Cardiology Flashcards
(407 cards)
1
Q
What are the five big risk factors for the development of cardiovascular disease?
A
Hypertension. Smoking. Diabetes mellitus. Hypercholesterolaemia. Family history.
2
Q
What is bradycardia?
A
HR < 60bpm
3
Q
What is tachycardia?
A
HR > 100bpm
4
Q
ECG interpretation: Presence of P waves.
A
Sinus rhythm.
5
Q
ECG interpretation: Absence of P waves.
A
Atrial fibrillation.
6
Q
ECG interpretation: PR interval constant, < 0.2s.
A
No heart block.
7
Q
ECG interpretation: PR interval constant, > 0.2s.
A
First degree heart block.
8
Q
ECG interpretation: PR interval increasing, then dropped QRS.
A
Second degree heart block (type 1 / Wenckebach).
9
Q
ECG interpretation: PR interval constant, then dropped QRS.
A
Second degree heart block (type 2).
10
Q
ECG interpretation: PR interval random, P waves not associated with QRS.
A
Third degree heart block (complete heart block).
11
Q
ECG interpretation: QRS < 0.12s.
A
No bundle branch block.
12
Q
ECG interpretation: QRS > 0.12s.
A
Broad complex.
Bundle branch block.
13
Q
ECG interpretation: QRS > 0.12s, V1 first deflection down, V6 first deflection up.
A
Left bundle branch block.
14
Q
ECG interpretation: QRS > 0.12s, V1 first deflection up, V6 first deflection down.
A
Right bundle branch block.
15
Q
ECG interpretation: ST segment elevated.
A
Infarction.
Pericarditis.
16
Q
ECG interpretation: ST segment depressed.
A
Ischaemia.
Infarction.
Digoxin treatment.
17
Q
ECG interpretation: T wave height > two-thirds of QRS height.
A
Hyperkalaemia.
18
Q
ECG interpretation: T wave inversion.
A
Normal in aVR and V1.
Old infarction.
Left ventricular hypertrophy.
19
Q
ECG: Which leads have T wave inversion normally?
A
aVR.
V1.
20
Q
Define atherosclerosis.
A
Plaque accumulation in the arteries of the body.
21
Q
Describe the mechanism of action of statins.
A
Inhibit the action of HMG-CoA reductase (enzyme in hepatic cholesterol synthesis).
22
Q
Who should receive a statin?
A
Established cardiovascular disease.
QRISK3 > 10%.
23
Q
What time of day should patients take a statin?
A
At night (this is when the majority of cholesterol synthesis takes place).
24
Q
What dose of atorvastatin is used in primary prevention and secondary prevention of cardiovascular disease?
A
Primary - 20mg.
Secondary - 80mg.
25
How should statin use be managed in pregnancy?
Pregnancy is a contraindication to statin use - stop three months before attempting pregnancy.
26
Define stage 1 hypertension.
Clinic blood pressure ≥ 140/90 mmHg.
| 24hr ABPM average ≥ 135/85 mmHg.
27
Define stage 2 hypertension.
Clinic blood pressure ≥ 160/100 mmHg.
| 24hr ABPM average ≥ 150/95 mmHg.
28
Define severe hypertension.
Clinic systolic blood pressure ≥ 180 mmHg.
| Clinic diastolic blood pressure ≥ 120 mmHg.
29
What is the difference between primary and secondary hypertension?
Primary develops due to complex physiological changes associated with ageing.
Secondary develops as a result of endocrine disease, renal disease, pharmacotherapy (inc. COCP) and pregnancy.
30
How does hypertension present?
Asymptomatic in most cases unless blood pressure is very high.
31
At what blood pressure do people develop symptoms of hypertension and what are they?
≥ 200/120 mmHg including headaches, visual disturbances and seizures.
32
What is ambulatory blood pressure monitoring?
A system that records blood pressure periodically (twice and hour) over a 24hr period - the preferred method for diagnosing hypertension.
33
It is important to assess someone with newly diagnosed hypertension for end-organ damage. What investigations should be performed?
```
Fundoscopy (hypertensive retinopathy).
Urine dipstick (renal disease).
Urea and electrolytes (renal disease).
HbA1c (diabetes mellitus).
ECG (LVH, IHD).
```
34
What lifestyle changes can be advised for people with hypertension?
Improving diet, more physical exercise, losing weight and stopping smoking.
35
When should pharmacological therapy begin in the management of hypertension?
If lifestyle measures fail to control blood pressure and there is evidence of end-organ damage or a QRISK3 of ≥ 10%.
36
What is first-line pharmacological therapy for hypertension in those under 55 or with T2DM?
Angiotensin-converting enzyme inhibitors such as ramipril.
37
Hypertension: What are side effects of ramipril / ACEi use?
Cough, angioedema and hyperkalaemia.
38
Hypertension: What pharmacological therapy should be used in those aged under 55 or with T2DM if ACEi cannot be tolerated?
Angiotensin 2 receptor blockers such as candesartan.
39
Hypertension: What are side effects of candesartan / ARB use?
Hyperkalaemia.
40
Hypertension: What monitoring is required in the use of ACE inhibitors?
Check urea and electrolytes before treatment and one-to-two weeks after starting. As well as after increasing dose.
41
Hypertension and ACEi: What changes in U&Es should be expected / acceptable?
Rise in serum creatinine, acceptable up to 30% from baseline.
Rise in serum potassium, acceptable up to 5.5mmol/l.
42
What is first-line pharmacological therapy for hypertension in those over 55 without T2DM, or those of Afro-Caribbean heritage with no diabetes mellitus?
Calcium channel blockers such as amlodipine.
43
Hypertension: What are side effects of amlodipine / CCB use?
Flushing, ankle swelling and headache.
44
What is the blood pressure target for people receiving pharmacological therapy?
< 80yrs: < 140/90mmHg.
| > 80yrs: < 150/90mmHg.
45
Hypertension: What is second-line pharmacological therapy if first-line fails to control BP?
Add a thiazide-like diuretic (indapamide) or ACEi/ARB depending on the pathways.
46
Hypertension: What are side-effects of thiazide-like diuretic use?
Hyponatraemia, hypokalaemia and dehydration.
47
Hypertension: What is third-line therapy is second-line fails to control BP.
Three medications: ACEi/ARB + CCB + thiazide-like diuretic.
48
Hypertension: What is fourth-line therapy if BP still uncontrolled on triple therapy?
If potassium ≤ 4.5 add low-dose spironolactone.
| If potassium > 4.5 add alpha-blocker or beta-blocker.
49
What is malignant hypertension?
Severe hypertension (≥180/120mmHg) with symptoms of acute organ injury such as papilloedema, retinal bleeding, headache + nausea, chest pain, haematuria and epistaxis.
50
Define orthostatic/postural hypotension.
Drop in blood pressure > 20/10mmHg within three minutes of standing.
51
What groups are at risk of orthostatic/postural hypotension?
Older people.
Neurodegenerative disease.
Diabetes.
Hypertension.
52
What are clinical features of orthostatic hypotension?
Presyncope (feeling faint) and syncope.
53
What is the management of orthostatic hypotension?
Midodrine (alpha1 agonist).
| Fludrocortisone (corticosteroid).
54
What are the four Ds of postural hypotension with compensatory tachycardia?
Deconditioning.
Dysfunctional heart (aortic stenosis).
Dehydration (disease, dialysis, drugs).
Drugs (levodopa, tamsulosin, etc.).
55
What is angina?
Chest pain that usually occurs due to insufficient blood flow to the myocardium (a result of coronary artery narrowing).
56
What is stable angina?
Chest pain that occurs during periods of stress (exercise) when the myocardium becomes ischaemic because oxygen supply cannot meet demand.
57
What relieves the chest pain associated with stable angina?
Rest or GTN spray.
58
What pharmacotherapy should patients with stable angina receive for immediate symptomatic relief?
Sublingual glyceryl trinitrate (GTN) spray PRN.
59
Stable angina: How often can a patient use a GTN spray during an angina attack?
Every 5 minutes. If ongoing for ten minutes call 999.
60
What pharmacological therapy is given for long-term symptomatic relief of stable angina?
Beta-blocker (atenolol) or calcium channel blocker (verapamil, diltiazem).
Or could try long-acting dihydropyridine calcium channel blocker (MR nifedipine).
61
What pharmacological therapy is offered for long-term symptomatic relief to those suffering from stable angina not controlled on a BB or CCB?
Long-acting nitrate (isosorbide mononitrate).
62
What pharmacological therapy is given for secondary prevention of cardiovascular disease in stable angina?
Aspirin 75mg.
Statin 80mg.
ACE inhibitor.
63
Stable angina management: How should standard-release isosorbide mononitrate be taken?
Asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours... to minimise the development of nitrate tolerance.
64
Stable angina management: What is an alternative to standard-release isosorbide mononitrate that reduces the risk of tolerance developing?
Once-daily modified release isosorbide mononitrate.
65
What is the gold-standard investigation for stable angina?
CT coronary angiography reveals stenosed (narrowed) coronary arteries.
66
What surgical interventions can be offered in the management of stable angina?
Percutaneous coronary intervention (PCI).
| Coronary artery bypass graft (CABG).
67
Stable angina: Describe the process of percutaneous coronary intervention.
A catheter is inserted into the brachial or femoral artery and guided to the coronary arteries using fluoroscopy... it then involves dilating the blood vessel with a balloon and/or inserting a stent.
68
Stable angina: Describe the process of coronary artery bypass graft.
It involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patients leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis.
69
Describe the recovery time of CABG vs PCI.
CABG have longer recovery and greater complication than PCI.
70
What is acute coronary syndrome?
An umbrella term covering a number of acute presentations in medicine that includes ST-elevation myocardial infarction, non-ST elevation myocardial infarction and unstable angina. The conditions usually result from occlusion of a coronary artery by a thrombus from an atherosclerotic plaque.
71
What mainly forms a thrombus in arteries?
Platelet activation.
72
What is the most common presenting feature of acute coronary syndrome?
Chest pain.
73
Describe the chest pain associated with acute coronary syndrome.
Central/left-sided, may radiate to the jaw or left arm, described as heavy or constricting.
74
What are clinical features of acute coronary syndrome other than chest pain?
Dyspnoea, sweating, nausea and vomiting, pallor and clamminess.
75
What is the mainstay of investigation in ACS?
Twelve-lead ECG.
| Serial troponins.
76
What are troponins?
Proteins found in cardiac muscle that are released as a result of myocardial ischaemia.
77
What is meant by 'serial' troponins?
Troponins monitored at baseline, six hours and twelve hours after the onset of symptoms.
78
Are troponins specific for ACS?
No - they are also raised in renal failure, sepsis, myocarditis, aortic dissection and pulmonary embolism.
79
What is the management of all patients with ACS?
```
Morphine (severe pain only).
Oxygen (sats < 94% only).
Nitrates.
Aspirin 300mg.
Remember: MONA.
```
80
How is STEMI diagnosed?
ST elevation or new left bundle branch block on ECG.
81
How is NSTEMI diagnosed?
Raised troponins and/or ST depression, T wave inversion, pathological Q waves.
82
ACS: What is the diagnosis if troponins are normal and there are no pathological ECG changes?
Unstable angina or musculoskeletal pain.
83
What risk assessment tool can inform the management of ACS?
GRACE (Global Registry of Acute Coronary Events).
84
What GRACE score indicates that patients with ACS should receive coronary angiography within 72 hours?
> 3%
85
What pharmacological therapy is given for acute NSTEMI?
```
Beta-blocker.
Aspirin.
Ticagrelor.
Morphine.
Anticoagulant (fondaparinux).
Nitrates (GTN).
Remember: BATMAN
```
86
Acute NSTEMI management: What alternative can be given to ticagrelor and under what circumstances?
Clopidogrel is given in those with a high bleeding risk (i.e. taking an oral anticoagulant).
87
What is the mechanism of action of fondaparinux?
Fondaparinux activates antithrombin III which potentiates the inhibition of coagulation factor Xa.
88
An anterolateral STEMI will result in ECG changes in which leads?
I
aVL
V3-V6
89
An anterolateral STEMI is associated with occlusion of which coronary artery?
Left coronary artery.
90
An anterior STEMI will result in ECG changes in which leads?
V1-V4
91
An anterior STEMI is associated with occlusion of which coronary artery?
Left anterior descending artery.
92
A lateral STEMI will result in ECG changes in which leads?
I
aVL
V5-V6
93
A lateral STEMI is associated with occlusion of which coronary artery?
Left circumflex artery.
94
An inferior STEMI will result in ECG changes in which leads?
II
III
aVF
95
An inferior STEMI is associated with occlusion of which coronary artery?
Right coronary artery.
96
What is the management of acute STEMI?
Percutaneous coronary intervention.
97
Which patients with acute STEMI should receive percutaneous coronary intervention?
Those presenting within twelve hours of symptom onset and if PCI is available within two hours.
98
Acute STEMI: What is the pharmacological management if PCI is planned?
Give dual anti platelet (aspirin + ticagrelor).
| Or if at high bleeding risk - clopidogrel.
99
Acute STEMI: What is the management if PCI unavailable?
Thrombolysis (tenecteplase).
100
How should acute STEMI be monitored following thrombolysis?
Aim for 50% resolution in ST elevation on ECG after 90 minutes.
101
What is secondary prevention pharmacological management following acute STEMI.
```
Dual-antiplatelet (aspirin, ticagrelor).
ACEi (ramipril).
Beta-blocker (bisoprolol).
Statin (atorvastatin).
Remember: DABS.
```
102
Give six examples of complications resulting from myocardial infarction.
```
Death.
Mitral regurgitation.
Heart failure.
Arrhythmia.
Aneurysm.
Dressler's syndrome.
```
Remember: DREAD
103
What memory aid can be used to remember the complications of MI?
DREAD.
| Death, rupture of heart septum or papillary muscles, oEdema, aneurysm + arrhythmia, Dressler's syndrome.
104
Describe the pathophysiology of mitral regurgitation post-MI.
Rupture of papillary muscles following infero-posterior myocardial infarction.
105
Describe the pathophysiology of Dressler's syndrome post-MI.
Localised immune réponse which results in pericarditis two-three weeks post-MI.
106
What is the presentation of Dressler's syndrome?
Pleuritic chest pain and low grade fever. 2-3 weeks post-MI.
107
What is heard on auscultation in Dressler's syndrome?
Pericardial rub.
108
How is a diagnosis of Dressler's syndrome made?
```
ECG (global ST elevation, T wave inversion).
Echocardiogram (pericardial effusion).
Inflammatory markers (raised CRP, ESR).
```
109
What is the management of Dressler's syndrome?
NSAIDs.
If more severe:
Steroids
Pericardiocentesis.
110
What is bundle branch block?
A complete or partial interruption of the electrical pathways inside the wall of the heart between the ventricles.
111
Describe the pathophysiology of right bundle branch block (RBBB).
Delayed electrical conduction to the right ventricle - the right ventricle contracts later and the heart ejects less blood.
112
What is the cause of RBBB?
Often a normal variant... the result of natural degeneration of the conduction system that occurs with age. Can be the result of PE, COPD, cardiomyopathy or heart defect.
113
What does ECG reveal in RBBB?
Widening of the QRS complex (> 0.12s) and a notched morphology of the QRS complex. V1 first deflection up, M morphology. V6 first deflection down, W morphology.
114
What is the cause of LBBB?
Underlying heart disease including myocardial infarction.
115
What does ECG reveal in LBBB?
Widening of the QRS complex (> 0.12s) and a notched morphology of the QRS complex. V1 first deflection down, W morphology. V6 first deflection up, M morphology.
116
Define heart block.
Interruption or delay of electrical conduction in the heart.
117
How is heart block classified?
Where the block occurs: sinoatrial node, atrioventricular node, at/below the bundle of His.
118
Describe sinoatrial node block.
Electrical impulse is delayed or blocked and atrial depolarisation is delayed.
119
Explain why sinoatrial node block rarely causes severe symptoms.
Secondary pacemaker (the atrioventricular node) stimulates a rate of 40-60bpm which is sufficient to retain consciousness in the resting state.
120
Describe atrioventricular node block.
Electrical impulse is delayed or blocked and ventricular depolarisation is delayed or completely blocked.
121
What are the three types of atrioventricular block?
First-degree.
Second-degree (type 1 and 2).
Third-degree.
122
Describe first-degree AV heart block.
Delay, but not disruption, as the electrical signal moves between the atrium and the ventricles through the atrioventricular node.
PR interval > 0.2s on ECG. No dropped or skipped beats.
123
Describe second-degree AV heart block (type 1 / Wenckebach).
Impairment of electrical conduction between the atria and ventricles that results in a failure to conduct an impulse, causing a skipped beat.
Progressive prolongation of PR interval, with resulting dropped beat.
124
Describe second-degree AV heart block (type 2).
Impairment of electrical conduction between the atria and ventricles that results in a failure to conduct an impulse, causing a sudden, unexpected dropped beat.
PR interval is unchanged from beat to beat, with a random skipped beat.
125
Describe third-degree AV heart block (complete).
Complete impairment of conduction between the atria and ventricles.
There is no relationship between P waves and QRS complexes.
126
What rate do the ventricles contract in complete AV heart block?
Ventricles produce their own signal to control rate at approx. 30-40 bpm.
127
What is the management of second-degree (type 2) and third-degree heart block?
Atropine 500 micrograms IV.
Repeat atropine up to 6 times (total 3mg).
Consider noradrenaline.
Consider transcutaneous cardiac pacing.
128
What is a pacemaker?
A device that delivers controlled electrical impulses to specific areas of the heart to restore the normal electrical activity and improve heart function.
129
What two components make up a pacemaker?
A pulse generator.
| Pacing leads.
130
What are three different types of pacemaker?
Single-lead chamber pacemaker.
Dual-chamber pacemaker.
Biventricular (triple-chamber) pacemaker.
131
Describe single-lead chamber pacemaker.
Leads in a single chamber - either the right atrium or right ventricle.
132
Describe dual-chamber pacemaker.
Leads in both the right atrium and right ventricle.
133
Describe biventricular (triple-chamber) pacemakers.
Leads in the right atrium, right ventricle and left ventricle.
134
How can you identify a pacemaker on ECG?
Sharp vertical line in all leads either before the P wave (if the lead is in the atria) and/or before the QRS complex (if the lead is in the ventricle).
135
What is heart failure?
Heart is unable to pump sufficiently to maintain blood flow to meet the body's needs.
136
What is the clinical presentation of heart failure?
Shortness of breath (worse with exercise or lying down), fatigue, peripheral oedema.
137
What are examination findings in heart failure?
Cyanosis, tachycardia, elevated JVP.
138
What is acute heart failure?
Sudden onset or worsening of the symptoms of heart failure.
139
What are the two types of acute heart failure?
De novo acute heart failure (no past history of HF).
| Decompensated acute heart failure (background history of HF).
140
How does right-sided heart failure classically present and why?
Peripheral oedema, ascites, hepatosplenomegaly as a result of blood backing up into the systemic circulation.
141
How does acute left ventricular failure classically present and why?
Shortness of breath, productive cough (frothy/pink sputum) as a result of pulmonary oedema.
142
What are examination findings in acute left ventricular failure?
Oxygen desaturation, tachypnoea, tachycardia and bilateral basal crackles on auscultation.
143
What clinical features may be present in acute left ventricular failure due to underlying cause?
```
Chest pain (MI).
Fever/cough (viral infection).
```
144
What hormone is useful in the investigation of heart failure?
N-terminal pro-B-type natriuretic peptide (NT-proBNP).
145
Describe the physiological function of NT-proBNP.
Hormone produced by the left ventricular myocardium in response to strain. BNP is a vasodilator and diuretic white attempts to reduce strain on the heart.
146
HF: Interpret raised levels (> 400 ng/L) of NT-proBNP.
Supportive of diagnosis of heart failure and indicate further investigation.
147
HF: Interpret very high levels (> 2000 ng/L) of NT-proBNP.
Poor prognosis and requires urgent treatment.
148
Describe the sensitivity and specificity of NT-proBNP.
Sensitive but not specific (raised in renal impairment, tachycardia, pulmonary embolism, COPD).
149
What are findings on CXR in patients with left ventricular failure?
```
Alveolar oedema ('bat wings').
Kerley B lines.
Cardiomegaly.
Dilated upper lobe.
Pleural effusions.
Remember ABCDE.
```
150
Other than NT-proBNP and CXR... what imaging investigation may be performed in LVF?
Echocardiogram.
151
Echocardiogram: What is normal ejection fraction?
50-70%.
152
Echocardiogram: What is reduced ejection fraction?
< 40%.
153
What is the management of acute left ventricular failure?
Stop intravenous fluids.
Sit the patient up.
Give oxygen.
Intravenous loop diuretics (40mg furosemide).
154
Why does sitting a patient upright improve their symptoms in left ventricular failure?
Upright fluid will cover a smaller surface area of lung making the upper zones clear for more efficient gas exchange.
155
What is chronic heart failure?
Impaired left ventricular contraction or left ventricular relaxation that leads to chronic back-pressure of blood trying to flow into and through the left side of the heart.
156
What are five characteristic clinical features of chronic heart failure?
```
Shortness of breath worse on exertion.
Cough.
Orthopnoea.
Peripheral oedema.
Paroxysmal nocturnal dyspnoea.
```
157
Define orthopnoea.
Difficulty breathing when lying down.
158
What is paroxysmal nocturnal dyspnoea?
Episodes of waking at night with a severe attack of shortness of breath and cough. Patients describe feeling suffocated.
159
Describe the potential mechanisms behind the development of paroxysmal nocturnal dyspnoea.
Fluid settles across a larger surface area of the lung when laid flat.
Less responsive respiratory centre during sleep leads to reduced respiratory rate and work of breathing = hypoxia.
Less adrenaline in sleep, myocardium more relaxed = worse cardiac output.
160
Describe Class I of the New York Heart Association (NYHA) heart failure classification.
No symptoms, no limitation.
161
Describe Class II of the NYHA heart failure classification.
Mild symptoms, ordinary physical activity causes breathlessness.
162
Describe Class III of the NYHA heart failure classification.
Moderate symptoms, less than ordinary activity causes breathlessness.
163
Describe Class IV of the NYHA heart failure classification.
Severe symptoms, breathless at rest, increased discomfort with physical activity.
164
Give four examples of causes of chronic heart failure.
Ischaemic heart disease.
Valvular heart disease (aortic stenosis).
Hypertension.
Arrhythmias (e.g. AF).
165
What is first-line pharmacological therapy for the treatment of chronic heart failure?
```
ACE inhibitor (ramipril).
Beta-blocker (bisoprolol).
```
166
What is second-line pharmacological therapy for chronic heart failure?
Aldosterone antagonist (spironolactone / eplerenone).
167
What pharmacological therapy can be given in chronic heart failure to improve symptoms (but has no effect on mortality)?
Furosemide (loop diuretic).
168
What positively inotropic agent can be prescribed in chronic heart failure?
Digoxin.
169
What is digoxin and its function?
A cardiac glycoside that increases the force of myocardial contraction and reduces conductivity within the AV node.
170
What are clinical features of digoxin toxicity?
Anorexia, nausea, vomiting, diarrhoea, malaise, weakness, palpitations, syncope, confusion, hallucinations, blurred vision and arrhythmias.
171
What investigation can be performed in suspected digoxin toxicity?
Plasma digoxin concentration - must be measured at least six hours after the last dose of digoxin.
172
Under what circumstances should digoxin dose be reduced?
Renal dysfunction (digoxin is renally excreted).
173
What is cor pulmonale?
Right-sided heart failure caused by respiratory disease.
174
Describe the pathophysiology of cor pulmonale.
Increased pressure and resistance to blood flow in the pulmonary arteries (pulmonary hypertension) results in right ventricular strain.
175
Give five causes of cor pulmonale.
COPD, pulmonary embolism, interstitial lung disease, cystic fibrosis and primary pulmonary hypertension.
176
What are the clinical features of bradycardia with haemodynamic compromise?
Shock (hypotension, pallor, sweating, clammy extremities, confusion / impaired consciousness), syncope.
177
What is the first-line pharmacological treatment of bradycardia with haemodynamic compromise?
Atropine 500 microgram intravenously (repeat up to 6 times, max. 3mg).
178
Describe the mechanism of action of atropine.
Antimuscarinic which inhibits the parasympathetic nervous system.
179
What are side effects of atropine use.
Pupil dilation, urinary retention, dry eyes, constipation.
180
Give three causes of narrow complex tachyarrhythmias.
Atrial fibrillation.
Atrial flutter.
Supraventricular tachycardia.
181
Give two causes of broad complex tachyarrhythmias.
Ventricular tachycardia.
| SVT with bundle branch block.
182
What is atrial flutter?
A form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves due to a re-entrant rhythm.
183
What is the clinical presentation of atrial flutter?
Palpitations, light-headedness and shortness of breath.
184
What does ECG reveal in atrial flutter?
Narrow complex (< 0.12s), regular tachycardia with 'sawtooth appearance'.
185
What is the atrial rate in atrial flutter?
Often 300bpm.
186
What determines the ventricular rate in atrial flutter (and what is most common)?
The degree of AV node block determines the rate. A 2:1 block is most common... resulting in a ventricular rate of 150bpm.
187
What is a supraventricular tachycardia (SVT)?
Result of an electrical signal re-entering the atria from the ventricles (tachycardia isn't ventricular in origin). It is a self-perpetuating loop without an end point.
188
What is the clinical presentation of SVT?
Palpitations, light-headedness.
189
What does ECG reveal in SVT?
Narrow complex (< 0.12s) tachycardia.
190
What is the first-line management of SVT?
Vagal manoeuvres (such as Valsalva or carotid sinus massage).
191
What is second-line management of SVT (after Vagal manoeuvres)?
Intravenous 6mg adenosine (or verapamil in asthmatics).
192
Describe the mechanism behind Vagal manoeuvres.
They stimulate the parasympathetic nervous system by acting the vagus nerves (stimulating lower heart rate).
193
What are the three main types of SVT?
Atrioventricular nodal re-entrant tachycardia (through AV node).
Atrioventricular re-entrant tachycardia (through accessory pathway).
Atrial tachycardia.
194
What is the mechanism of adenosine?
Adenosine slows cardiac conduction through the atrioventricular node to reset back to sinus rhythm.
195
How should adenosine be given for management of SVT?
6mg as a rapid bolus via a large proximal (antecubital fossa) cannula.
196
What should patients be warned of before giving adenosine?
Adenosine can cause a brief period of asystole or bradycardia... warn them they may feel a sense of "impending doom" // dying.
197
What is paroxysmal supraventricular tachycardia?
A situation where SVT reoccurs and remits in the same patient over time.
198
What is the long-term management of Paroxysmal supraventricular tachycardia?
Beta-blockers, calcium channel blockers, amiodarone.
| Radiofrequency ablation.
199
What is Wolff-Parkinson-White (WPW) syndrome?
WPW is a condition caused by the presence of a congenital accessory pathway that connects the atria and ventricles (called the Bundle of Kent).
200
What does ECG reveal in Wolff-Parkinson-White syndrome?
Delta wave.
QRS prolongation.
Shortened PR interval.
201
ECG: What is a delta wave?
Slurred upstroke of QRS (slow rise in the initial part of the QRS complex).
202
What is definitive treatment of Wolff-Parkinson-White syndrome?
Radiofrequency ablation.
203
Describe the process of radiofrequency ablation.
A catheter is inserted into the femoral veins along with a wire which is guided to the heart under fluoroscopy. The wire is placed against different areas to test the electrical signals... once an abnormal pathway is identified radifrequency ablation is applied to burn the abnormal area (scar tissue doesn't conduct electricity).
204
What is atrial fibrillation (AF)?
A chaotic, irregular atrial tachyarrhythmia that is characterised by fibrillatory waves on ECG.
205
AF: What are fibrillatory waves on ECG?
Random oscillations of the baseline.
206
What are causes of AF?
```
Sepsis.
Mitral valve stenosis.
Ischaemic heart disease.
Thyrotoxicosis.
Hypertension.
Remember: Mrs SMITH.
```
207
What is the difference between paroxysmal and persistent AF?
Paroxysmal AF terminates spontaneously (< 7 days, typically < 24 hours).
Persistent AF is continuous and cannot be cardioverted or it is determined that caridoversion is inappropriate.
208
What are the clinical features of AF?
Palpitations, shortness of breath, chest pain.
209
Give three causes of an irregularly irregular pulse.
Atrial fibrillation.
Ventricular ectopics.
Sinus arrhythmia.
210
How is atrial fibrillation distinguished from other causes of irregularly irregular pulse?
ECG.
211
What does ECG reveal in patients with AF?
Absent P waves, irregularly irregular QRS complex tachycardia.
212
What is valvular AF?
Atrial fibrillation in the presence of moderate-to-severe mitral stenosis or prosthetic heart valve.
213
What are the two stages of AF management?
Rate/rhythm control.
| Stroke risk reduction.
214
What is the management of a haemodynamically unstable patient with AF?
DC cardioversion (give prior sedation).
215
AF: Describe the rate control management approach.
Rate control is the predominant management approach in AF and aims to slow the heart rate down (allowing the ventricles to fill) to avoid the negative effects on cardiac function.
216
What pharmacological therapies make up AF rate control?
1st: Beta-blocker (atenolol).
2nd: Rate-limiting calcium channel blocker (diltiazem).
3rd: Digoxin (if BB or CCB don't work and only in sedentary people).
217
AF: Describe the rhythm control management approach.
Cardioversion: Aims to get the patient back into and maintain a normal sinus rhythm.
218
When should rhythm control be preferred over rate control in the management of AF (4 things)?
Reversible cause for the AF.
AF is new onset (< 48 hours).
AF is causing heart failure.
Patient remains symptomatic despite effective rate control.
219
What are the two options for cardioversion in AF?
Pharmacological cardioversion.
| Electrical cardioversion.
220
What drugs can be given for pharmacological cardioversion in AF?
1st: flecainide.
2nd: amiodarone.
221
AF: How should cardioversion be performed in someone with a short duration of symptoms (< 48 hours)?
Heparin is given then cardioversion attempted.
222
AF: How should cardioversion be performed in someone that has been in AF for > 48 hours?
Anticoagulation provided for three weeks before cardioversion attempted. Rate control given in the intermediate period.
223
Why do patients require anticoagulation for three weeks before attempted cardioversion in AF?
The moment of cardioversion presents the greatest risk of embolism leading to stroke (may mobilise a thrombus from the atrium into the circulation).
224
What scoring system is used for predicting stroke risk in AF patients?
CHA2DS2-VASc
225
What are the criteria for the CHA2DS2-VASc risk tool?
```
Congestive heart failure (1).
Hypertension (1).
Age > 75 (1), > 65 (1).
Diabetes (1).
Stroke/TIA hx (2).
Vascular disease (1).
Sex female (1).
```
226
How is CHA2DS2-VASc score interpreted?
0 - no anticoagulation.
1 - consider anticoagulation in males.
2 - offer anticoagulation.
227
What scoring system is used to assess bleed risk in anti coagulated AF patients?
HASBLED.
228
What are the criteria for the HASBLED risk tool?
```
Hypertension (1).
Abnormal renal/liver function (2).
Stroke hx (1).
Bleeding hx (1).
Labile INRs (1).
Elderly (1).
Drugs or alcohol (2).
```
229
How is HASBLED score interpreted?
≥ 3 is high risk of bleeding.
230
What management approach may be opted for in paroxysmal AF?
Pill in the pocket - terminate episodes when they become symptomatic (palpitations, shortness of breath) by taking flecainide.
231
Who is suitable for 'pill in the pocket' management in paroxysmal AF?
Those who have infrequent episodes and without underlying structural heart disease.
232
What is the mechanism behind warfarin?
Vitamin K antagonist. Vitamin K acts as a cofactor in the carboxylation of clotting factors.
233
Vitamin K is involved in the carboxylation in which clotting factors?
Factor II
Factor VII
Factor IX
Factor X
234
How is warfarin monitored?
INR.
235
What is INR?
International normalised ratio - the prothrombin time of the patient compared the prothrombin time of a normal healthy adult.
236
Warfarin: What is the target INR for AF?
2.5
237
Warfarin: What is the target INR for VTE?
2.5
238
Warfarin: What is the target INR for recurrent VTE?
3.5
239
What is the management of someone on warfarin therapy that presents with major bleeding?
Stop warfarin.
Give intravenous 5mg vitamin K.
Give prothrombin complex concentrate.
240
What is the management of someone on warfarin therapy that presents with INR > 8.0 and minor bleeding?
Stop warfarin.
Give intravenous 1-3g vitamin K.
Restart warfarin when INR < 5.
241
What is the management of someone on warfarin therapy that presents with INR > 8.0 and no bleeding?
Stop warfarin.
Give oral vitamin K 1-5mg.
Restart warfarin when INR < 5.
242
What is the management of someone on warfarin therapy that presents with INR 5.0-8.0 and minor bleeding?
Stop warfarin.
Give intravenous 1-3g vitamin K.
Restart warfarin when INR < 5.
243
What is the management of someone on warfarin therapy that presents with INR 5.0-8.0 and no bleeding?
Omit 1 or 2 doses of warfarin and reduce subsequent maintenance dose.
244
Warfarin: What can induce cP450 and lead to reduced INR?
```
Phenytoin
Carbamazepine
Barbituates
Rifampicin
Alcohol.
Sulfonylureas / St Johns wart
Remember: PC BRAS
```
245
Warfarin: What can inhibit cP450 and lead to raised INR?
```
Allopurinol
Omeprazole
Disulfiram
Erythromycin
Valproate
Isoniazid
Ciprofloxacin
Ethanol (acute).
Sulphonamides
Remember: AO DEVICES
```
246
What is ventricular tachycardia?
A broad-complex tachycardia originating from a ventricular ectopic focus.
247
Why does ventricular tachycardia require urgent treatment?
VT has the potential to precipitate into ventricular fibrillation (which results in cardiac arrest).
248
What are the two main types of ventricular tachycardia?
Monomorphic ventricular tachycardia (most commonly due to MI).
Polymorphic ventricular tachycardia (such as Torsades de Pointes).
249
What is the management of ventricular tachycardia?
Electrical cardioversion.
250
When should electrical cardioversion be performed in a person with VT?
Adverse signs e.g. sBP < 90, pulse > 100, chest pain, ischaemia on ECG, heart failure, syncope.
251
How is electrical cardioversion performed in the management of VT?
Provide sedation.
| Give three synchronised DC shocks.
252
Which electrolytes should be assessed following cardioversion in VT?
Potassium.
Magnesium.
Calcium.
253
What medication should be given following electrical cardioversion in VT?
Amiodarone 300mg IV over at least 20 minutes.
| Then amiodarone 900mg IV over 24 hours.
254
What is long QT?
Condition of delayed ventricular repolarisation that can lead to ventricular tachycardia and sudden death.
255
What is a normal QT interval?
< 440 ms.
256
What is long QT syndrome?
An inherited condition of QT prolongation.
257
Give examples of non-pharmacological causes of QT interval prolongation?
Myocardial infarction.
Hypokalaemia.
Hypomagnesaemia.
Hypocalcaemia.
258
Give examples of pharmacological causes of QT interval prolongation?
```
Methotrexate
Erythromycin
Terfenadine
Haloperidol
Clarithromycin
Amiodarone
TCAs
SRRIs
Remember: METH CATS
```
259
What is the management of long QT?
Avoid medications that can prolong QT.
Beta-blockers.
Implantable cardioverter defibrillator.
260
What is Torsades de Pointes (TdP)?
"Twisting of the points"... a form of polymorphic ventricular tachycardia associated with long QT interval.
261
Describe how a prolonged QT interval can lead to TdP.
Prolonged QT = prolonged repolarisation following contraction.
Prolonged repolarisation leads to spontaneous depolarisation in some myocytes.
Depolarisation spreads throughout ventricle and contraction occurs prior to repolarisation.
262
What are causes of Torsades de Pointes?
```
Hypothermia
Hypothyroidism
Hypocalcaemia
Hypomagnesaemia
Hypoakalemia
```
263
What is the management of Torsades de Pointes?
Intravenous magnesium sulphate.
| Correct underlying cause.
264
What are ventricular topics?
Premature ventricular complexes are premature beats caused by random electrical discharges outside the atria.
265
How do ventricular ectopics present?
Patients complain of random, brief palpitations.
266
How do ventricular ectopics appear on an ECG?
Broad QRS complex, premature to the expected next impulse, often followed by a compensatory pause.
267
What is bigeminy?
A type of ventricular ectopic where every other beat is a premature ventricular complex.
268
What is trigeminy?
A type of ventricular ectopic where every third beat is a premature ventricular complex.
269
What is the most likely congenital heart defect to be found in adulthood?
Atrial septal defect.
270
What is the presentation of atrial septal defect?
Fatigue and breathlessness
271
What is heard on auscultation of an atrial septal defect?
Ejection systolic murmur (heard loudest on inspiration) with fixed splitting of S2.
272
Explain why fixed splitting of S2 is heard in a patient with atrial septal defect.
Blood flows from L atrium to R atrium, more blood in the R atrium means more blood must be pumped out of the R ventricle... pulmonary valve closes later than the aortic valve.
273
What is seen on ECG in a patient with atrial septal defect?
RBBB.
274
What valve defect can be heard as a mid-diastolic murmur (louder on expiration) with a loud S1 opening snap.
Mitral stenosis
275
What is mitral stenosis?
Hardening of the mitral valve (between the L atrium and L ventricle).
276
What features (other than what is heard on auscultation) may present in mitral stenosis?
```
Low volume pulse.
Malar flush (plum red discolouration of cheeks).
```
277
Why do people with mitral stenosis develop malar flush?
Back-pressure of blood into pulmonary system causes rise in CO2 and vasodilation.
278
Mitral stenosis can cause what arrhythmia (and why)?
Atrial fibrillation - atrial strain results in electrical disruption.
279
What investigations can be performed in the assessment of mitral stenosis?
Echocardiography.
ECG.
CXR.
280
What might echocardiography show in mitral stenosis?
Reduced cross-sectional area of the mitral valve.
281
What might ECG show in mod-severe mitral stenosis?
Broad, notched/bifid P wave - a sign of left atrial enlargement.
282
What might CXR show in mitral stenosis?
Left atrial enlargement.
283
What is mitral regurgitation?
An incompetent mitral valve allows blood to flow back into the left atrium during ventricular contraction.
284
What causes mitral regurgitation?
Idiopathic weakening with age.
Ischaemic heart disease.
Rheumatic heart disease.
Connective tissue disorders (Ehlers Danlos, Marfans).
285
What is heard on auscultation in mitral regurgitation?
High-pitched pansystolic murmur (louder on expiration) best heard at the apex with the patient lying on their left.
286
What is heard on auscultation in tricuspid regurgitation?
High-pitched pansystolic murmur (louder on inspiration) best heard at the lower left sternal border.
287
What is aortic stenosis?
Narrowing of the aortic valve (at the exit of the left ventricle).
288
What is the most common cause of aortic stenos?
Age-related calcification (typically present between 65-75 years of age).
289
What are the clinical features of aortic stenosis?
Chest pain and exertional syncope.
290
What is heard on auscultation in aortic stenosis?
High-pitched ejection systolic murmur that radiates to the carotids.
291
Aortic stenosis leads to the development of...
Left ventricular hypertrophy and subsequent failure.
292
When should valve replacement be considered in aortic stenosis?
Symptomatic.
| Asymptomatic but pressure gradient of > 40mmHg across the aortic valve.
293
What are the two types of prosthetic valve?
Biological (bioprosthetic).
| Mechanical.
294
What are the advantages/disadvantages of biological heart valves over mechanical valves?
Adv: Don't require long-term anticoagulation.
Dis: Structural deterioration and calcification over time.
295
What are the advantages/disadvantages of mechanical heart valves over biological valves?
Adv: Low failure rate.
Dis: Increased risk of thrombosis and require long-term anticoagulation.
296
What is aortic regurgitation?
A condition of aortic incompetence whereby blood flows in the reverse direction during ventricular diastole.
297
How does aortic regurgitation present clinically?
Palpitations, exertional dyspnoea, orthopnoea and paroxysmal nocturnal dyspnoea.
298
What causes aortic regurgitation?
Rheumatic fever, infective endocarditis, connective tissue disease, bicuspid aortic valve.
299
What is found on examination in aortic regurgitation?
Collapsing pulse, wide pulse pressure, displaced hyperdynamic apex beat... on auscultation a high-pitched early diastolic murmur.
300
How is aortic regurgitation diagnosed?
Echocardiogram.
301
What is the inheritance pattern of hypertrophic obstructive cardiomyopath?
Autosomal dominant.
302
What is the pathophysiology of hypertrophic obstructive cardiomyopathy?
Disorder of muscle tissue caused by defects in the genes encoding the contractile proteins. Left ventricle hypertrophy results in decreased compliance and decreased cardiac output.
303
What is the most common cause of sudden cardiac death in the young?
Hypertrophic obstructive cardiomyopathy (HOCM).
304
How can hypertrophic obstructive cardiomyopathy present?
Exertional dyspnoea, angina, syncope or sudden death.
305
What does auscultation of hypertrophic obstructive cardiomyopathy reveal?
Ejection systolic murmur loudest at the lower left sternal edge.
306
What does echocardiogram reveal in hypertrophic obstructive cardiomyopathy?
Mitral regurgitation.
Systolic anterior motion.
Asymmetric hypertrophy.
Remember: Mr SAM ASH
307
What is the management of HOCM?
Amiodarone, beta-blocker/verapamil, cardioverter defibrillator, dual chamber pacemaker and endocarditis prophylaxis.
308
What is the second most common cause of cardiac death in the young?
Arrhythmogenic right ventricular dysplasia (ARVD).
309
What is the inheritance pattern of arrhythmogenic right ventricular dysplasia/cardiomytopathy?
Autosomal dominant.
310
Describe the pathophysiology of arrhythmogenic right ventricular dysplasia/cardiomyopathy.
Replacement of right ventricular myocardium with fatty and fibrofatty tissue.
311
What is the presentation of arrhythmogenic right ventricular dysplasia?
Palpitations, syncope and sudden cardiac death.
312
What may ECG reveal in arrhythmogenic right ventricular dysplasia?
```
T wave inversion (V1-V3).
Epsilon wave (terminal notch in QRS).
```
313
How is arrhythmogenic right ventricular dysplasia managed?
Sotalol.
Catheter ablation.
Implantable cardioverter-defibrillator.
314
What are causes of dilated cardiomyopathy?
Alcohol excess.
Coxsackie B virus.
Wet beriberi (thiamine deficiency).
Doxorubicin (chemo).
315
What is the pathophysiology of dilated caridomyopathy?
Dilation of heart chambers, especially left ventricle = systolic dysfunction.
316
What are causes of restrictive cardiomyopathy?
Amyloidosis.
Post-radiotherapy.
Loeffler's endocarditis.
317
When does peripartum cardiomyopathy present?
Between the last month of pregnancy and five months post-partum.
318
Which group is at greater risk of developing peripartum cardiomyopathy?
Older women.
Greater parity.
Multiple gestations.
319
What is Takotsubo cardiomyopathy?
Broken heart syndrome. A cardiomyopathy induced by stressful triggers such as bereavement.
320
What are the clinical features of Takotsubo cardiomyopathy?
```
Chest pain.
Heart failure (dyspnoea, oedema).
```
321
What does echocardiogram reveal in Takotsubo cardiomyopathy?
Apical ballooning of the myocardium.
322
What is peripheral arterial disease?
Atherosclerosis and subsequent stenosis of arteries (most commonly in the legs).
323
Which arteries are affected in peripheral artery disease (PAD)?
Most commonly the arteries in the legs (also arms, neck or kidneys).
324
What is the main clinical feature of peripheral artery disease?
Intermittent claudication.
325
PAD: What is intermittent claudication?
Muscle pain, ache, cramp that develops on mild exertion and is relieved by rest. Can affect the calf, thigh or buttock.
326
PAD: What is the claudication distance?
The distance an individual is able to walk before the onset of pain.
327
What examination findings are present in peripheral arterial disease?
```
Absent femoral, popliteal or foot pulses.
Cold legs.
Atrophic skin changes.
Skin ulcers.
Abnormal hair/nail growth.
```
328
What is the first-line investigation in peripheral arterial disease?
Colour duplex ultrasonography.
329
Peripheral arterial disease: What investigation is required before surgical intervention?
MR angiography to detail the extent and location of disease as well as the quality of distal vessels.
330
What is the initial management of peripheral arterial disease?
Risk factor modification: smoking cessation, blood pressure control, cholesterol control (statin) and antiplatelet. Provide supervised exercise programmes.
331
What surgical intervention can be performed in the management of peripheral arterial disease?
Percutaneous transluminal angioplasty (balloon inflated within a narrowed arterial segment).
Arterial reconstruction with bypass graft if distal run-off is good.
332
What is critical limb ischaemia?
A complication of peripheral arterial disease that develops when blood flow to the legs becomes severely restricted.
333
What are the clinical features of critical limb ischaemia?
Ulceration.
Gangrene.
Foot pain at rest ("burning").
334
What is acute limb ischaemia?
A medical emergency. The result of thrombosis in situ, emboli or graft occlusion.
335
What are the clinical features of acute limb ischaemia?
Pale, pulseless, painful, paralysed, parenthetic and perishingly cold.
336
What is the management of acute limb ischaemia?
Open surgery or angioplasty.
337
What is Buerger's disease?
Thromboangiitis obliterates (Buerger's disease) is a small and medium vessel vasculitis that causes thrombus formation.
338
What group of people are most commonly affected by Buerger's disease?
Male aged 25-35 that smokes cigarettes.
339
What is the characteristic presentation of thromboangiitis obliterans?
Painful blue discolouration of the fingertips or toes that is worse at night.
May progress to ischaemic ulcers and gangrene.
340
What is gangrene?
Death of tissue due to inadequate blood supply.
341
What does angiography reveal in Buerger's disease?
Corkscrew collaterals (collateral vessels which form to bypass the affected arteries).
342
What is the management of Buerger's disease?
Completely stop smoking and don't use nicotine replacement therapy.
343
Define aneurysm.
Artery with dilatation of more than 50% of its original diameter.
344
What causes aneurysms to develop?
Atheroma, trauma, infection, connective tissue disorders or inflammatory processes.
345
What is the difference between true and false aneurysms?
True aneurysms - abnormal dilatations that involve all layers of the arterial wall.
False aneurysms - involve a collection of blood in the outer layer (adventitia) only.
346
What are common sites of aneurysm?
Aorta (infrarenal), iliac arteries, femoral arteries, popliteal arteries.
347
What are complications of aneurysms?
```
Rupture.
Thrombosis.
Embolism.
Fistulae.
Pressure/compression on nearby structures.
```
348
Outline the abdominal aortic aneurysm screening programme in England.
All men aged 65 are invited for an ultrasound scan to identify and treat dangerously large aneurysms before rupture.
349
What is an abdominal aortic aneurysm?
Aneurysm of the abdominal aorta > 3cm across
350
How are aneurysms monitored?
Annual ultrasound.
351
What advice is given to reduce the risk of growth of AAA.
Smoking cessation, healthy diet, regular exercise, alcohol moderation.
352
When should people with AAA receive surgical intervention?
AAA > 5.5cm
353
What intervention is offered for AAA?
Endovascular aneurysm repair (EVAR).
354
What is the presentation of ruptured AAA?
Intermittent or continuous abdominal pain, collapse, expansile abdominal mass and shock.
355
What is aortic dissection?
Injury to the innermost layer of the aorta allows blood to flow between the layers of the aortic wall, forcing the layers apart.
356
What are the presenting features of aortic dissection?
Sudden tearing chest pain that radiates to the back. Vomiting, sweating and light-headedness.
357
How are aortic dissections classified?
Type A - involves ascending aorta, arch of the aorta (2/3 cases).
Type B - involves descending aorta distal to left subclavian origin.
358
By what process do the complications of aortic dissection develop?
Aortic dissection extends and branches of the aorta occlude sequentially. The dissection can also occlude proximally.
359
What features of aortic dissection may present as a result of branch occlusion?
Distal expansion: Hemiplegia (stroke), unequal arm pulses, unequal arm blood pressure, acute limb ischaemia, anuria.
Proximal expansion: murmur (aortic valve incompetence), MI and cardiac arrest.
360
What investigation confirms the diagnosis of aortic dissection?
CT angiogram shows a false lumen in the aorta.
361
What is the management of aortic dissection?
Control blood pressure with IV labetalol.
Give IV morphine for pain.
Refer for surgery.
362
What surgery is performed for aortic dissection?
Type A - open surgery.
| Type B - endovascular repair.
363
What is pericarditis?
Inflammation of the pericardium.
364
What is the pericardium?
Fibroelastic sac that surrounds the heart.
365
What cause pericarditis?
Infection (coxsackie, tuberculosis), trauma, post-MI, connective tissue disease, hypothyroidism, malignancy.
366
What are clinical features of pericarditis?
Chest pain, fever, non-productive cough, dyspnoea.
367
How may the chest pain in pericarditis be relieved?
Sitting forwards.
368
What is found on examination of pericarditis?
Tachypnoea, tachycardia, pericardial friction rub on auscultation.
369
What does ECG show in pericarditis?
Widespread saddle-shaped ST elevation.
370
What do troponins show in pericarditis?
Raised.
371
What is the management of acute pericarditis?
Treat underlying cause.
| Give ibuprofen.
372
What is constrictive pericarditis?
Condition that develops as a result of scarring and loss of elasticity of the pericardial sac... prevents normal filling and thus restricts cardiac output.
373
What is the presentation of constrictive pericarditis?
Poor exercise tolerance, exertional dyspnoea. Features of right heart failure (elevated JVP, ascites, oedema, hepatomegaly). Positive Kussmaul's sign.
374
Constrictive pericarditis: What is Kussmaul's sign?
Paradoxical rise in JVP on inspiration (should fall with inspiration due to reduced pressure in expanding thoracic cavity).
375
What may CXR show in constrictive pericarditis?
Pericardial calcification.
376
What is cardiac tamponade?
Pericardial effusion raises intrapericardial pressure... reducing ventricular filling and thus restricting cardiac output.
377
What is the diagnostic triad of cardiac tamponade?
Low blood pressure.
Raised JVP.
Muffled heart sounds on auscultation.
378
What does ECG show in cardiac tamponade?
Electrical alternans (alternation of QRS complex altitude).
379
What is the treatment of cardiac tamponade?
Urgent pericardiocentesis.
380
What is infective endocarditis?
Endocardial inflammation as a result of microbial infection... typically affecting the heart valves.
381
What are heart valves commonly affected in infective endocarditis?
Valves are a source of turbulent blood flow which damages the endocardial lining... thrombi develop on damaged surface and microorganisms attach to thrombi to form vegetations.
382
Assume infective endocarditis in which patients?
Fever + new murmur.
383
What pathogen most commonly causes infective endocarditis?
Staphylococcus aureus.
384
What are risk factors for infective endocarditis?
Skin breaches (dermatitis, intravenous lines, wounds), prosthetic valves, valvular disease, dental problems, renal failure, immunosuppression, diabetes mellitus.
385
In what order are the valves commonly affected in infective endocarditis?
```
Mitral.
Aortic.
Mitral + aortic.
Tricuspid.
Pulmonary.
```
386
What are the clinical features of infective endocarditis?
Fever, rigors, night sweats, malaise, weight loss, anaemia, splenomegaly, clubbing.
387
By what mechanism can infective endocarditis damage organs?
Vegetations can detach, become septic emboli and then cause abscesses in the relevant organ
388
Give examples of organ damage in infective endocarditis.
Skin (Janeway lesions).
Glomerulonephritis.
Roth spots (retinal haemorrhage)
Splinter haemorrhages
389
What criteria are used for diagnosing infective endocarditis?
Duke criteria
390
What are the Duke criteria for infective endocarditis?
Repeated blood cultures - three sets at different times from different sites.
If negative consider fungal endocarditis.
391
What blood tests may be performed in infective endocarditis (with results).
FBC - anaemia, neutrophilia.
ESR - raised.
CRP - raised.
Rheumatoid factor - positive.
392
What imaging can be performed in the investigation of infective endocarditis?
Transthoracic echocardiogram may be able to show vegetations > 2mm... transoesophageal echocardiogram is more sensitive.
393
What is the management of infective endocarditis?
Intravenous gentamicin.
394
What are varicose veins?
Dilated, tortuous, superficial veins that occur secondary to incompetent venous valves.
395
Where do varicose veins most commonly occur?
Great saphenous vein.
| Small saphenous vein.
396
What are risk factors for varicose veins?
Increasing age, female, pregnancy, obesity.
397
What is the presentation of varicose veins?
Cosmetic complaints (superficial dilated vessels). Some patients may have aching, throbbing or itching.
398
What are possible complications of varicose veins?
```
Varicose eczema.
Hyperpigmentation.
Hard/tight skin.
Hypopigmentation.
Bleeding.
Superficial thrombophlebitis.
Venous ulceration.
```
399
Define syncope.
Transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.
400
Give three causes of reflex syncope.
Vasovagal (triggered by emotion, pain or stress).
Situational (triggered by cough, micturition, gastrointestinal causes).
Carotid sinus syncope.
401
What are prodromal symptoms of reflex syncope?
Sweating, pallor, nausea + vomiting.
402
What are the causes of orthostatic hypotension?
```
Venous pooling (after exercise or during pregnancy).
Post-prandial (after meals).
Prolonged bed rest (deconditioning).
```
403
Define shock.
Circulatory failure that results in inadequate organ perfusion. sBP < 90mmHg, MAP < 65mmHg.
404
What two factors can contribute to shock?
```
Cardiac output (inadequate).
Systemic vascular resistance (inadequate).
```
405
What is the presentation of shock?
Reduced conscious level, agitation, cool peripheries, tachycardia, slow cap refill, tachypnoea, oliguria.
406
What are the three types of shock?
Hypovolaemic shock.
Cardiogenic shock.
Septic shock.
407
What are the eight reversible causes of cardiac arrest?
```
Hypothermia.
Hypoglycaemia, hypocalcaemia, hypokalaemia, hyperkalaemia.
Hypoxia.
Hypovolaemia.
Thrombosis.
Tension pneumothorax.
Tamponade.
Toxins.
```
