Cardiac Lecture Part 2 PDF

Chapter 29: Adrenergic Drugs (Vasopressors) Dr. Francisco Ayala DNP, MSN, APRN, FNP-C, CCRN Background • Shock – the result of significant decrease in cardiac output or abnormal distribution of blood volume. • Shock is a life-threatening condition due to not getting enough blood flow • 4 common c...

Chapter 29: Adrenergic Drugs (Vasopressors) Dr. Francisco Ayala DNP, MSN, APRN, FNP-C, CCRN Background • Shock – the result of significant decrease in cardiac output or abnormal distribution of blood volume. • Shock is a life-threatening condition due to not getting enough blood flow • 4 common culprits 1. Distributive (vasoplegic response, massive vasodilation, Sepsis) 2. Hypovolemic (Decreased blood* volume) 3. Cardiogenic (Decreased Pump Function) 4. Obstructive (barrier to perfusion – a clot, tamponade, pneumothorax) Rule #1 These drugs should not be given through the periphery. Not usually given through an IV. Why? Rule #2 • The patient should be optimally fluid resuscitated for pressors to have their maximal effect • You need to fill up the gas tank before you try to run the motor! • Improving the squeeze or the rate is useless if there is no fluid to move around (blood volume) Rule #3 • Vasopressors can cause tissue necrosis if extravasated. As such, they should be given through a central line. Rule #4 • An arterial line is commonly used in conjunction with vasopressors. • Why do you think we need an arterial line? Why are they given? Shock! Sepsis! Hypotension! Inotropic/Chronotropic Support • Examples: Cardiogenic Shock Drugs to know Norepinephrine (Levophed) Dobutamine (Dobutrex) Epinephrine Dopamine Phenylephrine Norepinephrine (Levophed • Used for Hypotension and Shock • Mimic the effect of the sympathetic nervous system (Norepinephrine) • SEVERE Alpha 1 agonist effect – Vasoconstriction - Raises blood pressure • MILD Beta 1 agonistic effect – negligible increase in heart rate (sometimes not at all) • Due to the profound vasoconstriction – patient is at increased risk for limb ischemia, organ failure (kidney/liver) • Medication can cause tissue necrosis if it extravasates (usually given via a central line and not an IV) Epinephrine (Adrenalin) • A drug that mimics the endogenous catecholamine of the same name. • A potent Alpha1, Beta1, and Beta 2 receptor agonist • Due to these effects, it will raise BP, Heart Rate, Systemic Vascular Resistance, Cardiac Index, and Stroke Volume • Especially useful in Anaphylaxis or Profound Refractory Hypotension. • A precursor of Epinephrine and Norepinephrine Dopamine • The action is dose dependent!! • Different receptors alpha vs Beta vs Dopaminergic are stimulated depending on how much or how little is given. Dopamine • 1-5mcg/kg/min – Increases renal blood flow • > 10mcg/kg/min – Stimulates beta receptors • 20 – 50 mcg/kg/min – Beta activity continues + alpha stimulation also occurs • So what does this mean? • At low doses there is little effect on heart rate or blood pressure but increased renal perfusion (increased urine output) • At higher doses it can increase heart rate • At max doses it can increase heart rate and blood pressure A sympathomimetic = Beta 1 agonist, MILD Beta 2, LITTLE to NONE Alpha stimulation Dobutamine Increases INOTROPY (contraction) but has minimal effect on CHRONOTROPY (heart rate) Used when an increase in Cardiac Output is needed without the increase in Blood Pressure Beta 1 Dobutamine • Caveat: The patient actually needs a little “extra” blood pressure because the vasodilating effects may cause hypotension • Less vascular activity than Dopamine Phenylephrine A synthetic adrenergic drug that stimulates ALPHA-adrenergic receptors to produce vasoconstriction Longer duration than epinephrine but less potent effects Can cause bradycardia Chapter 30: Heart Failure Dr. Francisco Ayala DNP, MSN, APRN, FNP-C, CCRN Drugs to know • RAAS Inhibitors – ACE/ARBs (”-pril” “-sartan”) • Sympatholytic Drugs – Beta Blockers (Metoprolol Succinate) • Neprilysin Inhibitor - Sacubitril • Inotropes - Cardiac Glycosides - Digoxin • Diuretics – Furosemide, Bumetanide, HCTZ, Sprinolactone • Inotropes - Milrinone Heart Failure Physiology • The heart fails due to structural damage, after a heart attack, improperly working heart valves, long standing hypertension, kidney problems Decreased Cardiac Output Cardiac Dysrhythmias Heart Failure Complications Edema Electrolyte imbalances Acute Exacerbations Death Drugs that make sense! • Drugs that reverse or assist the detrimental effects of the last slide. Problem Digoxin Decreased Cardiac Output X Edema (Fluid Overload) Diuretics Beta Blockers X RAAS Inhibitors Sacubitril X X SNS Activation X Neprilysin Inhibitors Amiodarone X Dysrhythmias RAAS Activation Milrinone X X X X Digoxin • Positive Inotrope • Indicated for use in heart failure with L. ventricular dysfunction • Second Line Drug • Narrow Therapeutic Index (0.8 – 2.0 ng/mL) • Interesting relationship with potassium In a patient with hypokalemia, digoxin toxicity can develop In a patient with hyperkalemia, digoxin can be ineffective Digoxin Toxicity • Common symptoms include lethargy, confusion, GI upset (nausea, vomiting, diarrhea) • Dysrhythmias (SVT, heart blocks, bradycardia) • Yellowish-green discoloration of the vision Antidote: Digibind: digoxin immune fab Digoxin Nursing Considerations • Check the apical pulse for one full minute prior to administering (hold if < 60 bpm) • Monitor serum electrolytes particularly potassium (< K > Toxicity) • Monitor for signs and symptoms of toxicity (vision changes, GI s/s) • Draw serum Digoxin levels to ensure therapeutic dose (6 hour after dose) • If patient is ill while on therapy, suspect toxicity, notify HCP, hold Digoxin. Diuretic Therapy • Loop Diuretic – POTENT diuretics (lots of urination, lots of risk for electrolyte imbalances (furosemide, bumetanide) • Thiazide Diuretics – They’re “mid” – get the job done but not as potent. Still some electrolyte imbalances (HCTZ) • Spironolactone – Potassium sparring (increase K+). Hold on to potassium. Low diuretic effects Loop Diuretics • Furosemide – Main use is for management of edema, fluid overload in patient’s with moderate to severe heart failure. • These drugs are very potent! • This means their effects are profound 1. Major diuresis 2. High potential for fluid-electrolyte imbalances 3. + ototoxicity + nephrotoxicity Loop Diuretics – Nursing Considerations • 1. Weigh the patient daily (Report weight gain > 2lb in 24 hours) • 2. Hold the medication if patient is hypokalemic, hypotensive, dehydrated or at risk for it (ex – patient is having vomiting and diarrhea) • 3. Monitor serum electrolytes especially potassium ( may need supplementation if low) • 4. Monitor renal function (BMP – BUN/Creatinine) Beta Blockers • Very important, linked to decreased mortality rate • Suppress Sympathetic Nervous System • Metoprolol Succinate (prototype for heart failure) • Prevent V. fib (dysrhythmias) • Reduces cardiac workload and oxygen consumption Positive Inotropic (Squeeeeze improvers) - Increased contractility Milrinone Systemic/pulmonary vasodilation – smooth muscle relaxation (decreased preload/afterload) Used for acute heart failure Angiotensin Receptor-Neprilysin Inhibitor Blocks RAAS effects + sustains natriuretic peptide activity Sacubitril/Valsartan (Entresto) Recommended when heart failure becomes more severe (EF < 40%) Risk of Angioedema (higher in African American patients) Black box warning – Pregnancy. Do not use!