarditis

A

Infection of heart valves or other endocardial lined structures within the heart
Types: left sided native (mitral or aortic), left sided prosthetic, right sided, device related (e.g., pacemakers, defibrillator)

192
Q

Describe the epidemiology of infective endocarditis

A

Elderly, young IV drug users, young with congenital heart disease, anyone with prosthetic valve

193
Q

Describe the aetiology for infective endocarditis

A

Bacteria: S. aureus (common in IVDU, T2DM, surgery), S. viridans (poor dental hygiene), enterococci/s. bovis, HACEK organisms, fungi (candida, aspergillus)

194
Q

Describe the risk factors for IE

A

Elderly, intra-venous drug users, prosthetic valves, rheumatic fever, surgery

195
Q

Describe the pathophysiology for IE

A
  1. Transient bacteraemia. 2. Damage to valvular tissue. 3. Formation of vegetation
    Pathogen enters bloodstream. Valve is damaged exposing endothelium, platelets and fibrin aggregate. Pathogen binds to platelet-fibrin matrix forming vegetation. This leads to cardiac valve distortion which can cause heart failure and sepsis.
196
Q

What are the key presentations for IE

A

Fever, heart new murmur, splinter haemorrhages (nails), Osler’s nodes (tender subcutaneous nodules on fingers), Janeway lesions (painless erythematous macules on the palms), Roth’s spots (retinal haemorrhage),

197
Q

Describe the clinical manifestations for IE

A

Signs: Embolism (stroke, MI, PE), valve dysfunction (arrhythmia, heart failure)
Symptoms: Fever, sweats, weight loss, fatigue

198
Q

What is the gold standard investigation for IE

A

Transoesophageal echocardiogram (vegetation)

199
Q

Describe the first line investigations for IE

A

Duke’s criteria: MAJOR – positive blood culture organisms typical of IE, evidence of endocardial involvement. MINOR – risk factors, fever, vascular phenomena, immune phenomena, blood cultures which aren’t major. Definitive IE: 2 major/1 major + 3 minor
Ix: blood cultures (positive), transthoracic echocardiogram (vegetation), FBC (anaemia, neutrophilia) raised ESR/CRP, ECG (prolonged PR interval)

Other: Fundoscopy (Roth’s spots)

200
Q

What are the differential diagnosis for IE

A

Rheumatic fever

201
Q

Describe the management for IE

A

1st line – antibiotics based on cultures.
S. aureus = beta lactam/vancomycin + rifampicin + gentamicin
S. viridans = beta lactam (penicillin)/vancomycin + gentamicin
S.bovis/enterococci = beta lactam/vancomycin + aminoglycoside
Surgery if antibiotics aren’t working, complications, to remove infected devices, to replace the valve, to remove large vegetations before they embolise

202
Q

Describe the complications for IE

A

Vegetations embolising to cause stroke, MI, PE, Heart failure, sepsis

203
Q

Define aortic stenosis

A

Obstruction of blood flow across the aortic valve due to narrowing so the left ventricle can’t eject blood properly in systole. Normal aortic valve 3-4cm2, symptoms occur when valve 1/4 size

204
Q

Describe the epidemiology of aortic stenosis

A

Most common valve defect

205
Q

Describe the aetiology for aortic stenosis

A

Congenital bicuspid aortic valve (normally tricuspid), congenital aortic stenosis. Acquired: Ageing calcification, rheumatic heart disease

206
Q

Describe the risk factors for aortic stenosis

A

Age > 60 years, congenital aortic valve defect, rheumatic heart disease

207
Q

Describe the pathophysiology for aortic stenosis

A

Aortic orifice is restricted so a pressure gradient develops between the LV and the aorta (increased afterload). Left ventricle function is initially maintained by compensatory hypertrophy. Over time this becomes exhausted, left ventricle function declines.

208
Q

What are the key presentations for aortic stenosis

A

SAD: syncope (exertional), angina, dyspnoea (exertion due to heart failure), ejection systolic crescendo-decrescendo murmur radiating to carotids

209
Q

Describe the clinical manifestations for aortic stenosis

A

Signs: Slow rising carotid pulse and decreased pulse amplitude, soft/absent 2nd heart sound, prominent S4 heart sound
Symptoms: Dyspnoea, fatigue, chest pain

210
Q

What is the gold standard investigation for aortic stenosis

A

Echocardiogram (+Doppler): assess LV size and function, doppler derived elevated aortic pressure gradient, assess valve area

211
Q

Describe the clinical manifestations for aortic stenosis

A

ECG (left ventricle hypertrophy and Q waves), chest x-ray (may show pulmonary congestion)

212
Q

What are the differential diagnosis for aortic stenosis

A

Hypertrophic cardiomyopathy, ischaemic heart disease

213
Q

Describe the management for aortic stenosis

A

Management 1st line – surgery if symptomatic, reduced ejection fraction or undergoing CABG with aortic stenosis. Lower risk patients: SAVR (surgical aortic valve replacement). Higher risk patients (e.g., age 75+): TAVI (transcatheter aortic valve implantation)
Good dental hygiene, IE prophylaxis, medical therapy limited role since AS is mechanical (statin, ACEi)

214
Q

Describe the complications for aortic stenosis

A

Heart failure, sudden cardiac death, IE

215
Q

Define aortic regurgitation

A

Leakage of blood into left ventricle during diastole due to ineffective closing of the aortic valve cusps

216
Q

Describe the aetiology for aortic regurgitation

A

Bicuspid aortic valve, rheumatic heart disease, infective endocarditis, connective tissue disorders (e.g., Marfan’s, Ehlers-Danlos)

217
Q

Describe the risk factors for aortic regurgitation

A

Bicuspid aortic valve, rheumatic heart disease, infective endocarditis, connective tissue disorders (e.g., Marfan’s, Ehlers-Danlos)

218
Q

Describe the pathophysiology for aortic regurgitation

A

Combined pressure and volume overload in left ventricle. Compensatory mechanisms: left ventricle dilation, left ventricle hypertrophy. Progressive dilation leads to heart failure.

219
Q

What are the key presentations for aortic regurgitation

A

Wide pulse pressure, diastolic blowing murmur at left sternal border, Austin flint murmur (rumbling diastolic murmur, fluttering of anterior mitral valve due to regurgitant streams), displaced hyperdynamic apical impulse

220
Q

Describe the clinical manifestations for aortic regurgitation

A

Signs: Diastolic blowing murmur, Austin flint murmur at apex, systolic ejection murmur, collapsing (water hammer/Corrigan’s) pulse (rapid rise and collapse in arterial pulse resulting in wide pulse pressure), Quincke’s sign (capillary pulsations), de Musset sign (head bobbing with heartbeat)
Symptoms: Dyspnoea on exertion, orthopnoea, palpitations, paroxysmal nocturnal dyspnoea

221
Q

What is the gold standard investigation for aortic regurgitation

A

Echocardiogram: LV size and function, aortic valve evaluation

222
Q

Describe the first line investigations for aortic regurgitation

A

ECG, Chest x-ray: enlarged cardiac silhouette and enlarged aortic root

223
Q

What are the differential diagnosis for aortic regurgitation

A

Mitral regurgitation, aortic stenosis, mitral stenosis, infective endocarditis

224
Q

Describe the management for aortic regurgitation

A

1st line – surgery if symptomatic or asymptomatic with ejection fraction <50% or LV end-systolic diameter >50mm. surgery: Aortic valve replacement (SAVR), or TAVI if unsuitable (transcatheter aortic valve implantation)
IE prophylaxis, inotropes, diuretics

225
Q

Describe the complications for aortic regurgitation

A

IE, heart failure, sudden cardiac death

226
Q

Define mitral stenosis

A

Obstruction to left ventricular inflow which prevents proper filling in diastole

227
Q

Describe the aetiology for mitral stenosis

A

Rheumatic heart disease, IE, valve calcification

228
Q

Describe the risk factors for mitral stenosis

A

Rheumatic heart disease (S.pyogenes infection)

229
Q

Describe the pathophysiology for mitral stenosis

A

Increased trans-mitral pressures leads to left atrial enlargement and atrial fibrillation. Left atrial dilation causes pulmonary congestion (reduced emptying) and progressive dyspnoea. Pulmonary hypertension causes right heart failure symptoms. Pulmonary hypertension causes rupture of bronchial vessels leading to haemoptysis.

230
Q

What are the key presentations for mitral stenosis

A

Malar flush, atrial fibrillation, low pitched mid-diastolic murmur (loudest at apex, best heard on expiration. Note: RHS best heard on inspiration. LHS = expiration)

231
Q

Describe the clinical manifestations for mitral stenosis

A

Signs: Prominent “a” wave in jugular venous pulsations, RHF signs, loud opening 1st heart sound snap
Symptoms: Dyspnoea, orthopnoea, haemoptysis, RHF symptoms, palpitations

232
Q

What is the gold standard investigation for mitral stenosis

A

Echocardiogram: assesses mitral valve mobility, gradient, and orifice area. Hockey stick shaped mitral deformity

233
Q

Describe the first line investigations for mitral stenosis

A

ECG: atrial fibrillation and left atrial enlargement, chest x-ray: left atrial enlargement (M shaped P waves), pulmonary vessel congestion

234
Q

What are the differential diagnosis for mitral stenosis

A

AF

235
Q

Describe the management for mitral stenosis

A

Medical therapy (MS is mechanical so medicine only relieves symptoms): diuretics to reduce LA pressure, BB, CCB, digoxin to prolong diastole for better filling.
Surgery: mitral balloon valvotomy, valve replacement. Infective endocarditis prophylaxis

236
Q

Describe the complications for mitral stenosis

A

AF, stroke, IE

237
Q

Define mitral regurgitation

A

Backflow of blood from the LV to the LA during systole

238
Q

Describe the epidemiology for mitral regurgitation

A

Mild MR seen in 80% of normal individuals

239
Q

Describe the aetiology for mitral regurgitation

A

Myxomatous degeneration (floppy valve), ischaemic mitral regurgitation, rheumatic heart disease, infective endocarditis, connective tissue disorders (Marfan’s, Ehlers-Danlos)

240
Q

Describe the risk factors for mitral regurgitation

A

Rheumatic heart disease, IE, mitral valve prolapse

241
Q

Describe the pathophysiology for mitral regurgiation

A

Left ventricular volume overload. Compensatory mechanisms: left atrial enlargement, left ventricular hypertrophy, and increased contractility. Progressive left atrial dilation and right ventricle dysfunction due to pulmonary hypertension. Progressive left ventricle volume overload leads to dilation and heart failure.

242
Q

What are the key presentations for mitral regurgitation

A

Pan-systolic high pitched, whistling murmur at apex radiating to axilla, dyspnoea on exertion

243
Q

Describe the clinical manifestations for mitral regurgitation

A

Signs: S3 heart sound, soft 1st heart sound, heart failure
Symptoms: Dyspnoea on exertion, exercise intolerance, heart failure symptoms, fatigue, orthopnoea

243
Q

What is the gold standard investigation for mitral regurgitation

A

Echocardiogram: estimation of LA, LV size and function. Valve structure assessment

244
Q

Describe the first line investigations for mitral regurgitation

A

ECG: LA enlargement (M shaped P waves), atrial fibrillation, left ventricular hypertrophy. Chest x-ray: LA enlargement, central pulmonary artery enlargement

245
Q

What are the differential diagnosis for mitral regurgitation

A

Aortic stenosis, mitral stenosis

246
Q

Describe the management for mitral regurgitation

A

1st line – surgery if symptomatic or asymptomatic with ejection fraction <60% or LV end-systolic diameter >40mm. Surgery: valve repair or replacement.
Medication: Rate control for AF (BB, CCB, digoxin), anticoagulation for AF, diuretics for fluid overload, infective endocarditis prophylaxis

247
Q

Describe the complications for mitral regurgitation

A

AF, congestive heart failure, IE

248
Q

Define shock

A

Medical emergency when the body isn’t getting enough blood flow to provide adequate substrate for aerobic cellular respiration. Types: cardiogenic, hypovolemic, septic, anaphylactic, neurogenic

249
Q

Describe the aetiology for shock

A

Cardiogenic: heart pump failure, MI, cardiac arrest. Reduced CO and MAP
Hypovolemic: due to blood loss/fluid loss. Reduced venous return, CO and MAP
Septic: toxins in blood. Reduced MAP
Anaphylactic: Severe allergic reaction. Histamine release, vasodilation, reduced MAP, hypoxia
Neurogenic: damage to CNS, loss of SNS causing vasodilation and low BP

250
Q

What are the key presentations for shock

A

All types: pulse weak + rapid, pale, sweaty, cold, low BP, reduced urine output, confusion

251
Q

Describe the clinical manifestations for shock

A

Symptoms: Cardiogenic: chest pain, oedema, raised JVP, slow cap refill, dyspnoea
Hypovolemic: hypotension, tachycardia, clammy skin, cyanosis
Septic: pyrexia, warm peripheries, diarrhoea, fever
Anaphylactic: urticaria, puffy face, hypotension, tachycardia, itching, wheeze
Neurogenic: bradycardia, instantaneous hypotension, warm flushed skin, priapism

252
Q

Describe the management for shock

A

Cardiogenic: ABCDE, resuscitation (whatever treats underlying cause, e.g., fluids, oxygen, CPR)
Hypovolemic: ABCDE, oxygen, IV fluids, vasodilator
Septic: ABCDE, broad spectrum antibiotics
Anaphylactic: ABCDE, IV adrenaline
Neurogenic: ABCDE, IV atropine

253
Q

Define ventricular septal defect

A

Congenital abnormal connection between the 2 ventricles

254
Q

Describe the aetiology for ventricular septal defect

A

Congenital - Down’s syndrome, turner’s syndrome

255
Q

Describe the pathophysiology for ventricular septal defect

A

Increased pressure in the right ventricle causes blood to flow from the right ventricle to the left ventricle, increasing blood flow through the lungs, therefore no cyanosis. This is following a left to right shunt but when right side becomes higher then left then becomes cyanotic (Eisenmenger syndrome).
A left to right shunt causes increased pressure in the pulmonary vessels leading to pulmonary hypertension. If this continues, the pressure in the right side of the heart will become greater than the left, resulting in blood shunting from the right to left ventricle, bypassing the lungs and causing cyanosis. This is Eisenmenger syndrome.

256
Q

What are the key presentations for ventricular septal defect

A

Small VSD – asymptomatic
Large VSD – high pulmonary blood flow, exercise intolerance, harsh pan-systolic murmur, breathless, poor feeding, failure to thrive, increased respiratory rate, tachycardia, may cause Eisenmenger’s.

257
Q

What is the gold standard investigation for ventricular septal defect

A

Echocardiogram (shows shunting across VSD)

258
Q

Describe the first line investigations for ventricular septal defect

A

Chest x-ray (pulmonary plethora, cardiomegaly), ECG

259
Q

What are the differential diagnosis for ventricular septal defect

A

ASD, PDA

260
Q

Describe the management for ventricular septal defect

A

Small + Asymptomatic = no treatment. Large + Symptomatic = surgical repair

261
Q

Describe the complications for ventricular septal defect

A

IE

262
Q

Define atrial septal defect

A

Abnormal connection between the 2 atria. Types: ostium primum, ostium secondum, patent foramen ovale

263
Q

Describe the aetiology for atrial septal defect

A

Congenital

264
Q

Describe the pathophsyiology for atrial septal defect

A

Greater pressure in the left atrium causes a left to right shunt pushing blood into the right atrium, increasing blood flow through the right heart and pulmonary vessels, therefore no cyanosis.
Increased blood flow through the right heart leads to right heart strain and RVH, causing pulmonary hypertension. This leads to Eisenmenger syndrome where the shunt reverses from left to right to right to left, bypassing the lungs causing cyanosis.

265
Q

Describe the clinical manifestations for atrial septal defect

A

Signs: Small = asymptomatic
Large = significant increase in blood flow through right heart and lungs, systolic ejection murmur, pulmonary hypertension, right heart dilatation, SOBOE, increased chest infections, fixed splitting of second heart sound
Symptoms: Dizziness, palpitations, dyspnoea, failure to thrive

266
Q

What is the gold standard investigation for atrial septal defect

A

Echocardiogram (shunt visualisation, shows blood flow pattern)

267
Q

Describe the first line investigations for atrial septal defect

A

ECG (tall P waves show right atrial enlargement), chest x-ray (enlarged heart and pulmonary arteries)

268
Q

What are the differential diagnosis for atrial septal defect

A

VSD, PDA

269
Q

Describe the management for ASD

A

Spontaneous closure otherwise surgical closure

270
Q

Describe the complications for ASD

A

Stroke from venous thromboembolism, atrial fibrillation, pulmonary hypertension, right heart failure, eisenmengers

271
Q

Define patent ductus arteriosus

A

Ductus arteriosus fails to close post birth

272
Q

Describe the aetiology for PDA

A

Congenital, prematurity, mother rubella infection

273
Q

Describe the pathophysiology for PDA

A

Pressure in the aorta is higher than in pulmonary vessels so blood flows from the aorta to the pulmonary artery creating a left to right shunt. This increases pressure in the pulmonary arteries leading to pulmonary hypertension, right heart strain and right ventricular hypertrophy. Increased blood flow to the left side of the heart can cause left ventricular hypertrophy.

274
Q

What are the key presentations for PDA

A

Small = asymptomatic
Large = continuous machinery like murmur, cardiomegaly, torrential flow from aorta to PA causing pulmonary hypertension and RVH, breathlessness, poor feeding, failure to thrive, risk of endocarditis

275
Q

What is the gold standard investigation for PDA

A

Echocardiogram (shows the shunt, can show ventricle hypertrophy)

276
Q

Describe the first line investigations for PDA

A

Chest x-ray (cardiomegaly), ECG (deep Q waves and R waves show left atrial enlargement)

277
Q

What are the differential diagnosis for PDA

A

ASD,VSD

278
Q

Describe the management for PDA

A

Spontaneous or surgical closure (percutaneous catheter). Indomethacin (prostaglandin inhibitor) may close the PDA

279
Q

Describe the complications for PDA

A

IE, respiratory distress syndrome

280
Q
A
281
Q

Define coarctation of aorta

A

Narrowing of the aorta at the site of insertion of the ductus arteriosus

282
Q

Describe the aetiology for coarctation of aorta

A

Congenital malformation, turner’s syndrome

283
Q

Describe the pathophysiology for coarctation of aorta

A

Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing. Narrowing of the aorta reduces the pressure of blood flowing to the arteries that are distal to the narrowing. It increases pressure in areas proximal to the narrowing, e.g., heart and first 3 branches of the aorta. This causes increased perfusion to upper body vs lower body.

284
Q

What are the key presentations for coarctation of aorta

A

Hypertension, different upper and lower body BP, diminished pulse in lower extremities

285
Q

Describe the clinical manifestations for coarctation of aorta

A

Tachypnoea, bruits over scapulae and back, systolic ejection murmur

286
Q

What is the gold standard investigation for coarctation of aorta

A

Echocardiogram (narrowing in thoracic aorta, pressure gradient across narrowing)

287
Q

Describe the first line investigation for coarctation of aorta

A

Chest x-ray (rib notching)

288
Q

What are the differential diagnosis for coarctation of aorta

A

Aortic stenosis, interrupted aortic arch

289
Q

Describe the management for coarctation of aorta

A

Surgical repair or stenting. Prostaglandin E to keep the ductus arteriosus open while waiting for surgery

290
Q

Describe the complications for coarctation of aorta

A

Coronary artery disease, systemic hypertension

291
Q

Define tetralogy of fallot

A

Congenital condition where there are 4 existing pathologies: 1. Ventricular septal defect. 2. Overriding aorta. 3. Pulmonary valve stenosis (RV outflow obstruction). 4. Right ventricular hypertrophy

292
Q

Describe the aetiology for tetralogy of fallot

A

Inherited mutations

293
Q

Describe the pathophysiology for tetralogy of fallot

A

VSD allows blood to flow between ventricles. Overriding aorta means the enrank to the aorta (aortic valve) is placed further to the right than usual, above the VSD. When the right ventricle contracts, it pushes deoxygenated blood through the aorta into the systemic circulation. Pulmonary stenosis causes resistance against blood flow from the right ventricle, creating a right to left shunt, pushing blood through the aorta and bypassing the lungs causing deoxygenated blood to enter the systemic circulation = cyanosis. Increased strain of the right ventricle trying to pump against resistance causes hypertrophy.

294
Q

What are the key presentations for tetralogy of fallot

A

Cyanotic, systolic ejection murmur, Tet spells (right to left shunt is temporarily worsened. Child may present in squat position/knees to chest which increases flow to pulmonary arteries - tet spells = suddenly turn bluish and may faint)

295
Q

Describe the clinical manifestations for tetralogy of fallot

A

Signs: tachypnoea, clubbing
Symptoms: Poor feeding, poor weight gain

296
Q

What is the gold standard investigation for tetralogy of fallot

A

Echocardiogram (shows blood flow route)

297
Q

Describe the first line investigations for tetralogy of fallot

A

Chest x-ray (boot shaped heart due to RV thickening)

298
Q

What are the differential diagnosis for tetralogy of fallot

A

Pulmonary stenosis, ventricular septal defect

299
Q

Describe the management for tetralogy of fallot

A

Full surgical repair within 2 years of life

300
Q

Describe the complications for tetralogy of fallot

A

Heart failure, cardiac death

301
Q

Define hypertrophic cardiomyopathy

A

Cardiomyopathy = group of myocardium diseases affecting the heart’s mechanical or electrical function. Hypertrophic CM = left ventricular hypertrophy causing obstruction of the outflow tract.

302
Q

Describe the epidemiology for hypertrophic caridomyopathy

A

Main cause of sudden cardiac death in young people

303
Q

Describe the aetiology for hypertrophic cardiomyopathy

A

Genetic autosomal domination mutation in sarcomere proteins – Troponin T, Beta-myosin

304
Q

Describe the risk factors for hypertrophic cardiomyopathy

A

Family history of HCM

305
Q

Describe the pathophysiology of HCM

A

Genetic dysfunction of sarcomere proteins leads to left ventricle hypertrophy which causes impaired diastolic filling and therefore reduced stroke volume and reduced cardiac output. It also causes an abnormal mitral valve which obstructs the left ventricle outflow tract.

306
Q

What are the key presentations for HCM

A

SUDDEN DEATH, chest pain, palpitations, syncope, dyspnoea

307
Q

Describe the clinical manifestations for HCM

A

Signs: Systolic ejection murmur, jerky carotid pulse, left ventricle lift (visible or palpable chest wall impulses)
Symptoms: Chest pain, palpitations, syncope, dyspnoea

308
Q

What is the gold standard investigation for HCM

A

Echocardiogram: LVH, asymmetrical septal hypertrophy

309
Q

Describe the first line investigations for HCM

A

1st line ECG: LVH - T wave inversion, Q waves, ST depression, chest x-ray: cardiomegaly

Other: Genetic testing

310
Q

What are the differential diagnosis for HCM

A

Athlete’s heart, LVH due to hypertension

311
Q

Describe the management for HCM

A

1st line – beta blockers, CCB (diltiazem/verapamil) (anti-arrhythmic) or DC cardioversion if haemodynamically stable
Prevention: Implantable cardioverter-defibrillator

312
Q

Describe the complications for HCM

A

Sudden cardiac death, infective endocarditis, atrial fibrillation

313
Q

Define dilated cardiomyopathy

A

Cardiomyopathy = group of myocardium diseases which affect the mechanical and electrical function of the heart. Dilated CM = left ventricle is dilated (enlarged), stretching the thick muscle wall stretches, becoming thinner and weaker so contracts weaker.

314
Q

Describe the epidemiology for dilated cardiomyopathy

A

Most common cardiomyopathy

315
Q

Describe the aetiology for dilated cardiomyopathy

A

Genetic, ischaemic heart disease, alcohol, thyroid disorder

316
Q

Describe the pathophysiology for dilated cardiomyopathy

A

Ventricular chamber enlargement and poor contraction. Dilation of the ventricle disrupts the hearts’ ability to contract leading to progressive heart failure. There is diffuse interstitial fibrosis and systolic dysfunction of the ventricles.

317
Q

What are the key presentations for dilated cardiomyopathy

A

Heart failure presentation: Dyspnoea, fatigue, peripheral oedema

318
Q

Describe the clinical manifestations for dilated caridomyopathy

A

Signs: Heart failure, arrhythmia, raised JVP, thromboembolism, peripheral oedema, 3rd/4th heart sounds
Symptoms: Shortness of breath, fatigue, weakness, chest pain

319
Q

What is the gold standard investigation for dilated cardiomyopathy

A

Echocardiogram: dilated ventricles

320
Q

Describe the first line investigations for dilated cardiomyopathy

A

ECG: tachycardia, LBBB, T wave inversion, Q waves. Chest x-ray: enlarged heart

321
Q

What are the differential diagnosis for dilated cardiomyopathy

A

Hypertrophic CM, restrictive CM, heart failure

322
Q

Describe the management for dilated cardiomyopathy

A

Treat causes and underlying conditions – heart failure (ABAL – ACEi, beta blocker, aldosterone antagonists, loop diuretic) and arrhythmias. Consider implantable cardioverter defibrillator for high risk arrhythmia patients

323
Q

Describe the complications for dilated cardiomyopathy

A

Heart failure, arrhythmia, thrombus

324
Q

Define restrictive cardiomyopathy

A

Cardiomyopathy = group of myocardium diseases which affect the mechanical and electrical function of the heart. Restrictive CM = scar tissue replaces the normal heart muscle and the ventricles become rigid so don’t contract properly.

325
Q

Describe the epidemiology for restrictive cardiomyopathy

A

Least common cardiomyopathy

326
Q

Describe the aetiology for restrictive cardiomyopathy

A

Granulomatous diseases (amyloidosis, sarcoidosis), idiopathic, end-myocardial fibrosis

327
Q

Describe the pathophysiology for restrictive cardiomyopathy

A

Decreased volume in ventricles causes bi-atrial enlargement. Rigid fibrous myocardium fills poorly and contracts poorly causing decreased cardiac output

328
Q

What are the key presentations for restrictive cardiomyopathy

A

Heart failure: dyspnoea, fatigue, peripheral oedema

329
Q

Describe the clinical manifestations for restrictive cardiomyopathy

A

Signs: S3+4 heart sounds, raised JVP, oedema, ascites, hepatomegaly
Symptoms: Dyspnoea, fatigue, orthopnoea, chest pain

330
Q

What is the gold standard investigation for restrictive cardiomyopathy

A

Cardiac catheterisation

331
Q

Describe the first line investigations for restrictive cardiomyopathy

A

ECG, chest x-ray (normal/small heart), echocardiogram: thickened ventricular walls, atria and septum

332
Q

What are the differential diagnosis for restrictive cardiomyopathy

A

Constrictive pericarditis, heart failure, hypertrophic cardiomyopathy

333
Q

Describe the management for restrictive cardiomyopathy

A

No treatment – poor prognosis. Treat underlying cause. Heart transplant

334
Q

Describe the complications for restrictive cardiomyopathy

A

Heart failure, arrhythmias

335
Q

Define rheumatic fever

A

Systemic infection from Lancefield group A beta-haemolytic strep (s. pyogenes)

336
Q

Describe the epidemiology for rheumatic fever

A

Developing countries

337
Q

Describe the aetiology for rheumatic fever

A

Group A beta-haemolytic streptococcus mainly S.pyogenes

338
Q

Describe the pathophysiology of rheumatic fever

A

Antibodies against streptococcus bacteria also attack body tissues. Commonly valves in heart - rheumatic heart disease

339
Q

What are the key presentations for rheumatic fever

A

Fever, joint pain, recent strep infection (tonsilitis)

340
Q

Describe the clinical manifestations for rheumatic fever

A

Signs: Tachycardia, murmur (esp mitral stenosis), pericardial rub, chorea (jerky movements), erythema marginatum (pink rings rash on torso/limbs)
Symptoms: Fever, arthritis, chest pain, dyspnoea, fatigue

341
Q

Describe the first line investigations for rheumatic fever

A

Jones criteria (2 major/ 1 major + 2 minor) JONES: joint pain, organ inflammation e.g., carditis, nodules, erythema marginatum rash, Sydenham’s chorea. FEAR: fever, ECG changes (prolonged PR), arthralgia (no arthritis), raised inflammatory markers (ESR/CRP)
Investigations: ESR/CRP raised, ECG (prolonged PR) chest x-ray + echo, throat swab for cultures, antistreptococcal antibodies

342
Q

Describe the management for rheumatic fever

A

1st line – antibiotics: IV benzylpenicillin then phenoxymethicillin for 10 days
NSAIDs for joints, aspirin + steroids for carditis, haloperidol for chorea. Ongoing penicillin prophylaxis

343
Q

Describe the complications for rheumatic fever

A

Valve disease (mitral stenosis), heart failure

344
Q

Define atrioventricular node re-entry tachycardia

A

Tachycardia due to the presence of 2 functionally and anatomically distinct conduction pathways in the AV node

345
Q

Describe the epidemiology for AVNRT

A

Most common supraventricular tachycardia

346
Q

Describe the aetiology for AVNRT

A

Cardiomyopathy, ischaemic heart disease, hyperthyroidism, cocaine, excess alcohol

347
Q

Describe the risk factors for AVNRT

A

Coronary artery disease, substance misuse

348
Q

Describe the pathophysiology for AVNRT

A

Electrical signal re-enters the atria from the ventricles through the AV node. Once the signal is back in the atria it travels through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point and results in fast narrow QRS complex tachycardia.

349
Q

What are the key presentations for AVNRT

A

Tachycardia, paroxysmal attacks (sudden onset/offset palpitations)

350
Q

Describe the clinical manifestations for AVNRT

A

Signs: Sudden onset/offset palpitations, neck pulsation, tachycardia (140-280bpm)
Symptoms: Chest pain, shortness of breath, fatigue, weakness

351
Q

What is the gold standard investigation for AVNRT

A

ECG: P waves are within the QRS complex, narrow QRS. QRS followed by T wave repeated

352
Q

What are the differential diagnosis for AVNRT

A

Atrial fibrillation, atrial flutter, sinus tachycardia

353
Q

Describe the management for AVNRT

A

1st line – vagal manoeuvres (Valsalva, carotid sinus massage). 2nd – IV adenosine
Prevention – beta blockers, CCB, flecainide

354
Q

Define brugada syndrome

A

Sodium channelopathy causing dangerously fast arrhythmias

355
Q

Describe the aetiology for brugada syndrome

A

Gene mutation

356
Q

What are the key presentations for Brugada syndrome

A

Syncope, palpitations, dyspnoea, chest pain

357
Q

What is the gold standard investigation for Brugada syndrome

A

ECG: Coved ST elevation in chest leads V1-3

358
Q

Describe the management for Brugada syndrome

A

Implantable cardiac defribillator

359
Q

Define bundle branch block

A

A block in the conduction of one of the bundle branches, so the ventricles don’t receive impulses at the same time

360
Q

Describe the aetiology of bundle branch blocks

A

RBBB: pulmonary embolism, ischemic heart disease, atrial or ventricular septal defect
LBBB: ischemic heart disease, valvular disease, cardiomyopathy, cardiac surgery

361
Q

Describe the risk factors for bundle branch blocks

A

Ischaemic heart disease, structural heart defects

362
Q

Describe the pathophysiology for bundle branch blocks

A

RBBB: depolarisation only occurs through the left bundle branch, LV depolarises as normal, RV walls are eventually depolarised by the left bundle branch in a slower, less effective pathway. This creates the second R wave in V1 and a slurred S wave (V5-6)
LBBB: depolarisation only occurs through the right bundle branch, RV depolarises as normal, LV walls are eventually depolarised y the right bundle branch in a slower, less effective pathway. This creates the second R wave in V6 and slurred S wave (V1-2)

363
Q

What are the key presentations for bundle branch blocks

A

Asymptomatic, syncope

364
Q

What is the gold standard investigation for bundle branch blocks

A

ECG
RBBB: MaRRoW – M in V1 (RSR), W in V6 (slurred S), wide QRS
LBBB: WiLLiaM – W in V1 (slurred S), M in V6 (RSR), wide QRS

365
Q

Describe the management for bundle branch blocks

A

Usually no treatment. Treat hypertension, pacemaker, cardiac resynchronisation therapy (CRT)

366
Q

Describe the complications for bundle branch blocks

A

Complete heart block

367
Q

Define deep vein thrombosis

A

Formation of a thrombus within the deep vein system. A type of venous thromboembolism along with pulmonary embolism

368
Q

Describe the aetiology for DVT

A

Virchow’s triad: reduced blood flow, endothelial injury, increases likelihood of clotting

369
Q

Describe the risk factors for DVT

A

Virchow’s triad: Venous stasis (immobility, long haul flights, surgery). Vascular injury (smoking, trauma). Hypercoagulability (pregnant, COPD, obesity, malignancy, oestrogen therapy, thrombophilia – predispose to clots, e.g. antiphospholipid syndrome)

370
Q

Describe the pathophysiology for DVT

A

The major of thrombi occur in the lower legs below the calf which can impede minor veins. More serious DVT occur above the calf and can occlude major veins, e.g., superficial femoral, impeding distal flow. The thrombus can embolise from the deep veins to the vena cava > right side of heart > pulmonary arteries and cause a pulmonary embolism.

371
Q

What are the key presentations for a DVT

A

Unilateral, calf swelling, tenderness, pitting oedema, dilated superficial veins, colour changes to leg, warm, erythema, cyanosis

372
Q

What is the gold standard investigation for a DVT

A

Doppler ultrasound (unable to compress vein = clot)

373
Q

Describe the first line investigations for a DVT

A

Wells score (risk of patient having DVT or PE. <2 = unlikely.) 1. If unlikely, order D-dimer test (looks for fibrin breakdown products and clotting problems). If D-dimer is raised, order doppler ultrasound of leg. 2. If DVT likely >2, order doppler. ultrasound.

374
Q

What are the differential diagnosis for DVT

A

Compartment syndrome, cellulitis, acute limb ischaemia

375
Q

Describe the management for a DVT

A

1st line – DOAC anticoagulation: apixaban or rivaroxaban.
Long term: LWMH, DOAC or warfarin, compression stockings, treat underlying cause.
LMWH 1st line in pregnancy

376
Q

Describe the monitoring for a DVT

A

Prevention – hydration, mobilisation, compression stockings, LMWH

377
Q

Describe the complications for a DVT

A

Pulmonary embolism

378
Q

Define pericardial effusion and cardiac tamponade

A

Accumulation of fluid in the pericardial sac. Cardiac tamponade is when the pericardial effusion is large enough to raise the inter-pericardial pressure leading to reduced filling of the ventricles during diastole, resulting in reduced cardiac output in systole.

379
Q

Describe the aetiology of pericardial effusion

A

Exudative effusions in pericarditis: virus, bacteria, autoimmune disease, neoplastic, metabolic, trauma, iatrogenic, idiopathic.
Transudative effusions from increased venous pressure causing restricted drainage of the pericardial space: congestive heart failure, pulmonary hypertension
Rupture of heart or aorta causing bleeding in pericardial space: MI, aortic dissection, trauma

380
Q

Describe the risk factors for pericardial effusion

A

Malignancy, aortic dissection, purulent pericarditis

381
Q

Describe the pathophysiology for pericardial effusion and cardiac tamponade

A

The potential space within the pericardial cavity fills with fluid which creates an inward pressure on the heart, making it more difficult to expand during diastole

382
Q

What are the key presentations for pericardial effusion and cardiac tamponade

A

Pericardial friction rub, dyspnoea, chest pain, Beck’s triad

383
Q

Describe the clinical manifestations for pericardial effusion and cardiac tamponade

A

Signs: Beck’s triad: hypotension, muffled heart sounds, raised JVP. Pulsus paradoxus (fall of systolic BP >10mmHg on inspiration), orthopnoea, raised pulse, (Cardiac tamponade -Kussmaul’s sign: paradoxical rise in JVP on inspiration)
Symptoms: Hiccups, nausea, hoarse voice, dysphagia

384
Q

What is the gold standard investigation for cardiac tamponade/ pericardial effusion

A

Echocardiogram (echo-free zone surrounding the heart)

385
Q

Describe the first line investigations for pericardial effusion

A

1st line: ECG (electrical alternans – varying QRS amplitudes due to heart bouncing back and forth in increased pericardial fluid), Chest x-ray (enlarged, globular heart)

Other: FBC (raised WBC count, raised ESR showing inflammation)

386
Q

What are the differential diagnosis for pericardial effusion

A

Constrictive pericarditis, congestive heart failure, Dressler’s syndrome

387
Q

Describe the management for pericardial effusion

A

Treat the underlying cause (e.g. infection). Pericarditis – aspirin NSAIDS, colchicine
Drain the effusion: needle pericardiocentesis or surgical drainage
For cardiac tamponade: Urgent pericardiocentesis. Sent fluid for culture.

388
Q

Describe the complications for pericardial effusion

A

Cardiac tamponade, haemodynamic compromise, and death

389
Q

Describe the prognosis for pericardial effusion

A

Depends on underlying cause - worse with infection

390
Q

Define Prinzmetal angina

A

Angina due to coronary artery spasm. AKA vasospastic angina

391
Q

Describe the aetiology for Prinzmetal angina

A

Does not correlate with exertion. May be precipitated by smoking, cocaine, marijuana, emotional stress, extreme cold weather

392
Q

Describe the pathophysiology for Prinzmetal angina

A

Coronary artery spasms and suddenly narrows

393
Q

What are the key presentations for Prinzmetal angina

A

Central crushing chest pain at rest which resolves with GTN spray

394
Q

Describe the clinical manifestations for prinzmetal angina

A

Dyspnoea, sweating, nausea

395
Q

What is the gold standard investigation for prinzmetal angina

A

Coronary angiography (ACh used to provoke spasm)

396
Q

Describe the first line investigations for prinzmetal angina

A

ECG (ST elevation during acute episode), biomarkers (not elevated)

397
Q

Describe the management for prinzmetal angina

A

1st line – GTN spray. Other: calcium channel blockers + long-acting nitrates. Stop smoking, reduce risk factors.

398
Q

Define pulmonary embolism

A

Blood clot forms in the pulmonary arteries, usually as a result of DVT in the legs which has embolised to the lungs. DVTs and PE are called thromboembolism

399
Q

Describe the aetiology for PE

A

Virchow’s triad: reduced blood flow, endothelial injury, increases likelihood of clotting

400
Q

Describe the risk factors of PE

A

Virchow’s triad: Venous stasis (immobility, long haul flights, surgery). Vascular injury (smoking, trauma). Hypercoagulability (pregnant, COPD, obesity, malignancy, oestrogen therapy, thrombophilia – predispose to clots, e.g. antiphospholipid syndrome)

401
Q

Describe the pathophysiology for PE

A

Clots in the pulmonary arteries block blood flow to lung tissue and create strain on the right heart. PE can cause cor pulmonale due to increased pulmonary resistance > increases strain on right heart > right ventricle hypertrophy > right heart failure.

402
Q

What are the key presentations for PE

A

Sudden onset pleuritic chest pain, dyspnoea, haemoptysis

403
Q

Describe the clinical manifestations for PE

A

Signs: Haemoptysis, pleuritic chest pain, hypoxia, tachycardia, tachypnoea, DVT (leg swelling and tenderness), hypotension, cyanosis,
Symptoms: Shortness of breath, cough, fever, dizziness, syncope

404
Q

What is the gold standard investigation for PE

A

CT pulmonary angiogram (direct visual of thrombus in pulmonary artery)

405
Q

Describe the first line investigations for PE

A

Wells score (risk of DVT or PE). 1. <4 = unlikely PE. Order d-dimer (looks for fibrin breakdown products and clotting problems). If d-dimer raised, order CT pulmonary angiogram (visual of thrombus). 2. >4 = likely PE. Order CTPA

Other: Ventilation-perfusion scan (area of lung not perfused), ECG (sinus tachycardia, S1Q3T3 pattern = cor pulmonale, T wave inversion V1-4), ABG (low o2 and Co2)

406
Q

What are the differential diagnosis for PE

A

MI, pneumonia, pneumothorax

407
Q

Describe the management for PE

A

Massive PE, haemodynamic compromise = thrombolysis (streptokinase/alteplase)
Non-massive PE = anticoagulation – apixaban, rivaroxaban or LMWH
Long term: LMWH, DOAC or warfarin. LMWH 1st line in pregnancy

408
Q

Describe the monitoring for PE

A

Prevention – LMWH, stop OCP or HRT, mobilisation, compression stockings

409
Q

Describe the complications for PE

A

Pulmonary infarction, cardiac arrest

410
Q

Define torsades de pointes

A

Polymorphic ventricular tachycardia in which the QRS amplitude varies and the QRS complexes appear to twist around the baseline. It is associated with prolonged QT interval. It will either terminate spontaneously and revert back to sinus rhythm or progress into ventricular tachycardia.

411
Q

What are the key presentations for torsades de pointes

A

Palpitations, dizziness, syncope, tachycardia

412
Q

What is the gold standard investigation for torsades de pointes

A

ECG: rapid irregular QRS complexes which twist around baseline

413
Q

Describe the management for torsades de pointes

A

Correct electrolyte imbalance or remove cause. Magnesium infusion (even if normal serum sodium), defibrillation if V-fib occurs

414
Q

Describe the complications for torsades de pointes

A

Ventricular fibrillation: ventricular muscle fibres contract randomly causing a complete failure of ventricular function > cardiac arrest. 1st line – DC cardioversion

Conditions (9 decks)

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