Cardiology Flashcards Preview

Medicine > Cardiology > Flashcards

Flashcards in Cardiology Deck (82):
1

What is pulsus paradoxus?

An abnormally large decrease in systolic blood pressure (>10 mmHg) and pulse wave amplitude during inspiration. (Normal fall <10mmHg)

2

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.

3

What are the five most common causes of congestive heart failure?

1. CAD
2. Hypertension
3. Idiopathic (often dilated cardiomyopathy)
4. Valvular (e.g. AS, AR and MR)
5. Alcohol (dilated cardiomyopathy)

4

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%

5

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.

6

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

7

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

8

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

5.Ssecond-line: Digoxin

9

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

10

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

3. Beta-blockers
e.g. cardioselective agents preferred - metoprolol and atenolol

4. Nitrates

11

Which conditions compose the acute coronary syndromes (ACS)? (3)

1. Unstable angina
2. NSTEMI
3. STEMI

12

Which cardiac enzyme is the most sensitive and specific marker of myocardial necrosis? Describe pattern of increase/decrease.

Cardiac troponin
Serum levels increase within 3-12 hours of chest pain onset, peak at 24-48h, and decrease to baseline over 5-14 days

13

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

14

What is the first-line choice for thrombolysis in acute MIs?

Tissue plasminogen activators - alteplase, reteplase or tenecteplase

(Tenecteplase used in BHS)

15

Post-MI, which medications should be the patient on?

SAAB - C

Statin
Aspirin
ACE-i
Beta-blocker
Clopidogrel

If large anterior MI - consider warfarin for 3 months as prophylaxis against systemic embolism from LV mural thrombus

16

When are CABGs performed? (4)

1. Left main stem disease
2. Multi-vessel disease
3. Failed angioplasty
4. Refractory angina

17

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

18

What is the most common cause of secondary hypertension?

Renal disease

19

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)

20

Which endocrine disorders can cause hypertension? (5)

Conn's, Cushing's, phaeochromocytoma, acromegaly, hyperparathyroidism

21

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

22

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

23

List 3 causes of aortic stenosis.

1. Congenital bicuspid valve
2. Rheumatic disease
3. Senile/calcific degeneration

24

What are triad of symptoms said to be most common aortic stenosis?

SAD

syncope
angina
dyspnoea

25

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

26

Apart from aortic stenosis, name three other causes of LV outflow obstruction.

1. Subaortic membrane
2. Hypertrophic cardiomyopathy
3. Supravalvular stenosis

27

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.

28

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

29

What is aortic sclerosis?

Senile degeneration of the valve. Ejection systolic murmur, normal volume and character of pulse, no radiation to carotids

30

How is pulse pressure calculated?

PP = SBP - DBP

Normal DBP = 40mmHg

31

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)

32

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

33

List 3 causes of acute aortic regurgitation

1. Infective endocarditis
2. Ascending aortic dissection
3. Trauma

34

List 4 causes of chronic aortic regurgitation

1. Congenital
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

35

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)

36

What kind of murmur is heard in aortic regurgitation?

Diastolic murmur (heard best in expiration, with patient sitting forward)

37

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

38

How is aortic regurgitation investigated? (3)

1. ECG - LVH
2. CXR - cardiomegaly, dilated ascending aorta, pulmonary oedema
3. Echo - diagnostic

39

List 3 causes of mitral stenosis

1. Rheumatic
2. Congenital
3. Prosthetic valve

40

List 6 symptoms of mitral stenosis

1. Dyspnoea
2. Fatigue
3. Palpitations - associated with AF
4. Chest pain
5. Systemic emboli
6. Haemoptysis

41

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

42

List 5 causes of mitral regurgitation

1. Rheumatic fever
2. Infective endocarditis
3. Mitral valve prolapse
4. Connective tissue disorders
5. Ruptured chordae tendinae

43

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

44

How is mitral regurgitation managed?

1. Control rate if AF
2. Anticoagulate
3. Diuretics improve symptoms
4. Surgery - for deteriorating symptoms; aim to repair of replace the valve before LV irreversibly impaired

45

What is the most common valvular abnormality?

Mitral valve prolapse

46

How is chronic AF managed? (3)

1. Rate control
2. Rhythm control
3. Anticoagulation

Usually rate > rhythm

47

Describe the rate control regimen in chronic AF

Beta blocker (atenolol or metoprolol) or CCB (diltiazem or verapamil)

Digoxin only OK in sedentary/elderly

48

What are the three clinical patterns of AF?

The three Ps

1. Paroxysmal AF -

2. Persistent AF -

3. Permanent or chronic AF -

49

What is paroxysmal AF?

episodes come on suddenly and generally revert spontaneously within the next 24-48h without any intervention

50

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

51

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)

52

In which conditions is emergency cardioversion indicated?

VF and pulseless/unstable VT

53

What constitutes a broad complex tachycardia?

Rate >100 and QRS complexes >120ms

54

How is stable VT managed? (6)

1. Oxygen
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

55

How can VT be prevented?

Implantation of ICD or radiofrequency ventricular tachycardia ablation in refractory cases

56

What constitutes a narrow complex tachycardia?

Rate of more than 100bpm, QRS less than 120ms

57

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

58

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

59

List 7 viral causes of acute myocarditis

Flu
Hepatitis
Mumps
Rubeola
Coxsackie
Polio
HIV

60

What is the leading cause of sudden cardiac death in the young?

Hypertrophic cardiomyopathy

61

What is hypertrophic cardiomyopathy?

LVOT obstruction from asymmetric septal hypertrophy. May present at any age. Autosomal dominant inheritance but 50% are sporadic.

62

What symptoms can occur in HCM? (5)

1. Sudden death could be first symptom
2. Angina, dyspnoea, palpitation, syncope

63

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

64

List 7 factors associated with dilated cardiomyopathy?

1. Alcohol
2. Hypertension
3. Haemochromatosis
4. Viral infection
5. Autoimmune
6. Peri- or postpartum thyrotoxicosis
7. Congenital (X-linked)

65

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)

66

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

67

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

68

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

OR

2. synchronised electrical cardioversion

69

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

OR warfarin/dabigatran

70

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)

71

Describe the JONES criteria

Major:
- J: Joints (migratory polyarthritis)
- O: pancarditis
- N: subcutaneous nodules
- E: erythema marginatum
- S: Sydenham' s chorea

Minor:
Arthralgia, fever, elevated ESR, prolonged PR interval on ECG, previous rheumatic fever

72

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

73

What is Kussmaul's sign?

Paradoxical rise in JVP during inspiration - seen in constrictive pericarditis BUT NOT CARDIAC TAMPONADE

74

List 5 causes of acute pericarditis.

1. Idiopathic
2. Infectious - viral - coxsackie most common; bactieral - s. pneumoniae; TB, fungal
3. Post-MI and cardiac surgery
4. Neoplasm
5. Connective tissue disorders - SLE, RA, scleroderma etc.

75

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

76

WHat is Beck's triad?

Cardiac tamponade

1. Muffled heart sounds
2. Hypotension
3. Distended neck veins

77

Which leads would be affected in an anteroseptal AMI?

V1- V4

78

Which artery is involved in an anteroseptal AMI?

LAD

79

Which leads are affected in an inferior AMI?

II, III, aVF

80

Which artery is involved in an inferor AMI?

RCA

81

What is the normal width of a QRS complex?

less than 0.12 secs (three small squares)

82

What is the normal width of a

0.12-2