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.
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)
3
Q
What are the risk factors for stable angina pectoris
A
Non-modifiable: age, gender, race.
Modifiable: diabetes, hypertension, obesity high LDL, smoking
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
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
6
Q
Describe the symptoms for stable angina pectoris
A
Dyspnoea, nausea, sweating, fainting
7
Q
What is the gold standard investigation for stable angina pectoris
A
CT angiography (presence of luminal narrowing, plaques)
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
9
Q
What are the differential diagnosis for stable angina pectoris
A
Unstable angina, STEMI, NSTEMI
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
11
Q
Describe the complications for stable angina pectoris
A
MI, stroke, heart failure
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.
13
Q
Describe the aetiology for unstable angina
A
Atherosclerotic plaque rupture and subsequent thrombosis and inflammation
14
Q
What are the risk factors for unstable angina
A
Non-Modifiable: age, gender, race. Modifiable: diabetes, hypertension, obesity, high LDL, smoking
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
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)
17
Q
Describe the clinical manifestations for unstable angina
A
Sweating, dyspnoea, nausea, fainting, palpitations
18
Q
What is the gold standard investigation for unstable angina
A
ECG (no ST elevation) + biomarkers (no troponin increase)
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
20
Q
What are the differential diagnosis for unstable angina
A
Stable angina, pericarditis, myocarditis
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
22
Q
What are the complications for unstable angina
A
MI, stroke, heart failure
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.
24
Q
Describe the aetiology for a STEMI
A
Rupture and thrombosis of plaque causing complete occlusion of major coronary artery lumen.
25
Describe the risk factors for a STEMI
Non-modifiable: age, gender, race. Modifiable: hypertension, diabetes, obesity, high LDL, smoking
26
Describe the pathophysiology for a STEMI
Atherosclerotic plaque rupture and thrombosis causes complete occlusion of coronary artery leading to transmural injury and infarct to the myocardium.
27
What are the key presentations for a STEMI
Central crushing chest pain radiating down arms jaw neck, not relieved by rest or GTN spray, persists >20 mins, impending doom feeling
28
Describe the clinical manifestations for a STEMI
Signs: Tachycardia, high/low BP, 4th heart sound
Symptoms: Sweating, N+V, dyspnoea, fatigue, palpitations
29
What is the gold standard investigation for a STEMI
ECG (ST elevation) + biomarkers (troponin elevated)
30
Describe the first line investigations for a STEMI
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
31
What are the differential diagnosis for a STEMI
Unstable angina, NSTEMI, pericarditis
32
Describe the management for a STEMI
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
33
What are the complications for a STEMI
Heart failure, rupture of infarcted ventricle, rupture of interventricular septum, heart block, arrhythmias, mitral regurgitation, post-MI pericarditis (Dressler’s syndrome)
34
Define an NSTEMI
Non-ST-elevated myocardial infarction is part of ACS. Acute ischaemic event causing myocardial cell necrosis and troponin release.
35
Describe the aetiology of an NSTEMI
Rupture and thrombosis of atherosclerotic plaque causing partial occlusion of major coronary artery or total occlusion of minor coronary artery.
36
Describe the risk factors for an NSTEMI
Non modifiable: age, gender, race. Modifiable: hypertension, diabetes, obesity, high LDL, smoking
37
Describe the pathophysiology for an NSTEMI
Atherosclerotic plaque rupture and thrombosis causes partial occlusion to coronary artery. This causes necrosis of cardiac tissue and infarction to sub endothelium.
38
What are the key presentations for an NSTEMI
Central crushing chest pain radiating down arms jaw neck, not relieved by rest or GTN spray, persists >20 mins, impending doom feeling
39
Describe the clinical manifestations for an NSTEMI
Signs: Tachycardia, high/low BP, 4th heart sound
Symptoms: Sweating, N+V, dyspnoea, fatigue, palpitations
40
What is the gold standard investigation for an NSTEMI
ECG (ST depression) + biomarkers (elevated troponin)
41
Describe the first line investigations for an NSTEMI
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
42
What are the differential diagnosis for an NSTEMI
STEMI, unstable angina
43
Describe the management for an NSTEMI
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
44
Describe the complications for an NSTEMI
Heart failure, ruptured infarcted ventricle, ruptured interventricular septum, mitral regurgitation, arrhythmias, heart block, post-MI pericarditis (Dressler syndrome)
45
Describe the types of MI
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
46
Define heart failure
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.
47
Describe the epidemiology for heart failure
10% of over 70s, male > women, increases with age, typical effects 1-2% developed world
48
Describe the aetiology for heart failure
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
49
Describe the risk factors for heart failure
Older, male, smoking, obesity, previous MI
50
Describe the pathophysiology for heart failure
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
51
What are the key presentations for heart failure
SOB, fatigue and oedema
52
Describe the clinical manifestations for heart failure
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
53
What is the gold standard investigation for heart failure
Echocardiogram (may confirm cause, e.g., MI, valvular heart disease, and can show LV dysfunction)
54
Describe the first line investigations for heart failure
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
55
What are the differential diagnosis for heart failure
COPD, pulmonary embolism
56
Describe the management for heart failure
1st line - ABAL. ACE inhibitor (ramipril), beta blocker (bisoprolol), aldosterone antagonist (spironolactone), loop diuretic (furosemide)
Consider cardiac resynchronisation therapy. Surgery: LVAD, cardiac transplantation
57
What are the complications for heart failure
Pleural effusion, acute kidney injury, sudden cardiac death
58
Describe the prognosis for heart failure
50% die within 5 years of diagnosis
59
Define hypertension
Blood pressure >140/90 in clinic, >135/85 with ambulatory or home readings
60
Describe the epidemiology for hypertension
Biggest risk factor for cardiovascular disease
61
Describe the aetiology for hypertension
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)
62
Describe the risk factors for hypertension
Non-modifiable: age, FHx, ethnicity (Afro-Caribbean). Modifiable: alcohol, sedentary lifestyle, diabetes, smoking, salt intake
63
Describe the pathophysiology for hypertension
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
64
What are the key presentations for hypertension
Asymptomatic
65
Describe the clinical manifestations for hypertension
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
66
What is the gold standard investigation for hypertension
Ambulatory BP (worn 24hrs) > 135/85 mmHg
67
Describe the first line investigations for hypertension
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)
68
What are the differential diagnosis for hypertension
Chronic kidney disease, Cushing syndrome, phaeochromocytoma
69
Describe the management for hypertension
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
70
Describe the monitoring for hypertension
Treatment targets: Age <80 = <140/90mmHg. Age >80 = <150/90mmHg
71
Describe the complications for hypertension
Ischaemic heart disease, cerebrovascular event (stroke, MI), heart failure, CKD
72
Define Cor Pulmonale
Right sided heart failure caused by respiratory disease
73
Describe the aetiology for Cor Pulmonale
COPD, pulmonary embolism, interstitial lung disease, cystic fibrosis, primary pulmonary hypertension
74
Describe the risk factors for Cor Pulmonale
Respiratory disease
75
Describe the pathophysiology for Cor Pulmonale
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.
76
What are the key presentations for Cor Pulmonale
SOB, peripheral oedema, chest pain
77
Describe the clinical manifestations for Cor Pulmonale
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,
78
What is the gold standard investigation for Cor pulmonale
Right heart catheterisation
79
Describe the first line investigations for Cor Pulmonale
ABG (hypoxia and hypercapnia), spirometry, chest CT, echocardiogram
80
What are the differential diagnosis for Cor Pulmonale
Primary pulmonary hypertension, pulmonary valve stenosis
81
Describe the management for Cor Pulmonale
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
82
Describe the complications for Cor Pulmonale
Tricuspid regurgitation, hepatic congestion and cardiac cirrhosis, death
83
Describe the prognosis for Cor Pulmonale
50% 5 year survival
84
Define atrial fibrillation
Atrial fibrillation is a supraventricular tachycardia caused by uncoordinated, rapid and irregular atrial activity, resulting in an irregularly irregular ventricular pulse
85
Describe the epidemiology for AF
Most common sustained cardiac arrhythmia, more males than females
86
Describe the aetiology for AF
Heart failure, hypertension, coronary artery disease, valvular disease (especially mitral valve stenosis), cardiac surgery, cardiomyopathy, idiopathic
87
Describe the risk factors for AF
Age 60+, hypertension, T2DM, heart failure, past MI
88
Describe the pathophysiology for AF
Contraction of the atria is uncoordinated, rapid and irregular due to disorganised electrical activity which overrides the sinoatrial node activity. 300-600bpm.
89
What are the key presentations for AF
Irregular pulse, tachycardia, palpitations, ECG: no P waves, irregularly irregular pulse and narrow QRS
90
Describe the clinical manifestations for AF
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
91
What is the gold standard investigation for AF
ECG: absent P waves, irregularly irregular pulse (irregular R-R intervals with narrow QRS)
92
Describe the first line investigations for AF
1st line ECG: absent P waves, irregularly irregular pulse (irregular R-R intervals with narrow QRS)
Other: FBC
93
What are the differential diagnosis for AF
Atrial flutter, Wolff-Parkinson-white syndrome, atrial tachycardia
94
Describe the management for AF
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
95
Describe the monitoring for AF
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.
96
Describe the complications for AF
Acute stroke, myocardial infarction, congestive heart failure
97
Describe the prognosis for AF
Double mortality risk and 5x stroke risk
98
Define atrial flutter
Macro re-entrant atrial tachycardia caused by organised electrical activity in the atrium with a rate of 250-350bpm. Less common than AF
99
Describe the aetiology of atrial flutter
Idiopathic, coronary heart disease, obesity, heart failure, hypertension, COPD, pericarditis
100
Describe the risk factors for atrial flutter
AF
101
Describe the pathophysiology for atrial flutter
Originates from a re-entrant circuit around the tricuspid valve annulus. Short circuit causes the atria to fire very rapidly
102
What are the key presentations for atrial flutter
ECG: flutter waves saw-tooth pattern, often 2:1 block (p-wave: QRS complex)
103
Describe the clinical manifestations for atrial flutter
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
104
What is the gold standard investigation for atrial flutter
ECG: saw-tooth pattern (flutter waves), often 2:1 block (2 P waves for every QRS)
105
Describe the first line investigations for atrial flutter
ECG: saw-tooth pattern (flutter waves), often 2:1 block (2 P waves for every QRS)
Other FBC
106
What are the differential diagnosis for atrial flutter
Atrial fibrillation, atrial tachycardia
107
Describe the management for atrial flutter
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)
108
Describe the monitoring for atrial flutter
CHA2SD2-VASc for risk of stroke in atrial fibrillation/flutter
109
Describe the complications for atrial flutter
Acute stroke, medication related bradycardia
110
Define heart block
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)
111
Describe the aetiology for heart block
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
112
Describe the risk factors for heart block
Coronary artery disease, cardiomyopathy, fibrosis
113
Describe the pathophysiology for heart block
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.
114
What are the key presentations for heart block
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
115
Describe the gold standard investigations for heart block
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)
116
What are the differential diagnosis for heart block
SVT, AF
117
Describe the management for heart block
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
118
Describe the complications for heart block
Sudden cardiac death
119
Define ventricular ectopics
Premature ventricular beats caused by random electrical discharges from the ventricles before an electrical impulse can be made by the atrium
120
What are the key presentations for ventricular ectopics
Random, brief palpitations, abnormal beat, syncope
121
What is the gold standard investigation for ventricular ectopics
ECG: individual random, abnormal, broad QRS complexes on a background of a normal ECG
122
Describe the management for ventricular ectopics
Reassurance and self-monitoring. Beta blocker or CCB. Ablation to stop abnormal signals
123
Describe the complications for ventricular ectopics
Bigeminy - ventricular ectopics occur so frequently that they happen after every sinus beat. ECG shows normal sinus beat followed by ectopic, normal, ectopic
124
Define long QT syndrome
Ventricular tachyarrhythmia characterised by prolonged QT interval on ECG >480ms
125
Describe the aetiology for long QT syndrome
Congenital channelopathy: Romano-Ward syndrome, hypokalaemia, hypocalcaemia, bradycardia, drugs (amiodarone, tricyclic antidepressants)
126
What are the key presentations for long QT syndrome
Syncope, palpitations, may progress to V-fib
127
What is the gold standard investigation for long QT syndrome
ECG: prolonged QT interval >480ms
128
Describe the management for long QT syndrome
Correct electrolyte disturbances and remove causative factors, give beta blocker, pacemaker or implantable defib
129
Describe the complications for long QT syndrome
Torsades de pointes
130
Define Wolff-Parkinson-White syndrome (AVRT)
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.
131
Describe the aetiology for Wolff-Parkinson-White syndrome
Congential abnormality, Epstein's anomaly
132
What are the risk factors for AVRT
Congenital heart defects
133
Describe the pathophysiology for AVRT
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.
134
What are the key presentations for AVRT
Palpitations, ECG: short PR interval, wide QRS, slurred upstroke of QRS complex = delta wave
135
Describe the clinical manifestations for AVRT
Signs: Tachycardia, ECG: short PR interval, wide QRS, slurred upstroke of QRS complex = delta wave
Symptoms: Palpitations, dizziness, dyspnoea
136
What is the gold standard investigation for AVRT
ECG: short PR interval, wide QRS, slurred upstroke of QRS complex = delta wave
137
Describe the first line investigations for AVRT
ECG: short PR interval, wide QRS, slurred upstroke of QRS complex = delta wave
138
What are the differential diagnosis for AVRT
AF, atrial flutter, AVNRT
139
Describe the management for AVRT
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)
140
Describe the complications for AVRT
Sudden cardiac death
141
Define abdominal aortic aneurysm
Dilation of the abdominal aorta >50% with a diameter greater than 3cm (aneurysm typically infrarenal)
142
Describe the epidemiology for AAA
Men affected more often and younger
143
Describe the aetiology of AAA
Mainly idiopathic, atheroma, trauma, infection, connective tissue disorders (Marfan’s and Ehlers-Danlos syndrome)
144
Describe the risk factors for AAA
Smoking, atherosclerosis, obesity, hypertension, increasing age
145
Describe the pathophysiology for AAA
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
146
What are the key presentations for AAA
Asymptomatic, palpable pulsatile abdominal mass
147
Describe the clinical manifestations for AAA
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
148
What is the gold standard investigation for AAA
Computed tomography angiography
149
Describe the first line investigations for AAA
1st line Abdominal Ultrasound (>3cm. ruptured = immediate management)
150
What are the differential diagnosis for AAA
Acute pancreatitis, diverticulitis, appendicitis
151
Describe the management for AAA
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
152
What are the complications for AAA
Ruptured aneurysm, thrombosis, embolism, abdominal compartment syndrome
153
Describe the prognosis for AAA
80% mortality if ruptured
154
Define aortic dissection
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)
155
Describe the epidemiology of aortic dissection
Men aged 50-70
156
Describe the aetiology for aortic dissection
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)
157
Describe the risk factors for aortic dissection
Hypertension, smoking, trauma, raised LDL, obesity, sedentary lifestyle, male, increasing age.
158
Describe the pathophysiology for aortic dissection
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.
159
What are the key presentations for aortic dissection
Sudden and severe ripping/tearing pain in chest
160
Describe the clinical manifestations for aortic dissection
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
161
What is the gold standard investigation for aortic dissection
CT angiogram or transoesophageal echocardiogram (intimal flap and false lumen)
162
Describe the first line investigations for aortic dissection
1st line ECG (ST depression may occur), chest x-ray (widened mediastinum), TTE echocardiogram (intimal flap in acute, two lumens in chronic)
Other: MRI
163
What are the differential diagnosis for aortic dissection
Myocardial infarction, cardiac arrest, pericarditis
164
Describe the management for aortic dissection
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
165
Describe the complications for aortic dissection
Cardiac tamponade, aortic regurgitation, pre-renal AKI
166
Describe the prognosis for aortic dissection
High mortality from rupture
167
Define peripheral vascular disease
Range of syndromes that are caused by atherosclerotic obstruction of lower-extremity arteries.
168
Describe the epidemiology for peripheral vascular disease
Very common, increases with age, more men
169
Describe the aetiology for peripheral vascular disease
Atherosclerosis
170
Describe the risk factors for peripheral vascular disease
Non-modifiable: age, gender, race. Modifiable: obesity, diabetes, hypertension, high LDL, smoking
171
Describe the pathophysiology for peripheral vascular disease
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
What are the key presentations for peripheral vascular disease
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
Describe the clinical manifestations for peripheral vascular disease
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
What is the gold standard investigation for peripheral vascular disease
CT angiogram (shows occlusions)
175
Describe the first line investigations for peripheral vascular disease
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
Describe the management for peripheral vascular disease
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
Describe the complications for peripheral vascular disease
Amputation, permanent limb weakness, gangrene
178
Define acute pericarditis
Inflammation of the pericardium with or without pericardial effusion
179
Describe the epidemiology for acute pericarditis
80-90% idiopathic, higher in young patients
180
Describe the aetiology for acute pericarditis
Viral (enteroviruses), bacterial (TB), autoimmune (rheumatoid arthritis, Sjogren syndrome), neoplastic, metabolic (uraemia), traumatic and iatrogenic, idiopathic, Dressler’s syndrome (post MI)
181
Describe the risk factors for acute pericarditis
Bacterial/viral infections, past MI, autoimmune disease, trauma
182
Describe the pathophysiology for acute pericarditis
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
What are the key presentations for acute pericarditis
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
Describe the clinical manifestations for acute pericarditis
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
What is the gold standard investigation for acute pericarditis
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
Describe the first line investigations for acute pericarditis
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
What are the differential diagnosis for acute pericarditis
MYOCARDIAL INFARCTION!!! Pneumonia, pulmonary embolus
188
Describe the management for acute pericarditis
Sedentary activity until symptoms resolve and ECG/CRP. 1 - NSAID or aspirin. + Colchicine (anti-inflammatory)
189
What are the complications for acute pericarditis
Pericardial effusion, cardiac tamponade, chronic constrictive pericarditis
190
Describe the prognosis for acute pericarditis
Pretty good with acute
191
Define infective endocarditis
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
Describe the epidemiology of infective endocarditis
Elderly, young IV drug users, young with congenital heart disease, anyone with prosthetic valve
193
Describe the aetiology for infective endocarditis
Bacteria: S. aureus (common in IVDU, T2DM, surgery), S. viridans (poor dental hygiene), enterococci/s. bovis, HACEK organisms, fungi (candida, aspergillus)
194
Describe the risk factors for IE
Elderly, intra-venous drug users, prosthetic valves, rheumatic fever, surgery
195
Describe the pathophysiology for IE
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
What are the key presentations for IE
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
Describe the clinical manifestations for IE
Signs: Embolism (stroke, MI, PE), valve dysfunction (arrhythmia, heart failure)
Symptoms: Fever, sweats, weight loss, fatigue
198
What is the gold standard investigation for IE
Transoesophageal echocardiogram (vegetation)
199
Describe the first line investigations for IE
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
What are the differential diagnosis for IE
Rheumatic fever
201
Describe the management for IE
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
Describe the complications for IE
Vegetations embolising to cause stroke, MI, PE, Heart failure, sepsis
203
Define aortic stenosis
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
Describe the epidemiology of aortic stenosis
Most common valve defect
205
Describe the aetiology for aortic stenosis
Congenital bicuspid aortic valve (normally tricuspid), congenital aortic stenosis. Acquired: Ageing calcification, rheumatic heart disease
206
Describe the risk factors for aortic stenosis
Age > 60 years, congenital aortic valve defect, rheumatic heart disease
207
Describe the pathophysiology for aortic stenosis
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
What are the key presentations for aortic stenosis
SAD: syncope (exertional), angina, dyspnoea (exertion due to heart failure), ejection systolic crescendo-decrescendo murmur radiating to carotids
209
Describe the clinical manifestations for aortic stenosis
Signs: Slow rising carotid pulse and decreased pulse amplitude, soft/absent 2nd heart sound, prominent S4 heart sound
Symptoms: Dyspnoea, fatigue, chest pain
210
What is the gold standard investigation for aortic stenosis
Echocardiogram (+Doppler): assess LV size and function, doppler derived elevated aortic pressure gradient, assess valve area
211
Describe the clinical manifestations for aortic stenosis
ECG (left ventricle hypertrophy and Q waves), chest x-ray (may show pulmonary congestion)
212
What are the differential diagnosis for aortic stenosis
Hypertrophic cardiomyopathy, ischaemic heart disease
213
Describe the management for aortic stenosis
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
Describe the complications for aortic stenosis
Heart failure, sudden cardiac death, IE
215
Define aortic regurgitation
Leakage of blood into left ventricle during diastole due to ineffective closing of the aortic valve cusps
216
Describe the aetiology for aortic regurgitation
Bicuspid aortic valve, rheumatic heart disease, infective endocarditis, connective tissue disorders (e.g., Marfan’s, Ehlers-Danlos)
217
Describe the risk factors for aortic regurgitation
Bicuspid aortic valve, rheumatic heart disease, infective endocarditis, connective tissue disorders (e.g., Marfan’s, Ehlers-Danlos)
218
Describe the pathophysiology for aortic regurgitation
Combined pressure and volume overload in left ventricle. Compensatory mechanisms: left ventricle dilation, left ventricle hypertrophy. Progressive dilation leads to heart failure.
219
What are the key presentations for aortic regurgitation
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
Describe the clinical manifestations for aortic regurgitation
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
What is the gold standard investigation for aortic regurgitation
Echocardiogram: LV size and function, aortic valve evaluation
222
Describe the first line investigations for aortic regurgitation
ECG, Chest x-ray: enlarged cardiac silhouette and enlarged aortic root
223
What are the differential diagnosis for aortic regurgitation
Mitral regurgitation, aortic stenosis, mitral stenosis, infective endocarditis
224
Describe the management for aortic regurgitation
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
Describe the complications for aortic regurgitation
IE, heart failure, sudden cardiac death
226
Define mitral stenosis
Obstruction to left ventricular inflow which prevents proper filling in diastole
227
Describe the aetiology for mitral stenosis
Rheumatic heart disease, IE, valve calcification
228
Describe the risk factors for mitral stenosis
Rheumatic heart disease (S.pyogenes infection)
229
Describe the pathophysiology for mitral stenosis
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
What are the key presentations for mitral stenosis
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
Describe the clinical manifestations for mitral stenosis
Signs: Prominent “a” wave in jugular venous pulsations, RHF signs, loud opening 1st heart sound snap
Symptoms: Dyspnoea, orthopnoea, haemoptysis, RHF symptoms, palpitations
232
What is the gold standard investigation for mitral stenosis
Echocardiogram: assesses mitral valve mobility, gradient, and orifice area. Hockey stick shaped mitral deformity
233
Describe the first line investigations for mitral stenosis
ECG: atrial fibrillation and left atrial enlargement, chest x-ray: left atrial enlargement (M shaped P waves), pulmonary vessel congestion
234
What are the differential diagnosis for mitral stenosis
AF
235
Describe the management for mitral stenosis
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
Describe the complications for mitral stenosis
AF, stroke, IE
237
Define mitral regurgitation
Backflow of blood from the LV to the LA during systole
238
Describe the epidemiology for mitral regurgitation
Mild MR seen in 80% of normal individuals
239
Describe the aetiology for mitral regurgitation
Myxomatous degeneration (floppy valve), ischaemic mitral regurgitation, rheumatic heart disease, infective endocarditis, connective tissue disorders (Marfan’s, Ehlers-Danlos)
240
Describe the risk factors for mitral regurgitation
Rheumatic heart disease, IE, mitral valve prolapse
241
Describe the pathophysiology for mitral regurgiation
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
What are the key presentations for mitral regurgitation
Pan-systolic high pitched, whistling murmur at apex radiating to axilla, dyspnoea on exertion
243
Describe the clinical manifestations for mitral regurgitation
Signs: S3 heart sound, soft 1st heart sound, heart failure
Symptoms: Dyspnoea on exertion, exercise intolerance, heart failure symptoms, fatigue, orthopnoea
243
What is the gold standard investigation for mitral regurgitation
Echocardiogram: estimation of LA, LV size and function. Valve structure assessment
244
Describe the first line investigations for mitral regurgitation
ECG: LA enlargement (M shaped P waves), atrial fibrillation, left ventricular hypertrophy. Chest x-ray: LA enlargement, central pulmonary artery enlargement
245
What are the differential diagnosis for mitral regurgitation
Aortic stenosis, mitral stenosis
246
Describe the management for mitral regurgitation
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
Describe the complications for mitral regurgitation
AF, congestive heart failure, IE
248
Define shock
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
Describe the aetiology for shock
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
What are the key presentations for shock
All types: pulse weak + rapid, pale, sweaty, cold, low BP, reduced urine output, confusion
251
Describe the clinical manifestations for shock
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
Describe the management for shock
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
Define ventricular septal defect
Congenital abnormal connection between the 2 ventricles
254
Describe the aetiology for ventricular septal defect
Congenital - Down's syndrome, turner's syndrome
255
Describe the pathophysiology for ventricular septal defect
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
What are the key presentations for ventricular septal defect
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
What is the gold standard investigation for ventricular septal defect
Echocardiogram (shows shunting across VSD)
258
Describe the first line investigations for ventricular septal defect
Chest x-ray (pulmonary plethora, cardiomegaly), ECG
259
What are the differential diagnosis for ventricular septal defect
ASD, PDA
260
Describe the management for ventricular septal defect
Small + Asymptomatic = no treatment. Large + Symptomatic = surgical repair
261
Describe the complications for ventricular septal defect
IE
262
Define atrial septal defect
Abnormal connection between the 2 atria. Types: ostium primum, ostium secondum, patent foramen ovale
263
Describe the aetiology for atrial septal defect
Congenital
264
Describe the pathophsyiology for atrial septal defect
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
Describe the clinical manifestations for atrial septal defect
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
What is the gold standard investigation for atrial septal defect
Echocardiogram (shunt visualisation, shows blood flow pattern)
267
Describe the first line investigations for atrial septal defect
ECG (tall P waves show right atrial enlargement), chest x-ray (enlarged heart and pulmonary arteries)
268
What are the differential diagnosis for atrial septal defect
VSD, PDA
269
Describe the management for ASD
Spontaneous closure otherwise surgical closure
270
Describe the complications for ASD
Stroke from venous thromboembolism, atrial fibrillation, pulmonary hypertension, right heart failure, eisenmengers
271
Define patent ductus arteriosus
Ductus arteriosus fails to close post birth
272
Describe the aetiology for PDA
Congenital, prematurity, mother rubella infection
273
Describe the pathophysiology for PDA
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
What are the key presentations for PDA
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
What is the gold standard investigation for PDA
Echocardiogram (shows the shunt, can show ventricle hypertrophy)
276
Describe the first line investigations for PDA
Chest x-ray (cardiomegaly), ECG (deep Q waves and R waves show left atrial enlargement)
277
What are the differential diagnosis for PDA
ASD,VSD
278
Describe the management for PDA
Spontaneous or surgical closure (percutaneous catheter). Indomethacin (prostaglandin inhibitor) may close the PDA
279
Describe the complications for PDA
IE, respiratory distress syndrome
280
281
Define coarctation of aorta
Narrowing of the aorta at the site of insertion of the ductus arteriosus
282
Describe the aetiology for coarctation of aorta
Congenital malformation, turner's syndrome
283
Describe the pathophysiology for coarctation of aorta
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
What are the key presentations for coarctation of aorta
Hypertension, different upper and lower body BP, diminished pulse in lower extremities
285
Describe the clinical manifestations for coarctation of aorta
Tachypnoea, bruits over scapulae and back, systolic ejection murmur
286
What is the gold standard investigation for coarctation of aorta
Echocardiogram (narrowing in thoracic aorta, pressure gradient across narrowing)
287
Describe the first line investigation for coarctation of aorta
Chest x-ray (rib notching)
288
What are the differential diagnosis for coarctation of aorta
Aortic stenosis, interrupted aortic arch
289
Describe the management for coarctation of aorta
Surgical repair or stenting. Prostaglandin E to keep the ductus arteriosus open while waiting for surgery
290
Describe the complications for coarctation of aorta
Coronary artery disease, systemic hypertension
291
Define tetralogy of fallot
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
Describe the aetiology for tetralogy of fallot
Inherited mutations
293
Describe the pathophysiology for tetralogy of fallot
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
What are the key presentations for tetralogy of fallot
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
Describe the clinical manifestations for tetralogy of fallot
Signs: tachypnoea, clubbing
Symptoms: Poor feeding, poor weight gain
296
What is the gold standard investigation for tetralogy of fallot
Echocardiogram (shows blood flow route)
297
Describe the first line investigations for tetralogy of fallot
Chest x-ray (boot shaped heart due to RV thickening)
298
What are the differential diagnosis for tetralogy of fallot
Pulmonary stenosis, ventricular septal defect
299
Describe the management for tetralogy of fallot
Full surgical repair within 2 years of life
300
Describe the complications for tetralogy of fallot
Heart failure, cardiac death
301
Define hypertrophic cardiomyopathy
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
Describe the epidemiology for hypertrophic caridomyopathy
Main cause of sudden cardiac death in young people
303
Describe the aetiology for hypertrophic cardiomyopathy
Genetic autosomal domination mutation in sarcomere proteins – Troponin T, Beta-myosin
304
Describe the risk factors for hypertrophic cardiomyopathy
Family history of HCM
305
Describe the pathophysiology of HCM
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
What are the key presentations for HCM
SUDDEN DEATH, chest pain, palpitations, syncope, dyspnoea
307
Describe the clinical manifestations for HCM
Signs: Systolic ejection murmur, jerky carotid pulse, left ventricle lift (visible or palpable chest wall impulses)
Symptoms: Chest pain, palpitations, syncope, dyspnoea
308
What is the gold standard investigation for HCM
Echocardiogram: LVH, asymmetrical septal hypertrophy
309
Describe the first line investigations for HCM
1st line ECG: LVH - T wave inversion, Q waves, ST depression, chest x-ray: cardiomegaly
Other: Genetic testing
310
What are the differential diagnosis for HCM
Athlete's heart, LVH due to hypertension
311
Describe the management for HCM
1st line – beta blockers, CCB (diltiazem/verapamil) (anti-arrhythmic) or DC cardioversion if haemodynamically stable
Prevention: Implantable cardioverter-defibrillator
312
Describe the complications for HCM
Sudden cardiac death, infective endocarditis, atrial fibrillation
313
Define dilated cardiomyopathy
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
Describe the epidemiology for dilated cardiomyopathy
Most common cardiomyopathy
315
Describe the aetiology for dilated cardiomyopathy
Genetic, ischaemic heart disease, alcohol, thyroid disorder
316
Describe the pathophysiology for dilated cardiomyopathy
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
What are the key presentations for dilated cardiomyopathy
Heart failure presentation: Dyspnoea, fatigue, peripheral oedema
318
Describe the clinical manifestations for dilated caridomyopathy
Signs: Heart failure, arrhythmia, raised JVP, thromboembolism, peripheral oedema, 3rd/4th heart sounds
Symptoms: Shortness of breath, fatigue, weakness, chest pain
319
What is the gold standard investigation for dilated cardiomyopathy
Echocardiogram: dilated ventricles
320
Describe the first line investigations for dilated cardiomyopathy
ECG: tachycardia, LBBB, T wave inversion, Q waves. Chest x-ray: enlarged heart
321
What are the differential diagnosis for dilated cardiomyopathy
Hypertrophic CM, restrictive CM, heart failure
322
Describe the management for dilated cardiomyopathy
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
Describe the complications for dilated cardiomyopathy
Heart failure, arrhythmia, thrombus
324
Define restrictive cardiomyopathy
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
Describe the epidemiology for restrictive cardiomyopathy
Least common cardiomyopathy
326
Describe the aetiology for restrictive cardiomyopathy
Granulomatous diseases (amyloidosis, sarcoidosis), idiopathic, end-myocardial fibrosis
327
Describe the pathophysiology for restrictive cardiomyopathy
Decreased volume in ventricles causes bi-atrial enlargement. Rigid fibrous myocardium fills poorly and contracts poorly causing decreased cardiac output
328
What are the key presentations for restrictive cardiomyopathy
Heart failure: dyspnoea, fatigue, peripheral oedema
329
Describe the clinical manifestations for restrictive cardiomyopathy
Signs: S3+4 heart sounds, raised JVP, oedema, ascites, hepatomegaly
Symptoms: Dyspnoea, fatigue, orthopnoea, chest pain
330
What is the gold standard investigation for restrictive cardiomyopathy
Cardiac catheterisation
331
Describe the first line investigations for restrictive cardiomyopathy
ECG, chest x-ray (normal/small heart), echocardiogram: thickened ventricular walls, atria and septum
332
What are the differential diagnosis for restrictive cardiomyopathy
Constrictive pericarditis, heart failure, hypertrophic cardiomyopathy
333
Describe the management for restrictive cardiomyopathy
No treatment – poor prognosis. Treat underlying cause. Heart transplant
334
Describe the complications for restrictive cardiomyopathy
Heart failure, arrhythmias
335
Define rheumatic fever
Systemic infection from Lancefield group A beta-haemolytic strep (s. pyogenes)
336
Describe the epidemiology for rheumatic fever
Developing countries
337
Describe the aetiology for rheumatic fever
Group A beta-haemolytic streptococcus mainly S.pyogenes
338
Describe the pathophysiology of rheumatic fever
Antibodies against streptococcus bacteria also attack body tissues. Commonly valves in heart - rheumatic heart disease
339
What are the key presentations for rheumatic fever
Fever, joint pain, recent strep infection (tonsilitis)
340
Describe the clinical manifestations for rheumatic fever
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
Describe the first line investigations for rheumatic fever
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
Describe the management for rheumatic fever
1st line – antibiotics: IV benzylpenicillin then phenoxymethicillin for 10 days
NSAIDs for joints, aspirin + steroids for carditis, haloperidol for chorea. Ongoing penicillin prophylaxis
343
Describe the complications for rheumatic fever
Valve disease (mitral stenosis), heart failure
344
Define atrioventricular node re-entry tachycardia
Tachycardia due to the presence of 2 functionally and anatomically distinct conduction pathways in the AV node
345
Describe the epidemiology for AVNRT
Most common supraventricular tachycardia
346
Describe the aetiology for AVNRT
Cardiomyopathy, ischaemic heart disease, hyperthyroidism, cocaine, excess alcohol
347
Describe the risk factors for AVNRT
Coronary artery disease, substance misuse
348
Describe the pathophysiology for AVNRT
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
What are the key presentations for AVNRT
Tachycardia, paroxysmal attacks (sudden onset/offset palpitations)
350
Describe the clinical manifestations for AVNRT
Signs: Sudden onset/offset palpitations, neck pulsation, tachycardia (140-280bpm)
Symptoms: Chest pain, shortness of breath, fatigue, weakness
351
What is the gold standard investigation for AVNRT
ECG: P waves are within the QRS complex, narrow QRS. QRS followed by T wave repeated
352
What are the differential diagnosis for AVNRT
Atrial fibrillation, atrial flutter, sinus tachycardia
353
Describe the management for AVNRT
1st line – vagal manoeuvres (Valsalva, carotid sinus massage). 2nd – IV adenosine
Prevention – beta blockers, CCB, flecainide
354
Define brugada syndrome
Sodium channelopathy causing dangerously fast arrhythmias
355
Describe the aetiology for brugada syndrome
Gene mutation
356
What are the key presentations for Brugada syndrome
Syncope, palpitations, dyspnoea, chest pain
357
What is the gold standard investigation for Brugada syndrome
ECG: Coved ST elevation in chest leads V1-3
358
Describe the management for Brugada syndrome
Implantable cardiac defribillator
359
Define bundle branch block
A block in the conduction of one of the bundle branches, so the ventricles don't receive impulses at the same time
360
Describe the aetiology of bundle branch blocks
RBBB: pulmonary embolism, ischemic heart disease, atrial or ventricular septal defect
LBBB: ischemic heart disease, valvular disease, cardiomyopathy, cardiac surgery
361
Describe the risk factors for bundle branch blocks
Ischaemic heart disease, structural heart defects
362
Describe the pathophysiology for bundle branch blocks
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
What are the key presentations for bundle branch blocks
Asymptomatic, syncope
364
What is the gold standard investigation for bundle branch blocks
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
Describe the management for bundle branch blocks
Usually no treatment. Treat hypertension, pacemaker, cardiac resynchronisation therapy (CRT)
366
Describe the complications for bundle branch blocks
Complete heart block
367
Define deep vein thrombosis
Formation of a thrombus within the deep vein system. A type of venous thromboembolism along with pulmonary embolism
368
Describe the aetiology for DVT
Virchow’s triad: reduced blood flow, endothelial injury, increases likelihood of clotting
369
Describe the risk factors for DVT
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
Describe the pathophysiology for DVT
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
What are the key presentations for a DVT
Unilateral, calf swelling, tenderness, pitting oedema, dilated superficial veins, colour changes to leg, warm, erythema, cyanosis
372
What is the gold standard investigation for a DVT
Doppler ultrasound (unable to compress vein = clot)
373
Describe the first line investigations for a DVT
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
What are the differential diagnosis for DVT
Compartment syndrome, cellulitis, acute limb ischaemia
375
Describe the management for a DVT
1st line – DOAC anticoagulation: apixaban or rivaroxaban.
Long term: LWMH, DOAC or warfarin, compression stockings, treat underlying cause.
LMWH 1st line in pregnancy
376
Describe the monitoring for a DVT
Prevention – hydration, mobilisation, compression stockings, LMWH
377
Describe the complications for a DVT
Pulmonary embolism
378
Define pericardial effusion and cardiac tamponade
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
Describe the aetiology of pericardial effusion
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
Describe the risk factors for pericardial effusion
Malignancy, aortic dissection, purulent pericarditis
381
Describe the pathophysiology for pericardial effusion and cardiac tamponade
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
What are the key presentations for pericardial effusion and cardiac tamponade
Pericardial friction rub, dyspnoea, chest pain, Beck's triad
383
Describe the clinical manifestations for pericardial effusion and cardiac tamponade
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
What is the gold standard investigation for cardiac tamponade/ pericardial effusion
Echocardiogram (echo-free zone surrounding the heart)
385
Describe the first line investigations for pericardial effusion
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
What are the differential diagnosis for pericardial effusion
Constrictive pericarditis, congestive heart failure, Dressler’s syndrome
387
Describe the management for pericardial effusion
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
Describe the complications for pericardial effusion
Cardiac tamponade, haemodynamic compromise, and death
389
Describe the prognosis for pericardial effusion
Depends on underlying cause - worse with infection
390
Define Prinzmetal angina
Angina due to coronary artery spasm. AKA vasospastic angina
391
Describe the aetiology for Prinzmetal angina
Does not correlate with exertion. May be precipitated by smoking, cocaine, marijuana, emotional stress, extreme cold weather
392
Describe the pathophysiology for Prinzmetal angina
Coronary artery spasms and suddenly narrows
393
What are the key presentations for Prinzmetal angina
Central crushing chest pain at rest which resolves with GTN spray
394
Describe the clinical manifestations for prinzmetal angina
Dyspnoea, sweating, nausea
395
What is the gold standard investigation for prinzmetal angina
Coronary angiography (ACh used to provoke spasm)
396
Describe the first line investigations for prinzmetal angina
ECG (ST elevation during acute episode), biomarkers (not elevated)
397
Describe the management for prinzmetal angina
1st line – GTN spray. Other: calcium channel blockers + long-acting nitrates. Stop smoking, reduce risk factors.
398
Define pulmonary embolism
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
Describe the aetiology for PE
Virchow’s triad: reduced blood flow, endothelial injury, increases likelihood of clotting
400
Describe the risk factors of PE
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
Describe the pathophysiology for PE
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
What are the key presentations for PE
Sudden onset pleuritic chest pain, dyspnoea, haemoptysis
403
Describe the clinical manifestations for PE
Signs: Haemoptysis, pleuritic chest pain, hypoxia, tachycardia, tachypnoea, DVT (leg swelling and tenderness), hypotension, cyanosis,
Symptoms: Shortness of breath, cough, fever, dizziness, syncope
404
What is the gold standard investigation for PE
CT pulmonary angiogram (direct visual of thrombus in pulmonary artery)
405
Describe the first line investigations for PE
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
What are the differential diagnosis for PE
MI, pneumonia, pneumothorax
407
Describe the management for PE
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
Describe the monitoring for PE
Prevention – LMWH, stop OCP or HRT, mobilisation, compression stockings
409
Describe the complications for PE
Pulmonary infarction, cardiac arrest
410
Define torsades de pointes
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
What are the key presentations for torsades de pointes
Palpitations, dizziness, syncope, tachycardia
412
What is the gold standard investigation for torsades de pointes
ECG: rapid irregular QRS complexes which twist around baseline
413
Describe the management for torsades de pointes
Correct electrolyte imbalance or remove cause. Magnesium infusion (even if normal serum sodium), defibrillation if V-fib occurs
414
Describe the complications for torsades de pointes
Ventricular fibrillation: ventricular muscle fibres contract randomly causing a complete failure of ventricular function > cardiac arrest. 1st line – DC cardioversion
