Cardio-Heartfailure

Question 1

what are some typical causes of heart failure?

Answer 1

myocardinal damage
hypertension
infection
genetic/congenital
abnormality
chemical toxicity

Question 2

what is the difference between a systolic heart failure and a diastolic heart failure.

Answer 2

systolic: reduced contractility
diastolic: reduced filing of the heart.

Question 3

how does the heart compensate for a decrease in CO?

Answer 3

increasing the SNS which increases HR and force of contraction and ^ PVR
increases the renin-angiotensin system, SNS activates the beta1 receptors, which increases vasoconstriction and Na+ and H2O retention, which increases blood volume and PVR
increases the force of contraction of the heart the fluid etention and the vasoconstriction will increase the contactility. (Frank-Starling Law)
ventricular hypertrophy
if CO is decreases due to chronic stress, the heart muscle cells increase in size to compensate

Question 4

what are some characteristics of a compensated heart?

Answer 4

it may function normally at rest but may fail due to exercise or stress. if the CO returns to normal levels, the renal output also returns to normal. If CO does not return to normal levels= decompensated heart failure.

Question 5

what is depompensated heart failure?

Answer 5

severely damaged heart cannot be compensated by SNS, renin-agotensis system or ventricular hypertrophy. Causes excessive stretching and excess fluid in venous system. high mortality

Question 6

what is congestive heart failure (CHF)

Answer 6

decompensated heart +edema

Question 7

what are the symptoms of CHF.

Answer 7

• tachycardia
• shortness of breath
• sweating
• peripheral/pulmonary edema
• decreased exercies toleerance
• enlargement of the heart
• hypotension

Question 8

What are the treatment strategies for heart failure?

Answer 8

1. reduced workload of heart
2. restrict Na+/stop smoking
3. diuretics
4. ACE inhibitors/ARB
5. cardiac glycosis
6. beta-blockers
7. vasodilators

Question 9

what is the treatment of mild heart failure?

Answer 9

ACE inhibitor (enalapril), ARB (losartan), thiazide dieuretic, swithc to look diuretic if more powerful agent required.

Question 10

what is the treatment for patients with left ventricular dysfunction but no edema?

Answer 10

ACE inhibitors (enalapril), ARB (losartan).

Question 11

what is the treatment for patient with edema ?

Answer 11

vasodilators (long-acting nitrates), diuretics

Question 12

what is the treatment for patients with excessive tachycardia?

Answer 12

low-dose-beta-blockers- but must be extremely cautious

Question 13

what is a cardiac glycosides (digoxin)

Answer 13

Used in patients who remain symptomatic following treatment or have CHF & atrial fibrillation or enlarged/ dysfunctional left ventricle

Question 14

what is the direct mechanism of of digoxin.

Answer 14

In cardiac muscle cells -> ^Na+ inside cells -> decrease in Ca2+ efflux out of cell -> ^ intracellular Ca2+ -> ^ interaction between actin and myosin -> ^cardiac contractility.

Question 15

what is the indirect mechanism of digoxin.

Answer 15

^ PSNS activity & decreased SNS activity from improved circulation -> decreased baroreceptor activation.

Question 16

how is digoxin dose controlled?

Answer 16

patients given large initial dose (digitalization) followed by daily maintenance dose. Maintenance dose adjusted for each individual via monitoring plasma digoxin levels.

Question 17

what is the toxicity of digoxin?

Answer 17

cardia toxicity: arrhythmias develop in patients with decreased with K+ level (from diuretics or diarrhea) can lead to tachycardia & fibrillation.
Quinidine reduces digoxin clearance -^ toxicity
GI: anorexia, nausea, vomiting and Diarrhea

Question 18

what is angina?

Answer 18

when coronary blood flow is insufficient -> O2 deprivation -> decrease in muscle strength -> acute heart failure.
muscle pain = angina

Question 19

what is angina pectoris

Answer 19

angina pectoris -> chest pain, caused by imbalance between O2 supply and demand.

Question 20

what is atherosclerotic angina pectoris?

Answer 20

-most common form
due to ‘irreversible’ atherosclerotic obstruction of coronary arteries
-precipitated by exertion

Question 21

what is vasospastic angina pectoris?

Answer 21

• spasm of part of coronary vessels

- can occur at any time

Question 22

what is unstable angina pectoris?

Answer 22

-atherosclerotic plaque + platelet aggregation + vasospasm

Question 23

how would you treat a decrease in O2 demand and an increase in O2 supply?

Answer 23

decrease by: decreasing HR/CO and PVR,

increase by O2 supply by: ^ coronary blood flow

Question 24

what is the pharmacokinetics mechanism of nitroglycerin?

Answer 24

its metabolized by liver, and therefore oral bioavailability low, multiple formulation available,

Question 25

what is the mechanism of nitroglycerin?

Answer 25

the nitrate group converted to NO -> ^ cGmp -> relaxation of smooth muscle cells in blood vessels = vasodilation.
this casues a decrease in venous return and PVR, and it dilated the coronary arteries.
there is a decrease in O2 requirement and ^ O2 delivery.

Question 26

what is the toxicity of nitroglycerin?

Answer 26

toxicity= hypotension, tachycardia, and headaches
tolerance= reduce effectiveness of same does following exposure to long acting nitrates.

Question 27

what is sildenafil?

Answer 27

inhibits phosphodiesterase therefore prevents breakdown of cGMP -> relaxation of smooth muscles.
potentiates effects of nitrates -> severe hypotension, myocardial infarction

Question 28

what is verapamil?

Answer 28

inhibits Ca2+ influx
=smooth muscle cells dilation,
= decrease in cardiac contractility

Question 29

what is the toxicities of verapamil?

Answer 29

cardiac depressions- can lead to bradycardia, heart failure, and cardiac arrest

Question 30

what are some examples of sympatholytics?

Answer 30

propranolol, metoprolol, they are beta-blockers, they decrease the rate and force of contraction of the heart, and thus decreases myocardial O2 requirements

Question 31

what is the clinical management of angina pectoris?

Answer 31

1. Acute attacks: subligual nitrates
2. maintenance monotherapy: hypertensive pareints- Ca2+ channel of beta blockers normotensive-long-acting-nitrate.
3. combination therapy: Ca2+ channel and beta-blockers