Shock & Heart Failure

Question 1

3 types of shock.

Answer 1

Hypovolemic
Distributive
Cardiogenic

Question 2

What is hypovolemic shock? Distributive? Cardiogenic?

Answer 2

Hypovolemic - decrease in blood volume due to blood loss via hemorrhage, fluid loss due to endothelial damage, secretions, dehydration

Distributive - vasodilation due to sepsis/toxic shock

Cardiogenic shock - inadequate filling of the arteries caused by cardiac pump failure (ie MI, valve rupture, pulmonary emboli, myocarditis, pericardial tamponade)

Question 3

What is vasovagal syncope usually caused by which type of shock?

Answer 3

Distributive shock; systemic vasodilation leads to decrease in HR, BP, and ultimately flow to the brain –> fainting

Question 4

What are the immediate consequences of shock? long-term consequences?

Answer 4

immediate: decrease in BP

long-term: poor tissue perfusion

Question 5

What are the immediate consequences of heart failure? long-term consequences?

Answer 5

immediate: impaired pump performance

long-term: progressive deterioration of the heart/death of myocardial cells

Question 6

What is ESPVR a measure of? EDPVR?

Answer 6

ESPVR: measure of ventricular stiffness at the end of systole, measure of ionotropy and contractility

EDPVR: measure of ventricular stiffness at the end of diastole; measure of lusitropy and relaxation

Question 7

How is ejection fraction calculated?

Answer 7

EF = SV/EDV

Question 8

What is heart failure?

How does heart failure precipitate itself?

Answer 8

Heart failure: malfunctioning ventricular filling/ejection of blood

Precipitation: cyclical Impaired ejection (systolic heart failure) impaired/reduced filling (diastolic heart failure)

Question 9

What is the pathophysiology of R heart failure? How is ejection fraction affected?
What is it also known as?

Answer 9

blood backs up and accumulates behind the heart (increased venous pressure) AND too little blood flows into pulmonary circulation

Ejection fraction is not affected

aka backward failure, diastolic HF

Question 10

What is the pathophysiology of L heart failure? What is it also known as?

Answer 10

too little blood flows into the systemic circulation/out of the heart AND flow backs up into pulmonary veins

Ejection fraction is reduced

aka forward failure, systolic HF

Question 11

How is EF affected in systolic vs diastolic HF?

Answer 11

Systolic = impaired EF (HFrEF; r = reduced)

Diastolic = Preserved EF (HFpEF; p = preserved)

Question 12

What are the causes of R heart failure? L heart failure?

Answer 12

RHF: failure of previous contraction to fully pump out all of the blood (ie due to COPD, pulmonary hypertension, congenital heart dz)

LHF: heart can’t generate enough pressure to pump blood out (ie due to ischemic heart disease, hypertensive heart disease, cardiomyopathies, valvular disease)

Question 13

What are the clinical manifestations of R heart failure? L heart failure?

Answer 13

RHF: JVP, peripheral edema, anasarca (fluid in body cavity), dropsy/edema

LHF: rales, dyspnea, orthopena (dyspnea in supine), PND, fatigue

Question 14

What are the structural manifestations of R heart failure? L heart failure?

Answer 14

RHF: concentric hypertrophy; EF is normal

LHF: eccentric hypertrophy; EF is low because the EDV is really high

Question 15

What are the two types of neurohumoral responses?

Answer 15

functional - short term responses that modify the function of existing structures

proliferative - long-term responses that modify cell size, shape, composition, survival

Question 16

What are the short term responses of neurohumoral signaling on:
cardiac stimulation?
vasoconstriction?
transcriptional activation?

What are the long-term responses of neurohumoral signaling on these 3 parameters?

Answer 16

Cardiac stimulation:
short-term (ie NE) changes HR, contractility, to modulate CO.
long-term - arrhythmias, increased energy demand, which can lead to cardiac myocyte death.

vasoconstriction
short-term: (ie NE) changes afterload to maintain BP
long-term: decrease CO, increased energy demand, which can lead to cardiac myocyte death.

Transcriptional activation
short-term: sarcomeres added to normalize wall stress and maintain CO
long-term: hypertrophy, remodeling; increased energy demand, which can lead to cardiac myocyte death.

Question 17

What role does the neurohumoral responses play in exercise?

Answer 17

cardiac stimulation + select vasoconstriction to maintain BP, CO, and redistribute blood

Question 18

What role does the neurohumoral responses play in shock? What does chronic neurohumoral responses result in?

Answer 18

cardiac stimulation + vasoconstriction + salt/h2o retention to maintain perfusion, CO, redistribute blood to vital organs.

BUT

chronic a1 –> decrease CO due to increased afterload

chronic b1 –> arrhythmias

chronic ADH –> kidney damage

Question 19

What role does the neurohumoral responses play in heart failure?

What do chronic neurohumoral responses result in?

Answer 19

Roles of neurohumoral responses:
maintain circulation
vasoconstriction - maintain afterload/BP
cardiac stimulation - increase HR/contractility
fluid retention - increase preload
proliferative signaling: reduces wall stress

Bad: all of these processes increase energy expenditure + increases energy starvation

Question 20

How are proliferative signaling good? bad?

Answer 20

increases the # of sarcomeres to normalize wall stress such that CO can be maintained, but long-term signaling can result in an increase in energy starvation, fetal gene expression, remodeling, and ultimately apoptosis.

Question 21

What hypertrophic phenotype does aortic insufficiency manifest as? aortic stenosis?

Answer 21

AI: eccentric (due to increased diastolic stress)

AS: concentric (due to increase systolic stress - not to be confused with increased systolic HF)

Question 22

What hypertrophic phenotype does a low EDV manifest as? high EDV?

Answer 22

low EDV: concentric

high EDV: eccentric

Question 23

What hypertrophic phenotype does ischemic/MI cardiomyopathy manifest as? hypertensive heart disease?

Answer 23

Ischemia/MI: eccentric

hypertensive heart disease: concentric

Question 24

What hypertrophic phenotype does endurance training cause? strength straining?

Answer 24

Endurance: eccentric

strength: eccentric, but with slightly thicker walls

Question 25

What’s the difference between physiological and pathological?

Answer 25

Physiological: no tendency for progressive deterioration and myocyte death. Expression of ADULT phenotype genes

Pathological: tendency for progressive deterioration and myocyte death. Expression of fetal phenotype.

Question 26

Systolic HF leads to:

Diastolic HF leads to:

Answer 26

Systolic HF: progressive dilation/remodeling

Diastolic HF: leads to concentric/increased risk of ischemia

Question 27

What signaling molecule is involved in eccentric hypertrophy?

concentric hypertrophy?

Answer 27

eccentric: Erk 5
concentric: Erk 1,2

Question 28

What is the recommended treatment for RHF? LHF?

Answer 28

RHF: diuretics - to decrease preload

LHF: Ace inhibitors, nitrates, b-blockers, aldosterone blockers

Question 29

Why do drugs that improve survival in systolic HF (eccentric) have less benefit than diastolic HF?

Answer 29

because diastolic HF rarely remodels

Question 30

What drugs inhibit remodeling?

Answer 30

ACE inhibitors and b-blockers