Cardio-Heartfailure Flashcards Preview

BIOM*3090. UOG > Cardio-Heartfailure > Flashcards

Flashcards in Cardio-Heartfailure Deck (31):
1

what are some typical causes of heart failure?

myocardinal damage
hypertension
infection
genetic/congenital
abnormality
chemical toxicity

2

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

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

3

how does the heart compensate for a decrease in CO?

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

4

what are some characteristics of a compensated heart?

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.

5

what is depompensated heart failure?

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

6

what is congestive heart failure (CHF)

decompensated heart +edema

7

what are the symptoms of CHF.

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

8

What are the treatment strategies for heart failure?

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

9

what is the treatment of mild heart failure?

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

10

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

ACE inhibitors (enalapril), ARB (losartan).

11

what is the treatment for patient with edema ?

vasodilators (long-acting nitrates), diuretics

12

what is the treatment for patients with excessive tachycardia?

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

13

what is a cardiac glycosides (digoxin)

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

14

what is the direct mechanism of of digoxin.

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

15

what is the indirect mechanism of digoxin.

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

16

how is digoxin dose controlled?

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

17

what is the toxicity of digoxin?

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

18

what is angina?

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

19

what is angina pectoris

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

20

what is atherosclerotic angina pectoris?

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

21

what is vasospastic angina pectoris?

- spasm of part of coronary vessels
-can occur at any time

22

what is unstable angina pectoris?

-atherosclerotic plaque + platelet aggregation + vasospasm

23

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

decrease by: decreasing HR/CO and PVR,
increase by O2 supply by: ^ coronary blood flow

24

what is the pharmacokinetics mechanism of nitroglycerin?

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

25

what is the mechanism of nitroglycerin?

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.

26

what is the toxicity of nitroglycerin?

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

27

what is sildenafil?

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

28

what is verapamil?

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

29

what is the toxicities of verapamil?

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

30

what are some examples of sympatholytics?

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

31

what is the clinical management of angina pectoris?

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