Heart failure and Cardiovascular Shock

Question 1

Preload

Answer 1

The volume of blood stretching the ventricles at the end of diastole, before the next contraction

Question 2

Afterload

Answer 2

-The peripheral resistance against which the left ventricle must pump

• Afterload depends on the size of the ventricle, wall tension, and arterial BP

Question 3

Contractility

Answer 3

• Ability of heart muscle to shorten or contract
• Contractility can be increased by Epinephrine and Norepinephrine released by the SNS

Question 4

Ejection Fraction

Answer 4

• Percentage of end-diastolic blood volume that is ejected during systole
• Ejection fraction provides information about the function of the left ventricle during systole and is a calculation used to determine the severity of heart failure on the left side

Question 5

Heart failure

Answer 5

A condition where the heart cannot pump blood effectively enough to meet the body’s needs
HF is caused by a loss of critical quantity of functional myocardial cells after injury to the heart from several different causes

Question 6

equation

Answer 6

Stroke Volume (SV) x Heart Rate (HR) = Cardiac Output (CO)

Question 7

Cardiovascular (Cardiogenic) Shock:

Answer 7

The heart is severely compromised that it cannot pump enough blood to supply vital organs

Question 8

left sided heart failure

Answer 8

Blood can’t be pumped out, which results in it backing up into the L. atrium and pulmonary veins

*most common

Question 9

left sided preload/ afterload

Answer 9

Increase in preload and an increase in afterload

Question 10

right sided heart failure

Answer 10

Blood backs up into the r. atrium and systemic venous circulation

Question 11

right side HF areas of blockage

Answer 11

Increases pressure in inferior vena cava and causes hepatic veins to become congested with blood and leads to hepatomegaly and systemic venous congestion

Question 12

right sided hf preload/ afterload

Answer 12

Decrease in preload and an increase in afterload

Question 13

systolic HF

Answer 13

Inability to pump blood forward, left ventricle is unable to eject blood properly

Increased preload and increased afterload

Question 14

diastolic HF

Answer 14

Impaired ability of ventricle to relax and fill during diastole

less blood fills into ventricles

Decreased preload and increased afterload

Question 15

structural change: thickening

Answer 15

decreased blood volume (holds less blood)-> heart is stiff and weak ->

prevention of proper filling (decreases amount of blood pumped out with each beat)

Question 16

structural change: Stiff heart (due to collagen accumulation)

Answer 16

impairs hearts ability to contract and relax (decreased contractile force of ventricle)
–> decreased SV and decreased CO

Question 17

structural change: thinning

Answer 17

dilation -> heart weak -> decreased contractility strength -> harder to pump blood out to the rest of the body (ineffective pumping) -> decreased CO -> decreased tissue perfusion -> increased fluid and sodium retention

Question 18

structural change: Abnormal valve function

Answer 18

increased pressure -> insufficient blood flow and increased workload on chamber

Question 19

cellular dysfunction: Sarcoplasmic reticulum disorganization

Answer 19

inefficient calcium handling -> impaired contractility (ultimately leading to decreased CO)

Question 20

cellular: mitochondrial dysfunction

Answer 20

impaired contractility and decreased CO

Question 21

cellular: cytoskeletal alterations

Answer 21

change in cell shape and stability -> impaired contractility

Question 22

patho order

Answer 22

damage to heart-> weakening of heart-> Improper filling and relaxing, or improper pumping and ejecting of blood (can have both) ->
decreased CO

Question 23

compensatory mechanisms: SNS

Answer 23

baroreceptors sense a decrease in arterial pressure, activating SNS, releasing NE, EP to stimulate beta- adrenergic receptors

result: Increase in HR and ventricular contractility

Increases CO (temporary fight or flight response)

Question 24

neurohormonal response

Answer 24

Juxtaglomerular Apparatus senses decrease in renal perfusion

activate raas system
result:
Vasoconstriction and increased B/P
Increased CO

Question 25

ventricular remodeling

Answer 25

initially increases contractility and CO

but Altered ventricle shape increases ventricular mass and wall tension due to myocyte hypertrophy
-Impaired contractility
-Ventricles become larger and less effective at pumping

Question 26

dilation

Answer 26

Enlargement of chambers/thinning of ventricular wall
-heart muscle stretches
increases: CO/contraction

Question 27

hypertrophy

Answer 27

Increased muscle mass/cardiac wall thickness (new development of tissue)
increases: CO/ contraction

Question 28

counter-regulatory mechansims

nitric oxide

Answer 28

released and…
Relaxes arterial smooth muscle  vasodilation and decreased afterload

Question 29

counter-regulatory mechansims

Natriuetic peptides

Answer 29

ANP (arterial natriuretic peptide) and BNP (b-type natriuretic peptide)
Released in response to increased blood volume in heart

Question 30

Natriuetic peptides result

Answer 30

Vasodilation -> decreased CO
Counteracts effects of SNS and RAAS

Question 31

cardiovascular shock

Answer 31

1.) Damage to heart
2.) Weakens heart
3.) Decreased CO
4.) Decreased organ perfusion