Flashcards in Cardiology Deck (82):
What is pulsus paradoxus?
An abnormally large decrease in systolic blood pressure (>10 mmHg) and pulse wave amplitude during inspiration. (Normal fall <10mmHg)
What does the Frank-Starling law say? What does the graph show during a failing heart?
As the stretch of the wall increases, so does the stroke volume.
In a failing heart, there is a decreased force of contraction as the heart is unable to keep up with an increase in stroke volume. Stroke volume eventually decreases.
What are the five most common causes of congestive heart failure?
3. Idiopathic (often dilated cardiomyopathy)
4. Valvular (e.g. AS, AR and MR)
5. Alcohol (dilated cardiomyopathy)
What is the difference between systolic versus diastolic failure?
Systolic failure - inability of the ventricle to contract normally, resulting in decreased cardiac output. EF is less than 40%
Diastolic failure - inability of the ventricle to relax and fill normally, causing increased filling pressures. EF is more than 50%
What is the difference between low-output vs high-output failure?
Low-output: cardiac output is decreased and fails to increase normally with exertion
High-output: output is normal or increased in the face of increased needs - failure occurs when cardiac output fails to meet these needs.
What is the difference between chronic stable angina and the acute coronary syndromes?
Chronic stable angina - most often due to a fixed stenosis caused by an atheroma
Acute coronary syndromes are the result of plaque rupture
What investigations are ordered if CHF is suspected? (3)
1. ECG - usually non-specific conduction abnormalities
2. CXR - cardiomegaly, pulmonary venous distribution, interstitial oedeama. Normal CXR does not exclude diagnosis
3. TTE - single most useful test
Pharmacological treatment of symptomatic CHF
1. ACEis (use AIIRBs if intolerant)
2. Beta-blockers (carvedilol, bisoprolol, metoprolol XR)
3. Diuretics - to achieve euvolaemia in fluid-overloaded patients.
4. Spironolactone for patients who remain severely symptomatic, despite appropriate doses of ACEIs and diuretics
Discuss the role of calcium-channel blockers in treating symptomatic CHF. (3)
CCBs have vasodilator and anti-ischaemic effects.
Non-dihydropyridine CCBs e.g. verapamil and diltiazem are direct negative inotropes therefore contraindicated in patients with systolic heart failure
Dihydropyridines (amlodipine and felodipine) have not shown survival benefits in systolic CHF but may be used to treat comorbidities
How is chronic stable angina managed? (first-line) (4)
1. General measures - lifestyle modification and treatment of risk factors e.g. statins and anti-hypertensives etc.
2. Anti-platelet therapy e.g. aspirin
e.g. cardioselective agents preferred - metoprolol and atenolol
Which conditions compose the acute coronary syndromes (ACS)? (3)
1. Unstable angina
Which cardiac enzyme is the most sensitive and specific marker of myocardial necrosis? Describe pattern of increase/decrease.
Serum levels increase within 3-12 hours of chest pain onset, peak at 24-48h, and decrease to baseline over 5-14 days
How should an acute MI be managed in emergency? (8)
1. Get ECG
2. IV access - FBE, U&E, glucose, lipids, cardiac enzymes (troponin > CK-MB)
3. Brief assessment - hx, ex, contraindications to PCI or fibrinolysis
4. Aspirin 300mg (if it hasn't been given by ambos already)
5. Morphine 5-10mg IV +/- metoclopramide
6. If STEMI on ECG and PCI available within 120min - do PCI
7. If no PCI available within 120 mins - do fibrinolysis
Consider instituting a beta-blocker, clopidogrel and ACE-i
What is the first-line choice for thrombolysis in acute MIs?
Tissue plasminogen activators - alteplase, reteplase or tenecteplase
(Tenecteplase used in BHS)
Post-MI, which medications should be the patient on?
SAAB - C
If large anterior MI - consider warfarin for 3 months as prophylaxis against systemic embolism from LV mural thrombus
When are CABGs performed? (4)
1. Left main stem disease
2. Multi-vessel disease
3. Failed angioplasty
4. Refractory angina
What is the difference between stable and unstable angina?
Nature of pain
Stable:induced by exercise, relieved by rest
Unstable: angina of increasing frequency or severity, occurs on minimal exertion or at rest, associated with increased risk of MI
What is the most common cause of secondary hypertension?
Which renal conditions can contribute to secondary hypertension? (2 categories)
Intrinsic renal disease (75%) - glomerulonephritis, polyarteritis nodosa, systemic sclerosis, PCKD, chronic pyelonephritis
Renovascular disease (25%) - renal artery stenosis, fibromuscular dysplasia (rare , mostly in young women)
Which endocrine disorders can cause hypertension? (5)
Conn's, Cushing's, phaeochromocytoma, acromegaly, hyperparathyroidism
Describe the grading of hypertensive retinopathy
I - tortuous arteries with thick shin walls - silver or copper wiring
II - AV nipping (narrowing where arteries cross veins)
III - Flame haemorrhages and cotton-wool spots
IV - Papilloedema
How is hypertension managed? (3)
1. Treat underlying cause if present
2. Lifestyle changes
3. Pharmacological - monotherapy (calcium channel blocker or thiazide in those over 55, ACE inhibitor in those under 55) or combination - ACEi + thiazide + CCB
List 3 causes of aortic stenosis.
1. Congenital bicuspid valve
2. Rheumatic disease
3. Senile/calcific degeneration
What are triad of symptoms said to be most common aortic stenosis?
How is aortic stenosis severity determined? What is mild/moderate/severe
Mean gradient and valve area (normal = 3cm squared)
Mild - less than 25mmHg and greater than 1.5cm squared
Moderate - 25-40 mmHg and 1-1.5 cm squared
Severe - more than 40mmHg, less than 1 cm2
Apart from aortic stenosis, name three other causes of LV outflow obstruction.
1. Subaortic membrane
2. Hypertrophic cardiomyopathy
3. Supravalvular stenosis
Describe the progression of symptoms in aortic stenosis. (3)
1. Loss of 50% to 70% of valve area can occur with no symptoms.
2. Symptoms occur when stenosis is moderately severe
3. Once symptoms occur, average survival 2-3 years with no surgical intervention - the only effective treatment is valvular replacement.
Describe the pulse, pulse pressure and murmur heard in aortic stenosis.
Slow rising pulse with narrow pulse pressure
Ejection systolic mumur heard at base, left sternal edge and aortic area and which radiates to the carotids
What is aortic sclerosis?
Senile degeneration of the valve. Ejection systolic murmur, normal volume and character of pulse, no radiation to carotids
How is pulse pressure calculated?
PP = SBP - DBP
Normal DBP = 40mmHg
Describe the pathophysiology behind narrow pulse pressure
Narrow pulse pressure (<20mmHg)
Caused by decreased cardiac output and increased systemic resistance (i.e. anything that will cause a decrease in SBP or increase in DBP)
List 3 common and 2 less common conditions that may be characterised by narrow pulse pressure
common: HF, aortic stenosis, hypovolaemia - shock
less common: HOCM, mitral stenosis
List 3 causes of acute aortic regurgitation
1. Infective endocarditis
2. Ascending aortic dissection
List 4 causes of chronic aortic regurgitation
2. Connective tissue disorders (Marfan's, Ehlers-Danlos)
3. Seronegative arthritis and rheumatic disorders (AS, Reiter's syndrome, SLE)
4. Aortitis - syphilis, takayasu's arteritis
What kind of murmur is heard in aortic stenosis?
Ejection systolic murmur (heard at the base, left sternal edge and the aortic area, radiates to the carotids)
What kind of murmur is heard in aortic regurgitation?
Diastolic murmur (heard best in expiration, with patient sitting forward)
How can aortic regurgitation be managed? (2)
1. Medical - goal to reduce systolic hypertension - ACEi.
2. Surgical (aortic valve replacement) - if increasing symptoms, enlarged heart on CXR/echo
How is aortic regurgitation investigated? (3)
1. ECG - LVH
2. CXR - cardiomegaly, dilated ascending aorta, pulmonary oedema
3. Echo - diagnostic
List 3 causes of mitral stenosis
3. Prosthetic valve
List 6 symptoms of mitral stenosis
3. Palpitations - associated with AF
4. Chest pain
5. Systemic emboli
How is mitral stenosis managed? (5)
1. Rate control if AF
2. Anticoagulation with warfarin
3. Diuretic to decrease preload and pulmonary venous congestion
4. Surgical: ballon vavuloplasty (if pliable, non-calcified valve), open mitral valvotomy or valve replacement
5. SBE/IE prophylaxis for GI/GU infected procedures
List 5 causes of mitral regurgitation
1. Rheumatic fever
2. Infective endocarditis
3. Mitral valve prolapse
4. Connective tissue disorders
5. Ruptured chordae tendinae
How is mitral regurgitation investigated? (3)
1. ECG: AF +/- P mitrale if in sinus rhythm,LVH
2. CXR: enlarged LA + LV, mitral valve calcification, pulmonary oedema
3. Echo: to assess LV function and aetiology
How is mitral regurgitation managed?
1. Control rate if AF
3. Diuretics improve symptoms
4. Surgery - for deteriorating symptoms; aim to repair of replace the valve before LV irreversibly impaired
What is the most common valvular abnormality?
Mitral valve prolapse
How is chronic AF managed? (3)
1. Rate control
2. Rhythm control
Usually rate > rhythm
Describe the rate control regimen in chronic AF
Beta blocker (atenolol or metoprolol) or CCB (diltiazem or verapamil)
Digoxin only OK in sedentary/elderly
What are the three clinical patterns of AF?
The three Ps
1. Paroxysmal AF -
2. Persistent AF -
3. Permanent or chronic AF -
What is paroxysmal AF?
episodes come on suddenly and generally revert spontaneously within the next 24-48h without any intervention
What is persistent AF?
similar abrupt onset but episodes persist for days to weeks unless active measures are taken to revert the patient to sinus rhythm
What is permanent/chronic AF?
inability of patient to sustain sinus rhythm for any length of time, or a decision has been made not to attempt cardioversion because of other factors (e.g giant atria)
In which conditions is emergency cardioversion indicated?
VF and pulseless/unstable VT
What constitutes a broad complex tachycardia?
Rate >100 and QRS complexes >120ms
How is stable VT managed? (6)
2. IV access
3. 12 lead ECG
4. Amiodarone IVI
5. If polymorphic (torsades de pointes) - magnesium sulphate 2g over 5 min
6. If this fails, or if cardiac arrest, use DC shock
How can VT be prevented?
Implantation of ICD or radiofrequency ventricular tachycardia ablation in refractory cases
What constitutes a narrow complex tachycardia?
Rate of more than 100bpm, QRS less than 120ms
How is SVT managed? (2)
1. If haemodynamically stable - vagal maneouvres 1st line - breath-holding, valsalva, carotid massage
2. IV adenosine - 1st line; if fails, verapamil
What is Wolff-Parkinson-White syndrome and what would an ECG show? (3)
Caused by congenital accessory conduction pathway between atria and ventricles
ECG: short PR interval, wide QRS complex (due to slurred upstroke or 'delta wave') and ST-T changes
List 7 viral causes of acute myocarditis
What is the leading cause of sudden cardiac death in the young?
What is hypertrophic cardiomyopathy?
LVOT obstruction from asymmetric septal hypertrophy. May present at any age. Autosomal dominant inheritance but 50% are sporadic.
What symptoms can occur in HCM? (5)
1. Sudden death could be first symptom
2. Angina, dyspnoea, palpitation, syncope
How is HCM managed? (4)
1. B-blockers or verapamil for symptoms (aim is reducing ventricular contractility)
2. Amiodarone for arrhythmias (AF, VT)
3. Anticoagulate for paroxysmal AF or systemic emboli
4. Surgical/invasive: defibrillator, dual=chamber pacing, septal myomectomy
List 7 factors associated with dilated cardiomyopathy?
4. Viral infection
6. Peri- or postpartum thyrotoxicosis
7. Congenital (X-linked)
Describe the pulse, pulse pressure, and murmur heard in aortic regurgitation
Collapsing (water-hammer) pulse, wide pulse pressure, early diastolic murmur (heard best in expiration, with patient sitting forward)
What needs to be considered in cardioverting patients with AF?
If the patient has severe symptoms or a compromised haemodynamic state, cardioversion should always be considered immediately
UNLESS THIS IS THE CASE, careful consideration of the RISK OF THROMBOEMBOLISM
When is it generally safe to electively cardiovert a patient with AF? Why?
If the episode has lasted less than 48 hours
If there is doubt as to duration of AF, or if clear that episode has lasted more than 48 hours, DO NOT ATTEMPT to cardiovert until steps are taken to minimise thromboembolic risk (due to atrial 'stunning' that can occur following cardioversion
What can be involved in cardioverting a patient with AF? (2)
*Make sure less than 48h - risk of thromboembolism
1. Pharmacological - IV or oral amiodarone or flecainide
2. synchronised electrical cardioversion
How can thromboembolic risk post-cardioversion be reduced? (2)
1. Perform transoesophageal echo - if thrombus present, cardioversion should not be attempted until patient has been fully anticoagulated for 3 weeks
2. Drugs that can be used - dalteparin, enoxaparin or unfractionated heparin
What is the diagnostic criteria for rheumatic fever?
Evidence of preceding GAS infection (positive throat culture, elevated strep antibody titre) and 2 major or 1 major and 2 minor manifestations (JONES criteria)
Describe the JONES criteria
- J: Joints (migratory polyarthritis)
- O: pancarditis
- N: subcutaneous nodules
- E: erythema marginatum
- S: Sydenham' s chorea
Arthralgia, fever, elevated ESR, prolonged PR interval on ECG, previous rheumatic fever
How is rheumatic fever treated? (5)
1. Bed rest
2. Benpen then pen V
3. Analgesia for carditis/arthritis - aspirin or NSAIDs, can add oral pred
4. Haloperidol or diazepam for chorea
5. Ongoing penicillin prophylaxis - ranging from 5 years to lifelong
What is Kussmaul's sign?
Paradoxical rise in JVP during inspiration - seen in constrictive pericarditis BUT NOT CARDIAC TAMPONADE
List 5 causes of acute pericarditis.
2. Infectious - viral - coxsackie most common; bactieral - s. pneumoniae; TB, fungal
3. Post-MI and cardiac surgery
5. Connective tissue disorders - SLE, RA, scleroderma etc.
List three clinical features of acute pericarditis.
1. Chest pain - pleuritic, alleviated by sitting up and forward
2. Friction rub
3. ECG - diffuse elevated ST segments +/- depressed PR segment
WHat is Beck's triad?
1. Muffled heart sounds
3. Distended neck veins
Which leads would be affected in an anteroseptal AMI?
Which artery is involved in an anteroseptal AMI?
Which leads are affected in an inferior AMI?
II, III, aVF
Which artery is involved in an inferor AMI?
What is the normal width of a QRS complex?
less than 0.12 secs (three small squares)