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MRCP > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Draw the JVP wave form

A
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2
Q

What is a wave of JVP

A

Due to atrial contraction – actively push up superior vena cava (SVC) and into the right ventricle
(may cause an audible S4).

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3
Q

What is the c wave of JVP

A

An invisible flicker in the x descent due to closure of the tricuspid valve, before the start of
ventricular systole

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4
Q

What is the x decent of JVP

A

Downward movement of the heart causes atrial stretch and a drop in pressure.

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5
Q

What is the V wave of JVP

A

Due to passive filling of blood into the atrium against a closed tricuspid valve

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6
Q

What is the y descent?

A

Opening of the tricuspid valve with passive movement of blood from the right atrium to the right
ventricle (causing an S3 when audible).

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7
Q

What are causes of raised JVP with normal wave form?

A

Heart failure- biventricular or isolated R heart failure
Fluid overload of any cause
Severe bradycardia

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8
Q

What is kussmaul’s sign?

A

Raised JVP upon inspiration and drops with expiration, opposite of health and implies R heart chambers cannot increase in size to accommodate increased venous return. This can be due to pericardial disease (constriction) or fluid in pericardial space (pericardial effusion and cardiac tamponade)

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9
Q

Raised JVP with loss of normal pulsations causes?

A

SVC syndrome

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10
Q

What are the features of complete heart block?

A

Syncope
HF
Regular bradcycardia
Wide pulse pressure
JVP: cannon waves in neck
Variable intensity of S1

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11
Q

What is the relationship between S1 sound and PR

A

There is an inverse relationship
So when the PR interval increases the S1 sound decreases
PR interval reduced, S1 Increases

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12
Q

What is the first heart sound?

A

Closure of mitral and tricuspid valves

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13
Q

What is the second heart sound?

A

Closure of the aortic and then pulmonary valves (.05 seconds apart)

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14
Q

When is splitting of SE normal?

A

During inspiration

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15
Q

What is S3? third heart sound

A

It is caused by diastolic filling of the ventricle
It is considered normal if <30 years old, may persist in woman up to 50 years old
Heard in left ventricular failure e.g dilated cardiomyopathy, constrictive pericarditis (pericardial knock) and mitral regurgitation, VSD

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16
Q

What is S4 fourth heart sound?

A

Heard is aortic stenosis, HOCM, hypertension, LVH, amyloid
Caused by atrial contraction vs. stiff ventricle- therefore coinsides with p wave on ECG
HOCM double apical impulse may be felt as a result of palpable S4

17
Q

What are causes of a loud S1

A

Mobile mitral stenosis, hyperdynamic states, tachycardia states, L to R shunts, short PR intervals

18
Q

What are causes of soft S1

A

Immobile mitral stenosis, hypodynamic states, mitral regurgitation, poor ventricular function, long PR intervals

19
Q

What are causes of split S1

A

RBBB, LBBB, VT, Inspiration, ebstein’s anomaly

20
Q

What are causes of variable S1

A

AF, Complete heart block

21
Q

What are causes of loud S2

A

Systemic hypertension (loud A2), Pulmonary hypertension (loud P2), Tachycardic states, ASD (loud P2)

22
Q

What are causes of soft or absent S2

A

Severe aortic stenosis

23
Q

What are causes of fixed splitting of S2

A

ASD

24
Q

What are causes of widely split S2

A

RBBB, Pulmonary stenosis, deep inspiration, mitral regurgitation

25
Q

What are causes of single s2?

A

Severe pulmonary stenosis/aortic
stenosis
Hypertension
Large VSD
Tetralogy of Fallot
Eisenmenger’s syndrome
Pulmonary atresia
Elderly

26
Q

What are causes of reserved split S2?

A

LBBB
Right ventricular pacing
PDA
Aortic stenosis

27
Q

What is prinzmetal angina

A

Prinzmetal (vasospastic) angina is a rare form of angina in which pain is experienced at rest rather than during activity. It is caused by narrowing or occlusion of proximal coronary arteries due to spasm and cannot be diagnosed by coronary angiography. Beta blockers should not be used in
this form of angina because they may worsen the coronary spasm. Patients with this condition may be treated effectively with a dihydropyridine derivative CCB such as amlodipine.

28
Q

What are some examples of Glycoprotein IIb/IIIa receptor antagonists

A

abciximab
eptifibatide
tirofiban

It does this by binding to the GP IIb/IIIa receptors on the surface of platelets, preventing fibrinogen from binding to these receptors and thus blocking platelet aggregation. This reduces thrombus formation in the coronary arteries and improves blood flow, making it an effective treatment for acute coronary syndrome.

29
Q

How long should warfarin be continued after successful defibrilliation

A

4 weeks

30
Q

What drug should be avoided in VT

A

VERAPAMIL

MRCP (2 decks)

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