Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHARMACOLOGY - 2 > 15a – Cardiovascular Pharmacology > Flashcards

15a – Cardiovascular Pharmacology Flashcards

1
Q

Hemodynamic considerations for heart failure: preload

A

-pressure form venous system
o Needs to be sufficient to fill R. and L. side of heart
o *need a MINIMUM
o Don’t want too much=excessive amount of blood (stretch too much and weaken muscles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hemodynamic considerations for heart failure: afterload

A

-pressure in arteries
o If too constricted=more difficult to generate enough pressure to push the blood forwards
o Want to try and reduce it so blood can be pushed out with reduced workload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

2 types of cardiomyopathy

A
  • Hypertrophic cardiomyopathy
  • Dilated cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hypertrophic cardiomyopathy

A
  • Most common form of heart failure in CATS
  • *lots of muscle that can generate lots of FORCE but volume in chamber is smaller and walls can be STIFFER (lower preload)
  • *want to try and relax the muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Dilated cardiomyopathy

A
  • Most common form of heart failure in DOGS
  • Certain breeds predisposed (ex. Boxers)
  • Cats develop it if diet low in taurine (not seen often anymore)
  • Grain-free diets? (no genetic component)
  • *Sarcomeres are added in series=large ventricle that is thinner=can not generate as much FORCE
    o NEED TO MAKE IT GENERATE MORE FORCE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cardiac insufficiency/failure due to

A
  • Reduced SV or CO secondary to other reasons
  • Abnormal rates (bradycardia, tachycardia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are reasons that SV or CO may be reduced? (causing cardiac failure)

A
  • Reduced preload (hypovolemia, hypertrophic cardiomyopathy or pericardial effusion)
  • Impaired contractility (dilated cardiomyopathy)
  • Increased afterload (severe hypertension, aorta/pulmonic stenosis)
  • Inadequate valve function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is something that can cause bradycardia?

A
  • Third degree AV block
    o Excitations not going through
  • *decreased HR=CO can’t be high enough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some things that can cause tachycardia?

A
  • Atrial fibrillation
  • Ventricular tachycardia
  • *no longer ADAPTIVE: even though increased HR, getting decreased SV and CO will be decreased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Heart failure symptoms: chronic

A
  • Cardiomegaly
  • R. vs. L. ventricular failure
  • *failure on one side eventually leads to failure on OTHER SIDE
  • Arrhythmias (especially tachycardia): risk of SUDDEN death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

L. ventricular failure symptoms

A
  • Blood accumulates in lungs
  • Pulmonary edema
  • Poor peripheral perfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

R. ventricular failure symptoms

A
  • Leads to edema in venous side
  • Subcutaneous edema
  • Ascites (make them have a lower appetite: cachexia)
  • Hepatojugular reflex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Consequences, complications and compensations in heart failure: IN THE HEART

A
  • Decrease contractility or reduced SV=insufficient CO
    o Decrease BP=decrease baroreceptor activity (less stretch)=increase sympathetic activity (decrease PS stimulation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Consequences, complications and compensations in heart failure: increased S leads to

A

o Vasoconstriction=increase TPR=increased afterload=more work heart needs to do
 *makes situation worse (normally would fix BP in an acute response)
o Increases HR and contractility
 *makes situation worse)
o Increase ADH=increase blood volume=venous pressure=return to ventricles (OVERFILLING: forcing it to work harder!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Consequences, complications and compensations in heart failure: decreased renal blood flow

A

o Increase renin (S stimulation also contributes)=activation of RAAS cascade
 Vasoconstrict=increase afterload
 Increased ADH
 *increased aldosterone: retain more Na and expand blood volume=even more into the failing heart to work more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

If too high HR

A
  • Tachycardia
  • Can’t fill enough during diastole
  • Handled better in dilated vs. hypertrophic cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some positive inotropic agents?

A
  • Pimobendan (‘inodilator’)
  • Digoxin
  • Dobutamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pimobendan (‘inodilator’)

A
  • Phosphodiesterase inhibitor (relative of Viagra)
  • Positive inotrope (increase contractility) and arterial VASODILATOR
  • May enhance sensitivity of cardiac contractile proteins to calcium
  • Induces ‘well-being’ and INCREASES appetite
  • **Shown to increase survival in dogs with DCM or mitral valve insufficiency (double or triple)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pimobendan actions in heart (cardiomyocyte)

A
  • Accumulation of cAMP=increase sensitivity of contractile elements to Ca2+
  • *mimics beta-1 adrenergic receptor like effect in all cardiomyocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Pimobendan actions in vascular smooth muscle (arteriol size)

A
  • Accumulation of cAMP(cGMP)=vasodilation=reduce peripheral resistance=decreased afterload
  • *Decreases work that the heart needs to do to get a good SV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Digoxin

A
  • Digitalis glycosides isolated from FOXGLOVE
  • Inhibits Na/K ATPase (want PARTIAL INHIBITION)
  • Positive inotropic effect
  • Negative chronotropic (decrease HR) and dromotropic (decrease speed on conduction) effect
  • *one of most highly TOXIC drugs used clinically
  • Secondarily: leads to increased peripheral tissue perfusion (Ex. increased renal output)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Digoxin actions on cardiomyocytes

A
  • Inhibits Na/K pump=increased Na inside
  • Excess Na removed by Na/Ca exchanger=working harder=more Ca inside
  • *Ca-induced Ca release=more Ca=enhanced contraction
  • SECONDARY EFFECT OF INCREAED CALCIUM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Na/K pump role in cardiomyocytes

A
  • Maintain resting membrane potential
  • *can NOT inhibit them all
    o Why digoxin can be toxic
24
Q

Digoxin actions in conductor cells and Purkinje fibers

A
  • Decrease conduction velocity
  • Increased refractory period
    o Take longer to ‘reset’ resting membrane potential (Na/K pumps)
  • *more difficult to spread excitation
25
Q

Digoxin actions on baroreceptor reflex

A
  • Enhanced sensitivity to stretch=decrease sympathetic activation
    o GOOD: no overactivation of sympathetic in heart failure
26
Q

Digoxin vs. Pimobendan

A
  • Cheaper, but does NOT
    o Improve appetite
    o Increase survival
  • “reduces effects’
27
Q

Other good effects of Digoxin

A
  • Increased PS tone
  • Decreased S tone (baroreceptor: sense increased stretch more easily)
28
Q

Side effects of Digoxin

A
  • Death
  • Anorexia (CNS effects)
  • Vomiting and diarrhea
  • AV block or ventricular arrhythmias
  • *Hypokalemia can precipitate arrhythmias
  • **follow up after putting an animal on it
29
Q

Hypokalemia and arrhythmias even in absence of Digoxin

A
  • no K to exchange for Na in the cell=’inhibiting/reducing’ Na/K pump ability to function
30
Q

What blocks Digoxin effects?

A
  • Hyperkalemia
    o K is ‘forced’ into cells=more Na can be exchanged than normal
    o *would take a lot more Digoxin to overcome the force
  • *NEED a balance of K in the body (hypo- and hyper- kalemia are NOT great)
31
Q

Dobutamine (or Dopamine)

A
  • Beta1 and beta2 agonist
  • Emergency use only:
    o ARRHYTHMOGENIC=more likely to get an arrhythmia
    o Get heart working well enough to get blood around (also then give diuretics to get rid of edema)
  • Exerts positive inotropic actions via beta1-adrenergic receptor AGONIST action
32
Q

Dobutamine effects on cardiomyocyte

A
  • Increase beta1 adrenergic receptor response=increase cAMP=increase
  • *if use dopamine=increase renal blood flow as well
33
Q

When are beta-blockers useful in heart failure?

A
  • Chronic treatment of hypertrophic cardiomyopathy
  • *both in HCM and CM due to INHIBITION of beta1 stimulated renin release
    o Prevent RAAS and expansion of blood volume=reduces preload
  • Ex. used in cats
34
Q

Why are beta-blockers useful in chronic treatment of HCM?

A
  • Positive inotropes generally contraindicated
  • Often HR so high and heart wall so rigid that diastolic filling is IMPAIRED
  • *blocks effects of compensatory overactivation of heart by SNS
    o Try and reduce HR: allow more filling in diastole
35
Q

What beta-blockers are preferable and what is an example?

A
  • Beta1 selective antagonists
  • Ex. metoprolol (particularly in asthmatic patients)
36
Q

What is an example of a mixed beta1 and alpha1 antagonist?

A
  • Carvedilol
  • Alpha1 inhibition=reduces afterload=better for heart to function and provide adequate CO
  • HCM and DCM
  • *increasingly being used
37
Q

When do you use Digoxin?

A
  • Heart failure
  • Atrial fibrillation
38
Q

Digoxin for atrial fibrillation

A
  • Impairs ability of resting membrane to recover
  • *profound affect to block AV node
39
Q

What are 2 main types of vasodilators?

A
  • ACE inhibitors
  • Angiotensin type 1 receptor antagonists
40
Q

ACE inhibitors

A
  • Enalapril, benazepril, or imidipril
  • *prevent formation of Ang II from Ang I by inhibiting angiotensin converting enzyme (ACE)
41
Q

Angiotensin type 1 receptor (ARBs) antagonists

A
  • Valsartan or telmisartan
  • Block Ang II actions!
42
Q

Both ACE inhibitors and AT1 receptor blockers

A
  1. Cause vasodilation: reduce venous and arterial pressure, therefore edema
  2. Prevent aldosterone release: decrease fluid retention/edema
    *when get rid of edema=alleviate distress syndromes=improves quality of life
43
Q

Enalapril (ACE inhibitor)

A
  • show to significantly decrease clinical symptoms
  • extend survival time by 92% in dogs
44
Q

RAAS system: different drug actions

A
  • stop the whole pathway=beta-adrenergic receptor antagonists in kidneys
  • ARBs: prevent Ang II actions (no aldosterone or vasoconstriction)
  • ACE: prevent getting Ang II and also break down of bradykinin (leads to more vasodilation)
45
Q

Side effect of ACE inhibitors (humans for sure, maybe dogs+cats?)

A
  • Tickle cough can develop within first few weeks
  • *due to increased Bradykinin
  • Animals: need to distinguish between cough they get from heart failure (PRODUCTIVE COUGH: removing fluid from lungs) OR if sudden (NON-PRODUCTIVE COUGH)
46
Q

What are some other vasodilators that can be used for acute treatment and/or in severe cases?

A
  • Nitroglycerin
  • Sodium nitroprusside
  • *both are broken down into NO! (NO dilates all vasculature)
47
Q

Nitroglycerin

A
  • Venodilator
48
Q

Sodium nitroprusside

A
  • Arteriolar and venodilator
49
Q

What are some other vasodilators that are older (but cheap)?

A
  • Alpha-blockers: proazosin (mainly arteriolar, some venodilation)
  • Direct acting arteriolar dilators: hydralazine (veno and arteriolar dilator)
    o Decrease Ca=decrease contraction
50
Q

All vasodilators (except the main ones) may cause (LONG TERM)

A
  • Excessive hypotension
  • Reflex tachycardia
  • Activation of RAAS system
    *worsen situation
51
Q

Nitro-vasodilators

A
  • Have what could become an NO groups
  • *rapidly metabolized in vascular space to free NO!
    o NO bypasses endothelium and goes into vascular smooth muscle=increase cGMP=vasodilation
  • *especially venodilation!
52
Q

Nitroprusside caution!

A
  • Also has cyanide!
    o Over a certain amount of time can limit ability to use it
  • *don’t be afraid of it: just don’t use long term (no more than a couple days!)
53
Q

Example: if taken a drug (ex. Sildenafil or Viagra) that inhibits phosphodiesterase, and take a nitro-vasodilator

A
  • *massive vasodilation effects! (coming from 2 streams!)
54
Q

Diuretics in heart failure therapy

A
  • Treatment of pulmonary edema
    *want to get ride of excessive fluid, but NOT dehydrate the animal
55
Q

When using diuretics in heart failure therapy beware of

A
  • excessive diuresis leading to EXCESSIVE LOSS OF VENOUS RETURN
  • HYPOkalemia potentiating digoxin action

PHARMACOLOGY - 2 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions