Heart Failure

Question 1

What is heart failure?

Answer 1

Chronic or acute state resulting from failure of the heart to meet oxygen demands of the body

Question 2

What are the 2 ways the heart is unable to deliver oxygen to the rest of the body

Answer 2

♣ Heart cannot pump properly
♣ Heart cannot fill with enough blood

Question 3

What is the difference between chronic and acute heart failure

Answer 3

• Acute: heart failure occurs due to a clot where HT develops rapidly, backs up blood into the heart and causes heart failure
• Chronic: close progressive onset of heart failure

Question 4

What are some underlying issues of heart failure?

Answer 4

• LV Dysfunction
  ♣ Failure for the left ventricle (LV) to pump blood to the rest of the body
• Neuroendocrine Activation
  ♣ Recognizes hear is not pumping properly so these hormones aim to increase the size of the heart
  
  • In doing do, it makes the situation worse
  • Prevents or delays remodeling

Question 5

Describe Systolic Heart Failure:

Answer 5

Systolic HF is the inability of the LV to eject blood during a contraction.
o Ejection fraction is insufficient in systolic HF i.e. the left side of the heart has trouble pumping blood around the rest of the body

Question 6

When does Systolic Heart Failure Occur:

Answer 6

Occurs in patients following a heart attack which leaves the ventricle damaged or occurs due to long-standing HT

Question 7

Describe Diastolic Heart Failure:

Answer 7

Diastolic HF is due to a deficit in the filling capacity of the heart because of the reduced preload

Question 8

When does Diastolic Heart Failure Occur:

Answer 8

Occurs in patients with long-standing HT which causes hypertrophy and a reduction in ventricular volume

Question 9

Congestive Heart Failures

Question 10

What does the Frank-Starling Law of the Heart Describe

Answer 10

The Frank-Starling law describes the relationship between the diastolic pressure of the heart
(the preload, so the pressure in the atrium) and the amount of work done by the heart
(described by stroke volume, how much blood is pumped out of the ventricles).

Normally, the preload changes and this results in a change in stroke volume. Quite a small change in
preload results in quite a large change in stroke volume.

Question 11

In athletes, what does the Frank-Starling Law look like?

Answer 11

In athletes, this relationship is steeper where there is a bigger increase in SV for the same change in preload

Question 12

What does the Frank-Starling Law look like in those who experience heart failure?

Answer 12

The relationship between SV and preload becomes less and less steep:
♣ For the same increase in preload, there is smaller increase in SV (less blood is pumped out)
* The heart does less work (lower SV) because size of ventricle and the muscle capacity is reduced the heart physically cannot work more
* So not enough blood circulates the body

Question 13

What are some lethal diseases states that follow heart failure?

Answer 13

o Uncontrolled HT (asymptomatic)
o Diabetes (greater changes of developing HF)
o Myocardial infarction
o Valve dysfunction (can be treated by surgery but if goes unnoticed –> HF)
o Viral myocarditis

Question 14

What are the 4 classes of heart failure?

Answer 14

CLASS 1 - symptoms only w exercise
CLASS 2 - slight limitation on ordinary activity (fatigue, palpitations)
CLASS 3 - limitation on less than ordinary activity
CLASS 4 - symptoms at rest

Question 15

Progression of HF: What are the primary effects of HF and what are they associated with

Answer 15

• Primary Effects are associated with the hemodynamic model of the CVS and include:
  o Reduced CO
  o Excessive sympathetic discharge
  ♣ Not enough blood is being pumped so there is an attempt to increase BP
  o Salt + water retention to increase BP

Question 16

Progression of HF: What are the secondary effects of HF and what are they associated with

Answer 16

• Secondary Effects are associated with the neuroendocrine activity of the CVS and include:
  o Remodeling
  o Cardiac hypertrophy (larger in size)
  o Cardiac apoptosis (some cardiac muscle is replaced by other kinds of tissue)

Question 17

Cardiac output during heart failure:
1) Preload

Answer 17

a. Preload is the atrial pressure
b. Increased in HF due to increase blood volume and venous tone

Question 18

Cardiac output during heart failure:
1) Afterload

Answer 18

a. Afterload aka vascular resistance is the pressure that must be overcome to force blood out of the heart (increased in HF bc of inability to pump properly)
b. Increased due to reflex sympathetic outflow + renin-angiotensin system to increase BP
i. However, elevated afterload can also further reduce cardiac output

Question 19

Cardiac output during heart failure:
1) Contractility

Answer 19

a. Reduction in intrinsic contractility because of remodeling of the heart and therefore reduction in pump performance

Question 20

Cardiac output during heart failure:
1) Heart Rate

Answer 20

a. Increases through sympathetic NS compensation
b. Body does its best to catch up by increasing HR
i. This reduces preload and afterload because blood doesn’t have time to build up in the heart

Question 21

What are the 2 ways decreased cardiac output IN HEART FAILURE is detected?

Answer 21

1) Reduced carotid sinus firing
2) Reduced renal blood flow

Question 22

When reduced cardiac output is detected, what are the 2 different compensatory mechanisms

Answer 22

1) Reduced carotid sinus firing –> increased sympathetic discharge
♣ increased force, rate, preload + afterload
2) Reduced renal blood flow –> increase renin release
♣ increased remodeling, preload + afterload

Question 23

Positive Inotropic Drugs:
1) Drugs class and example
2) Mechanism of action:
3) Indication
4) Side effects

Answer 23

1) Drugs: Cardiac Glycosides
- EXAMPLE: Digoxin
- Come from digitalis + other plants

2) Mechanism: Blocks Na+/K+ ATPase
- Positive inotropic effect on heart muscle meaning heart muscle contracts harder and increases CO

3) Indication:
i. Primarily for HF
ii. Atrial fibrillation
- Because it is also has cardiac parasympathetic effects (slows AV conduction)

4) Side effects:
i. Very toxic
ii. Causes cardiac arrhythmias
iii. GI upset
iv. Neuroendocrine effect

Question 24

Diuretics:
1) Example
2) Mechanism of action:
3) Indication
4) Side effects

Answer 24

1) Furosemide

2) Mechanism:
i. Lowers blood volume

3) Indications
i. Useful in almost all HF patients
ii. Loop diuretics: edema, chronic HF
iii. Thiazides: mild-chronic failure
iv. Spironolactone (aldosterone antagonist)

4) Side effects
i. Hypokalemia
1. Too much K+ is excreted

Question 25

Angiotensin Antagonists:
1) Drugs class (2 types) and example for each
2) Mechanism of action:
3) Indication
4) Side effects

Answer 25

1) Drugs:
i. ACE inhibitors
1. Captopril
ii. Receptor antagonists
1. Losartan
2) Mechanism:
i. ACE inhibitors: Reduce angiotensin II synthesis
ii. Angiotensin receptor inhibitors: Block AT-1 type receptors

3) Indications:
i. First time agents (with diuretics) in HF and HT
1. AT-1 type receptor antagonists used If ACE inhibitors are not tolerated

4) Side effects:
i. Renal damage (ACE inhibitors)
ii. Contraindicated in pregnancy (AT-1 type receptor antagonists)

Question 26

BETA BLOCKERS:
1) Example
2) Mechanism

Answer 26

1) Metoprolol
2) Mechanism unknown but may involve reduces renin secretion

Question 27

BETA AGONISTS:
1) Example
2) Selective for what beta-receptor under what conditions
3) What does it do (2 different things)

Answer 27

1) Dobutamide
2) Beta-1 selective for severe HF
3) increases cardiac output AND reduces afterload that comes with increasing cardiac output

Question 28

PHOSPHODIESTERASE INHIBITORS:
1) Example
2) Indication
3) Mechanism of action

Answer 28

1) Theophylline
2) Acute decompensation in HF
3) Increases cAMP levels in cardiac + vascular tissue
1. Increases cAMP which is involved in adrenergic pathway therefore for the same stimulus, can get more of a contraction

Question 29

VASODILATORS:
1) Example
2) Indication
3) What does it do to preload and afterload?

Answer 29

1) Nitroglycerin
2) Acute decompensation in HF
3) Reduce afterload which increases ejection fraction

Reduce preload which reduces myocardial O2 requirement because the heart is working less and therefore requires less O2

Question 30

Drugs for acute vs chronic heart failure

Answer 30

Question 31

1) What are the 3 instances of cardiac hypertrophy
2) Describe the muscle mass and structure of the heart in each instance

Answer 31

1)
a) cardiac dilation
b) pathological hypertrophy
c) physiological hypertrophy

2)
a) Cardiac Dilation:
♣ Myocyte death while there is an increase in size of the heart and a thinning of the muscle wall cardiac dysfunction
b) Pathological Hypertrophy
♣ Fibrosis of heart and increase in mass but by non-cardiac muscle cells
♣ Leads into cardiac dilation
c) Physiological hypertrophy
♣ During pregnancy
♣ No fibrosis and increase in mass due to cardiac muscle
♣ No cardiac dysfunction

Question 32

Positive Inotropic Drugs:
1) How does the cardiac action potential opens voltage ion channels normally (i.e. how does action potential translate to muscle contraction through the Na+/K+ ATPase)

Answer 32

o Cardiac action potential opens voltage gated Ca2+ channels (Ca2+ in)
♣ Voltage gated Ca2+ channels bring Ca2+ inside cytoplasm of cardiac muscle cells
♣ Calcium causes contraction by acting on muscle fibers
o The calcium is brought into the cytoplasm because the intracellular [Ca2+] is decreased by the Na+/Ca2+ exchanger (Na+ in, Ca2+ out)
♣ Calcium is taken out of the cytoplasm by Na+/Ca2+ exchanger
* The export of Ca2+ depends on intracellular [Na+]
o If there is too much intracellular [Na+], the Ca2+ will not be exported because the export means more Na+ in, which is not needed right now
o If there is too little intracellular [Na+], the Ca2+ will be exported whereas Na+ is imported
* This increase in intracellular Na+ (due to the Na+/Ca2+) is exchanged for K+ by the Na+/K+ ATPase to hyperpolarize the cell and await another AP (Na+ out, K+ in)

Question 33

Positive Inotropic Drugs:
1) How does the inotropic intervention work

Answer 33

1) The Na+/K+ ATPase is blocked by the drug (Digoxin) which causes a build-up of intracellular Na+
♣ If there is too much intracellular [Na+], the Ca2+ will not be exported because the export means more Na+ in
♣ If the export of Ca2+ is not done then the cell remains in contracted state
o Inotropic drugs increase contractility
♣ Increases intracellular [Ca2+] for the same cardiac membrane potential/AP longer contraction
♣ Too much intracellular [Ca2+] can cause ectopic AP and contractions because the calcium is not properly buffered by the Na+/Ca2+ exchanger