3.3.4. Positive Ionotropic Drugs Flashcards

1
Q

Cardiac performance is determined by what four factors?

A

preload, afterload, contractility, heart rate

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2
Q

what is another way to describe ‘contractility ‘?

A

“inotropic state”

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3
Q

list 5 things that can increase contractility

A
  • neural input (NE)
  • circulating catechols (Epi, NE)
  • Digoxin
  • (+) inotropic drugs
  • increased intracellular [Ca]
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4
Q

Acidosis, ischemia, (-) inotropic drugs, Ca-channel blockers, and beta-blockers all do what?

A

DECREASE contractility

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5
Q

what is cardiogenic shock?

A

When the blood pressure is too low to meet the needs of the vital organs due to cardiogenic pump failure
(inadequate CO)

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6
Q

two physiological factors that define cardiogenic shock

A

SBP < 100 mmHg; Cardiac Index < 1.8 L/min/m2

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7
Q

what are the symptoms of cardiogenic shock?

A

Poor urine output, cool extremities (due to vasoconstriction in an attempt to shunt more blood), confusion, and acidosis

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8
Q

of oral and IV agents, which do you use first? last?

A

Use oral agents FIRST when there is chronic heart failure with symptoms; IV agents are a last resort

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9
Q

list the two classes of sympathomimetic agents that can be used as positive inotropic agents

A

1) beta adrenergic AGONISTS; 2) catechols (NE, dopamine, dobutamine)

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10
Q

what other category of positive ionotropic agent inhibits intracellular enzymes?

A

phosphodiesterase (PDE) inhibitors - these guys prevent cAMP breakdown, allowing for a greater force of contraction

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11
Q

When might you PDE inhibitors for a patient w/heart failure?

A

If they’re on beta-blockers that aren’t showing any signs of improvement. (Recall that sympathomimetics - beta agonists - wouldn’t be logical to use if the beta blockers the Pt is on would counteract them anyway)

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12
Q

Describe the symptoms of cardiogenic shock for a Pt that would indicate the use of DOBUTAMINE

A

Asymptomatic, SBP 70-100 mmHg

AKA, mildly low BP with no symptoms

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13
Q

Describe the symptoms of cardiogenic shock for a Pt that would indicate the use of DOPAMINE

A

Symptomatic, SBP 70-100 mmHg

When symptoms exist, you need to give something with more alpha agonistic activity

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14
Q

Describe the symptoms of cardiogenic shock for a Pt that would indicate the use of NOREPINEPHRINE

A

SBP < 70 mmHG

NE has a slight reduction for cardiac arrhythmias

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15
Q

What are the dangers of using positive inotropic agents (other than digoxin)?

A

Because they increase mortality (arrhythmias, MI), you need to continually monitor the patient’s BP and evaluate ECGs.

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16
Q

describe the clinical uses of digoxin, and when it is indicated

A
  • Symptomatic CHF (in systolic dysfunction only; with or without atrial fibrillation)
  • Supraventricular arrhythmias (to control ventricular rate)
17
Q

what is a CONTRAINDICATION of digoxin (specifically relating to pharmacokinetics)?

A

because digoxin is eliminated by the kidney (some GI), anyone with HF likely has kidney problems as well. This can lead to digoxin toxicity

18
Q

what is a consideration you must take when administering digoxin?

A

Combining digoxin with any drug that decreases clearance, volume of distribution, or both, is extremely dangerous (puts the Pt in the toxic range).

For example: Propafenone, quinidine, verapamil, amiodarone

19
Q

what does taking digitalis/digoxin do for your patients in the long run?

A

It eventually restores the angiotensin-renin system and instead relies on increased contractility, i.e. inotropy. While it alleviates HF symptoms and keeps Pts out of the hospital, IT DOES NOT PROLONG LIFE

20
Q

Describe digoxin’s mechanism of action

A
  • digoxin blocks the Na-K-ATPase, causing an increase in cytosolic Na
  • the increase in intracellular [Na] prevents Ca efflux via the Ca-Na antiporter (because the Na gradient is equalized)
  • increased intracellular [Ca] causes increased contractility at the level of the sarcomere
21
Q

What are the ABSOLUTE contraindications of digoxin use?

A
  1. AV NODAL block is greater than first degree (don’t want to give a drug that makes conduction worse unless they have a pacemaker)
  2. Wolff-Parkinson-White (WPW) syndrome (will increase conduction through the “wrong” pathway, increasing the risk for severe arrhythmia)
  3. Hypertrophic or restrictive cardiomyopathy (Digoxin increases the tension in the heart)
  4. Cardiac amyloidosis
22
Q

What are the RELATIVE contraindications of digoxin use?

A

Renal insufficiency, hypokalemia, hyperthyroidism, acute coronary syndrome, normal systolic cardiac function

23
Q

list the signs of digoxin toxicity

A

Nausea, vomiting, diarrhea, Blurred vision, scotomas and yellow-green (halo) vision, Bi-directional VTach (doesn’t cause Torsades)

24
Q

How do you treat digoxin toxicity?

A

Stop the drug and admit for ECG monitoring.
Correct electrolytes (low [K+] or [Mg2+] common; high [K+] is more dangerous).
Give Fab Digibind, correct electrolytes, and MgSO4.
Cardioversion, calcium, CCB are relatively contraindicated.
Give Lidocaine and phenytoin if VTach seen.

25
Q

in two general situations, when is digoxin indicated?

A

Digoxin is used in symptomatic systolic dysfunction and poorly controlled atrial fibrillation

26
Q

in general, contractility and SV INCREASE with what four things?

A
  • Catecholamines (increase activity of the Ca++ pump in sarcoplasmic reticulum)
  • digitalis (increased intracellular Na+, causing increased intracellular Ca++)
  • decreased extracellular Na+
  • increased intracellular Ca++
27
Q

in general, contractility and SV DECREASE with what four things?

A
  • beta-1 blockade
  • heart failure
  • narcotic overdose
  • hypoxia/hypercapnia
  • acidosis