HEART FAILURE PHARMACOLOGY NURS 203 General Pharmacology Danita - PowerPoint PPT Presentation

University of Hawai‘i Hilo Pre - Nursing Program HEART FAILURE PHARMACOLOGY NURS 203 – General Pharmacology Danita Narciso Pharm D 1

LEARNING OBJECTIVES  Understand the effects of heart failure in the body  Understand how one gets heart failure  Understand how each of the medications work to relive the symptoms of heart failure  Know which medications help prevent cardiac remodeling  Know digoxin and nesiritide 2

WHAT IS HEART FAILURE - WHEN THE VENTRICLES CANNOT PUMP OUT ENOUGH BLOOD TO MEET THE DEMANDS OF THE BODY Diastolic Systolic Ventricular filling (enlargement/stiffness) Ventricular pumping (contractility)/ejection) Right sided Left sided Back up of blood into the venous system Back up of blood into the pulmonary system 3

RISK FACTORS FOR HEART FAILURE 4

WHAT CAUSES HEART FAILURE? Diastolic *PRESERVED EF Systolic *DECREASED EF Increased ventricular stiffness Damaged or reduced heart muscle (MI) Mitral or tricuspid valve stenosis Dilated cardiomyopathy Pericardial disease Ventricular hypertrophy  Pressure overload  Volume overload Usually from prolonged uncontrolled hypertension Ischemic heart disease (MI) Uncontrolled risk factors 5

WHAT HEART FAILURE CAUSES 6

THE HEART TRIES TO COMPENSATE 7

PROBLEMS ASSOCIATED WITH HEART FAILURE Remodeling  Refers to the structural damage that can take place in the heart after prolonged stress  Chamber dilation, fibrosis, abnormal cells, reduction in cardiac muscle cells Compensation  Your body’s attempt to make up for the lack of oxygen and nutrients to the tissues Decompensation  When your body cannot fill the void any longer 8

STRATEGIES FOR TREATING HEART FAILURE Reduce Preload Reduce Afterload • Venous return of blood to • Reduce Heart Rate Arteries the heart • • Regulate SNS Regulate SNS • Blood volume • RAAS • RAAS 9

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ACEI & ARBS PREVENT/REVERSE REDUCE PRELOAD REDUCE AFTERLOAD REMODELING • • • Reduced aldosterone release Relaxation of arterial smooth Decrease in SNS tone • • Dilate veins (long-term use muscle EPI causes fibrotic effect) processes in the heart • Angiotensin II receptors in the heart cause hypertrophy • Angiotensin I receptors in the heart ACEI ARB 11

BETA BLOCKERS  Three beta blockers have been studied to show decrease in morbidity and mortality with their use in heart failure  Metoprolol succinate How BB work in HF ADRs  Cavedilol • • Caution – may reduce cardiac Bronchial constriction  Bisoprolol • output Reduced cardiac output • Decreased concentrations of • Ventricular failure • catecholamines Fatigue • • Upregulation of beta Reduced exercise tolerance • receptors Unpleasant dreams, insomnia, • Decrease heart rate depression • Decreased hypertrophy & • Deleterious effect on lipid panel • remodeling Withdrawal - taper 12

DIURETICS Thiazide Loop PS • • • Mild HF Marked fluid retention Adjunct • • Edema of lungs & Increase diuresis • limbs Correct electrolyte imbalance Potassium Sparing Therapeutic effects in HF treatment (thiazide & • Reduce morbidity & loops) mortality • Reduce preload • Reduction in aldosterone • Reduced blood volume action • Reduce cardiac size • All with mod/severe HF 13

DIGOXIN Increase the refractory period – negative chronotropic Are from PSN effects Decrease conduction velocity – negative dromotropic Increase contractility of the heart – positive inotropic Next slide 14

DIGOXIN Increase contractility of the heart – positive inotropic 3 1. The Na/K ATPase pump moves Na against 2 its concentration gradient outside the cell 2. A Ca/Na exchanger allows Na to flow into 1 the cell, in exchange for a calcium (driven by concentration gradient) 3. This creates a charge gradient and maintains a concentration gradient for Ca to follow • Sodium UNDER NORMAL CIRCUMSTANCES  Potassium  Calcium 15

DIGOXIN Increase contractility of the heart – positive inotropic 3 UNDER NORMAL CIRCUMSTANCES 2 1 1. The Na/K ATPase pump is inhibited 2. Less Ca is lost in the Ca/Na exchanger 3. Ca still moves in • Sodium the cell – higher  Potassium Ca levels are  Calcium maintained WITH DIGOXIN 16

DIGOXIN – NARROW THERAPEUTIC WINDOW Kinetics ADRs • At high/toxic doses, SNS outflow • 65-80% bioavailability • Arrhythmia – too much calcium in heart • Distributes well, CNS • Bigeminy • Excreted unchanged by kidneys • AV block • Dose adjust • Ventricular tachycardia • Ventricular fibrillation • Diarrhea & vomiting • CNS – Halos, disorientation & hallucinations 17

DIGOXIN – EXTRA BEATS Too much calcium  Delayed after depolarization  Potassium increase = more positive resting membrane potential Normal sinus rhythm Premature Ventricular Beats (PVB) - bigeminy 18

DIGOXIN – DRUG INTERACTIONS Digoxin interacts with the following substances:  Potassium  Hyperkalemia – decreases the effects of digoxin  Hypokalemia – Increases he effects of digoxin  Thiazide and loop diuretics  Cause hypokalemia  Potassium sparing diuretics  Cause hyperkalemia  Calcium supplementation  Magnesium supplementation Antidote = Potassium or anti-digoxin antibody 19

DIGOXIN – DIGIFAB CALCULATIONS Page 514 in your book 20

HYDRALAZINE - VASODILATOR Therapeutic effects ADRs Dilated arteries (reduce afterload) Headache Reduce remodeling – long-term effect Nausea Increase cardiac output Palpitations Used in patients with Lupus like symptoms  High peripheral vascular resistance  Arthralgia, myalgia, skin rash  Low ventricular output Fever Peripheral neuropathy 21

NITRATES- ISOSORBIDE DINITRATE Therapeutic effects ADRs Dilated veins(reduce preload) Headache Reduce remodeling – long-term effect Orthostatic hypotension Used in patients with: Tachycardia  High ventricular filling pressure  Pulmonary congestion & SOB 22

NESIRITIDE Non-selective dilation of vessels Brain Natriuretic Peptide (BNP) What is BNP  Substances released in HF patients to attempt to balance the activation of the RAAS system What does BNP (with ANP in the body) do?  Natriuresis  Diuresis  Vasodilation  Decreased aldosterone  Decreased hypertrophy  Inhibition of SNS and RAAS 23

NISIRITIDE Uses/ADRs Kinetics Uses: Used as continuous IV infusion – very short half life  Reduce preload and afterload  Acute decompensated heart failure Metabolized by vascular enzymes and excreted in the urine ADRs:  Severe hypotension  Ventricular arrhythmias  Renal damage 24

QUESTIONS 25