Exam II: CV Drugs Inotropes Flashcards by Linsley Lloyd

Q

Plant family from which many ___ ___are derived.

[Digitalis]

A

cardiac glycosides

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Q

Inotrope used for patients with ___ and to slow ventricular response of patients with ___(PAT, afib, aflutter).

[Digitalis]

A

congestive heart failure, supraventricular tachydysrhythmias

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Q

Digoxin decreases the risk of ___ due to heart failure, but increases the incidence of ___ ___(arrhythmias).
[Digitalis]

A

death, sudden death

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Q

Digoxin probably still plays a role in patients with ____ with evidence of congestion who are unable to tolerate ___ ___ of disease-modifying agents due to borderline blood pressure/renal function.

[Digitalis]

A

severe HF, high doses

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Q

Digoxin should be used with the aim of ___ ___ ___, while SDC and ___ and ___levels should be closely monitored to minimize the risk of toxicity.

[Digitalis]

A

reducing hospital readmissions, creatinine and potassium

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Q

In the treatment of SVT, ___ can be given in combination with a ___-___ at smaller doses of each and yet obtain more rapid control.

[Combination therapy]

A

digoxin, beta-antagonist

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Q

Contraindications:
Wolff-Parkinson-White – ___% develop ___ from increased ___ down the alternate path

[Combination therapy]

A

30, Vfib, conduction

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Q

Contraindications:
Hypertrophic cardiomyopathy (subaortic stenosis) –___

[Combination therapy]

A

increased obstruction with increased contractility

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Q

Contraindications:
Acute myocardial infarction – increase ___ ___ with increased ____
[Combination therapy]

A

oxygen demand, contractility

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Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

Digoxin has been shown to improve ____ without any benefit on _____.

A

morbidity
mortality

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Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

Digoxin may act by ____ sympathetic activity.

A

decreasing

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Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

Digoxin may not be effective in patients who have normal ___ ___ ____ function.

A

left ventricular systolic

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Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

The benefits of digoxin therapy are greatest in patients with ___ ___ ____, an enlarged heart and a ___ ___ ____ ____.

A

severe heart failure
3rd heart sound gallop

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Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

Digoxin may be used in patients with mild to moderate heart failure if they do not respond to an ___-___ ___ ___ or a ___ ____.

A

angiotensin-converting enzyme inhibitor
beta blocker

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Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

___ dosages of digoxin can be effective.

A

Low

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Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

___ function and possible ___ ____ must be considered in deciding on an appropriate dosage of digoxin.

A

Renal
drug interactions

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Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

In general, digoxin therapy should be _____ in the acute phase after myocardial infarction.

A

avoided

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Q

Digoxin MOA:
___ Effects
Inhibition of ______ ion transport system – causing increased Na inside the cell
Increased intracellular Na then affects the Na/Ca exchanger and ___ ____ is taken out of the cardiac cell.
More ___ inside the cell accounts for increased contraction force.

A

Direct
Na/K ATPase
less Ca++
Ca++

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Q

Decrease (less negative) resting membrane potential (automaticity)
Increases in the slope of phase 4 (automaticity)
Decrease in duration of action potential due to shortening of phase 2 (corresponds to vent contraction)

A

Decreased resting membrane potential (less negative) and increased automaticity are due to changes in the potassium gradient.

Phase 2 reflects closure of sodium ion channels and inward flux of calcium ions through specific slow calcium ion channels. Phase 2 corresponds to ventricular contraction.

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Q

Digoxin ANS activity -
Enhanced _____ activity
___ node activity decreased
Slowed conduction through the ___ node

A

PNS
SA
AV

(Enhanced PNS - activation of vagal nuclei and the nodose ganglion in the CNS. Results in slowed HR – especially with a fib)

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Q

Digoxin CV effects: Increased ____ ____, ____, decreased heart ____, ____, ______

A

myocardial contractility, SV
size, preload, LVED pressure

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Q

Digoxin CV: increased CO, ____ perfusion, and diuresis of newly ___ ____

A

renal
metabolized edema

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Q

Digoxin CV effects: Improved ____ perfusion, decreased _____ outflow, decreased ____ (____) leading to even better SV

A

tissue
sympathetic
SVR (afterload)

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Q

Digoxin CV: increased PNS activity, slowed HR - negative ____ and negative ____

A

chronotropic
dromotropic

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Digoxin CV: In the normal heart, increased contractility is offset by decreases in ___ and direct _____ in the arterial smooth muscle. Cardiac output may remain unchanged or even ____.

HR vasoconstriction decrease

Digoxin CV: In the failing heart, no change in HR with positive inotropic effects - decreased p____, a____, wall tension, and oxygen c_____.

preload, afterload consumption

Cardiac glycosides cause changes shown on the EKG: Prolonged ___ – delay through the AV node

PR

Cardiac glycosides cause changes shown on the EKG: Shortened QT – more rapid ____ ____

ventricular repolarization

Cardiac glycosides cause changes shown on the EKG: ___ segment depression – decreased slope of ___ ___

ST phase 3

Cardiac glycosides cause changes shown on the EKG: Smaller or inverted __ wave – decreased slope and duration of phases __ and __

T 2 and 3

Digoxin - Dose: Onset: Route: Clearance: Elimination 1/2 life:

Dose: up to 10 mcg/kg over 30 minutes Onset: 5 to 30 minutes Route: IV Clearance: 35% excreted daily via kidneys Elimination ½ life: 31-33 hours

Dig - Prolonged with ___ failure to up to ___ days

renal 4.4 days

Dig - ___% bound to protein (skeletal muscle) – decreased muscle mass in ___

25% elderly

Digitalis Toxicity: ____ therapeutic range 0.5 – 2.5 ng/ml

narrow TC says we dont need to know this range

Digitalis Toxicity: Incidence: __% of patients on digoxin will have some form of toxicity

20%

Digitalis Toxicity: MOA - inhibition of ____ ion transport system; Ca accumulates in the cell causing ____.

Na/K ATPase dysrhythmias

Digitalis Toxicity: Causes: most commonly ____ dysfunction; hypo____ (due to diuretic) increases myocardial ____ of drug (may also be due to hyperventilation); increased sympathetic activity related to hypo___; hyper____, hypo____, decreased muscle mass (elderly).

renal hypokalemia binding hypoxemia; hypercalcemia, hypomagnesia

Digitalis Toxicity: Hyperventilation related to hypokalemia – for every __ mm Hg decrease in PaCO2, serum potassium decreases an average of __ mEq/L On the other hand, increased serum potassium ___ ___ of cardiac glycosides to the ____ enzyme complex

10 0.5 inhibits binding Na-K ATPase

Digitalis Toxicity: Symptoms Arrhythmias – first symptom of arrhythmia is worsening of pre-existing CHF (8)

PVCs junctional tachycardia Wenckebach’s AV block sinus bradycardia or arrest atrial tachycardia – most common w dig toxicity bidirectional Vtach – two different foci Atrial flutter Vfib – most frequent cause of death with dig toxicity

Digitalis Toxicity: what one specific EKG change confirms toxicity?

No one specific EKG change confirms toxicity Increased automaticity, delayed AV conduction

Digitalis Toxicity: ____ symptoms seen most commonly in the elderly.

CNS

Digitalis Toxicity: GI symptoms -

Nausea and vomiting, diarrhea, increased salivation

Digitalis Toxicity: CNS symptoms. -

fatigue, confusion, delirium, blurred vision, green halos (CNS symptoms seen in elderly)

Digitalis Toxicity: Life-threatening ____ – with severe toxicity, related to paralysis of Na/K pump and leakage of ___ out of cell.

hyperkalemia K

Digitalis Toxicity: Treatment - ___ ____ unless most urgent until toxicity is corrected.

postpone case

Digitalis Toxicity: treatment - ___ digoxin

stop

Digitalis Toxicity: treatment - check _____

electrolytes

Digitalis Toxicity: Treatment - Correction of cause (hypo____, hypo____, arterial hypo____)

(hypokalemia, hypomagnesemia, arterial hypoxemia) *supplement K only after checking level

Digitalis Toxicity: Treatment - Anti-arrhythmic administration (3)

lidocaine, atropine, digibind Per Dr. Cahoon's notes: Lidocaine 1-2 mg/kg IV Phenytoin 0.5-1.5 mg/kg IV over 5 mins Atropine 35-70 mcg/kg IV Propranolol – suppress increased automaticity – but may increase AV node refractoriness

Digitalis Toxicity: Treatment - temporary ____ (complete ___ ___)

pacemaker AV block

Prophylactic Digitalis for Surgical Procedures: ___ ____, ____ signs of failure, the diagnosis of cause of arrhythmias might be muddy.

Healthy hearts, without (Events common under anesthesia that increase risks of toxicity – altered renal function, hyperventilation causing hypokalemia, increased sympathetic activity during anesthetic)

Prophylactic Digitalis for Surgical Procedures: Thoracic/abd surgery – in elderly patients, __ mg over ___ doses the day before and am of surgery decreased ___ incidence.

1 mg four doses SVT

Prophylactic Digitalis for Surgical Procedures: Cardiac disease – decreased incidence of ___ ____ ____ in patients with ___ during recovery

impaired cardiac function CAD

Prophylactic Digitalis for Surgical Procedures: ___ continue digitalis therapy esp. if for HR control

DO

Drug interactions with Digitalis: ______ – additive parasympathetic effect or cause dysrhythmias due to catecholamine release (theoretical)

Succinylcholine

Drug interactions with Digitalis: Beta-adrenergic ____ – (pavulon) – increased cardiac dysrhythmias.

agonists

Drug interactions with Digitalis: C____ ____ – dysrhythmias

Calcium IV

Drug interactions with Digitalis: Diuretics causing loss of K + lead to digitalis toxicity due to _____

hypokalemia

Drug interactions with Digitalis: Halothane – ______

Halothane – dysrhythmias

Drug interactions with Digitalis: F____, e____, i____ – decrease automaticity

Fentanyl, enflurane, isoflurane – decrease automaticity

Selective phosphodiesterase inhibitors (PDE III): non_____, non_____

Noncatecholamine, nonglycoside

Selective phosphodiesterase inhibitors (PDE III): MOA: decreased hydrolysis of ___ & ____, increasing the ___ & _____ in the myocardium and vascular smooth muscle

cAMP and cGMP cAMP and cGMP

Selective phosphodiesterase inhibitors (PDE III): Effect: ___ ____ effect with diastolic _____ and vascular smooth muscle _____

positive inotropic relaxation relaxation

Selective phosphodiesterase inhibitors (PDE III): clinical use: ___ ____ ____

Clinical use: acute cardiac failure

Selective phosphodiesterase inhibitors (PDE III): Increases cAMP, increases intracellular Ca and contractility in the myocardium In vascular smooth muscle, increased cAMP decreases intracellular Ca by facilitating the uptake of Ca into the ___ ____, leading to smooth muscle ____ & _____.

sarcoplasmic reticulum relaxation and vasodilation

Selective phosphodiesterase inhibitors - Amrinone: ____ effect and vaso____

Inotropic effect and vasodilation

Selective phosphodiesterase inhibitors - Amrinone: increases CO within __ ____

5 mins

Selective phosphodiesterase inhibitors - Amrinone: Initial dose ___-___ mg/kg IV, then infusion of __-__ mcg/kg/min

0.5-1.5 mg/kg IV 2-10 mcg/kg/min

Selective phosphodiesterase inhibitors - Amrinone: Side effect: ____ due to vasodilation, t______, dysrhythmogenic

hypotension thrombocytopenia

Selective phosphodiesterase inhibitors - Amrinone: Advantage: Safety with therapeutic index is 100:1 compared to 1.2:1 for ____ ____.

cardiac glycosides

Selective phosphodiesterase inhibitors - Milrinone (Primacor): ____ effect and vasodilation ____ effect on HR and myocardial oxygen consumption

inotropic little

Selective phosphodiesterase inhibitors - Milrinone (Primacor): Use: acute ___ ____ ____ after cardiac surgery; used in weaning from CBP

left ventricular dysfunction

Selective phosphodiesterase inhibitors - Milrinone (Primacor): Bolus ___ mcg/kg, infusion of ___ mcg/kg/min

50 0.5

Selective phosphodiesterase inhibitors - Milrinone (Primacor): __X the inotropic potency of amrinone w less side effects

30

Nonselective phosphodiesterase inhibitors - Inhibits all fractions of PDE isoenzymes __-__

I-V

Nonselective phosphodiesterase inhibitors - Theophylline: Uses: treatment of ____ (recommended to reserve the use of theophylline after beta2 agonists and corticosteroids have been tried)

bronchospasm

Nonselective phosphodiesterase inhibitors - Theophylline: Side effects: can cross ____, may relax ____ sphincter, narrow therapeutic range of __-__ mcg/ml; toxic effects: dysrhythmias

placenta GE 10-20

Nonselective phosphodiesterase inhibitors - Theophylline: Metabolism: liver metabolism negatively affected by ____, _____ or extremes of age; smoking (____ metabolism)

alcoholism, cimetidine smoking

Calcium: Inotropic effect of increased ___, decreased ____ pressure (especially in hypocalcemic)

SV LVED

Calcium: ___ and ___ decrease

HR and SVR

Calcium: Be careful when patient receiving digitalis and also _____; can cause arrhythmias

hypokalemic

Calcium: Uses: coming off ____ (cardioplegia with K, citrate in blood, sodium bicarbonate)

CPB

Calcium: CaCl contains more calcium than _____

CaGluconate

Calcium: ____ – effect

NMB increased contractility causes reflex decrease svr. "a number of signals (acetylcholine, bradykinin, calcium)" stimulate constitutive nitric oxide synthase in the endothelial cells of the vascular wall (which converts arginine to NO-->-->smooth muscle relaxation.)

Cardiac contractility (_____) is the intrinsic ability of the myocardium to pump in the absence of changes in preload or afterload. Contractility is related to the rate of myocardial muscle ____, which is, in turn, dependent on the ____ ____ _____ during systole. Increases in heart rate can also enhance contractility under some conditions, perhaps because of the increased availability of intracellular Ca2+.

inotropy shortening intracellular Ca++ concentration

Glucagon: ___ ___ produced in the pancreas

Polypeptide hormone

Glucagon: Stimulates the formation of ____

cAMP

Glucagon: Causes the release of ______ – secondary

catecholamines

Glucagon: Increases the contractility* and HR in the presence of ___ ____

beta blockers

Glucagon: Can cause tachycardia – significantly high enough to interfere with ___ and offsetting ability to increase ___

filling CO tachycardia esp if atrial fib

Glucagon: “In summary, the available evidence is against a positive inotropic effect of glucagon in the human heart. Thus, it should not be given as an inotropic agent for treating ___ ____ ___ ___ such as acute heart failure or cardiogenic shock. However, experimental and clinical evidence supports its positive _____ effect, which could prove useful for treating symptomatic bradycardia, particularly in cases of calcium or β-receptor antagonist overdose.”

low cardiac output states chronotropic

Glucagon: adult dose

1 – 5 mg rapid bolus

Glucagon: Elimination ½ time is ___-____

Elimination ½ time is 3-6 mins

Glucagon: side effects

May cause n & v, hyperglycemia, paradoxical hypoglycemia, hypokalemia

Glucagon: In smooth muscle, increased cAMP decreases intracellular Ca by facilitating the uptake of Ca into the ___ ____, leading to smooth muscle _____

sarcoplasmic reticulum relaxation

Methylene Blue: Potent inhibitor of ___ ___ (__) synthase in vascular endothelial cells; resulting in decreased ___ ____ and increased ____

nitric oxide (NO) NO release SVR

Methylene Blue: Binds to guanylate cyclase (GC) in the vascular smooth muscle – blocking ___ action in the ____ ___ ____

cGMP vascular smooth muscle

Methylene Blue: Useful in septic shock, endocarditis, transplant, protamine reaction, post ____ to counteract excessive ____ of vasoplegic syndrome

CPB vasodilation

Methylene Blue: dosing Bolus __ mg/kg over __ mins, followed by ____ mg/kg/hr if needed

Bolus 2 mg/kg over 30 mins, followed by 0.5-1 mg/kg/hr if needed