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7. Vascular > Lecture 4: failing heart > Flashcards

Lecture 4: failing heart Flashcards

1
Q

Describe the pressure-volume loop of the heart

A
  1. End-systolic volume means lowest pressure and volume; mitral valve opens
  2. Ventricles fill but pressure stays the same
  3. End-diastolic volume, mitral valve closes
  4. Isovolumetric contraction
  5. Aortic valve opens, ventricular ejection
  6. Aortic valve closes, isovolumetric relaxation
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2
Q

What factors determine the size of an infarct?

A
  1. The size of the area at risk
  2. Level of collateral flow
  3. Duration of ischaemia
  4. Rate of cell death
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3
Q

What is the benefit of ischaemic preconditioning?

A

Slows down the rate at which cells die

Ischaemia for short time, re-perfusion, ischaemia etc etc until you have a longer pathological period of ischaemia

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4
Q

In ischaemic injury, how can cells survive for a prolonged period of time?

A

High levels of anaerobic ATP

After around 10 minutes, glycogen runs out and ATP levels drop and cells will start to die and apoptise

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5
Q

How do biomarkers for ACS develop?

A

When the cardiac cell membrane ruptures soluble proteins leak out into the circulation. Circulating cardiac-specific proteins such as troponin (cTnI and cTnT) or cMyC used as biomarkers for the number of myocytes killed (infarct size)

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6
Q

Explain the progression of an infarct

A
  1. Subendocardial area first
  2. “Wavefront” of death spreads transmurally toward the epicardium
    - > After 3 hours, all necrotic tissue has developed
  3. The transmural wave spreads
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7
Q

When is interventiion during ACS useful?

A

In the first 2-3 hours, afterwards there is very little benefit

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8
Q

What are the main causes of heart failure?

A
  1. Pressure overload
  2. Volume overload
  3. Contractile dysfunction
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9
Q

What can cause pressure overload?

A
  • Hypertension

- Aortic stenosis

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10
Q

What can cause volume overload?

A

Aortic and mitral valve regurgitation

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11
Q

What can cause contractile dysfunction?

A
  • Ischaemic heart disease
  • Myocardial infarction
  • Pregnancy
  • Inherited or acquired cardiomyopathies
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12
Q

What are the main types of inherited cardiomyopathies?

A
  1. Dilated cardiomyopathy (problem with cytoskeletal proteins)
  2. Hypertrophic cardiomyopathy (problems with sarcomeric proteins)
  3. Arrythmogenic right ventricular cardiomyopathy (problems with desmosomal proteins)
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13
Q

What are the symptoms of mitral stenosis?

A

Palpitations
Murmurs
Dyspnoea
Heart failure

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14
Q

What are the symptoms of aortic stenosis?

A

Chest pain
Murmurs
Dyspnoea
Heart failure

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15
Q

What are the symptoms of mitral regurg?

A

Murmurs
Dyspnoea
Heart failure

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16
Q

What are the symptoms of aortic regurg?

A

Murmurs
Dyspnoea
Heart failure

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17
Q

What is the main cause of mitral stenosis?

A

Rheumatic heart disease

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18
Q

What is the main cause of aortic stenosis?

A

Calcification

Old age

19
Q

What is the main cause of mitral regurg?

A

Old age

20
Q

What is the main cause of aortic regurg?

A

Idiopathic
Marfan’s
Ehlers Danloss

21
Q

What cardiac remodeling changes happen in heart failure?

A
  1. LV remodelling
  2. Cellular changes
  3. Myocyte death
  4. Disruption of extracellular matrix
  5. Reduced perfusion of myocytes
22
Q

How is diastolic heart failure defined?

A

Diastolic HF is defined as heart failure in which the ejection fraction is >40%.

It’s often referred to as HF with preserved ejection fraction

23
Q

What cardiac benefits does ACE-I have?

A
  1. ↓ symptoms (exercise intolerance, oedema)
  2. Slow progression of disease
  3. Lengthen survival, ↓ hospitalisation
24
Q

What are the side effects of ACE-Is?

A
  1. Chronic cough
  2. Hypotension
  3. renal failure
  4. Hyperkalaemia
25
Q

What are the contraindications for ACE-I?

A
  1. Renal failure
  2. Bilateral renal stenosis
  3. Angioedema
  4. Pregnancy
26
Q

What cardiac benefits do ß-blockers have?

A
  • Prolong survival
  • ↓ sudden death by ventricular fibrillation (which accounts for ~50% of CHF mortality)
  • ↓ symptoms of HF
  • ↓ cardiac remodelling, ↓ renin release so inhibit the RAAS
27
Q

What cardiac benefits does spironolactone have?

A
  • ↓ mortality in severe HF when added to standard therapy

- ↓ fibrosis/remodelling of heart

28
Q

How does digoxin work?

A

Positive inotropes; increase myocyte [Ca2+] by blocking the Na+ pump, this increases intracellular [Na+] which reduces Ca2+ extrusion by the Na+/Ca2+ exchanger.

29
Q

What do you do in digoxin toxicity?

A

Treat toxicity with digibind, a digoxin antibody fragment.

30
Q

What is the mechanism of action of ivabradine?

A

Ivabradine lowers HR by blocking the ‘funny current’ in the SA node.

31
Q

How do diuretics help in heart failure?

A

A mainstay of CHF treatment because they ↓preload, oedema and dyspnoea, ↑exercise capacity.

Loop diuretics mainly used for CHF; thiazide-like diuretic can be added if oedema is not sufficiently controlled

32
Q

What are the adverse effects of diuretics?

A

Key side effects: Loop diuretics and thiazides can cause excess K+ loss→ arrhythmias; also hypotension.

Hypokalaemia is ameliorated by spironolactone, ACEI, ARBs, ENaC blockers (e.g. amiloride) or K+ supplements

33
Q

What is cardiorenal syndrome?

A

Heart failure leads to acute or chronic renal dysfunction

Close monitoring of renal function and plasma electrolytes is essential, watch out for hyperkalaemia

34
Q

What is the NYHA heart failure classification?

A
  1. Cardiac disease, but no symptoms and no limitation in ordinary physical activity
  2. Mild symptoms and slight limitation in ordinary physical activity
  3. Signification limitation in ordinary physical activity due to symptoms, comfortable only at rest
  4. Severe limitations, symptoms even at rest
35
Q

What are the modes of death in heart failure?

A
  1. Progressive (Progressive multi-organ failure as a result of heart failure)
  2. Sudden (often hypertrophic cardiomyopathy leading to VF)
36
Q

What is a first degree heart block?

A

Increased PR interval (normal limit is 120-200 ms)

Usually no symptoms

37
Q

What is a Mobitz 1 heart block?

A

Increasing PR interval until P wave is not followed by a QRS complex

Most patients do not have symptoms, would treat if symptomatic

38
Q

What is a Mobitz 2 heart block?

A

Dropped QRS complexes and PR prolongations are unpredictable

More serious than Mobitz 1; suggests the block is often further down the His bundle

Only treat if symptomatic, but is often symptomatic

39
Q

What is a complete heart block?

A

Complete dissociation between P wave and QRS complex

Morphologically, P wave and QRS complex look normal

Leads to severe bradycardia

40
Q

How would you treat symptomtic bradycardia?

A

Pacemaker

Pass trough subclavian vein; Wire in right ventricle and right atrium

41
Q

What are the 5 causes of ventricular arrhythmias?

A
  1. Ischaemia (most common)
  2. Cardiomyopathy
  3. Drugs
  4. Electrolyte disturbance
  5. Congenital cardiac abnormality
42
Q

What can VT lead to?

A

Can cause haemodynamic compromise, however can be compatible with standing up and talking

IF haemodynamically compromised → SHOCK

43
Q

What is an ICD?

A

Implantable cardioverter defibrillator

When it senses a VT, the device will try to eliminate the VT. If this is unsuccessful, it will shock

44
Q

Who would benefit from cardiac resynchronisation therapy?

A

Benefit to people with LVEF <35%, LBBB, those with heart failure symptoms

7. Vascular (15 decks)

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