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Inotrope
ATRENDYNURSE
Inotrope
• An inotrope is an agent that alters the force or
energy of muscular contractions.
• Negatively inotropic agents weaken the force
of muscular contractions.
• Positively inotropic agents increase the
strength of muscular contraction.
Positive inotropic agents
• Positive inotropic agents increase myocardial
contractility, and are used to support cardiac
function in conditions such as decompensated
congestive heart failure, cardiogenic shock,
septic shock, myocardial infarction,
cardiomyopathy, etc.
Examples of positive inotropic agents
include:
• Calcium sensitisers
– Levosimendan
• Catecholamines
– Dopamine
– Dobutamine
– Epinephrine (adrenaline)
– Isoprenaline (isoproterenol)
– Norepinephrine (noradrenaline)
• Digoxin
• Phosphodiesterase inhibitors
– Milrinone
– Amrinone
Negative inotropic agents
• Negative inotropic agents decrease myocardial
contractility, and are used to decrease cardiac
workload in conditions such as angina. While
negative inotropism may precipitate or
exacerbate heart failure, certain beta blockers
(e.g. carvedilol, bisoprolol and metoprolol)
have been believed to reduce morbidity and
mortality in congestive heart failure.
Examples of negative ionotropic
agents
• Beta blockers (e.g. carvedilol, bisoprolol and
metoprolol)
• Calcium channel blockers
– Diltiazem
– Verapamil
Risks Benefits
Risks and Benefits of Inotropes
BENEFITS
• Improves cardiac
performance
• Improves contractility of
myocardium
• Increase blood pressure
RISK
• Increased heart rate causing
further deterioration of
failing heart pump
• Increases myocardial
oxygen requirements
• Potentially arrythmogenic
• Can increase ischaemia
DOBUTAMINE (Dobutrex)
Mechanism of action:-
Synthetic catecholamine.
Stimulates Beta 1 and Alpha-adrenergic receptors.
Increases myocardial contractility, stoke volume and
cardiac output.
Decreases preload and afterload (Vasodilatation)
Increase renal and mesenteric blood flow by increasing
cardiac output.
• Initial dose: -
2 to 3 mcg/kg/minute.
• Usual dose: -
2.5 to 10 mcg/kg/minute.
Maximum dose: -
20 mcg/kg/minute.
• Contraindication:-
Idiopathic, hypertrophic subaortic stenosis.
• Nursing implication: -
Monitor for hypertension, tachycardia, chest pain,
and premature ventricular contractions.
Monitor cardiac output, pulmonary artery pressure
ECG
Correct hypovolemia before treating with this drug.
Adverse effects:-
 Tachycardia
 Arrhythmias
 Blood pressure fluctuation
 Myocardial ischemia
DOPAMINE
A chemical precursor of epinephrine.
 Possessing alpha and beta and dopaminergic
receptor – simulating actions.
The specific effects are related to the dose
delivered.
LOW DOSE :- 0.5- 2mcg/kg/minute
(Dopaminergic effect).
Vasodilation of renal and mesenteric arteries.
Promote blood flow and increased GFR
(glomerular filtration rates in patients who
become resistant to diuretics).
Urine output may increase without significant
effect on blood pressure or heart rate.
INTERMEDIATE DOSE:- 2 to 10 mcg/kg/minute
Beta-adrenergic receptor activity is increased in
the heart.
Partial antagonism of alpha – adrenergic
receptors will mediate vasoconstriction.
Modest increase in systemic vascular resistance
increases cardiac output & CVP
Indication:-
 Renal protection.
 Hypotention/haemodynamic compromise due to MI,
trauma, sepsis, CCF.
 Increases mesenteric flow in mesenteric ischaemia.
Contraindication: -
Pregnancy.
Tachyarrhythmias.
Occlusive vascular disease.
Adverse effect:-
Tachycardia
Supraventricular tachycardia
Ventricular arrhythmias
Pulmonary congestion
Nausea
Vomiting
EPINEPHRINE
Mechanism of action: -
Stimulation of alpha and beta-adrenergic receptors causes
vasoconstriction.
Increases heart contractility and rate.
Causes bronchodilation.
Antagonizes histamine effect.
• Dosage: -
Initial dose 0.5-1mg IV.
Or
1.5-3mg via ETT.
Maintain drip of 1-4 mcg/minute. Titrate to BP.
Common contraindication: -
Hypertension.
Caution with heart failure angina and hyperthyroidism.
Adverse effects: -
Cardiac Arrhythmias
 Palpitations
Tachycardia
 Sweating
 Nausea and vomiting
Respiratory difficulty
Pallor
Dizziness
Weaknes
Nursing implication: -
Monitor ECG.
Observe for ventricular ectopy.
NOREPHINEPHRINE
Mechanism of action: -
Potent alpha – receptor antagonist, leads to arterial
and venous constriction.
Minimal effect on beta 2 receptors.
Increases myocardial contractility due to its beta 1
adrenergic effects.
Effective in septic shock and neurogenic shock after
adequate hydration.
 Initial dose: - 0.5 mcg/minute to 1 mcg/minute
Titrate to desired effect
 Average dose:-2 to 12 mcg/minute
Doses greater than 30 mcg/minute
might be required during shock.
Contraindications:-
Hypovolemic and cardiogenic shock (because potent
vasoconstriction is already occurring).
Pregnancy.
Hypoxia.
Hypovolemia secondary to fluid deficit.
Caution with hypertension and hyperthyroidism.
Nursing implication:-
Extravasations produces ischemic necrosis and sloughing
of superficial tissues.
Use of a central line is recommended due to the risk of
extravasations into surrounding tissue.
Rebound hypotension occurs if it is discontinued
abruptly.
Its use should be temporary.
Monitor for bradycardia or arrhythmias.
Isoprenaline
Has nearly pure beta-adrenergic receptor activity.
Increase heart rate and contractility and cause peripheral
vasodilation.
Used for temporary control of symptomatic bradycardia.
Increases myocardial oxygen requirements and the
possibility of inducing or exacerbating myocardial
ischemia is present.
The risk of arrhythmias is also increased.
It is not the first treatment of choice for bradycardias.
• Atropine, epinephrine or pacing should be
initiated first.
DOSE: -
 Initial dose of 2 mcg/minute
 Titrate dose to a maximum of 10 mcg/min. or heart rate
is 60 or greater.
 Decrease the rate if blood pressure is >120/60
 Decrease rate if PVC’s or Ventricular tachycardia is
noted.
Adverse effects: -
Arrhythmias.
Ventricular tachycardia.
Ventricular fibrillation.
Warning:-
 May exacerbate tachyarrhythmias due to digitalis toxicity.
 May precipitate hypokalemia.
DIGOXIN
Digoxin is the most commonly prescribed cardiac
glycoside
Convenient pharmacokinetics,
Alternative routes of administration
Widespread availability of serum drug level
measurement.
DIGOXIN ADMINISTRATION
Digoxin can be administered intravenously or orally.
DIGOXIN LOADING DOSE
 Loading doses of Digoxin range from 10 – 15mcg/kg.
 Digoxin can be given orally, but with a slower onset of
action and peak effect.
DIGOXIN MAINTENANCE DOSE:-
Initial therapy of Digoxin is usually started at 0.125 to
0.375mg/day.
NOTE: DRAW A SERUM DIGOXIN LEVEL AT LEST SIX
HOURS AFTER THE LAST DOSE!
SIDE EFFECTS ASSOCIATED WITH TOXICITY:-
 GASTROINTESTINAL: Anorexia, nausea, vomiting,
diarrhea Rare: abdominal pain, hemorrhagic
necrosis of the intestines.
 CNS: visual disturbances, (blurred or yellow vision),
headache, weakness, dizziness, apathy and psychosis.
 OTHER: Skin rash, gynecomastia
MILRINONE (Primacor)
 Milrinone is about 10 fold more potent than Amrinone.
 A positive inotropic agent that increases cardiac output
and decreases systemic vascular resistance.
 Because of its vasodilating effect, Milrinone is not
generally associated with an increase in myocardial
oxygen demand.
 Milrinone can be diluted in dextrose or saline solution.
LOADING DOSE:-
50 mcg/kg given IV over 10 minutes
MAINTENANCE DOSE:-
0.375 to 0.75 mcg/kg/minute
Warning; -
DOSES TO HIGH CONCENTRATION CAN CAUSE
HYPOTENSION AND TACHYCARDIA.
MILRINONE IS INCOMPATIBLE WITH
LASIX!
ADVERSE EFFECTS:
 Supraventricular tachycardia
 Ventricular arrhythmias
 Ventricular ectopy
 Increased ventricular rate in atrial
fibrillation/flutter
 Headache
 Hypokalemia
 Tremors
 Thrombocytopenia
CONCLUSION
Inotropes are very effective drugs when
administered properly.
Patients receiving inotropes should be
monitored closely including blood pressure,
cardiac monitoring, intake and output, and
laboratory tests that have been ordered by the
physician.
Knowledge of desired effects and side effects is
critical to the administration of inotropes.
I HAVE GIVEN YOU THE KEY
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Inotropic agents, or inotropes, are medicines that change the force of your heart's contractions.

  • 2. Inotrope • An inotrope is an agent that alters the force or energy of muscular contractions. • Negatively inotropic agents weaken the force of muscular contractions. • Positively inotropic agents increase the strength of muscular contraction.
  • 3. Positive inotropic agents • Positive inotropic agents increase myocardial contractility, and are used to support cardiac function in conditions such as decompensated congestive heart failure, cardiogenic shock, septic shock, myocardial infarction, cardiomyopathy, etc.
  • 4. Examples of positive inotropic agents include: • Calcium sensitisers – Levosimendan • Catecholamines – Dopamine – Dobutamine – Epinephrine (adrenaline) – Isoprenaline (isoproterenol) – Norepinephrine (noradrenaline) • Digoxin • Phosphodiesterase inhibitors – Milrinone – Amrinone
  • 5. Negative inotropic agents • Negative inotropic agents decrease myocardial contractility, and are used to decrease cardiac workload in conditions such as angina. While negative inotropism may precipitate or exacerbate heart failure, certain beta blockers (e.g. carvedilol, bisoprolol and metoprolol) have been believed to reduce morbidity and mortality in congestive heart failure.
  • 6. Examples of negative ionotropic agents • Beta blockers (e.g. carvedilol, bisoprolol and metoprolol) • Calcium channel blockers – Diltiazem – Verapamil
  • 8. Risks and Benefits of Inotropes BENEFITS • Improves cardiac performance • Improves contractility of myocardium • Increase blood pressure RISK • Increased heart rate causing further deterioration of failing heart pump • Increases myocardial oxygen requirements • Potentially arrythmogenic • Can increase ischaemia
  • 9. DOBUTAMINE (Dobutrex) Mechanism of action:- Synthetic catecholamine. Stimulates Beta 1 and Alpha-adrenergic receptors. Increases myocardial contractility, stoke volume and cardiac output. Decreases preload and afterload (Vasodilatation) Increase renal and mesenteric blood flow by increasing cardiac output. • Initial dose: - 2 to 3 mcg/kg/minute. • Usual dose: - 2.5 to 10 mcg/kg/minute. Maximum dose: - 20 mcg/kg/minute.
  • 10. • Contraindication:- Idiopathic, hypertrophic subaortic stenosis. • Nursing implication: - Monitor for hypertension, tachycardia, chest pain, and premature ventricular contractions. Monitor cardiac output, pulmonary artery pressure ECG Correct hypovolemia before treating with this drug. Adverse effects:-  Tachycardia  Arrhythmias  Blood pressure fluctuation  Myocardial ischemia
  • 11. DOPAMINE A chemical precursor of epinephrine.  Possessing alpha and beta and dopaminergic receptor – simulating actions. The specific effects are related to the dose delivered. LOW DOSE :- 0.5- 2mcg/kg/minute (Dopaminergic effect). Vasodilation of renal and mesenteric arteries. Promote blood flow and increased GFR (glomerular filtration rates in patients who become resistant to diuretics). Urine output may increase without significant effect on blood pressure or heart rate.
  • 12. INTERMEDIATE DOSE:- 2 to 10 mcg/kg/minute Beta-adrenergic receptor activity is increased in the heart. Partial antagonism of alpha – adrenergic receptors will mediate vasoconstriction. Modest increase in systemic vascular resistance increases cardiac output & CVP Indication:-  Renal protection.  Hypotention/haemodynamic compromise due to MI, trauma, sepsis, CCF.  Increases mesenteric flow in mesenteric ischaemia.
  • 13. Contraindication: - Pregnancy. Tachyarrhythmias. Occlusive vascular disease. Adverse effect:- Tachycardia Supraventricular tachycardia Ventricular arrhythmias Pulmonary congestion Nausea Vomiting
  • 14. EPINEPHRINE Mechanism of action: - Stimulation of alpha and beta-adrenergic receptors causes vasoconstriction. Increases heart contractility and rate. Causes bronchodilation. Antagonizes histamine effect. • Dosage: - Initial dose 0.5-1mg IV. Or 1.5-3mg via ETT. Maintain drip of 1-4 mcg/minute. Titrate to BP. Common contraindication: - Hypertension. Caution with heart failure angina and hyperthyroidism.
  • 15. Adverse effects: - Cardiac Arrhythmias  Palpitations Tachycardia  Sweating  Nausea and vomiting Respiratory difficulty Pallor Dizziness Weaknes Nursing implication: - Monitor ECG. Observe for ventricular ectopy.
  • 16. NOREPHINEPHRINE Mechanism of action: - Potent alpha – receptor antagonist, leads to arterial and venous constriction. Minimal effect on beta 2 receptors. Increases myocardial contractility due to its beta 1 adrenergic effects. Effective in septic shock and neurogenic shock after adequate hydration.  Initial dose: - 0.5 mcg/minute to 1 mcg/minute Titrate to desired effect  Average dose:-2 to 12 mcg/minute Doses greater than 30 mcg/minute might be required during shock.
  • 17. Contraindications:- Hypovolemic and cardiogenic shock (because potent vasoconstriction is already occurring). Pregnancy. Hypoxia. Hypovolemia secondary to fluid deficit. Caution with hypertension and hyperthyroidism. Nursing implication:- Extravasations produces ischemic necrosis and sloughing of superficial tissues. Use of a central line is recommended due to the risk of extravasations into surrounding tissue. Rebound hypotension occurs if it is discontinued abruptly. Its use should be temporary. Monitor for bradycardia or arrhythmias.
  • 18. Isoprenaline Has nearly pure beta-adrenergic receptor activity. Increase heart rate and contractility and cause peripheral vasodilation. Used for temporary control of symptomatic bradycardia. Increases myocardial oxygen requirements and the possibility of inducing or exacerbating myocardial ischemia is present. The risk of arrhythmias is also increased. It is not the first treatment of choice for bradycardias. • Atropine, epinephrine or pacing should be initiated first.
  • 19. DOSE: -  Initial dose of 2 mcg/minute  Titrate dose to a maximum of 10 mcg/min. or heart rate is 60 or greater.  Decrease the rate if blood pressure is >120/60  Decrease rate if PVC’s or Ventricular tachycardia is noted. Adverse effects: - Arrhythmias. Ventricular tachycardia. Ventricular fibrillation. Warning:-  May exacerbate tachyarrhythmias due to digitalis toxicity.  May precipitate hypokalemia.
  • 20. DIGOXIN Digoxin is the most commonly prescribed cardiac glycoside Convenient pharmacokinetics, Alternative routes of administration Widespread availability of serum drug level measurement. DIGOXIN ADMINISTRATION Digoxin can be administered intravenously or orally. DIGOXIN LOADING DOSE  Loading doses of Digoxin range from 10 – 15mcg/kg.  Digoxin can be given orally, but with a slower onset of action and peak effect.
  • 21. DIGOXIN MAINTENANCE DOSE:- Initial therapy of Digoxin is usually started at 0.125 to 0.375mg/day. NOTE: DRAW A SERUM DIGOXIN LEVEL AT LEST SIX HOURS AFTER THE LAST DOSE! SIDE EFFECTS ASSOCIATED WITH TOXICITY:-  GASTROINTESTINAL: Anorexia, nausea, vomiting, diarrhea Rare: abdominal pain, hemorrhagic necrosis of the intestines.  CNS: visual disturbances, (blurred or yellow vision), headache, weakness, dizziness, apathy and psychosis.  OTHER: Skin rash, gynecomastia
  • 22. MILRINONE (Primacor)  Milrinone is about 10 fold more potent than Amrinone.  A positive inotropic agent that increases cardiac output and decreases systemic vascular resistance.  Because of its vasodilating effect, Milrinone is not generally associated with an increase in myocardial oxygen demand.  Milrinone can be diluted in dextrose or saline solution. LOADING DOSE:- 50 mcg/kg given IV over 10 minutes MAINTENANCE DOSE:- 0.375 to 0.75 mcg/kg/minute Warning; - DOSES TO HIGH CONCENTRATION CAN CAUSE HYPOTENSION AND TACHYCARDIA.
  • 23. MILRINONE IS INCOMPATIBLE WITH LASIX! ADVERSE EFFECTS:  Supraventricular tachycardia  Ventricular arrhythmias  Ventricular ectopy  Increased ventricular rate in atrial fibrillation/flutter  Headache  Hypokalemia  Tremors  Thrombocytopenia
  • 24. CONCLUSION Inotropes are very effective drugs when administered properly. Patients receiving inotropes should be monitored closely including blood pressure, cardiac monitoring, intake and output, and laboratory tests that have been ordered by the physician. Knowledge of desired effects and side effects is critical to the administration of inotropes.
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