CVS Session 9 - Heart Failure Flashcards Preview

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Flashcards in CVS Session 9 - Heart Failure Deck (40):

Define heart failure. 

- 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 commensurate with 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.


Outline the aetiology of heart failure. 

- Ischaemic Heart Disease (IHD) is the primary cause of Systolic HF

- Hypertension

- Dilated Cardiomyopathy:

I. Bugs (Viral/ Bacterial / Mycobacteria)

II. Alcohol / Drugs / Poisoning

III. Pregnancy

IV. Idiopathic


- Valvular Heart Disease / Congenital

- Restrictive Cardiomyopathy e.g. amyloidosis

- Hypertrophic Cardiomyopathy

- Pericardial disease

- High-Output Heart Failure

- Arrhythmias


Outline the progression of Heart Failure - Class I. 

Class I – No symptomatic limitation of physical activity


Outline the progression of Heart Failure - Class II.

Class II

- Slight limitation of physical activity

- Ordinary physical activity results in symptoms

- No symptoms at rest


Outline the progression of Heart Failure - Class III.

Class III:

- Marked limitation of physical activity

- Less than ordinary physical activity results in symptoms

- No symptoms at rest


Outline the progression of Heart Failure - Class IV

Class IV:

I. Inability to carry out any physical activity without symptoms

II. May have symptoms at rest

III. Discomfort increases with any degree of physical activity


Outline the physiology of the heart. 

- Cardiac Output ~ 5 litres/min

- Stroke Volume ~ 75 ml / beat

- LV end systolic volume ~ 75 ml

- LV end diastolic volume ~ 150 ml

- Ejection Fraction 50% plus

- Weight ~ 330 g


What are the factors affecting cardiac output?

- Heart rate

- Venous capacity (LV preload)

- Myocardial contractility

- Arterial and Peripheral impedance (after load)


State Starling's Law of the Heart and describe the graph. 

"The force developed in a muscle fibre depends on the degree to which the fibre is stretched."


Outline the pathophysiology of Left Ventricular Systolic Dysfunction. 

- Increased LV capacity

- Reduced LV cardiac output

- Thinning of the myocardial wall

I.  Fibrosis and necrosis of myocardium

II.  Activity of matrix proteinases


- Mitral valve incompetence

- Neuro-hormonal activation

- Cardiac Arrhythmias


Discuss the Structural Heart Changes. 

- Loss of muscle

- Uncoordinated or abnormal myocardial contraction

- Changes to the ECM:

I. Increase in collagen (III>I) from 5% to 25%

II. Slippage of Myocardial fibre orientation


- Change of cellular structure and function

I. Myocytolysis and vacuolation of cells

II. Myocyte hypertrophy

III. Sarcoplasmic reticulum dysfunction

IV. Changes to Calcium availability and/or receptor regulation


Outline Ventricular remodeling after acute infarction. 

- Initial infarct. 

- Expansion of infarct (hours to days) 

- Global remodeling (days to months) 



Outline Ventricular remodeling in diastolic and systolic heart failure 

- Normal Heart 

- Hypertrophied heart (diastolic heart failure) 

- Dilated heart (systolic heart failure)


Label the following images. 

- Fig 5.2: Normal heart.

- Fig 5.3: Concentric Hypertrophy of left ventricular wall

- Fig 5.4: Eccentric hypertrophy of left ventricular wall

- Fig 5.5: Global dilatation  


Outline the pathophysiology of Heart Failure with Preserved Ejection Fraction (HFpEF)

- Previously Diastolic Heart Failure or HFnEF

- Almost 50% of heart failure patients

- Key factors:

I. Frequently elderly and female

II. Often history of hypertension / diabetes / obesity


- Normal LV function with concentric remodelling

- Hospitalisation and mortality similar to systolic HF

- Diagnosis is less clear cut

- Little clinical outcome study data to guide therapy

- Reduced LV compliance and impaired myocardial relaxation:

I. Thicker and shorter cardiomyocytes

II. Increased deposition of collagen


- Impaired diastolic LV filling (with increased LA and PA pressures)

- LV filling becomes dependent on high LA pressure

- RV dysfunction can result from high LA and PA pressure

- Triggers neuro-hormonal activation as per systolic heart failure


Outline the clinical syndromes of heart failure. 

- Left Sided Heart Failure

- Right Sided Heart Failure

- Biventricular (congestive) cardiac failure

- LVSD (‘pump failure’)

- HFpEF (‘failure of LV relaxation’)


Identify the signs and symptoms of Left Heart Failure 


I. Fatigue

II. Exertional dyspnoea

III. Orthopnoea

IV. 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:

I. Tachycardia

II. Cardiomegaly (displaced apex beat, may be sustained)

III. 3rd or 4th heart sound (‘Gallop rhythm’)

IV. Functional murmur of mitral regurgitation

V. Basal pulmonary crackles (fluid in the lungs)

VI. Peripheral oedema


Outline the aetiology of Right Heart Failure. 

- Chronic lung disease

- 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 = Congested or Biventricular Heart Failure


What are the signs and symptoms of Right Heart Failure? 

Relate to distension and fluid accumulation in areas drained by the systemic veins:

- Fatigue, dyspnoea, anorexia, nausea

- ↑ JVP

- Tender, smooth hepatic enlargement

- Dependent pitting oedema

- Ascites

- Pleural effusion


Describe the features of neuro-hormonal activation. 

- Sympathetic Nervous System

- Renin-Angiotensin-Aldosterone System

- Natriuretic Hormones

- Anti-Diuretic Hormone

- Endothelin

- Prostaglandins / Nitric Oxide

- Kallikrien System

- Tissue Necrosis Factor – α


Outline the involvement of the Sympathetic Nervous System in heart failure. 

- Baroreceptor-mediated response

- Early compensatory mechanism to improve CO:

I. Cardiac contractility

II. Arterial and venous vasoconstriction

III. Tachycardia

  • However long-term deleterious effects:
  1. β-adrenergic receptors are down-regulated / uncoupled
  2. Noradrenaline
  1. Induces cardiac hypertrophy / myocyte apoptosis and necrosis via α-receptors
  2. Induce up-regulation of the RAAS
    • Reduction in heart rate variability (reduced paraSNS and increased SNS)


When is RAAS commonly activated in Heart Failure?

- Reduced renal blood flow

- SNS induction of renin from macula densa


Outline the effects of elevated Angiotensin II. 

Elevated Angiotensin II:

- Potent vasoconstrictor

- Promotes LVH and myocyte dysfunction

- Promotes aldosterone release

- Promotes Na+ /H2O retention

- Stimulates thirst by central action?


Explain how Angiotensin II plays a key role in organ damage. 

- Brain: Atherosclerosis -> Stroke 

- Vessels: Vasoconstriction, Vascular hypertrophy, Endothelial dysfunction -> Hypertension 

- Heart: LV hypertrophy, Fibrosis, Remodeling, Apoptosis -> Heart failure (MI) 

- Kidney: Decreased GFR, Increased Proteinuria, Increased Aldosterone release Glomerular sclerosis -> Renal failure 


All can progress to death. 


Outline the Renin-Angiotensin-Aldosterone System


Outline the effect of Natriuretic Hormones. 

- Atrial: stretch (A&V):

I. Predominate renal action – constricts afferent and vasodilates efferent arterioles

II. Decreases Na+ reabsorption in the collecting duct

III, Inhibits secretion of renin and aldosterone

IV. Systemic arterial and venous vasodilatation


- Brain: stretch (V) – similar effects

- C-Type: CNS and endothelium – limited effects

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

- Role as sensitive marker for HF (low false negative)


Outline the effect of ADH (Vasopressin)

- Hyponatraemia results from H2O in excess of Na+ retention and can be due to:

I. Increased H2O intake (thirst)

II. Action of ADH on V2 receptors in the collecting duct


- Normally hyponatraemia / hypoosmolality inhibits ADH release – but ADH is increased in HF:

I. Increased H2O retention

II. Tachycardia and reduced systemic resistance resulting in increased CO


Outline the effect of Endothelin. 

- 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)


Outline the effect of other chemicals:

- Prostaglandin E2 and I2

- Nitric Oxide

- Bradykinin

- Tumour Necrosis Factor (α-TNF) 

- Prostaglandin E2 and I2:

I. Stimulated by NA and RAAS

II. Act as vasodilators on afferent renal arterioles to attenuate effects of NA / RAAS

III. NSAID Rx blocks de novo PG synthesis


- Nitric Oxide

I. Usually potent vasodilator produced by endothelial cells via NO synthase

II. NO synthase may be blunted in HF

III. Loss of vasodilatation balance


- Bradykinin:

I. Promotes natriuresis and vasodilatation

II. Stimulates production of PGs


- Tumour Necrosis Factor (α-TNF)

I. Increased in HF

II. Depresses myocardial function

III. Stimulates NO synthase??

IV. Role in cachexia?


What is Oedema?

- Oedema is the excessive volume of fluid within the tissues:

I. Interstitial

II. Intracellular


- Heart failure is one cause

- Changes to capillary dynamics leads to oedema

- Don’t forget about the RAAS


Explain what is meant by:

Net Filtration Pressure = Hydrostatic Pressure – Osmotic Pressure


Explain the role of the vascular endothelium in heart failure. 

- Increase in peripheral arterial resistance:



III. Reduced NO

IV. Increased endothelin


- Alterations in vascular tone exacerbate the clinical deterioration

- Leads to skeletal muscle changes, renal effects, anaemia


Outline the skeletal muscle changes associated with changes in the vascular endothelium. 

- Reduced skeletal muscle blood flow


- Reduction in skeletal muscle mass (cachexia) – Affects all muscle including:

I. Limbs

II. Respiratory eg diaphragm


- Abnormalities of structure and function

- Contribute to fatigue and exercise intolerance


Outline the renal effects associated with changes in the vascular endothelium. 

- GFR is maintained in early HF by haemodynamic changes at the glomerulus

- Increased Na+ /H2O retention due to neurohormonal 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


Outline the anaemia associated with changes in the vascular endothelium. 

- Contributes to symptoms

- Common and easily treated

- Multi-factorial aetiology:

I. Chronic inflammatory disease

II. Expanded plasma volume

III. Drug therapy (ACEi / Aspirin)

IV. Iron malabsorption

V. Chronic renal failure




Outline the manifestations of a diseased myocardium. 

Diseased myocardium – Ischaemic Heart Disease:

- Myocardial scar

- Myocardial stunning/hibernation

- Epicardial coronary artery disease

- Abnormal coronary microcirculation

- Endothelial dysfunction


Outline abnormal loading conditions. 

- Hypertension

- Valve and myocardium structural defects

I. Acquired – Mitral, aortic, tricuspid and pulmonary valve diseases

II. Congenital – atrial and ventricular septum defects and others


- Toxic damage

I. Recreational substance abuse – alcohol, cocaine, amphetamine, anabolic steroids

II. Heavy metals – copper, iron, lead, cobalt

III. Medications – cytostatic drugs, antidepressant drugs, NSAID’s, anaesthetics

IV. Radiation


Outline, briefly, the clinical signs and symptoms of chronic heart failure. 

- Clinical signs

I. Pulmonary congestion

II. Venous congestion

III. Dependent oedema


- Symptoms

I. Dyspnoea

II. Lethargy

III. Orthopnoea


Outline the Vicious Cycle of Heart Failure


Outline how the overactivation of the RAAS and SNS is detrimental in HFrEF and underpins the basis of therapy