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20 Cards in this Set

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  • Back
Outline the New York Heart Association's functional classification of congestive heart failure.
Class I: No limitation during ordinary activity.
Class II: "Slight". Fatigue or dyspnoea with moderate exertion.
Class III: "Marked". Light activity produces symptoms. (20% annual mortality rate.)
Class IV: Symptoms at rest. (60% annual mortality rate.)
What are some common causes of systolic dysfunction?
Ethanol abuse
Long-standing hypertension
Viral myocarditis, Chagas disease
Idiopathic dilated cardiomyopathy.
What are some common causes of diastolic dysfunction?
A 'stiff' LV, caused by:
Chronic hypertension
LV hypertrophy
What are some causes of high-output CHF?
↓ oxygenation:
▹ Severe anaemia
▹ AV shunting

↑ demand:
▹ Paget disease
▹ Thyrotoxicosis
▹ Beriberi
Outline nonpharmacological CHF management.
Oxygen, pleurocentesis if required (in acute pulmonary oedema)
1. Physical activity (staying active; supervised exercise training; rest when symptoms are severe)
2. Weight reduction (well-balanced diet low in saturated fat)
3. Sodium restriction
4. Fluid restriction
What are the standard elements of pharmacological CHF management?
Combination therapy using an ACE inhibitor, beta-blocker, and diuretic.
Why are diuretics used in CHF?
Diuretics reduce plasma volume, thereby relieving the symptoms of circulatory congestions such as dyspnoea. They are the only treatment that acutely produces symptomatic benefits and improves exercise capacity.
Why are ACE inhibitors used in CHF?
They produce arterial and venous dilation, and decrease the secretion of aldosterone and antidiuretic hormone. These actions reduce the plasma volume, venous pressure, and level of oedema, and increase cardiac output by reducing arterial pressure and cardiac afterload.
ACE inhibitors also counteract the adverse effects of antiogensin that contribute to cardiac remodelling.
Why are β-adrenoceptor antagonists used in CHF?
Excessive SNS activity contributes to cardiac remodeling in 3 ways:
1. SNS → tachycardia & ↑O2 demand → ischemia/infartion → remodelling
2. SNS → ↑RAAS activation → remodelling
3. SNS → ↑production of cardiac cytokines such as TNF-alpha and interleukins → remodelling
Thus, despite their negative inotropic effect, β-blockers are of prognostic benefit.
What is 'pulsus parvus et tardus'? What other signs and symptoms might it be accompanied by?
A delayed, slow-rising carotid upstroke -- a classical sign of aortic stenosis.
Other signs and symptoms include:
1. Soft, absent, or paradoxically split S2
2. Harsh systolic murmur (sometimes with thrill along left sternal border, often radiating to the neck)
3. Exertional dyspnoea
4. Exertional angina pectoris
5. Exertional syncope
Name at least 7 risk factors for DVT/PE.
▹ Past confirmed history of DVT/PE
▹ Elderly (>65)
▹ Cancer
▹ Lying around (bed-rest), Lower limb immobilisation)
▹ Obesity, OCP
▹ Thrombophilia, Trauma
▹ Surgery
1. What does mitral stenosis sound like on auscultation?

2. What is a sign of the severity of the stenosis?

3. What is the most common cause of mitral stenosis?
1. Loud S1, opening snap following S2, followed by a low-pitched diastolic rumble (best heard @ apex).

2. As the severity of the stenosis increases, the interval between S2 and the opening snap decreases.

3. Almost all cases of mitral stenosis in adults are 2º to rheumatic heart disease.
What are the conventional drugs used to control AF?

Which patients should you never use those drugs in?

What is the first step in treatment if the patient is haemodynamically unstable?
AV-node blockers:
▹ ß-blockers
▹ Calcium channel blockers (eg. verapamil)
▹ Digoxin.

These drugs all slow AV nodal conduction, so they must be avoided in patients with Wolff-Parkinson-White syndrome, as they may cause a paradoxical tachycardia (the accessory pathway is unaffected by them).

If the patient is haemodynamically unstable, DC cardioversion is the treatment of choice.
What are some causes of atrial fibrillation?

▹ Pulmonary disease, esp. PE
▹ Hypertension *
▹ Atherosclerosis *
▹ Rheumatic heart disease, esp. involving mitral stenosis
▹ Medications (theophylline, caffeine, digitalis)
▹ Alcohol consumption (holiday heart syndrome, alcoholic cardiomyopathy)
▹ Congenital heart disease, eg. ASD
▹ Inflammatory disease (pericarditis, myocarditis)
▹ Surgery (post-bypass, post-valvular surgery)
▹ Thyrotoxicosis

* Most common
What are some causes of aortic regurgitation?
Rheumatic heart disease
Aortic dissection/Aortic root dilation
What are four antiarrhythmics that slow AV node conduction?
Ca-channel blockers, eg. verapamil
What are 5 cyanotic heart diseases?
Mnemonic: 1-2-3-4-5 T's

Truncus arteriosus (1 big vessel)
Transposition of the (2) great vessels
Tricuspid atresia
Tetralogy of fallot
Total anomalous pulmonary venous return (which has 5 words, yuk-yuk-yuk!)
What are some causes of S3?

Of S4?
Mnemonic: FIPPY SHIT
Incompetence (mitral/tricuspid)

Stenosis (aortic/pulmonary)
Hypertension/Heart block
Ischaemic heart disease
What are the criteria for diagnosis for rheumatic fever?
The Jones Criteria.

Subcutaneous nodules
Erythema marginatum
Signs of carditis (eg. new murmur on echocardiography)

Lab findings (↑ESR, ↑CRP, ↑antistreptolysin O)
↑PR interval on ECG
Previous RF/RHD
What are the signs of an ischaemic limb?
Poikilothermia ("perishing" cold)
Paralysis (later sign)