Positive inotropic medications

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Positive inotropic medications

Cardiovascular system

Antihypertensives

ACE inhibitors, ARBs and direct renin inhibitors

Thiazide and thiazide-like diuretics

Calcium channel blockers

Adrenergic antagonists: Beta blockers

Antianginals

cGMP mediated smooth muscle vasodilators

Calcium channel blockers

Adrenergic antagonists: Beta blockers

Antiarrhythmics

Class I antiarrhythmics: Sodium channel blockers

Class II antiarrhythmics: Beta blockers

Class III antiarrhythmics: Potassium channel blockers

Class IV antiarrhythmics: Calcium channel blockers and others

Lipid-lowering medications

Lipid-lowering medications: Statins

Lipid-lowering medications: Fibrates

Miscellaneous lipid-lowering medications

Positive inotropic medications

Positive inotropic medications

Assessments

Positive inotropic medications

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Positive inotropic medications

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Anti-digoxin Fab fragments p. 249

Digoxin p. NaN

antidote for p. 120

contractility effects of p. 292, 293

for dilated cardiomyopathy p. 317

sodium-potassium pump inhibition p. 47

therapeutic index of p. 235

toxicity treatment p. 363

Digoxin immune Fab p. 120

Vision change/loss

digoxin p. NaN

Transcript

Content Reviewers

Yifan Xiao, MD

Contributors

Kaia Chessen, MScBMC

Samantha McBundy, MFA, CMI

Maria Emfietzoglou, MD

Sam Gillespie, BSc

Positive inotropic medications, as their name implies, are a diverse group of medications that increase the strength of heart muscle contraction.

As a result, they increase the stroke volume and thus, the cardiac output.

Positive inotropic medications include cardiac glycosides, like digoxin; beta agonists, like dobutamine; and phosphodiesterase inhibitors, like milrinone.

They are used in conditions where the heart can’t pump enough blood to the body’s tissues, like in systolic heart failure.

Alright, the heart needs to squeeze out a certain volume of blood each minute, called the cardiac output, which can be rephrased as the heart rate multiplied by the stroke volume, which is the volume of blood squeezed out with each heartbeat.

Okay, now the stroke volume depends on the preload, or the amount of blood that returns to the heart; the afterload, or peripheral resistance; and the strength of the contraction, or contractility, of the cardiac muscle.

Now, muscle contraction is initiated with an action potential which modifies receptors allowing calcium ions to flow from the sarcoplasmic reticulum into the sarcoplasm.

This allows myosin heads to bind to the actin.

These two proteins are ultimately responsible for cell contraction.

In order for a muscle to relax, calcium ions must be pumped back into the sarcoplasmic reticulum.

When the frequency of stimulation is increased, more calcium ions accumulate in the sarcoplasm, and the strength of contraction increases.

Alright, now there are conditions in which the strength of the heart’s contraction is impaired, and the heart can’t pump out enough blood to meet the body’s demands, this is called heart failure.

Summary

Positive inotropic medications are medications that increase the force of muscle contraction of the heart, resulting in an increased cardiac output. Examples of positive inotropic medications include digoxin, dobutamine, and milrinone. These medications are generally used to treat systolic heart failure, cardiogenic shock, and other heart-related conditions.

Sources

  1. "Katzung & Trevor's Pharmacology Examination and Board Review,12th Edition" McGraw-Hill Education / Medical (2018)
  2. "Rang and Dale's Pharmacology" Elsevier (2019)
  3. "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)
  4. "Digoxin in Heart Failure with a Reduced Ejection Fraction: A Risk Factor or a Risk Marker?" Cardiology (2016)
  5. "Inotropic agents and vasodilator strategies for the treatment of cardiogenic shock or low cardiac output syndrome" Cochrane Database of Systematic Reviews (2018)
  6. "Treatments targeting inotropy" European Heart Journal (2018)
  7. "Therapeutic achievements of phosphodiesterase inhibitors and the future" European Heart Journal (1989)
Elsevier

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