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Yr 2 - Cardiology System > Systolic Heart Failure, MI, PE > Flashcards

Systolic Heart Failure, MI, PE Flashcards

1
Q

What is systolic heart failure?

A

Left ventricle (sometimes right too) loses ability to contract properly

Heart gradually loses ability to pump enough blood to meet body’s metabolic needs –> loses its ‘pumping reserve’

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2
Q

What are structural abnormalities of systolic heart failure?

A
  • Ventricles may be dilated, thinned or thickened
  • Valve regurgitations (leaking of blood backwards)
  • Mitral or tricuspid regurgitation may result from ventricular dilation due to stretching of valve ring
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3
Q

What are common prior events to systolic heart failure?

A
  • Most common is myocardial infarction
  • Viral myocarditis
  • Use of chemo drugs which poison heart muscle as unwanted side effect
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4
Q

What is viral myocarditis?

A

Viral infection causes inflammation of heart muscle

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5
Q

What are symptoms of systolic heart failure?

A
  1. Tiredness (fatigue)
  2. Breathlessness (dyspnoea)
  3. Breathlessness when lying flat (orthopnoea)
  4. Sudden breathlessness in the night (paroxysmal nocturnal dyspnoea)
  5. Passing excess urine at night (nocturia)
  6. Ankle swelling (oedema)
  7. Rapid respiration (tachypnoea)
  8. High jugular venous pressure (JVP)
  9. Tachycardia
  10. Hypotension
  11. Cachexia (loss of skeletal muscle mass)
  12. Anorexia
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6
Q

What would echocardiogram show in systolic heart failure?

A

Reduced pumping function of heart. Dilation of ventricle. Valves can be assessed.

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7
Q

What would a blood test of BNP (brain natiuretic peptide) show in systolic heart failure

A

Raised

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8
Q

Why would an ECG normally be abnormal in systolic heart failure?

A

Due to underlying disease

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9
Q

What drugs can be used to treat systolic heart failure?

A
  1. ACE-inhibitor
  2. Beta blocker
  3. Mineralocorticoid receptor antagonists
  4. Combination therapy with angiotensin II receptor blocker and a Neprilysin inhibitor (ARNI)
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10
Q

What other treatments can be used in systolic heart failure?

A
  • Loop diuretics such as furosemide are used to treat symptoms of fluid overload but do not have intrinsic prognostic benefit
  • Some patients benefit from a special pacemaker that “resynchronises” the
    right and left ventricle systolic contraction
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11
Q

What are 1ary/2ary preventions for systolic heart failure?

A
  1. Diagnose any underlying disease that might be treated directly (e.g. narrowing of coronary arteries, hypertension) 2. Secondary prevention may involve an implanted cardioverter defibrillator (ICD) to reduce the risk of sudden cardiac death due to ventricular arrhythmia
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12
Q

What is myocardial infarction?

A

Medical name for a heart attack. Occurs when blood flow to the heart muscle is abruptly cut off, causing tissue damage. This is usually the result of a blockage in one or more of the coronary arteries.

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13
Q

What anatomical structures are affected in MI?

A
  • Left coronary artery with branches (left anterior descending artery and circumflex artery) and also the left main stem
  • Right coronary artery with branches - posterior descending artery
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14
Q

What physiology does MI affect?

A

Delivery of blood with oxygen and nutrients to the myocardial tissues

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15
Q

What structural abnormalities lead to MI?

A
  • Narrowing of arteries as a result of coronary atheroma

- Coronary thrombosis

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16
Q

What is coronary atheroma?

A

Cholesterol deposits in the wall of the artery – called “plaques” or “stenoses”

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17
Q

Wha is coronary thrombosis?

A

Blockage of artery due to blood clot

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18
Q

What does MI lead to?

A
  1. Ischaemia (reduced blood supply) leading eventually to necrosis (death of cells also called infarction) of heart muscle (myocardium)
  2. Impaired contraction of myocardium
  3. Abnormal electrical activity of heart cells
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19
Q

What are risk factors of MI?

A
  • More common in men and elderly
  • Family history of heart disease
  • Smoking, high blood pressure, high cholesterol, obesity, diabetes
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20
Q

What are symptoms of MI?

A
  1. Severe crushing central / generalised chest pain – sudden onset that often pain spreads to arm(s) or neck
  2. Nausea, vomiting, sweatiness, breathlessness
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21
Q

What are clinical signs of MI?

A
  1. Patient is clearly distressed due to the pain (unless given morphine)
  2. Blood pressure may be low and heart rate fast
  3. Breathlessness may be obvious with fluid heard on lungs during inspiration due to pulmonary oedema (fluid in alveoli of lungs)
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22
Q

What is ECG like in MI?

A

ST segment elevation –> if coronary artery is completely blocked

23
Q

What does blood test show in MI?

A

Raised levels of heart protein ‘troponin’

24
Q

What does echocardiogram show in MI?

A

Reduced contraction of area affected

25
Q

What does coronary angiogram show in MI?

A

Shows an artery

blocked by atheromatous stenosis and by blood clot (thrombosis)

26
Q

What is a coronary angiogram?

A

X-ray test of heart arteries

27
Q

What is treatment for MI?

A
  • 999
  • Pain relief (morphine)
  • Thrombolytic drugs (dissolve clot) have been replaced by primary percutaneous intervention
28
Q

What is primary percutaneous intervention?

A

Through a thin tube in arm or leg, clot is removed and a small balloon is used to open the narrowed artery and a metal “stent” placed to hold artery open

29
Q

What are 1ary/2ary treatments for MI?

A

1ary –> reduce risk factors

2ary –> Aspirin, Ticagrelor or Clopidogrel, Betablockers, Statins, ACE-inhibitors

30
Q

How does aspirin aid in MI?

A

Antiplatelet action to prevent blood clot

31
Q

How does Ticagrelor or Clopidogrel aid in MI?

A

Antiplatelet action to prevent blood clot especially when a coronary stent present

32
Q

How do beta blockers aid in MI?

A

Lower heart rate and blood pressure through blocking effects of adrenaline and noradrenaline

33
Q

How do statins aid in MI?

A

HMG-CoA reductase inhibitors that lower blood cholesterol

34
Q

How do ACE inhibitors aid in MI?

A

Block angiotensin converting enzyme to prevent production of angiotensin II

35
Q

What is pulmonary embolus (PE)?

A

Blockage of part of the pulmonary arterial tree as a result of embolism of blood clot (movement of clot from another part of body)

Can be caused by blockage of deep veins of leg or abdomen by blood clot

36
Q

What does PE affect?

A

Gaseous exchange in the alveoli of lungs. Impaired perfusion of alveoli/lungs resulting in low oxygen levels in blood

37
Q

What are prior events to PE?

A

Usually the source of the thrombus (blood clot) that moves to the lungs – is in the deep veins of the legs

Check prior events to DVT (e.g. immobility)

38
Q

What are symptoms of PE?

A
  1. Sudden-onset dyspnoea (shortness of breath)
  2. Tachypnoea (rapid breathing) 3. Chest pain of a “pleuritic” nature (worsened by breathing)
  3. Cough and haemoptysis (coughing up blood)
39
Q

How may cases of sudden death are attributable to PE?

A

15%

40
Q

What are clinical signs of PE?

A
  1. Sinus tachycardia
  2. Collapse, and circulatory instability
  3. Pleural friction rub heard over affected area
  4. Strain on right ventricle detected (felt on chest wall)
  5. Raised jugular venous pressure (seen in neck)
41
Q

What is collapse and circulatory instability due to in PE?

A

Decreased blood flow

through the lungs and into the left side of the heart may be initial presentation in severe cases

42
Q

How many cases of PE are 2ary to DVT?

A

90%

43
Q

What would O2 saturation (measured from ear or finger) be for PE?

A

Low O2 saturation

Low oxygen on blood gases (hypoxaemia)

44
Q

What would D-dimer be for PE?

A

Elevated

45
Q

What would VQ (ventilation/perfusion) lung scan show

A

Lack of blood flow to part of lung

46
Q

What would CT scan show in PE?

A

Blood clot in pulmonary artery

47
Q

What is initial treatment for PE?

A
  1. Oxygen given at a high flow rate

2. Thrombolytic drugs may given by intravenous infusion to dissolve the blood clot in life-threatening cases

48
Q

What is 2ary treatment for PE?

A

Anticoagulants are used immediately and for some months (initially low molecular weight heparin by injection and later oral anticoagulant e.g. Apixaban/ Warfarin)

49
Q

What is ventricular fibrillation?

A

Electrical activity becomes disorganised and chaotic. Heart ‘quivers’ but does not beat. No blood is pumped to lungs or body causing rapid loss of consciousness

50
Q

What structural abnormalities are present in VF?

A
  • Heart may appear to have normal structure
  • Ventricles may be hypertrophied (more muscle) due to high blood pressure or genetic disease
  • Ventricles can be dilated and scarred (after MI or viral myocarditis)
51
Q

What are prior events to VF?

A
  • No warning, sudden cardiac death
  • Commonly occurs after MI (coronary thrombosis leading to heart attack)
  • Heart failure
52
Q

Clinical signs of VF?

A
  1. Patient is motionless, unresponsive to verbal command or shaking, has slow / deep snoring or no signs of breathing
  2. No pulse can be detected
  3. Collapse is sudden and dramatic
53
Q

What is medical intervention with VF?

A

ABC strategy:
A - Airway
B - Breathing (oxygen)
C - Circulation (external cardiac massage)

DC electrical shock (defibrillation) one rhythm determined

54
Q

2ary treatment for VF?

A
  1. Beta-blockers are sometimes used to reduce the risk of ventricular rhythm
    abnormalities
  2. Implanted Cardioverter Defibrillators (ICD) can be implanted like a pacemaker
    for patients who survive or who are at high risk of a first event

Yr 2 - Cardiology System (25 decks)

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