Cardiovascular Flashcards
The primary pathways by which the cardiovascular system can increase or decrease the
cardiac output include:
- Changes in heart rate
- Adjustments in myocardial contractility
- Optimization of vascular size
The physiological control is via
1. __________ sensors
2. _______ and ______ nervous system
3. ____-______-_______ system
The drugs often provide their effect via _______ or ________ these systems
The physiological control is via
1. Pressure sensors
2. Sympathetic and parasympathetic nervous system (SNS and PSNS)
3. Renin-angiotensin-aldosterone system (RAAS)
The drugs often provide their effect via stimulating or blunting these systems
The ANS regulates the cardiovascular system by adjusting:
* Heart rate –> ______ receptor
* Vascular volume –> ______ in vasculature
* Myocardial __________
The ANS regulates the cardiovascular system by adjusting:
* Heart rate –> Beta 1
* Vascular volume –> alpha in vasculature
* Myocardial contractility
The intrinsic heart rate is determined via _________ of both arms of the ______
The intrinsic heart rate is determined via blockade of both arms of the ANS
When an animal is at rest, the ______ system is likely dominant
→ The resting heart rate is ______ than the intrinsic heart rate
When an animal is at rest, the PSNS is likely dominant
→ The resting heart rate is lower than the intrinsic heart rate
Patients with heart failure often have higher ________ heart rates → ____ is likely dominant over the _____
Patients with heart failure often have higher resting heart rates → SNS is likely dominant over the PSNS
The sympathetic stimulation of cardiac muscle ________ the force of contraction
The sympathetic stimulation of cardiac muscle ↑ the force of contraction
A change in contractile strength that is independent of muscle _________ is referred to as a change in _________ or _________
A change in contractile strength that is independent of muscle length is referred to as a change in contractility or inotropy
In the presence of inotropic stimulation by the SNS, cardiac output is _________ over
the basal state
In the presence of inotropic stimulation by the SNS, cardiac output is enhanced over
the basal state
Parasympathetic nerves exert the effects on cardiac output by ________ heart rate
and with that _____ ventricular filling time
Parasympathetic nerves exert the effects on cardiac output by slowing heart rate
and with that ↑ ventricular filling time
Cardiac output: ________ of blood pumped each ________ by ____ ventricle
Cardiac output: volume of blood pumped each minute by one ventricle
List the organizations involved in classifying cardiac disease in dogs.
Comparing classes between institutions is pretty similar.
Recognize organizations and their classification. Associated clinical symptom of patient with stages, you can be more sure of the treatment to use.
What plant is pictured below?
Digitalis purpurea
Digoxin is derived from?
Derived from the purple foxglove plant (Digitalis purpurea)
In patients with failing heart, digitalis glycosides cause:
- It increases myocardial ________ (________)
- Increased cardiac _______
- Increased ______ with reduction of ______ secondary to a _______ in sympathetic tone
- _________ in heart rate
- No change in the myocardial _______ consumption
Digitalis glycosides: Digoxin
* It increases myocardial contractility (inotropism)
* Increased cardiac output
* Increased diuresis with reduction of edema secondary to a decrease in sympathetic tone
* Reduction in heart rate
* No change in the myocardial oxygen consumption
What is the MOA of digoxin?
Inhibition of Na+, K+-ATPase (sodium pump) in the cardiac myocytes
* The Na+, K+-ATPase is the cellular receptor for digitalis glycosides
* The ability of the pump to transport K+ inward and Na+ outward fails
* Increased Na+ intracellular augments transmembrane exchange of intracellular Na+ for extracellular Ca++ → increased intracellular Ca++
Increased Ca++ is stored in the sarcoplasmic reticulum
→ increases amount of Ca++ released by each action potential
Normally K+ comes in and Na+ out.
Digoxin: K+ won’t come inside the cell. Na+ will be more inside –> allow exchange with Ca ++.
Digoxin increases contractility in both _______ and ______ myocardium, but ouput of the ______ heart increases minimally
Digoxin increases contractility in both normal and failing myocardium, but output of the normal heart increases minimally
Digoxin also _______ increases ______ vagal tone (________ _________ effect) and decreases ________ nervous activity
Digoxin also indirectly increases efferent vagal tone (cholinergic parasympathomimetic effect) and decreases sympathetic nervous activity
Digoxin possesses negative _________ characteristics resulting from ________ stimulation
Digoxin possesses negative chronotropic characteristics resulting from parasympathetic stimulation
Digoxin is well absorbed after ______ administration → ______ > _______
Digoxin is well absorbed after oral administration → Elixir > tablets
The drug Digoxin is distributed _______ throughout the body
The drug Digoxin is distributed widely throughout the body
What is the most important route of elimination for Digoxin?
Urinary excretion is the most important route of elimination
Digitalis glycosides and their biotransformation products can follow the ____________ cycle
enterohepatic
- Digoxin is sufficiently absorbed by the oral route. The parenteral administration rarely used
- Digoxin is indicated in congestive heart failure → 0.005 - 0.02 mg/Kg q 12, dogs
- Supraventricular tachyarrhythmias → 0.0025 - 0.004 mg/Kg q 12, cats
- Dilated cardiomyopathy (DCM) → 0.005 - 0.008 mg/Kg q 12, dogs; 0.003 - 0.004 mg/Kg q
12, cats
dont study numbers
List the clinical signs of Digitalis toxicity.
In dogs, Digoxin concentrations from 0.8 to 2.4 ng/ml have been considered ___________,
whereas serum drug concentrations (SDCs) greater than 2.5-3 ng/ml are associated with
increased probability of _______
In dogs, Digoxin concentrations from 0.8 to 2.4 ng/ml have been considered therapeutic,
whereas serum drug concentrations (SDCs) greater than 2.5-3 ng/ml are associated with
increased probability of toxicosis
Dobutamine and dopamine are ____________ agents.
Sympathomimetic
Dobutamine
* It produces improvement in cardiac performance by binding ____ myocardial receptors. Through second messengers → increase ______cellular ________
* Dobutamine has a weak action on ____-receptors
* It has a very _______ half-life (1-2 min) → usually administered by ?
* The major indication → short term _____ in dogs and cats with _____ myocardial failure emergency
* Doses: 2.5 to 20 mcg/Kg/min in dogs; 0.5-5 mcg/Kg/min in cats
Dobutamine
* It produces improvement in cardiac performance by binding β1 myocardial receptors. Through second messengers → increase intracellular calcium
* Dobutamine has a weak action on α-receptors
* It has a very short half-life (1-2 min) → usually administered by constant-rate infusion (CRI)
* The major indication → short term inotropic in dogs and cats with acute myocardial failure emergency
* Doses: 2.5 to 20 mcg/Kg/min in dogs; 0.5-5 mcg/Kg/min in cats
Dopamine
* It has wide spectrum of effects. At intermediates dosages dopamine has positive effects on cardiac ________, heart ____, and cardiac _____ → 2 to 10 mcg/Kg/min
* Dopamine can only be administered ___ with a ____
* At low doses causes _______
* Activates ___ and ____ receptors
* Effects are always in sync with _____ used
Dopamine
* It has wide spectrum of effects. At intermediates dosages dopamine has positive effects on cardiac contractility, heart rate, and cardiac output → 2 to
10 mcg/Kg/min
* Dopamine can only be administered IV with a CRI
* At low doses causes vasodilation
* Activates beta and alpha receptors
* Effects are always in sync with amount used
___________ (Vetmedin®)
Agents that have both _________ and ______ ionotropic properties
* Pimobendan is an agent useful in the clinical management of canine heart failure caused by _____. Data on the use of pimobendan in _____ are limited
Pimobendan (Vetmedin®)
Agents that have both vasodilatory and positive inotropic properties
* Pimobendan is an agent useful in the clinical management of canine
heart failure caused by DCM. Data on the use of pimobendan in cats
are limited
What is the MOA of Pimobendan?
- Pimobendan increases the myocardial contractility by increasing affinity for Ca++
- It inhibits phosphodiesterase III (PDE III)→ responsible for vasodilating properties
Pimobendan
Pharmacokinetics
* The absorption is rapid after _____ administration
* Pimobendan is metabolized to an active metabolite → potent inhibitor of ____ ____
* It is excreted into ___, and eliminated in the _____
Pimobendan
Pharmacokinetics
* The absorption is rapid after oral administration
* Pimobendan is metabolized to an active metabolite → potent inhibitor of PDE III
* It is excreted into bile, and eliminated in the feces
What are the adverse effects of Pimobendan?
- Pimobendan is well tolerated in dogs
- At accidental overdosing, adverse signs are modest in severity
- The primary adverse effect are GI effects →reduced appetite, diarrhea
As for all positive inotropic agents, pimobendan is contraindicated in patients
with ?
outflow tract obstruction
Cytokines have been shown to depress ?
myocardial contractility
Elevated levels of circulating cytokines have been reported in patients with?
heart failure
List some examples of cytokines that are reported in patients with heart failure.
e.g.
* Tumor necrosis factor (TNF-α)
* Interleukin (IL-1β)
* Interleukin (IL-6)
The production of TNF-α, IL-1β, and IL-6 in the heart tissue was reduced
significantly by?
pimobendan
Pimobendan can only be given orally. This study showed how can we administerr it rectally. Consdering that if you are facing a patient that is in cirticaly stage and can be difficult to pill, did this studio and the most important thing they found is that for all the drugs, maybe you can find an IV presentation? But in the US there is no IV presentation for this drug. They found the amt of drug was similar and found metabolites in the serum. Importnat consideration: they have to give a little more amt of drug rectally than orally. normally 0.25 mg/kg ?
First pass metabolism: it is bypassed here, but they found a part of the rectum does not bypass first pass metabolism. The metabolite is active, Demethyol Pimobendan
What is the MOA of ACEIs?
when renin i released, angio converted into angio 1. ACE enzyme converts to angio 2. This is a situation that happens in our body and under normal condition, inder hypertensions and not heart failure, if we acauvate he sysem by heart failure it is bad for the patient
How is angiotensin II blocked?
remodeling, after some time heart has to change myocytes it has and the amt of ?????
ACEIs work on what stages of heart failure?
List the different types of Tachyarrhythmias
PE: Phenylephrine
