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ESA2 CVS > Session 11 > Flashcards

Session 11 Flashcards

1
Q

Give the definition of Heart Failure

A

A state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure

A pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate matching requirements of the metabolising tissues

A clinical syndrome caused by an abnormality of the heart and recognised by a characteristic pattern of haemodynamic, renal, neural and hormonal responses.

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2
Q

What is the Aetiology of Heart Failure?

A

Ischaemic Heart Disease is the primary cause of Systolic HF

Other causes of HF:

Hypertension

Dilated Cardiomyopathy (heart muscle becomes stretched and thin so unable to pump blood efficiently): due to bugs (viral/ bacterial/ mycobacteria), alcohol/drugs/poisoning, pregnancy, idiopathic

Valvular heart disease / congenital

Restrictive cardiomyopathy (restricted filling) e.g. amyloidosis

Hypertrophic cardiomyopathy

Pericardial disease

High-output heart failure (demand of the body outstrips the heart) e.g. due to Paget’s Disease

Arrhythmias

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3
Q

Discuss basic heart physiology

A

Cardiac Output ~5L/min

Stroke Volume ~75ml/beat

LV end systolic volume ~75ml

LV end diastolic volume ~150ml

Ejection Fraction 50% plus (~55% is normal, <10% is not compatible with life)

Weight ~330g

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4
Q

How does Heart Failure affect Cardiac Output?

A

Starling’s Law of the Heart: “the force developed in a muscle fibre depends on the degree to which the fibre is stretched”

With gross failure, you get reduced CO as end diastolic pressure increases; there is a narrow margin between dehydration (decreases CO) and overfilling (also decreases CO). This is important for management.

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5
Q

What is Systolic Dysfunction?

A

Increased LV capacity

Reduced LV cardiac output

Thinning of the myocardial wall e.g. due to previous MI: fibrosis and necrosis of myocardium occurs due to activity of matrix proteinases

Mitral valve incompetence

Neuro-hormonal incompetence

Cardiac arrhythmias

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6
Q

What are the structural changes of Systolic Dysfunction?

A

Loss of muscle e.g. after acute infarction,global remodelling around infarct occurs

Uncoordinated or abnormal myocardial contraction (ECG changes)

Changes to the extracellular matrix: increase in collagen (III > I) from 5% to 25% and slippage of myocardial fibre orientation

Change of cellular structure and function:

~Myocytolysis and vacuolation of cells

~Myocyte hypertrophy

~Sarcoplasmic reticulum dysfunction

~Changes to calcium availability and/or receptor regulation

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7
Q

How is vascular remodelling after an acute infarction different to vascular remodelling after systolic and diastolic failure? And what does a hypertrophied heart and a dilated heart indicate?

A

ventricular modelling after acute infarction is asymmetrical and ventricular remodelling in diastolic and systolic heart failure is symmetrical.

Hypertrophied heart = diastolic heart failure

Dilated heart = systolic heart failure

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8
Q

What is meant by Neuro-hormonal Activation?

A

Sympathetic Nervous System

Renin-Angiotensin-Aldosterone System

Natriuretic Hormones

Anti-diuretic Hormone

Endothelin

Prostaglands / Nitric Oxide

Kallikrien System

Tissue Necrosis Factor - alpha

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9
Q

Describe the effect of the Sympathetic Nervous System in Heart Failure

A

Baroreceptor-mediated response

Early compensatory mechanism to improve CO: cardiac contractility, arterial and venous vasoconstriction, tachycardia

However long-term deleterious effects: β-adrenergic receptors are down-regulated / uncoupled and Noradrenaline induces Cardiac Hypertrophy / Myocyte Apoptosis and necrosis via α-receptors and induce up-regulation of the RAAS

Reduction in heart rate variability (reduced paraSNS and increased SNS)

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10
Q

What is RAAS and its activity in Heart Failure?

A

The Renin-Angiotensin-Aldosterone System

Angiotensin II plays a Key role in organ damage.

When it binds to AT1 receptor it causes atherosclerosis, vasoconstriction, vascular hypertrophy and endothelial dysfunction in blood vessels which leads to hypertension which leads to stroke or heart failure.

Heart: Angiotensin II causes LV hypertrophy, fibrosis, remodelling and apoptosis which lead to heart failure and MI

Kidney decreases glomerular filtrate rate, proteinuria, increases aldosterone release and glomerular sclerosis which lead to renal failure.

Stroke, hypertension, Heart failure (MI) and renal failure all could lead to death

The RAAS is commonly activated in HF as reduced renal blood flow activates SNS indication of renin from macula densa – increases production of renin

Elevated ATII is a potent vasoconstrictor, promotes LVH and myocyte dysfunction, promotes aldosterone release, promotes Na+/H2O retention and stimulates thirst by central action

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11
Q

Summarise the RAAS

A
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12
Q

What are Natriuretic Hormones?

A

Stretch or increase in cardiac chamber volume leads to release of natriuretic peptides: predominate renal action – constricts afferent and vasodilates efferent arterioles. Vasodilatation increases urinary sodium excretion

  • Decreases Na+ reabsorption in the collecting duct
  • Inhibits secretion of renin and aldosterone
  • ? Systemic arterial and venous vasodilation

Brain: stretch (V) – similar effects, released from ventricles

C-Type: CNS and endothelium – limited effects

These peptides balance the effects of the RAAS on the vascular tone and the Na+/H2O balance

Role as a sensitive marker

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13
Q

Describe the effect of Anti-Diuretic Hormone (Vasopressin) in Heart Failure

A

Hypo-natraemia (low serum sodium) results from H2O in excess of Na+ retention and can be due to:

increased H2O intake (thirst)

action of ADH on V2 receptors in the collecting duct.

Normally hypo-natraemia / hypo-osmolality inhibits ADH release – but ADH is increased in HF.

This increases H2O retention.

Tachycardia and reduced systemic resistance results in increased CO.

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14
Q

Describe the effect of Endothelin

A

Endothelin is secreted by vascular endothelial cells.

Potent system and renal vasoconstrictor acting via autocrine (local) activity thus activating RAAS.

Evidence of increased levels in some patients with HF

Correlates with indices of severity (poor prognostic sign)

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15
Q

What are the benefits of Prostaglandin E2 and I2?

A

Stimulated by NA and RAAS
Act as vasodilators on afferent renal arterioles to attenuate effects of NA / RAAS
NSAID Rx blocks de novo PG synthesis

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16
Q

Describe the role of Nitric Oxide in HF

A

Usually potent vasodilator produced by endothelial cells via NO synthase
NO synthase may be blunted in HF
Loss of vasodilatation balance

17
Q

What is the effect of Bradykinin?

A

Promotes natriuresis and vasodilatation

Stimulates production of PGs

18
Q

What is the role of Tumour Necrosis Factor (alpha-TNF)?

A

Increased in HF

Depresses myocardial function

?? stimulates

NO synthase

?role in cachexia

19
Q

What happens in vascular endothelium?

A

SNS, RAAS, reduced NO and increased Endothelinlead to an increase in peripheral arterial resistance.

Alteratiosn in vascular tone exacerbate the clinical deterioration.

Lead to skeletal muscle changes:

  • Reduced skeletal muscle blood flow
  • Reduction in skeletal muscle mass (cachexia) which affects all muscle including limbs and respiratory e.g. diaphragm
  • Abnormalities of structure and function
  • Contribute to fatigue and exercise intolerance
20
Q

What are the Renal Effects in Heart Failure?

A

GFR (Glomerular Filtration Rate) is maintained in early HF by haemodynamic changes at the glomerulus
Increased Na+/H2O retention due to neuro-hormonal activation
However in severe HF, renal blood flow falls leading to reduced GFR and a subsequent rise in serum urea and creatinine

This can be exacerbated by treatment inhibiting the actions of Angiotensin II

21
Q

Describe how Anaemia can occur in HF

A

Anaemia may occur as heart failure progresses

Contributes to symptoms

Common and easily treated

Multi-factorial artiology: chronic inflammatory disease, expanded plasma volume, drug therapy (ACEi/Aspirin), Iron malabsorption, Chronic renal failure [note ACE inhibitors have a bone marrow suppressing effect in certain individuals and Aspirin can cause erosive gastritis]

22
Q

What happens in Diastolic Dysfunction?

A

20-50% of heart failure patients
Key Factors: frequently elderly and female, often history of hypertension/diabetes/obesity
Normal LV function but concentric Left Ventricle
Hypertrophy
Hospitalisation and mortality similar to systolic HF
Diagnosis is less clear cut
Little clinical outcome study data to guide therapy
Reduced LV compliance – it is stiff
Impaired myocardial relaxation
Impaired diastolic LV filling with increased LA and PA pressures
Unable to compensate by increasing LV EDP (end diastolic pressure) [Frank Starling Law]

Low cardiac output results

Triggers neuro-hormonal actrivation as per systolic heart failure

23
Q

What are the Clinical Syndromes of the heart?

A

In clinical practice, heart failure is often divided into:
Right Sided Heart Failure
Left Sided Heart Failure
Biventricular (congestive) Cardiac Failure
Systolic Heart Failure (‘pump failure’)
Diastolic Heart Failure (‘failure of relaxagtion’)

It is rare for any part of the heart to fail in isolation

24
Q

What are the Symptoms/Signs of Left Heart Failure?

A
  • Fatigue, exertional dysponea (SOB), orthopnoea (when lying flat), paroxysmal nocturnal dyspnoea (PND)

In mild left sided heart failure, there may be few clinical signs but as the heart failure progresses you may see

  • Tachycardia
  • Cardiomegaly (displaced apex beat, may be sustained)
    3rd or 4th heart sound (‘gallop rhyth
  • Functional murmur of mitral regurgitation (systolic murmur)
  • Basal pulmonary crackles (due to pulmonary oedema)
  • Peripheral oedema (pitting oedema – NOTE; Right heart failure causes this but if left heart failure is severe enough, it could cause right heart failure)
25
Q

What is the Aetiology of Right Heart Failure?

A

Chronic Lung Disease (of any cause)
Pulmonary embolism / pulmonary hypertension

Pulmonary / tricuspid valvular disease
Left – to –right shunts (ASD, VSD)
Isolated right ventricular cardiomyopathy
The most frequent cause is SECONDARY TO LEFT HEART FAILURE

26
Q

What are the Symptoms / Signs of Right Heart Failure?

A

Relate to distension and fluid accumulation in areas drained by the systemic veins
Fatigue, dyspnoea (SOB – but generally seenised JVP
Tender, smooth hepatic enlargement
Dependent pitting oedema
Ascites
Pleural effusion

27
Q

What are the management principles of heart failure?

A

Correct underlying cause

Non-pharmacological measures

Pharmacological therapy:

  1. Symptomatic improvement
  2. Delayed progression of heart failure
  3. Reduce mortality

Treat complications / associated conditions / cardiovascular risk factors e.g. arrhythmias

28
Q

What does Lifestyle management mean?

A

Reduce salt

Decrease alcohol

Increase aerobic exercise

Decrease blood pressure

29
Q

What Pharamcological drugs could you use in heart failure?

A

Diuretics

ACE inhibitors

Hydralazine / Nitrate

Beta-blockers

Spironolactone

(Digoxin) – cardiac glycoside

Inotropes – acute setting

Phosphodiesterase inhibitors – acute setting

Antiarrhythmics

30
Q

What does Cardiac Surgery mean? And what implantable pacemakers can be used?

A

Cardiac Surgery:
Heart transplantation
Mechanical assist devices
Underlying cause – valve surgery, revascularisation
Implantable pacemakers: biventricular pacing (for coordination of both sides of the heart leading to increased cardiac output)
Implantable Defibrillators: to prevent sudden death, particularly if patient has malignant arrhythmias

31
Q

How do ACE inhibitors work?

A

ACE inhibitors block the ACE-mediated production of angiotensin II from angiontensin I therefore reduce the angiotensin II effects mediated via both AT1 and AT2 receptors (does not abolish effects because angiontensin II can also be produced via non-ACE pathways that are unaffected by ACE inhibitors)

ACE also catalyzes the degradation of bradykinin.

Bradykinin produces vasodilation by stimulating the production of nitric oxide and prostaglandin in the endothelium therefore accumulation of bradykinin during ACE-inhibitor therapy makes an important contribution to the anti-hypertensive efficacy of these agents.

Accumulation of bradykinin has been implicated in the cough that is a side effect of ACE inhibitors.

32
Q

How do you calculate blood pressure?

A

BP = Cardiac Output x Total Peripheral Resistance

ESA2 CVS (14 decks)

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