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Human Diseases > Pathophysiology of heart failure > Flashcards

Pathophysiology of heart failure Flashcards

1
Q

Physiological definition of heart failure?

A

Heart fails to deliver enough blood for the needs of the body

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2
Q

Clinical definition of heart failure?

A

Syndrome with multiple causes. Symptoms including breathlessness, fatigue and oedema

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3
Q

Describe blood flow through the heart?

A

de-oxygenated blood from the body into the superior and inferior vena cava. Into the right atrium, through tricuspid valve into right ventricle. Through pulmonary valve into pulmonary artery to the lungs..
Oxygenated blood from lungs into pulmonary veins into the left atrium through mitral valve into left ventricle, through aortic valve into aorta

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4
Q

What surrounds the heart?

A

Myocardium

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5
Q

List the 4 types of heart failure?

A

Acute or chronic

Right or left sided

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6
Q

How do right and left sided heart failure dffer?

A 
Right = peripheral oedema ad raised jugular venous pressure
Left = pulmonary venous pressure raised and pulmonary oedema
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7
Q

What can aggravate chronic heart failure?

A

Dysfunctional neuro-hormonal regulation

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8
Q

What is a complication of chronic heart failure regarding medical procedures?

A

Complications of GA

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9
Q

Cardiac causes of heart failure?

A

Heart itself is damaged or its function is restricted - heart muscle disease (ischaemic heart disease)
Abnormal rhythm

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10
Q

Non-cardiac causes of heart failure syndrome?

A

Excessive demand in high output heart failure - anaemia

Fluid overload from other causes - renal failure, IV therapy

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11
Q

LIst the 4 most common causes of heart failure

A

Ischaemic heart disease
Hypertension
Valvular heart disease
Chronic obstructive pulmonary disease

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12
Q

Symptoms of heart failure? and causes

A

Breathlessness (pulmonary oedema)
Oedema (fluid retention)
Fatigue (poor cardiac output)

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13
Q

Investigations of heart failure?

A

ECG

Echocardiogram

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14
Q

How does reduced cardiac output resemble dehydration?

A 
Reduced blood pressure = low blood volume.
Physiological process (activation of renin-angiotensin-aldosterone system) retain salt and water = dehydration
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15
Q

Reduced cardiac output leads to the activation of the renin-angiotensin-aldosterone system to retain salt and water. What else is activated by renin-angiotensin-aldosterone system?

A

Activates sympathetic nervous system to vasoconstrict (maintain BP) and stimulate heart (maintain cardiac output)

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16
Q

Why is the activation of the renin-angiotensin-aldosterone system and sympathetic nervous system conflicting in chronic heart failure?

A

Chronic heart failure - excessive adrenaline (from sympathetic NS) causes overdrive of the heart
and renin-angiotensin-aldosterone system causes fluid retention = symptoms of chronic heart disease

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17
Q

Activation of renin-angiotensin-aldosterone system and sympathetic NS is compensatory in what type of heart disease?

A

Acute

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18
Q

How do stretch receptors cause a conflicting compensatory response?

A

Increased intracardiac pressures detected by stretch receptors = signla fluid overload = peptides released to stimulate sodium excretion = opposite tot he other effects = hormones fighting each toher

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19
Q

Result of renin-angiotensin-aldosterone system?

A

Increased circulatory volume, oedema, vasoconstriction

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20
Q

What hormones activate sympathetic NS?

A

Adrenaline and noradrenaline

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21
Q

Effects of sympathetic NS?

A

Stimulate HR and contractility
Vasocontriction
Increase BP

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22
Q

Consequences of sympathetic NS in the long term?

A

Fluid retention and oedema
Vasoconstriction increases the resistance against which the heart has to work
Continuous sympathetic stimulation damages heart muscle

23
Q

Mechanism of action of ACE inhibitors?

A

Stop production fo angiotensin II from angiotensin I - prevents the effects of angiotensin - vasoconstriction, oedema, increased volume, sympathetic NS activation - these are intially compensatory but then exacerbate symptoms of heart failure

24
Q

What activates renin-angiotensin-aldosterone system?

A

Renal hypoperfusion

25
Q

Effects of angiotensin II?

A

Vasoconstriction and aldosterone secretion = Increase HR and BP, activate sympathetic NS and retain NA and water which raises BP

26
Q

Mechanism of action of angiotensin II receptor blockers?

A

Prevents action of angiotensin II = exacerbates symptoms of chronic heart failure

27
Q

Mechanism of action of aldosterone antagonists?

A

Prevents action of aldosterone = sympathetic NS, increase BP, HR, retain Na (increase BP 0 = exacerbate symptoms of heart failure

28
Q

Mechanism of action of beta blockers?

A

Block the effect of adrenaline and noradrenaline on the heart = decrease HR and contractility = decrease fluid retention = decreased oedema, vasodilation = heart has to work less

29
Q

What drugs are used when a patient has fluid overload, how do these works?

A

Loop diuretics - make kidney get rid of salt and water

30
Q

Mechanism of action of sacubitril valsartan treatment?

A

Blocks ATI receptor and neprilysin (enzyme that degrades vasoactive peptides)

31
Q

List 2 non-pharmacological treatments for heart failure?

A 
Cardiac resynchronisation pacemaker
Cardiac surgery (valve replacement, repair, transplant)
32
Q

How does left sided heart failure present?

A

Pulmonary oedema

33
Q

How does left sided heart failure cause pulmonary oedema?

A

As the left ventricle fails, blood dams back in the pulmonary veins where venous pressure rises casuing alveoli in lungs to fill with fluid

34
Q

What is dyspnoea and orthopneoea?

A

Laboured breathing on effort and at rest

Caused by pulmonary oedema

35
Q

Effects of right sided heart failure?

A

Congestion of the systemic and portal veins = subcutaneous oedema, fatigue, abdominal distension and discomfort

36
Q

Main difference between effects of right vs left sided heart failure?

A 
Right = systemic symptoms
Left = pulmonary
37
Q

What normally governs the heart rate? where is this found?

A

Sinoatrial node - right atrium

38
Q

What causes the left and right atria to contract?

A

Depolarisation of sino-atrial node

39
Q

What ensures there is a pause between the contraction of the atria and the ventricles?

A

Depolarisation fo the atrioventricular node

40
Q

What causes a coordinated contraction fo the ventricles?

A

Depolarisation of the His-Purkinje system

41
Q

ECG composed of P QRS and T wave, what do this signify?

A 
P = atrial contraction
QRS = ventricular contraction
T = ventricular repolarisation
42
Q

What is tachycardia?

A

HR too fast - greater than 100bpm

43
Q

What is bradycrdia?

A

HR too slow - less than 60bpm

44
Q

What triggers sinus tachycardia? How does it look on ECG?

A

Normal response to exercise or emotion
Hyperthyroidism, heart failure
Normal P waves visible, just more of them

45
Q

What is atrial fibrillation?

A

Tachcardia due to uncoordinated and ineffectual atrial contraction = rapid and irregular ventricular rate

46
Q

Effect of atrial fibrillation?

A

Reduce efficiency of heart = heart failure

47
Q

What type of tachycardia is associated with ischaemia hear disease?

A

Ventricular tachycardia

48
Q

How does ventricular tachycardia display in ECG?

A

Complexes are wide since not conducted by His-Purkinje system

49
Q

What can cause sinus bradycardia?

A

Athletes

50
Q

What is extracsystoles?

A

Single extra beats arising from atria or ventricles

51
Q

What kind of heart rate disturbance causes cardiac arrest?

A

Ventricular fibrillation or asystole

52
Q

Effect of ventricular fibrillation?

A

Uncoordinated and ineffective electrical activity of ventricles = no cardiac output = cardiac arrest

53
Q

Common cause of ventricular fibrillation?

A

Acute coronary ischaemia (MI)

54
Q

Treatment of arrhythmias?

A

Anti-arrhythmic drugs
Direct current cardioversion
Pacemakers (bradycardia)
Implantable defibrillators

Human Diseases (37 decks)

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