One of the most important factors in affecting the strength of the heart’s muscular contractions is the level of calcium in the fluid inside the heart’s muscle cells. Positive inotropes: ~Beta-agonists ~Digitalis compound ~ Phosphodiesterase inhibitors ~Calcium-sensitizing drugs Negative ~ Beta-blockers ~Calcium channel blockers ~ Centrally acting sympatholytics – tx of HTN
Pharmacologic Beta blockade is superior to Calcium channel blockade regarding chronotropic properties of the myocardium . Titration of a Beta Blocker to a desired heart rate is decidedly easier than titration of a non dihydropyridine CCB
~ decreased venous return, which decreased preload
On-set: 5 minutes Half-life: 2 mins Monitoring Parameters Blood pressure, ECG, heart rate, CVP, RAP, MAP, urine output; if pulmonary artery catheter is in place, monitor Cl, PCWP, SVR, and PVR
Dopamine is most frequently used for treatment of hypotension because of its peripheral vasoconstrictor action. In this regard, dopamine is often used together with dobutamine and minimizes hypotension secondary to dobutamine-induced vasodilation. Thus, pressure is maintained by increased cardiac output (from dobutamine) and vasoconstriction (by dopamine). It is critical neither dopamine nor dobutamine be used in patients in the absence of correcting any hypovolemia as a cause of hypotension. Low-dose dopamine is often used in the intensive care setting for presumed beneficial effects on renal function. However, there is no clear evidence that low-dose dopamine confers any renal or other benefit. Indeed, dopamine may act on dopamine receptors in the carotid bodies causing chemoreflex suppression. In patients with heart failure, dopamine may inhibit breathing and cause pulmonary shunting. Both these mechanisms would act to decrease minute ventilation and oxygen saturation. This could potentially be deleterious in patients with respiratory compromise and patients being weaned from ventilators.
Extravasation management: Due to short half-life, withdrawal of drug is often only necessary treatment. Use phentolamine as antidote. Mix 5 mg with 9 mL of NS; inject a small amount of this dilution into extravasated area. Blanching should reverse immediately. Monitor site. If blanching should recur, additional injections of phentolamine may be needed
Peak effect: 10-20 mins Half-life: 2 mins Monitoring Parameters Blood pressure, ECG, heart rate, CVP, RAP, MAP, urine output; if pulmonary artery catheter is in place, monitor CI, PCWP, and SVR; also monitor serum potassium Additional Information Dobutamine lowers central venous pressure and wedge pressure but has little effect on pulmonary vascular resistance. Dobutamine therapy should be avoided in patients with stable heart failure due to an increase in mortality. In patients with intractable heart failure, dobutamine may be used as a short-term infusion to provide symptomatic benefit. It is not known whether short-term dobutamine therapy in end-stage heart failure has any outcome benefit. Dobutamine infusion during echocardiography is used as a cardiovascular stress. Wall motion abnormalities developing with increasing doses of dobutamine may help to identify ischemic and/or hibernating myocardium Particularly useful in low cardiac output states where filling pressures are elevated
Aortic stenosis: Ineffective therapeutically in the presence of mechanical obstruction such as severe aortic stenosis. • Atrial fibrillation: Patients with atrial fibrillation may experience an increase in ventricular response. • Hypovolemia: If needed, correct hypovolemia first to optimize hemodynamics. • Myocardial infarct (post): Use with caution in patients post-MI; can increase myocardial oxygen demand
increases in intracellular ionized calcium and contractile force in cardiac muscle, as well as with cAMP dependent contractile protein phosphorylation and relaxation in vascular muscle. sodium-potassium adenosine triphosphatase activity as do the digitalis glycosides. 12% of pts will have v arrhythmias
- Avoid in valve disease (obstructive disease) inotropic effect will worsen obstrstrcutive disease - Concerns related to adverse effects: • Arrhythmias: Observe for arrhythmias in this very high-risk patient population. Ventricular or atrial arrhythmias may persist even after discontinuation of inamrinone especially in patients with renal dysfunction. Ensure that ventricular rate is controlled in atrial fibrillation/flutter before initiating; may increase ventricular response rate. In heart transplant candidates, institute appropriate measures to protect patient against risks of sudden cardiac death. • Hepatic effects: Discontinue therapy if dose-related elevations in LFTs and clinical symptoms of hepatotoxicity occur; monitor liver function. • Hypotension: Monitor blood pressure/ heart rate closely. Mean arterial pressure decreases by ?5% at doses between 0.375-5 mcg/kg/minute and by 17% at 0.75 mcg/kg/minute (includes loading doses ranging between 37.5-75 mcg/kg). Infusion may require reduction in dose or temporary discontinuation if hypotension occurs. Hypotension may be prolonged especially in patients with renal dysfunction. Vigorous diuresis may contribute to hypotension; cautious administration of fluids may be required to prevent hypotension. - Monitoring Parameters Platelet count, CBC, electrolytes (especially potassium and magnesium), liver function and renal function tests; ECG, CVP, SBP, DBP, heart rate; infusion site If pulmonary artery catheter is in place, monitor cardiac index, stroke volume, systemic vascular resistance, pulmonary capillary wedge pressure and pulmonary vascular resistance.
The only absolute contraindications to the administration of amiodarone is allergic reaction (ie: anaphylaxis ) to the compound. However, because of the wide spectrum of the mechanism of action of amiodarone and the numerous side effects possible, there are a number of groups for which care should be taken when administering the drug. Individuals who are pregnant or may become pregnant are strongly advised to not take amiodarone. Since amiodarone can be expressed in breast milk, women taking amiodarone are advised to stop nursing. It is contraindicated in individuals with sinus nodal bradycardia, atrioventricular block, and second or third degree heart block who do not have an artificial pacemaker . Individuals with baseline depressed lung function should be monitored closely if amiodarone therapy is to be initiated.
- Cardizem can increase the effects of anesthetics
Leads to increased in intrcellular Na concentration. & increased in intracellular calcium as sodium-calcium exchange is stimulated by high intracellular Na concentrations. Increased calcium leads to greater activation of contractile protiens Mechanism of Action: The influence of digitalis glycosides on the myocardium is dose-related, and involves both a direct action on cardiac muscle and the specialized conduction system and indirect actions on the cardiovascular system medicated by the autonomic nervous system. The indirect actions mediated by the autonomic nervous system involve a vagomimetic action, which is responsible for the effects of digitalis on the sino-atrial (SA) and atrioventricular (AV) nodes; and also baroreceptor sensitization which results in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increment in mean arterial pressure. The pharmacologic consequences of these direct and indirect effects are: 1) an increase in the force and velocity of myocardial systolic contraction (positive inotropic action); 2) a slowing of heart rate (negative chronotropic effect); and 3) decreased conduction velocity through the AV node. In higher doses, digitalis increases sympathetic outflow from the central nervous system (CNS) to both cardiac and peripheral sympathetic nerves. This increase in sympathetic activity may be an important factor in digitalis cardiac toxicity. Most of the extracardiac manifestations of digitalis toxicity are also mediated by the CNS Heart Failure: The increased cardiac output resulting from the inotropic action of digoxin ameliorates the disturbances characteristic of heart failure (venous congestion, edema, dyspnea, orthopnea and cardiac asthma). Digoxin is more effective in &quot;low output&quot; (pump) failure than in &quot;high output&quot; heart failure secondary to arteriovenous fistula, anemia, infection or hyperthyroidsm. Digoxin is usually continued after failure is controlled, unless some known precipitating factor is corrected. Studies have shown, however that even though hemodynamic effects can be demonstrated in almost all patients, corresponding improvement in the signs and symptoms of heart failure is not necessarily apparent. Therefore, in patients in whom digoxin may be difficult to regulate, or in whom the risk of toxicity may be great (e.g patients with unstable renal function or whose potassium levels tend to fluctuate) a cautious withdrawal of digoxin may be considered. If digoxin is discontinued, the patient should be regularly monitored for clinical evidence of recurrent heart failure. Atrial Fibraillation: Digoxin reduced ventricular rate and thereby improves hemodynamics. Palpitation, precorring distress or weakness are relieved and concomitant congestive failure ameliorated. Digoxin should be continued in doses necessary to maintain the desired ventricular rate. Atrial Flutter: Digoxin slows the heart and regular sinus rhythm may appear. Frequently the flutter is converted to atrial fibrillation with controlled ventricular response. Digoxin treatment should be maintained if atrial fibrillation persists. (Electrical cardioversion is often the treatment of choice for atrial flutter. See discussion of cardioversion in PRECAUTIONS.) Paroxysmal Atrial Tachycardia (PAT): Digoxin may convert PAT to sinus rhythm by slowing conduction through the AV node. If heart failure has ensued or paroxyms recur frequently, digoxin should be continued. In infants, digoxin is usually continued for 3 to 6 months after a single episode of PAT to prevent recurrence.
Cardiac Medications Margaret Glembocki RN, MSN, ACNP-CSC Acute Care Nurse Practitioner
Objectives <ul><li>To define drug classes specific to cardiovascular system </li></ul><ul><li>To be able to verbalize safe administration of cardiac medications. </li></ul><ul><li>To be able to verbalize safe titration of cardiac medications </li></ul><ul><li>To identify potential outcomes and side effects of cardiac medication </li></ul>
It is our duty and responsibility as nursing professionals to ensure health care quality and patient safety. According to The Institute of Medicine, “Medical errors cause as many as 98,000 deaths at costs up to $29 billion a year in hospitals alone.” Alarming isn’t it?
5 Rights of Medication Administration <ul><li>Right Patient </li></ul><ul><li>Right Route </li></ul><ul><li>Right Dose </li></ul><ul><li>Right Time </li></ul><ul><li>Right Medication </li></ul>
How do Inotropic Drugs work?? <ul><li>Alters the force or strength of the heart’s muscular contractions. </li></ul><ul><li>2 types: Negative and Positive </li></ul><ul><ul><li>Negative Inotropic drugs make the heart beat less strongly </li></ul></ul><ul><ul><li>Positive Inotropic drugs make the heart beat more strongly </li></ul></ul>
Calcium Channel Blockers (-) <ul><li>Decrease the force of contraction of the myocardium. </li></ul><ul><li>Slow down the conduction of electrical activity within the heart by blocking the calcium channel during the plateau phase of the action potential of the heart. </li></ul><ul><li>This results in a negative chronotropic effect resulting in a lowering of the heart rate and the potential for heart block. </li></ul>
Thinkers….. <ul><li>It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with __________________. </li></ul><ul><li>The negative chronotropic effects of calcium channel blockers make them a commonly used class of agents in individuals with _____________________ in whom control of the heart rate is an issue. </li></ul>
Beta receptors….. <ul><li>Stimulation of β1 receptors by epinephrine induces a positive chronotropic and inotropic effect on the heart & increases cardiac conduction velocity and automaticity. </li></ul><ul><li>Stimulation of β1 receptors on the kidney causes renin release. </li></ul><ul><li>Stimulation of β2 receptors induces smooth muscle relaxation, induces tremor in skeletal muscle, and increases glycogenolysis in the liver and skeletal muscle. </li></ul><ul><li>Stimulation of β3 receptors induces lipolysis. </li></ul>
What Beta-blockers do… <ul><li>Beta blockers inhibit these normal epinephrine-mediated sympathetic actions. </li></ul><ul><ul><li>Reduce the effect of excitement/physical exertion on heart rate & force of contraction </li></ul></ul><ul><ul><li>Dilation of blood vessels </li></ul></ul><ul><ul><li>Opening of bronchi </li></ul></ul><ul><ul><li>Reduce tremor </li></ul></ul><ul><ul><li>Reduce breakdown of glycogen </li></ul></ul>
Renin-Angiotensin-Aldosterone System (RAAS) <ul><li>This system is activated in response to hypotension, decreased sodium concentration in the distal tubule, decreased blood volume and renal sympathetic nerve stimulation. </li></ul><ul><li>In such a situation, the kidneys release renin which cleaves the liver-derived angiotensinogen into angiotensin I. Angiotensin I is then converted to angiotensin II via the ACE in the pulmonary circulation as well as in the endothelium of blood vessels in many parts of the body. </li></ul><ul><li>The system in general aims to increase blood pressure </li></ul>
A ngiotensin- C onverting E nzyme Inhibitors (ACE inhibitors) <ul><li>Lower arteriolar resistance and increase venous capacity; increase cardiac output and cardiac index, stroke work and volume, lower renovascular resistance, and lead to increased natriuresis (excretion of sodium in the urine). </li></ul><ul><li>Indications for ACE inhibitors include: CHF, HTN, LV dysfunction, prevention of nephropathy in DM </li></ul><ul><li>Captopril, Norvasc, Lotensin </li></ul>
Case Study <ul><li>52 y/o female with history of HTN, EF= 50% and diet controlled DM presented to the ED with fatigue. Admitted for observation and stress test the following day. Home meds: Lisinopril and MVI. </li></ul><ul><li>Now c/o nausea and diaphoretic. 12- lead EKG ST inversion in Lateral leads…Call the doctor & get ready for________. </li></ul>
What should we prepare for? <ul><li>Cath lab bound….. </li></ul><ul><li>Blood work pending </li></ul><ul><li>Consent </li></ul><ul><li>Oxygen </li></ul><ul><li>Morphine </li></ul><ul><li>Anti-Platelets: Aspirin (COX inhibitor) and Plavix (ADP) </li></ul>
Heparin <ul><li>Anticoagulation action by accelerating the activity of antithrombin III to inactive thrombin. Does NOT lyse existing clots. </li></ul><ul><li>Measures: aPTT goal 1.5-2 times control (50-70) </li></ul><ul><li>25,000 units in 250mL of D5W. Concentration: 100units/mL. Dosing: units/hour </li></ul>
Integrilin (Eptifibatide) <ul><li>Inhibits platelet aggregation, with specificity for the platelet receptor GP IIb-IIIa. Initial onset of inhibition of platelet aggregation was observed within 15 minutes after the IV bolus. </li></ul><ul><li>Reversible: platelet function was restored toward baseline (<50% inhibition) within 4 hours of discontinuation of infusion. Primarily renally excreted </li></ul><ul><li>Indications: MI, PCI, USA </li></ul><ul><li>Dose: </li></ul><ul><ul><li>180mcg/kg bolus (max 22.6mg) </li></ul></ul><ul><ul><li>2mcg/kg/min </li></ul></ul><ul><li>CrCL <50: reduce maintenance to 1mcg/kg/min </li></ul>
Metoprolol (Lopressor) <ul><li>Beta 1-receptor: decrease in heart rate, decrease in both systolic and diastolic blood pressure (chron). Decreased CO (-) </li></ul><ul><li>Indications: MI, angina, atrial fibrillation and flutter, HF, HTN </li></ul><ul><li>Dose: </li></ul><ul><ul><li>25-100mg po twice daily </li></ul></ul><ul><ul><li>2.5-5mg IV </li></ul></ul>
Amiodarone <ul><li>Antiarrhythmic with predominant class III effects of lengthening cardiac action potential and blocking myocardial potassium channels leading to slowed conduction and prolonged refractoriness.” </li></ul><ul><li>Slows SR, increases PR & QT intervals, decreases PVR. Peripheral line ok to use. </li></ul><ul><li>Indications: A-fib/flutter, V-tach/fib, Cardiac arrest, PSVT, WPW </li></ul><ul><li>Dose: 450mg in 250 D5W </li></ul><ul><ul><li>Load: 150mg IVBP over 10 mins </li></ul></ul><ul><ul><li>Maintenance: 1mg/min x 6 hrs, then 0.5mg/min x 18hrs </li></ul></ul>
Diltiazem <ul><li>Calcium channel blocker that blocks calcium ion influx during depolarization of cardiac and vascular smooth muscle. </li></ul><ul><li>Decreases PVR and causes relaxation of the vascular smooth muscle resulting in a decrease of both systolic and diastolic blood pressure </li></ul><ul><li>Indications: A-fib, HTN, angina, </li></ul><ul><li>Dose: 125mg in 125 D5W (1:1) </li></ul><ul><ul><li>Load: 0.25mg/kg over 2mins repeat: 0.35mg/kg </li></ul></ul><ul><ul><li>Maintenance: 5-15mg/hr </li></ul></ul>
Diltiazem Adverse Reaction <ul><li>Hypotension </li></ul><ul><li>Flushing </li></ul><ul><li>Peripheral edema </li></ul><ul><li>Heart failure </li></ul><ul><li>Bradycardia </li></ul><ul><li>May see pronounced bradycardia if given concurrently with digoxin or beta-blockers. </li></ul>
Digoxin <ul><li>Inhibits Na-K ATPase membrane pump. </li></ul><ul><li>Indications: Atrial fibrillation/flutter, HF, PSVT </li></ul><ul><li>Dose: 10-15mcg/kg IV or PO in 3 divided doses q6-8 hrs with first dose = ½, then po q6 x2 (ie: 500mcg x1, then 250mcg q6 x2. Then 125-350mcg per day </li></ul>