The document discusses various inotropic agents used to increase the force of cardiac muscle contractions including cardiac glycosides like digoxin, sympathomimetic drugs such as epinephrine, dopamine, and dobutamine, and phosphodiesterase inhibitors like amrinone. It provides details on the mechanisms of action, dosages, administration, and side effects of these different classes of inotropic drugs used to enhance cardiac contractility and output in patients with heart failure or shock.
This document discusses various inotropes and vasoactive agents used to support hemodynamics. It describes the classification of agents as inotropes, chronotropes, vasopressors, or vasodilators. Key agents covered include dopamine, dobutamine, adrenaline, noradrenaline, milrinone, vasopressin, nitroglycerine, and sodium nitroprusside. For each agent, the document discusses receptor physiology, hemodynamic effects, indications, dosing, side effects, and monitoring considerations. It concludes with describing a vasoactive inotrope score used to quantify cardiovascular support.
Noradrenaline is used to treat hypotension, bronchospasm, and cardiac arrest. It works by causing smooth muscle relaxation in the airways and contraction in the arterioles and increasing cardiac contractability. The document provides formulas for calculating infusion rates of various inotropes like noradrenaline, dopamine, dobutamine, and nitroglycerin based on desired dose, patient weight, and drug concentration. Potential adverse effects include hypertension, bradycardia, and arrhythmias. When administering inotropes, nurses must follow ten rights, continuously monitor blood pressure and ECG, and be aware of drug interactions and precautions.
This document discusses inotropic agents, which are drugs that affect the strength of contraction of the heart muscle. It describes positive inotropes that increase contraction and negative inotropes that decrease contraction. The choice of inotrope depends on its pharmacological effects and the specific cardiovascular condition. Positive inotropes discussed include calcium, calcium sensitizers like levosimendan, catecholamines, cardiac glycosides, and others. Negative inotropes include beta blockers, calcium channel blockers, and antiarrhythmics. The mechanisms and effects of various catecholamines like dopamine, dobutamine, epinephrine, and dopexamine are also outlined.
The term inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle (myocardial contractility). However, it can also refer to pathological conditions. For example, enlarged heart muscle (ventricular hypertrophy) can increase inotropic state, whereas dead heart muscle (myocardial infarction) can decrease it.
Dobutamine is a positive inotropic drug that acts directly on cardiac beta-1 receptors to increase myocardial contractility and enhance stroke volume, resulting in increased cardiac output and decreased pulmonary capillary wedge pressure within 1-2 minutes. Common adverse reactions include nausea, headache, respiratory distress, angina, palpitations, tachycardia, hypertension and ventricular ectopic beats. Dobutamine is contraindicated in atrial fibrillation, ventricular arrhythmias and phaeochromocytoma.
Noradrenaline is a potent vasoconstrictor used to treat profound hypotension, usually in combination with dopamine, when other inotropes have failed in sepsis patients. It is administered by IV infusion at an initial dose of 0.05-0.1 microgram/kg/minute, titrated up to a maximum of 1-1.5 microgram/kg/minute. The drug comes in 2mg/2mL ampoules and is diluted for infusion based on the baby's weight to achieve a rate of 0.1 microgram/kg/minute, administered over 24 hours and monitored for potential side effects like hypertension and local tissue damage from extravasation.
THE USE OF INOTROPIC DRUGS IN CARDIAC SURGERYThierry Yunishe
This document provides information on various inotropic drugs used in cardiac surgery, including their indications, mechanisms of action, dosages, and side effects. It discusses sympathomimetic drugs like dopamine, dobutamine, and adrenaline that have positive inotropic effects by stimulating cardiac contraction directly. It also mentions the negative inotrope propranolol and vasopressors like adrenaline and noradrenaline. The aim of using inotropes in cardiac surgery is to optimize cardiac output while using the minimum effective dose to achieve desired outcomes and allow weaning off the drugs.
This document summarizes several vasopressors and inotropes used to treat hypotension including dopamine, adrenaline, noradrenaline, phenylephrine, vasopressin, dobutamine, and milrinone. It describes their mechanisms of action, metabolism/excretion, indications, dosing, and potential adverse effects. Dopamine is recommended for hypotension due to conditions like heart failure or trauma. Noradrenaline is first-line for septic shock. Dobutamine is used for cardiogenic shock or septic shock with myocardial dysfunction. Milrinone has inotropic and vasodilatory properties but is not recommended for septic shock.
Dopamine and dobutamine are endogenous catecholamines used to increase cardiac output and blood pressure. Dopamine acts through dopamine, adrenergic, and beta receptors. At low doses it increases renal blood flow but at higher doses causes vasoconstriction. Dobutamine is a synthetic catecholamine that directly stimulates beta receptors, increasing contractility and output while causing vasodilation. Both are given by continuous IV infusion and used to treat shock, heart failure, and hypotension. Side effects include arrhythmias for dopamine and hypertension for both.
Vasopressors are drugs that induce vasoconstriction and elevate blood pressure. This document discusses the history, physiology, classification, and pharmacology of various vasopressors used in the ICU setting. It describes how vasopressors act on different adrenergic receptors to increase blood pressure by either increasing cardiac output, systemic vascular resistance, or both. The document reviews commonly used vasopressors like norepinephrine, epinephrine, dopamine, phenylephrine, dobutamine, and ephedrine - outlining their indications, mechanisms of action, pharmacokinetics, and adverse effects.
Amiodarone is a potent antiarrhythmic agent that is used as a first-line treatment for cardiac arrest due to refractory ventricular fibrillation or pulseless ventricular tachycardia. It works by prolonging the action potential in cardiac tissues through its effects on sodium, potassium, and calcium channels. For stable wide-complex tachycardia with a pulse, amiodarone is administered in doses of 150mg over 10 minutes, which can be repeated if needed. For ventricular fibrillation or pulseless ventricular tachycardia, the initial dose is 300mg administered via IV push, which can be repeated at 150mg if there is no response.
Digoxin & Nitroglycerin by Dr. Sanaullah Aslam (Complete)Sanaullah Aslam
Digoxin is a drug derived from foxglove that increases the strength of heart contractions and regulates heart rhythm. It is used to treat heart failure and abnormal heart rhythms. Digoxin works by increasing the amount of calcium available to heart muscles to improve contraction. Common side effects include nausea, vomiting, and heart palpitations. In cases of toxicity, treatment includes administering digoxin immune fab to remove digoxin from the bloodstream.
Nitroglycerin is a vasodilator that relaxes blood vessels. It is used to treat angina by dilating coronary arteries and reducing the workload on the heart. Nitroglycerin is administered sublingually as a tablet or spray for
1) The document provides information on inotropes and vasopressors including their classification, sites of action, clinical effects, indications, and doses. It discusses catecholamines like adrenaline, noradrenaline, dopamine, and dobutamine. It also covers phosphodiesterase inhibitors, vasopressin, ephedrine, metaraminol, phenylephrine, methoxamine, and digoxin.
2) The document concludes with recommendations on first and second line vasopressor/inotropic agents for different clinical situations like septic shock, heart failure, cardiogenic shock, anaphylactic shock, and anesthesia-induced hypotension.
New pharmocological agents in the management of angina nicorandilJerin Kuruvilla
Nicorandil is a potassium channel activator used to treat angina. It works by dilating both epicardial coronary arteries through its nitrate-like properties as well as peripheral coronary arterioles through potassium channel activation. This dual mechanism of action decreases myocardial oxygen demand and increases supply. Nicorandil has been shown to be effective in treating stable and unstable angina, improving outcomes in acute myocardial infarction when administered before reperfusion, and preventing the no-reflow phenomenon during percutaneous coronary intervention. It provides cardioprotection through ischemic preconditioning with a good safety profile.
This document discusses vasoactive drugs, which affect vasomotor tone by causing vasoconstriction or vasodilation. It describes several classes of vasoactive drugs including vasodilators like hydralazine and nitroglycerin that work by different mechanisms in the arteries and veins. Vasoconstrictors like phenylephrine and vasopressin are also discussed. Many vasoactive drugs have direct effects on the heart by acting on receptors in the cardiovascular system. Inodilators like milrinone cause both vasodilation and increased cardiac contractility. Specific drugs such as dopamine, norepinephrine, and epinephrine are explained in terms of their vascular and cardiac effects.
Dobutamine and dopamine are commonly used inotropic agents that increase cardiac output by increasing stroke volume, though dopamine can increase afterload at higher doses. Epinephrine and norepinephrine also increase contractility through beta-1 agonism but have greater vasopressor effects. Dobutamine is preferred over dopamine when treating cardiogenic shock due to its more predictable cardiac effects. In septic shock, dobutamine with norepinephrine is recommended to increase cardiac output while maintaining blood pressure, though epinephrine is an alternative. The effects of inotropes on tissue oxygen utilization must also be considered, as agents like dopamine may impair splanchnic perfusion despite increasing cardiac output.
This document summarizes various inotropic drugs used to increase cardiac contractility including cardiac glycosides like digoxin, catecholamines like dopamine and dobutamine, phosphodiesterase inhibitors like milrinone, and calcium sensitizers like levosimendan. It provides details on their mechanisms of action, pharmacokinetics, uses, dosages, and side effects. The document focuses on the inotropic and hemodynamic effects of these drugs and their roles in treating low cardiac output states and heart failure.
Digoxin is a cardiac glycoside that has positive inotropic effects on the heart, increasing the force of contraction and maintaining stroke volume even at high impedance. It slows heart rate by increasing vagal tone through reflex and direct stimulation of the vagus nerve and sensitization of the SA node. It also has direct depressant effects on the SA and AV nodes. Digoxin increases excitability and conduction time in the AV node while reducing the effective refractory period of ventricles. It can cause ECG changes like decreased T wave amplitude, increased PR interval, and ST segment depression. Side effects include cardiac arrhythmias if potassium is low.
This document provides information on various drugs used in emergency situations:
- Oxygen is essential to prevent brain death within 6 minutes of hypoxia. The ideal oxygen saturation is 95% or higher.
- Nitroglycerin is a vasodilator used for angina and myocardial infarction. Morphine sulfate is used for chest pain associated with myocardial infarction.
- Atropine sulfate, isoproterenol, and epinephrine are used to treat bradycardia, asystole, AV block, and hypotension.
- Sodium bicarbonate is used for acidotic states from cardiac arrest. Antiarrhythmics include adenosine, amiodarone,
Nitroglycerin is a vasodilator used to treat angina pectoris, heart failure, and myocardial infarction. It works by relaxing blood vessels, reducing the workload on the heart. It is rapidly absorbed through the skin or oral mucosa and has a quick onset of action within 1-3 minutes. Nitroglycerin is administered sublingually for acute angina attacks or before exertion. It can also be given intravenously to treat heart attacks or control blood pressure during surgery. Common side effects include headaches, dizziness, and hypotension.
The document discusses various inotropic agents used to increase the force of cardiac muscle contractions. It describes three main classes of inotropes - cardiac glycosides like digoxin, sympathomimetics like dopamine and dobutamine, and phosphodiesterase inhibitors like amrinone. For each drug, it provides details on mechanisms of action, dosages, administration, indications, contraindications, side effects and nursing considerations. The document provides an in-depth review of inotropic drugs used clinically to enhance cardiac contractility and output.
This document discusses various inotropic agents used to increase the contractility of the heart. It describes the mechanisms and indications for commonly used inotropes including digitalis glycosides like digoxin, sympathomimetics like dopamine and dobutamine, and phosphodiesterase inhibitors like amrinone. It provides dosing guidelines and lists potential adverse effects and nursing considerations for each type of inotrope.
This document discusses the adrenergic system including adrenoceptor physiology, adrenergic agonists and antagonists. It describes the different types of adrenoceptors (alpha and beta), their locations and responses. It then discusses various adrenergic agonists like epinephrine, norepinephrine, phenylephrine, clonidine and dexmedetomidine and provides their mechanisms of action and dosages. Finally it covers various adrenergic antagonists like phentolamine, labetalol, esmolol, metoprolol and propranolol, describing their receptor selectivities, durations of action and dosages.
Dopamine is a chemical precursor of norepinephrine that stimulates alpha, beta, and dopaminergic receptors. At low doses, it causes vasodilation and increased renal blood flow. At intermediate doses, it increases heart rate and cardiac output. At high doses, it increases blood pressure through alpha receptor stimulation. Dobutamine is a synthetic catecholamine that stimulates beta1 and beta2 receptors, causing increased contractility and cardiac output without affecting renal blood flow. Nitroglycerin dilates coronary arteries to improve blood flow and reduces preload, helping to lower blood pressure and myocardial oxygen demand in conditions like hypertension and heart failure.
This document discusses various inotropes and vasopressors used to treat low blood pressure. It describes how vasopressors like norepinephrine work by causing vasoconstriction to raise blood pressure, while inotropes like dobutamine increase cardiac contractility. Several catecholamines are discussed in detail, including their mechanisms of action, clinical uses, dosing, and side effects. Dobutamine is an inotrope that increases heart rate and stroke volume but may increase cardiac work. Dopamine has dose-dependent effects including renal and cardiac stimulation. Epinephrine stimulates both alpha and beta receptors to increase blood pressure and heart rate. Norepinephrine is a potent vasop
This document provides an overview of the pharmacology of various cardiovascular agents, including cholinergic drugs, adrenergic drugs, catecholamines, and vasodilators. It discusses the mechanisms and therapeutic uses of specific drugs from each class, such as neostigmine, phenylephrine, dobutamine, milrinone, and levosimendan. The document also compares the effects and clinical applications of different catecholamines like norepinephrine and epinephrine.
A 28-year-old female presented with palpitations, presyncope and an abnormal ECG strip. The ECG shows a narrow complex tachycardia. Adenosine can be used both diagnostically and therapeutically to help determine if the arrhythmia is dependent on the atrioventricular node by attempting to terminate or cause transient heart block. If the arrhythmia terminates or heart block occurs, it suggests the arrhythmia involves the AV node and is likely a supraventricular tachycardia. If adenosine has no effect, it makes ventricular tachycardia more likely.
The document discusses various vasopressor drugs used to treat low blood pressure, including dobutamine, dopamine, epinephrine, and norepinephrine. It describes the mechanisms of action, clinical uses, dosing regimens, and adverse effects of each drug. Key points are that norepinephrine is preferred for septic shock due to fewer side effects, though clinical outcomes are similar across vasopressors. The document provides detailed information on hemodynamic effects and recommendations for use of different vasopressors in various clinical situations.
The document discusses drugs commonly used in cardiac catheterization laboratories. It describes the uses, mechanisms of action, dosages, and side effects of various drugs including lidocaine for local anesthesia, heparin and glycoprotein IIb/IIIa inhibitors for anticoagulation during procedures like percutaneous coronary intervention, nitrates like glyceryl trinitrate for vasodilation, inotropes like dopamine and dobutamine, antiarrhythmics like amiodarone, and contrast agents like iohexol. The document provides an overview of how these drugs are utilized during different cardiac procedures performed in cath labs.
Emergency medications are used to treat life-threatening conditions and save patients' lives. They work quickly to control symptoms and stabilize vital functions. This document outlines several emergency drugs including adrenaline, noradrenaline, dopamine, dobutamine, nitroglycerin, and others. It describes their mechanisms of action, indications, side effects, and important nursing considerations for safe administration. Understanding these critical care medications is important for emergency treatment of patients.
This document provides information on several medications including atropine, epinephrine, hydrocortisone, dopamine, furosemide, digoxin, digoxin immune fab, naloxone, phenytoin, phenobarbitone, and potassium chloride. For each medication, the document outlines indications, dosages, cautions, adverse effects, and monitoring as applicable. The document also provides treatment protocols for conditions like status asthmaticus and anaphylactic shock.
This document provides information on various medications including their indications, dosages, cautions, and adverse effects. It discusses drugs used to treat conditions like cardiac arrest, shock, seizures, and electrolyte abnormalities. The medications described include atropine, epinephrine, hydrocortisone, dopamine, furosemide, digoxin, phenytoin, phenobarbitone, potassium chloride, sodium bicarbonate, and calcium gluconate. Precise dosages are provided for neonatal and pediatric patients.
The document summarizes recent trends in the management of heart failure. It discusses the epidemiology and classification of heart failure. The mainstay of treatment involves neurohumoral modulation using ACE inhibitors, ARBs, beta-blockers, and MRAs. Other management principles include preload and afterload reduction, increasing contractility cautiously, and reducing heart rate. Newer drugs like sacubitril/valsartan, dapagliflozin, and vericiguat are improving outcomes, while others like omecamtiv mecarbil and istaroxime are under investigation.
Dr. Viraj Shinde's document provides an overview of sympathommimetic drugs. It defines them as drugs that mimic the actions of norepinephrine or epinephrine. It discusses the sympathetic and parasympathetic nervous systems, classification of sympathommimetic drugs, examples like epinephrine, mechanisms of action, therapeutic uses, and adverse effects. Receptor types, locations, agonists, and antagonists are outlined. The document also covers neurotransmitters, their criteria and the neurotransmission process. Specific drugs discussed include dopamine, isoproterenol, dobutamine, fenoldopam, phenylephrine, clonidine, and beta-2 selective agents.
Dr. Viraj Ashok Shinde's document discusses sympathommimetic drugs. It defines them as drugs that partially or completely mimic the actions of norepinephrine or epinephrine. It describes the sympathetic and parasympathetic nervous systems, classifications of sympathommimetic drugs, examples like epinephrine, mechanisms of action, therapeutic uses, and side effects. The summary provides an overview of the key topics covered in the document.
This document provides guidelines for post-arrest care in pediatric patients. It outlines recommendations for respiratory care to maintain oxygen saturation between 94-99% and use of inotropic drugs like milrinone and epinephrine for cardiac care. It also discusses guidelines for neurological care, ongoing assessment, and treatment of hypotension. Specific recommendations are provided for ventilation, drug therapies including epinephrine, dopamine, norepinephrine and factors influencing outcomes. Targeted temperature management and control of blood glucose are also addressed.
This document provides an overview of pediatric pharmacology of the cardiovascular system. It discusses drug therapies for hypertension, heart failure, arrhythmias, and other conditions. Specific drug classes covered include ACE inhibitors, calcium channel blockers, nitrates, and vasodilators. For each drug class, example medications are given along with their indications, dosages, administration instructions, and side effects. The learning objectives are to understand the pharmacotherapy of various pediatric cardiovascular conditions.
Adrenaline and noradrenaline are catecholamines that act as hormones and neurotransmitters. They are synthesized from tyrosine and phenylalanine through a series of enzymatic reactions. Adrenaline acts on alpha-1, alpha-2, and beta receptors and causes effects like increased heart rate, vasoconstriction, bronchodilation and glycogenolysis. Noradrenaline predominantly acts on alpha-1 and beta-1 receptors, causing potent vasoconstriction with little bronchodilation. Both are used to treat hypotension, cardiac arrest and anaphylaxis. Their administration must be closely monitored due to risks of hypertension, arrhythmias and tissue necrosis from vasoconstrict
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2. INTRODUCTION
An inotrope is an agent, which increases or decreases
the force or energy of muscular contractions.
In 1785 the first inotrope-Digitalis was discovered &
used for CCF.
As science advanced, other inotropes were developed
which were more potent and have different chemical
properties and physiological effects.
All inotropes are successful because they increase the
myocardial contractility of the heart.
By enhancing myocardial contractility, cardiac output,
the amount of blood ejected by the heart with each
beat, will also increase.
4. CARDIAC GLYCOSIDES
The first line of inotropes include all digitalis derivatives
Digitalis Glycosides have
A direct effect on cardiac muscle and the conduction
system.
An indirect effect on the cardiovascular system regulated
by the autonomic nervous system which is responsible for
the effect on the sino-atrial (SA) and atrioventricular (AV)
nodes.
5. The result of these direct and indirect
effects are: -
An increase in force and velocity of
myocardial contractility (positive inotrope
effect).
Slowing of heart rate (negative
chronographic effect).
Decreased conduction velocity through the
AV node.
6. 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.
IV injection should be carried out over 15 minutes
to avoid vasoconstriction responses.
Intramuscular Digoxin is absorbed unpredictably,
causing local pain, and is not recommended.
7. DIGOXIN LOADING DOSE
Loading doses of Digoxin range from 10 – 15mg/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 LEAST SIX
HOURS AFTER THE LAST DOSE!
8. 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
9. SYMPATHOMIMETICS (ADRENERGIC)
Sympathomemetic drugs exert potent inotropic
effects by stimulating beta (B1 & B2),alpha(A1 & A2)
and dopaminergic receptors in the myocardium, blood
vessels, and sympathetic nervous system.
10. ALPHA 1 (A1):
A1 receptors are in vascular smooth muscle & also in
the myocardium, which mediate positive inotropic
and negative chronotropic effects.
Stimulation of A1 receptors leads to vasoconstriction.
ALPHA 2 (A2):-
A2 receptors are located in large blood vessels.
Stimulation of A2 receptors mediates arterial and
venous vasoconstriction.
11. BETA 1 (B1):-
Beta 1 receptors increase heart rate and myocardial
contractility.
BETA 2 (B2):-
Beta 2 receptors enhance vasodilation; relax bronchial,
uterine and gastrointestinal smooth muscle
DOPAMINERGIC: Related to the effect of dopamine.
12. DOPAMINE (INTROPIN)
(200MG/5ML AMPULE).
A chemical precursor of epinephrine.
Possessing alpha and beta and dopaminergic
receptor – simulating actions.
The specific effects are related to the dose
delivered.
13. 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.
14. 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
15. DOPAMINE ADMINISTRATION
CONCENTRATIONS
Remove 5ml from 100ml 5% Glucose,
add 200 mg Dopamine, final
concentration 2000mcg/ml.
OR
Make the concentration half with 50
ml of 5% Dextrose.
17. WARNING:
Correct hypovolaemia prior to administration.
Do not infuse peripherally.
Extravasations can cause severe tissue necrosis.
Monitor the patient carefully for decreased
circulation in the extremities.
If extravasates into tissues-
The infusion should be immediately stopped.
Infiltrate with 0-15ml 0.9% Sodium Chloride containing
5-10mg Phentolalmine.
Regitine is then administered SQ in the four
90°quadrants around the site of extravasations.
19. DOBUTAMINE (DOBUTREX)
(250MG IN 20ML AMPULE)
Drug class:-
Catecholamine.
Mechanism of action:-
Chemically related to dopamine.
Synthetic catecholamine.
Stimulates Beta 1 and Alpha-adrenergic receptors.
Increases myocardial contractility, stoke volume
and cardiac output.
Decreases preload and afterload (Vasodilatation)
Produces mild chronotropic, hypotensive and
arrhythmogenic effects.
Increase renal and mesenteric blood flow by
increasing cardiac output.
Does not affect renal blood flow like dopamine.
20. Initial dose: -
2 to 3 mcg/kg/minute.
Usual dose: -
2.5 to 10 mcg/kg/minute.
Desired effects include:
1. Increased cardiac output
2. Increased stroke volume
This dose will not increase heart rate or cause
vasoconstriction.
21. Maximum dose: -
20 mcg/kg/minute.
Dobutamine administration
concentrations: -
Infusion pump: 500 mg per 250 cc normal saline
Syringe pump: 250 mg (20cc) in total 50 cc
normal
saline (5 mg per cc)
22. 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.
Patient with aterial fibrillation should be digitalized before giving
this drug to prevent ventricular tachycardia.
23. Warning: -
Increasing the rate past 20
mcg/kg/minute could be detrimental
because myocardial oxygen consumption
can cause tachycardias.
Adverse effects:-
Tachycardia
Arrhythmias
Blood pressure fluctuation
Myocardial ischemia
Headache
Nausea
Tremors
Hypokalemia
24. NOREPHINEPHRINE (LEVOPHED)
Drug class: -
Catecholamine.
Endogenous catecholamine released from nerve cells, synthesized by
adrenal medulla.
Metabolized mainly by the liver.
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 neuroginic shock after adequate
hydration.
Increases blood flow to the major organs including the kidneys and
helps in increases urine output.
25. 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.
Norepinephrine administration
concentration:-
Infusion pump:
4 mg per 250 c crystalloid (16 mcg/cc)
26. Contraindications:-
Hypovolemic and cardiogenic shock
(because potent vasoconstriction is
already occurring).
Pregnancy.
Hypoxia.
Hypovolemia secondary to fluid deficit.
Caution with hypertension and
hyperthyroidism.
27. 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.
28. EPINEPHRINE
Drug class: -
Catecholamine.
Endogenous catecholamine, produced,
stored, and released by the adrenal medulla.
Mainly eliminated via kidneys.
Mechanism of action: -
Stimulation of alpha and beta-adrenergic receptors causes
vasoconstriction.
Increases heart contractility and rate.
Causes bronchodilation.
Antagonizes histamine effect.
29. 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.
Pheochromocytoma.
Caution with heart failure angina and
hyperthyroidism.
31. ISOPROTERENOL (ISUPREL)
Has nearly pure beta-adrenergic receptor activity.
Increase heart rate and contractility and cause peripheral
vasodilation.
Used for temporary control of symptomatic bradycardia.
Initial drug of choice for heart transplant.
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.
32. 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.
Isoporterenol administration concentration: -
1 mg in 250 cc crystalloid (4 mcg/cc).
33. Adverse effects: -
Arrhythmias.
Ventricular tachycardia.
Ventricular fibrillation.
Warning:-
May exacerbate tachyarrhythmias due
to digitalis toxicity.
May precipitate hypokalemia.
34. PHOSPHODIESTERASE INHIBITORS
Powerful positive inotropic agents.
The action is not fully understood.
Inhibits phosphodiesterase, an enzyme that degrades (CAMP)
Cyclic Adenosine Monophosphate.
There is no effect on alpha or beta-receptors.
Increase contractile force and velocity of relaxation of cardiac
muscle.
Increasing cardiac output without increasing myocardial
oxygen consumption.
They cause vasodilation and a decrease in SVR (systemic
vascular resistance) and PVR (Pulmonary vascular
resistance & in afterload (resistance to ventricular ejection)
35. AMRINONE (INOCOR)
Has a hemodynamic effect similar to Dobutamine.
Increase cardiac output and decrease pulmonary
vascular resistance.
It should be used with caution in patients with
ischemic heart disease because it can exacerbate
ischemia.
It should be considered for use in patients with
severe congestive heart disease, which is no longer
responsive to other inotropes, diuretics, and
vasodilators.
It is also used after aorto-coronary bypass surgery.
It is recommended that the lowest dose that
produce the desired hemodynamic effect to be used.
36. LOADING DOSE:
0.5 TO 0.75 mg/kg given over 2-3 min. IV
DO NOT EXCEED 1 mg/kg.
Maintenance dose:
5 to 10 mcg/kg/min
Maximum dose:
10mg/kg/24hours.
Doses higher than 15 mcg/kg/minute can
produce tachycardia
37. NEVER DILUTE WITH DEXTROSE!
(Chemical reaction occurs)
Syringe pump: Use Straight Solution
Concentration 5 mg/cc
Adverse reaction: -
Thrombocytopenia occurs in 10% of all patients seen 48 – 72
hours after infusion and resolves when drug is discontinued.
Gastrointestinal upset
Myalgia
Fever
Hepatic dysfunction
Ventricular irritability
38. Nursing implication: -
Monitor for arrhythmias, hypotension, thrombocytopenia
& hepatotoxicity.
Monitor cardiac output, pulmonary artery pressure and
heart rate.
Effects last for 2 hours after drip is discontinued.
The loading dose may be given over 2 to 5 minutes, but to
prevent Hypotension it is recommended the loading dose be
given over 10 to 15 minutes.
39. 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.
40. LOADING DOSE:-
50 mcg/kg given IV over 10 minutes
MAINTENANCE DOSE:-
0.375 to 0.75 mcg/kg/minute
Warning; -
DOSES TO HIGH CAN CAUSE
HYPOTENSION AND TACHYCARDIA.
41. MILRINONE IS INCOMPATIBLE WITH L ASIX!
ADVERSE EFFECTS:
Supraventricular tachycardia
Ventricular arrhythmias
Ventricular ectopy
Increased ventricular rate in atrial
fibrillation/flutter
Headache
Hypokalemia
Tremors
Thrombocytopenia
42. EASY FORMULAS FOR DRUG CALCULATIONS FOR INFUSION
PUMPS
TO DETERMINE DESIRED RATE:-
(Remember 1 mg = 1000 mcg)
(Desired mcg) X kg. X 60 ÷ mcg/cc (in solution)
Example:- Give Dopamine 5 mcg/kg/min to a patient who weights 65 kg.
5 X 65 X 60 ÷ (800 mg in 500 cc)
(5 mcg) X (65 kg) X 60 ÷ (800 mg ÷ 500 cc = 1.6 mg. X 1000) = 1600 mcg
19500 ÷ 1600 = 12.18 cc
Example: Give Dopamine 2.5 mcg/kg/min to a patient who weight 55 KG.
2.5 X 55 X 60 ÷ 1600
(2.5 mcg) X (55 kg) X 60 ÷ 1600 = 5.15 cc
43. TO DETERMINE MCG/KG/CC INFUSING:
Example: You have a patient that weighs 85 kg who has a
dopamine drip infusion at 8cc per hour and you want to
determine how many mcg/kg/min the patient is receiving.
The dopamine is mixed at 1600 mcg per cc.
MCG/CC X RATE ÷ 60 ÷ KG
1600 X 8 ÷ 60 ÷ 85 = 2.5 mcg/kg/minute
Example: You have a patient that weighs 102 kg who has a
Dobutamine drip infusing at 12 cc per hour and you want to
determine how many mcg/kg/min the patient is receiving.
The Dobutamine is mixed at 500 mg in 250 cc = 2000 mcg per
cc.
(500 mg ÷ 250 = 2 X 1000 = 2000)
2000 X 12 ÷ 60 ÷ 102 = 3.92 mcg/kg/min.
44. 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.
45. CONCLUSION
CONT…
A thorough grasp of the pharmacology of
inotropes is crucial to understand the rationale
for drug therapy of heart failure.
Inotropes continue to improve through scientific
research.
Oral forms of inotropes are now being
investigated to manage congestive heart failure
at home.
46. BIBLIOGRAPHY
ACLS, Emergency Cardiovascular Care Program, American
Heart Association, 1997-1998, pp. 7.3-7.4, 8.3-8.8.
Braunwald; Heart Disease, 1998, W. B. Saunders Company,
pp. 9468-9470, 9477-9481, 9492-9502.
Critical Care Nursing-Diagnosis and Management, Second
Edition. L. Thelan, et al. Mosby-Year Book, Inc. 1994. pp 346-
347
Physician’s Desk Reference, 1997, pp. 1116-1118.
Mrs Florence Segaran , Associate Professor , College of
Nursing CMC, Vallore.