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IMED3001 > Heart Failure: Aetiology, Pathophysiology and clinical assessment > Flashcards

Heart Failure: Aetiology, Pathophysiology and clinical assessment Flashcards

1
Q

What is heart failure?

A

A clinical syndrome resulting from inability of heart to meet demands for CO placed on it by the body

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2
Q

What can heart failure result from?

A

Decrease in supply - The pump becomes weakened.

Increase in demand - Body is stressed

Abnormal compliance or restriction to filling of the heart

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3
Q

How many people have chronic heart failure in Australia?

A

> 300000 approximately

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4
Q

How many new cases of heart failure is there in Australia every year?

A

30000

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5
Q

What ethnic group suffers most from hospitalization and deaths from heart failure?

A

Aboriginal and torres strait islanders

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6
Q

What is the 5 year survival rate for heart failure?

A

45% in men and 37% in women

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7
Q

What happens to mortality rate with increasing age?

A

It increases

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8
Q

What is NYHA class?

A

New York Heart Association heart failure class. It is based on functional status of the heart.

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9
Q

Why is heart failure expected to increase dramatically?

A

Aging population and increased prevalence of diabetes and obesity.

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10
Q

What is the cost of the high amount of heart disease?

A

Heart failure hospitalisations and some treatments are expensive. 10% of total costs attributable to CVD, 4th behind coronary heart disease, hypertension, and stroke

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11
Q

Who is most commonly affected by rheumatic fever in Australia?

A

Aboriginal populations

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12
Q

Why do we need to understand pathogenesis of heart disease?

A

To do something about it

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13
Q

How is pathogenesis understood better?

A

Multidisciplinary approach is taken; dieticians, exercise physiologists/physiotherapists, doctors, psychologists, etc..

Understanding the non-pharmacological measures that can be taken, the drug treatments, and avoidance of drugs that can make things worse, and developing new therapies for heart failure.

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14
Q

What are some non-pharmacological measures that can be taken to reduce heart failure?

A

NaCl reduction, H2O restriction, monitoring symptoms and signs, reducing alcohol, and exercise.

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15
Q

What are some drug treatments that can be looked at?

A

Drugs targetting aspects of neurohormonal activation known to be important in heart failure.

Correcting fluid overload

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16
Q

What drugs can worsen heart failure?

A

NSAIDs, steroids, glitizones

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17
Q

What causes heart failure?

A

Heart failure is the end result of a wide range of conditions that result in reduced heart function despite a increase in demand for cardiac output.

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18
Q

What conditions increase demand on the heart?

A

Anaemia (Oxygen carrying capacity is reduced meaning heart needs to perfus tissue more for same effect thus making hear need more effort)

Sepsis (Reducing vascular resistance and activates cytokines which causes blood to clot causing things like ischaemia)

Thyroid disease (Heart rate expected to increase due to heightened sensitivity to catecholamines, increased HR, and arrhythmias, also increased metabolism means there is an increased need for nutrition)

Pregnancy (increased circulating blood volume with reduced peripheral resistance)

Medications (eg. NSAIDs, may alter renal auto-regulation and contribute to salt and fluid retention)

Renal failure (reduced excretion of toxins, acid/base disturbance, impaired excretion of NaCl and H2O meaning there is fluid overload and anaemia)

Respiratory failure (Reduced arterial O2 saturation, increased CO2, and more work from breathing)

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19
Q

How does anaemia increase demand on the heart?

A

Heart is less filled with nutrition = more blood must be pumped to same tissues = increase demand on the heart

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20
Q

How does sepsis increase demand on the heart?

A

Sepsis causes a decreases in peripheral vascular resistance and salt and fluid retention.

Less peripheral resistance means more blood volume needs to be pumped to the open areas.

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21
Q

How does thyroid disease increase demand on the heart?

A

Thyroid disease increases sensitivity to catecholamines. Meaning heart has to be beat faster and harder.

Thyroid disease also promotes arrhythmias (atrial fibrillation in particular)

Thyroid disease increases metabolic rate meaning tissues need more nutrients which increases demand on the heart for more CO

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22
Q

How does pregnancy increase demand on the heart?

A

More blood vessels = more blood volume + reduced peripheral vascular resistance.

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23
Q

How can medications increase demand on the heart?

A

Renal auto-regulation may be affected by drugs like NSAIDs and prednisolone which contribute to salt and fluid retention

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24
Q

How does renal failure increase demand on the heart?

A

Renal failure reduces excretion of toxins, water, and NaCl which means more fluid is in the blood which means the heart has to work harder to move it around.

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25
Q

How does respiratory failure increase demand on the heart?

A

Reduced arterial O2 saturation, increased CO2, increased work of breathing

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26
Q

How does Disseminated malignancy increase demand on the heart?

A

Increased metabolic rate from tumour load resulting in an increase in amount of blood reaching the tumours.

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27
Q

How does Paget’s disease increase demand on the heart?

A

Increased blood volume and reduced PVR due to the high blood supply that diseased bone requires.

28
Q

What is paget’s disease?

A

Bone replacement disorder where new bone is made slower than old bone is breaking down faster than it can be replaced and so the body compensates by producing more bone ASAP resulting in fragile bones that are in constant pain.

29
Q

Which diseases result in heart failure from a decreased supply of blood from the heart?

A

Coronary artery disease

Valvular disease

Hypertension

Arrhythmia

Cardiomyopathy of all types

Chemical toxins

Infection (eg. adenovirus)

Metabolic diseases

Pulmonary embolism

30
Q

What are the types of cardiomyopathy?

A

Idiopathic

Genetic

Familial

31
Q

What percentage of people have hypertension?

A

30 - 40% of people over the age of 50

32
Q

What does cardiomyopathy mean?

A

Weakening of the heart muscle

33
Q

What can cause reduced pump function in the heart?

A

A fall in contractility of the myocardium.

An increase in stiffness/reduced compliance of the heart

34
Q

What is the most common form of heart failure?

A

Systolic heart failure

35
Q

What causes systolic heart failure?

A

Atherothrombotic occlusion of a coronary artery results in regional myocardial infarction.

Myocardium is replaced by scar tissue so contractile function is reduced.

36
Q

What is the most important cause of heart failure in developed countries?

A

Coronary artery disease

37
Q

Can cardiac muscles regenerate?

A

No very small active stem cells

38
Q

What kind of narrowing causes coronary artery occlusion?

A

Atherosclerotic (>70%)

39
Q

Can myocardium recover fully if blood supply is restored to area of MI?

A

Yes (eg through angioplasty)

*Coronary artery disease results in regional impairment of ventricular function

40
Q

What does dilated cardiomyopathy look like?

A

Global impairment of ventricular function

Left ventricle muscle weakens and chambers become larger. More blood enters ventricle.

41
Q

What causes dilated cardiomyopathy?

A

Familial/genetic dilated cardiomyopathy

Viral cardiomyopathy

Alcoholic cardiomyopathy

Toxic cardiomyopathy

Peri-partum cardiomyopathy

42
Q

What is hypertrophic cardiomyopathy?

A

It is often inherited as an autosomal dominant condition and can cause death from arrhythmia

43
Q

What materials can infiltrate cardiac layers in infiltrative cardiomyopathies?

A

Amyloid

Sarcoid

Haemocromatosis in wilson’s disease (iron and copper)

Eosinophils in Loeffler’s endocarditis

44
Q

What is heart failure with preserved ejection fraction?

A

Heart failure with preserved ejection fraction. Heart failure with preserved ejection fraction (HFpEF) is a form of congestive heart failure where in the amount of blood pumped from the heart’s left ventricle with each beat (ejection fraction) is greater than 50%.

45
Q

What causes systolic heart failure?

A

Heart muscle diseases causing weaker contractions of the heart.

Reduced blood supply to cardiomyocytes resulting in ischaemic death and fibrosis of tissue reducing ability to eject blood adequately.

Valve diseases such as regurgitation in mitral and tricuspid valves and stenosis of aortic/pulmonary valves

Arrhythmias = too slow too fast and uncoordinated pumping ability

46
Q

What happens to ejection fraction in systolic heart failure?

A

it is severely reduced

47
Q

What is the pathophysiology of diastolic failure?

A

Reduced compliance of ventricle resulting in elevated filling pressures. (more work from atria so atrial hypertrophy)

Pulmonary venous pressure increases due to hold up of blood in the left atrium (results in pulmonary oedema and pleural effusions)

Vena cava pressure increases due to right ventricle non-compliance and so pressure in right atrium is elevated.

48
Q

Why is tachycardia bad for diastolic heart failure?

A

Due to need for higher effort to fill up the ventricles, a fast heart rate will give less time for blood to enter making the heart less efficient.

49
Q

Why is atrial fibrillation bad for diastolic heart failure?

A

Atrial contraction assists in late diastolic ventricular filling and so loss of coordinated contraction is bad

50
Q

What symptoms does the clinical syndrome of heart failure?

A

Breathlessness (this is used for NYHA classification system)

Fatigue / tiredness / reduced exercise capacity

Nocturnal dyspnoea (waking up short of breath)

Orthopnoea (shortness of breath lying down)

Bendopnoea (shortness of breath when bending over)

Peripheral / dependent oedema (swelling of the lower limbs) and abdominal swelling

Weight gain and loss in end-stage

51
Q

What are the NYHA classes and what do they mean?

A

They are classes used to describe overall condition of patient’s heart;

class I means no breathlessness on usual activitities

Class II means breathlessness on moderate exertion

Class III means breathlessness on minimal exertion

Class IV means breathlessness at rest

52
Q

What should clinical examination of heart failure patients show?

A

Weak/irregular pulse

Low BP

Raised jugular venous pulse

Conjunctival pallor and central cyanosis

Displaced apex beat

Heart murmurs (leaking mitral and tricuspid valves and added sounds (S3, S4)

Pleural effusions

Inspiratory crepitations (fluid in alveoli)

Hepatomegaly and ascites

Pitting oedema

53
Q

What are some ways of assessing fluid overload?

A

the jugular venous pressure. (The internal jugular vein is connected to the right atrial pressures)

54
Q

What kind of pulsation does the jugular vein show in patients of heart failure?

A

The flicker waveform which consists of the A wave and c wave.A wave is from the contraction of the right atrium and c wave from contraction of ventricle

55
Q

What tests are done to prove a condition is heart failure?

A

ECG (document HR; SR vs AF/Aflutter, ectopy)

CXR (good for diagnosing pulmonary oedema which is indirectly associated with heart failure.)

B-type natriuretic protein - high negative predictive value in acute setting and less valuable in chronic HF. (BNP is induced by ventricle)

Exercise test (exacerbate symptoms to know more)

Testing Hb, Fe, TFT

Sleep study

56
Q

What basis is targeted treatment done on?

A

5 Rs

Revascularise (PTCA, CAGB surgery)

Revert (anti-arrhythmics, DC cardioversion, PPM, AICD)

Re-synchronize (if bundle branch block / dys-syncrony consider bi-ventricular pacemakekr

Replace (mitral or aortic valve

57
Q

Pharmacological treatment of HF?

A

ACE inhibitors [potential hyperkaelemia be wary]

AtII type I receptor antagonists (people intolerant of ACEI) [potential hyperkaelemia be wary]

Aldosterone antagonists [potential hyperkaelemia be wary; risk higher than ACE1 inhibitors]

Beta adrenergic blockers [could exacerbate asthma symptoms, cause bradycardia/heart block, etc]

Diuretics [can cause hypokalaemia, intravascular fluid depletion, RAAS activation in overuse, great acutely but bad in long term]

Ivabradine (If channel blocker in SA node) [precaution with low HR, heart block, phosphene]

Digoxin [second or third line therapy. Range of side effects including arrhythmias, sometimes lethal]

Nitrates (relax smooth muscles around the body) [ not a big player with heart failure therapy]

Antiplatelet drugs and anticoagulation (atrial fibrillation or ischaemic heart disease is a result of coagulation, the blood thinning is not affected by the heart failure itself)

Omega 3 fatty acids

58
Q

What are some non-pharmacological treatments of chronic heart failure?

A

Low NaCl

Fluid restriction

Avoid NSAIDs, COXII, prednisolone

Alcohol reduction (low level is ok)

Smoking reduction

Exercise: aerobic or circuit

Heart failure service

59
Q

How is heart failure with preserved EF treated?

A

Non-pharmacologically through sodium and fluid restriction while encouraging moderate aerobic exercise.

Maintain atrial contraction to prevent tachycardia

Prevent / treat hypertension, ventricular hypertrophy

Prevent / treat myocardial ischaemia

60
Q

How can heart failure be prevented?

A

Long term optimal treatment for risk factors of vascular disease

Avoid cigarettes and ethanol excess and consuming less NaCl.

Regular exercise and maintaining a healthy weight

Early and optimal investifation and treatment of asymptomatic LV systolic impairment

Optimal management of CAD (coronary artery disease), arrhythmias, OSA, diabetes

With early aggressive management the prognosis of HD is steadily improving but many patients are deprived of effective therapy

61
Q

What is “broken heart syndrome”?

A

taka subo cardiomyopathy (stress caused heart disease)

62
Q

How do patients present in broken heart syndrome?

A

With clinical picture suggestive of acute MI: anginal-type chest pains, ischaemic ECG changes, and elevated troponin

63
Q

What is the pathophysiology of broken heart syndrome?

A

The stress causing it is often mild.

Thought to reflect a sympathetic nervous system and/or catecholamine mediated condition

64
Q

How is broken heart syndrome treated?

A

Same medications as HF. Beta blockers and ACEI inhibitors

65
Q

Who else can have symptoms similar to broken heart syndrome?

A

People on amphetamines or people with subarachnoid haemorrhages

66
Q

What causes mortality in heart failure patients?

A

2 main causes:

Cardiac deterioration with progressive pump failure

Sudden cardiac death caused by lethal arrhythmias

IMED3001 (46 decks)

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