Mechanisms Of Heart Failure Flashcards
Define heart failure
Heart’s inability to meet metabolic needs of the peripheral tissues, or instances when the heart can only do so in the presence of increased filling pressures
Forward failure means
Poor cardiac output
Characteristics of forward failure
(4)
Weakness
Exercise intolerance
Hypothermia
Decreased tissue perfusion
What does backward failure mean?
Congestion
Characteristics of backward failure
Increased venous filling pressure
Pulmonary edema/pleural effusion
Ascites
What are the Neurohormonal pathways involved in heart failure?
Renin-angiotensin-aldosterone system
Sympathetic nervous system
Natriuretic peptides
Endothelin/vasopressin systems
Draw the RAAS system
See image below
What is the Primary trigger for activation of the RAAS system?
Heart’s inability to provide normal renal perfusion
Decreased renal blood flow and NaCl delivery to the distal nephron induces renin release from the macular densa in the kidney.
What happens next?
Renin converts angiotensinogen (from liver) to angiotensin 1
Angiotensin I is converted to angiotensin II via
ACE in pulmonary vasculature
What are the functions of angiotensin II?
Renal Na/H2O retention
Production of aldosterone
Myocardial apoptosis
Cardiac/vascular remodeling/fibrosis
Increase thirst
ADH release
Vasoconstriction
What are the main effectors of the SNS (sympathetic nervous system)?
(2)
Epinephrine
Norepinephrine
What are the main results of
What are the main results of SNS activation?
Increased HR
Increased CO
Increased blood flow
What is the SNS short term response?
Chronic activation
Adrenergic receptor downregulation
Persistent tachycardia
Increased myocardial o2 demand
Myocyte necrosis
**further cardiac damage
Myocardial tissues produce 2 main hormones that induce natriuesis/diuresis/vasodilation
1- Atrial natriuretic peptide (ANP)
2- B-type natriuretic peptide (BNP)
What are ANP and BNP primarily produced in response to?
Stretch/stress of the myocardial tissue
What is the Natriuretic Peptide System counter-regulatory to?
RAAS/SNS
Circulatory ANP/BNP are increased with _____ ______
Heart disease
Beneficial effects become overwhelmed
Receptor downregulation
Inappropriate/inadequate production
Increased clearance/degradation
Describe Endothelin-1
Potent vasoconstrictor produced by vascular endothelial cells
Endothelin-1 is produced by vascular endothelial cells in response to : (3)
1- Shear stress
2- Angiotensin II
3- Cytokines
Endothelin-1 causes ______/______
And alters _____ ______ handling within muscles
Causes : vasoconstriction/increased after load
Alters : normal calcium
Vasopressin increases reabsorption of ____ ____ within the renal collecting ducts
Free water
Excessive vasopressin contributes to the development of
(3)
Fluid overload
CHF
Dilutional hyponatremia
What molecules are responsible for cardiac hypertrophy and altered cardiac architecture
(3)
Angiotensin II
Norepinephrine
Aldosterone
Concentric hypertrophy is
Pressure overload
Concentric hypertrophy is in response to conditions causing _____ _____
Pressure overload
*Concentric hypertrophy:
Increased afterload triggers the replication of sarcomeres in parallel
Resulting in increased relative thickness of
The ventricle walls
Eccentric hypertrophy is
Volume overload
*Eccentric hypertrophy :
Sarcomere replication in series
Elongation of myocytes and dilation of
Ventricular chamber
