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BW VTS ECC STUDY DECK > Mechanisms Of Heart Failure > Flashcards

Mechanisms Of Heart Failure Flashcards

1
Q

Define heart failure

A

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

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2
Q

Forward failure means

A

Poor cardiac output

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3
Q

Characteristics of forward failure
(4)

A

Weakness
Exercise intolerance
Hypothermia
Decreased tissue perfusion

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4
Q

What does backward failure mean?

A

Congestion

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5
Q

Characteristics of backward failure

A

Increased venous filling pressure
Pulmonary edema/pleural effusion
Ascites

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6
Q

What are the Neurohormonal pathways involved in heart failure?

A

Renin-angiotensin-aldosterone system
Sympathetic nervous system
Natriuretic peptides
Endothelin/vasopressin systems

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7
Q

Draw the RAAS system

A

See image below

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8
Q

What is the Primary trigger for activation of the RAAS system?

A

Heart’s inability to provide normal renal perfusion

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9
Q

Decreased renal blood flow and NaCl delivery to the distal nephron induces renin release from the macular densa in the kidney.
What happens next?

A

Renin converts angiotensinogen (from liver) to angiotensin 1

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10
Q

Angiotensin I is converted to angiotensin II via

A

ACE in pulmonary vasculature

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11
Q

What are the functions of angiotensin II?

A

Renal Na/H2O retention
Production of aldosterone
Myocardial apoptosis
Cardiac/vascular remodeling/fibrosis
Increase thirst
ADH release
Vasoconstriction

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12
Q

What are the main effectors of the SNS (sympathetic nervous system)?
(2)

A

Epinephrine
Norepinephrine

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13
Q

What are the main results of

A
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14
Q

What are the main results of SNS activation?

A

Increased HR
Increased CO
Increased blood flow

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15
Q

What is the SNS short term response?
Chronic activation

A

Adrenergic receptor downregulation
Persistent tachycardia
Increased myocardial o2 demand
Myocyte necrosis
**further cardiac damage

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16
Q

Myocardial tissues produce 2 main hormones that induce natriuesis/diuresis/vasodilation

A

1- Atrial natriuretic peptide (ANP)
2- B-type natriuretic peptide (BNP)

17
Q

What are ANP and BNP primarily produced in response to?

A

Stretch/stress of the myocardial tissue

18
Q

What is the Natriuretic Peptide System counter-regulatory to?

A

RAAS/SNS

19
Q

Circulatory ANP/BNP are increased with _____ ______

A

Heart disease

20
Q

Beneficial effects become overwhelmed

A

Receptor downregulation
Inappropriate/inadequate production
Increased clearance/degradation

21
Q

Describe Endothelin-1

A

Potent vasoconstrictor produced by vascular endothelial cells

22
Q

Endothelin-1 is produced by vascular endothelial cells in response to : (3)

A

1- Shear stress
2- Angiotensin II
3- Cytokines

23
Q

Endothelin-1 causes ______/______
And alters _____ ______ handling within muscles

A

Causes : vasoconstriction/increased after load
Alters : normal calcium

24
Q

Vasopressin increases reabsorption of ____ ____ within the renal collecting ducts

A

Free water

25
Q

Excessive vasopressin contributes to the development of
(3)

A

Fluid overload
CHF
Dilutional hyponatremia

26
Q

What molecules are responsible for cardiac hypertrophy and altered cardiac architecture
(3)

A

Angiotensin II
Norepinephrine
Aldosterone

27
Q

Concentric hypertrophy is

A

Pressure overload

28
Q

Concentric hypertrophy is in response to conditions causing _____ _____

A

Pressure overload

29
Q

*Concentric hypertrophy:
Increased afterload triggers the replication of sarcomeres in parallel
Resulting in increased relative thickness of

A

The ventricle walls

30
Q

Eccentric hypertrophy is

A

Volume overload

31
Q

*Eccentric hypertrophy :
Sarcomere replication in series
Elongation of myocytes and dilation of

A

Ventricular chamber

BW VTS ECC STUDY DECK (11 decks)

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