CVS Session 9 - Heart Failure Flashcards Preview

- 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

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

- Sympathetic Nervous System

- Renin-Angiotensin-Aldosterone System

- Natriuretic Hormones

- Anti-Diuretic Hormone

- Endothelin

- Prostaglandins / Nitric Oxide

- Kallikrien System

- Tissue Necrosis Factor – α

- 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)

- Reduced renal blood flow

- SNS induction of renin from macula densa

Elevated Angiotensin II:

- Potent vasoconstrictor

- Promotes LVH and myocyte dysfunction

- Promotes aldosterone release

- Promotes Na⁺ /H₂O retention

- Stimulates thirst by central action?

- 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. 

- 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)

- 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

- 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)

- 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?

- 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

- Increase in peripheral arterial resistance:

I. SNS

II. RAAS

III. Reduced NO

IV. Increased endothelin

- Alterations in vascular tone exacerbate the clinical deterioration

- Leads to skeletal muscle changes, renal effects, anaemia

- 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

- 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

- 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

Diseased myocardium – Ischaemic Heart Disease:

- Myocardial scar

- Myocardial stunning/hibernation

- Epicardial coronary artery disease

- Abnormal coronary microcirculation

- Endothelial dysfunction

- 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

- Clinical signs

I. Pulmonary congestion

II. Venous congestion

III. Dependent oedema

- Symptoms

I. Dyspnoea

II. Lethargy

III. Orthopnoea