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Medicine > Cardiology > Flashcards

Cardiology Flashcards

0
Q

Hyperkalaemia

Values
Signs/symptoms
ECG changes
Management

A

Management = calcium gluconate, nebulised salbutamol, insulin n dextrose

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1
Q

9 types of congenital heart defects (3 x 3)

A

3 holes - VSD, ASD, PDA
3 blocked pipes - Pulmonary and Aortic stenosis, Coarctation of aorta
3 Blue Babies - Tetralogy of Fallot, Transposition of great arteries, Complex CHD

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2
Q

Best way to mend a broken heart? (MI)

A 
B - bloods/beta blocker
R - reassurance
O - oxygen
M - morphine
A  - aspirin, 300mg
N  - nitrates (eg. GTN)
C  - clopidogrel/catheterisation
E  - enoxaparin
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3
Q

Describe the chest pain associated with MI

A

Crushing/gripping/heavy retrosternal pain radiating to neck, shoulder or jaw. May be assoc with pain/paraesthesia in arms, commonly left.

Worsened by exercise, relieved by rest or short acting nitrates

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4
Q

What pain is associated with aortic dissection?

A

Severe central chest pain radiating to back and down arms

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5
Q

What pain is associated with pleural disease?

A

Localised sharp pain, worse on breathing and coughing. Associated with tenderness at costochondral junction.

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6
Q

What is associated with shoulder tip pain?

A

Diaphragmatic pleural irritation

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7
Q

What pain is associated with oesophageal disease?

A

Central retrosternal chest pain/heartburn

Worse on bending over, stooping or lying down

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8
Q

What pain is associated with MSK disease?

A

Local tenderness, made worse with certain movements, Hx trauma

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9
Q

What is the pathophysiology of unstable angina?

A

Fissuring of plaques –> sudden onset angina of increasing frequency and severity.

Risk of subsequent total vessel occlusion means 5-8% die within 6/12 from MI

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10
Q

What is the most common form of MI?

A

Regional myocardial infarction (90%)

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11
Q

What are the types of MI?

A

Regional myocardial infarction
Regional subendocardial infarction
Circumferential subendocardial infarction

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12
Q

What is the pathophysiology of subendocardial infarction?

A

Some perfusion despite presence of clot (eg collateral supply present) OR rapid thrombolysis of clot

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13
Q

Where do the majority of infarcts affect?

A

Left ventricle and septal region

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14
Q

What is the primary cause of death in an MI?

A

Ventricular fibrillation - either caused by arrythmia from muscles adjacent to MI scar or ischaemia –> arrythmia

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15
Q

What are the characteristic changes on an ECG of an MI?

A

Few minutes = tall, pointed T waves, ST segment elevation

Few hours = T waves invert, Q waves develop

Few days = ST segment to normal

Few weeks = T waves return to normal, Q wave remains

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16
Q

ECG changes in which leads = A. MI?

A

V1, V2, V3

17
Q

ST elevation in which leads = I. MI?

A

II, III, AVF

18
Q

ST elevation in which leads = L. MI?

A

I, AVL, V5/6

19
Q

ST elevation in which leads suggests P. MI?

A

V5/V6

nb ST depression in leads V1-3 may be present

20
Q

What percentage of MI have a normal ECG?

A

20%

21
Q

What are the cardiac enzyme markers?

A

CK, AST, LDH, Troponin

Best = troponin T, peaks at 12-24hrs and elevated for 1/52

22
Q

What is the emergency management for suspected MI?

A

Aspirin 300mg chewed
Sublingual GTN
Morphine IV & Metoclopramide IV

Consider beta blocker for ongoing chest pain, hypertension and tachycardia

STEMI = Thrombolysis if no CI

23
Q

What dose of low molecular weight heparin would you give to a patient with a NSTEMI?

A

1mg/kg BD, SC for 2-8 days

24
Q

What long term management would you consider in an MI patient?

A

Daily 12-lead ECG, U&E, cardiac enzymes for 2-3/7
Thromboprophylaxis = Aspirin 75mg daily, warfarin 3/12 if large A. MI
Beta blocker
ACEi
Statin
Discharge after 5-7 days

25
Q

What are the indications for thrombolysis?

A

ST elevation >2mm in 2 or more chest leads
ST elevation > 1mm in 2 or more limb leads
P. Infarction (ST depression V1-3)
New onset left bundle branch block

26
Q

What are the CI to thrombolysis?

A 
Risk of bleeding (aortic dissection, trauma, CVA)
Acute pancreatitis
Active lung disease
Severe liver disease
Severe hypertension
Cerebral neoplasm
27
Q

What is streptokinase?

A

Purified fraction from haemolytic strep

Forms complex with plasminogen –> plasmin and breaking down clots

NB it is ANTIGENIC!!!

28
Q

What arrhythmias are complications of MI?

A

VT/VF
AF
Bradyarrhythmia
AV block

29
Q

What are the short term complications of MI?

A 
Pulmonary oedema
Cardiogenic shock
Thromboembolism
Ventriculo-septal defect
Rupture chordae tendinae/ventricular (2-10 days post-infarct)
30
Q

What are the symptoms of pulmonary oedema?

A 
Dyspnoea
Wheezing
Crackles
Frothy, blood coloured sputum
Anxious
31
Q

What is the pathogenesis of post-MI pulmonary oedema?

A

Chambers fail to empty completely at systole

  • -> Rise in Pa in heart
  • -> Pa reflected back into chamber or vessels
  • -> veins
  • -> organs
32
Q

What are the long term complications of MI?

A

Heart failure

Dressler’s syndrome

33
Q

What are the symptoms of heart failure?

A

Left = fatigue, exertional dyspnoea, orthopnoea, paroxysmal nocturnal, cardiomegaly, gallop rhythm, crackles at lung bases

Right = fatigue, breathlessness, anorexia, nausea, jugular vv distension, smooth hepatic enlargement, pitting oedema, ascites, pleural transudates

34
Q

What is Dressler’s syndrome and what are its symptoms?

A

Immune-mediated pericarditis associated high ESR occurring 2-10/12 after infarction.

Sharp central chest pain worsened by movement, respiration and lying down, radiating to neck and shoulders. Relieved by sitting forwards.

Classical sign = pericardial friction rub (biphasic to and fro rub)

35
Q

What advice should be given regarding driving, employment etc. post-MI?

A 
Work = return after 2/12
Sex = avoid 1/12
Travel = avoid air travel 2/12
Driving = stop for 1/12
36
Q

What is angina?

A

Episodic pain taking place when there is increased demand for increased myocardial work in the presence of impaired perfusion by blood

37
Q

What is stable angina and what is its pathogenesis?

A

Low flow in atherosclerotic coronary arteries. At least one stenosis >50%.

Stenosis = eccentric plaques, rich in lipid, improvement of flows achieved by vasodilator drugs OR concentric plaques, collagenous, affect the whole arterial wall, drug therapy CANNOT improve flow

38
Q

What is unstable angina and what is its pathogenesis?

A

Acute coronary syndrome largely caused by complicated atheroma. Fissuring of plaques –> sudden onset of angina —> increasing Hz/severity

Similar presentation to MI BUT no troponin elevation!!

39
Q

What are the consequences of atherosclerosis to the vascular structure?

A

Reduction in the size of the lumen
Changes in structure of tunica intima predisposing to thrombus formation
Changes in structure of tunica media –> loss of vessel wall easticity

40
Q

Which vessels are affected by atheroma?

A

Large and medium aa ONLY

Aorta, coronary, carotid, mesenteric, iliac, femoral, cerebral

Medicine (9 decks)

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