PHARM: HF, angina, anti cholesterol

Cause of Left-sided heart failure

Left ventricle fails to pump blood effectively to systemic circulation

Patho of Light-sided heart failure

Blood backs up into the lungs causing pulmonary congestion

Manifestation of Left-sided Heart Failure

Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pulmonary crackles, fatigue, reduced exercise tolerance, cough with pink frothy sputum

Patho of pulmonary crackles

Fluid in alveoli

Cause of right-sided HF

Right ventricle fails to pump blood effectively into pulmonary circulation

Patho of right-sided HF

Blood backs up into the systemic venous system

Manifestations of right-sided HF

Peripheral edema, acites, hepatomegaly, jugular venous distension (JVD), fatigue and weakness

Systolic HF

Contraction Problem with heart, ventricular pumping

Patho of systolic HF

Decreased contraction leads to reduced stroke volume and cardiac output

Diastolic HF

Problem with heart relaxation and the filling of the ventricles, reduced EJECTION FRACTION

Patho of diastolic HF

Stiff, noncompliant ventricle leads impaired filling during diastolic, normal EJECTION FRACTION but decreased stroke volume

Cardiac output

Volume of blood the heart pumps per minute, SV X HR=CO

Stroke volume

Volume of blood the heart pumps per beat, normal 4-8L per min

Ejection Fraction

% of blood pumped out of left ventricle each beat, (EF=SV / EDV) x 100, normal: 55-70%

Reduced Ejection Fraction leads to

Systolic HF

Increased EF leads to

Diastolic HF

Afterload

The pressure or resistance the ventricle must work against to eject blood

Preload

The stretch the ventricular muscle at the end of diastole (ventricular filling)

Systemic vascular resistance (SVR)

The resistance the left ventricle must overcome to pump blood into systemic circulation, influenced by vessel diameter and blood viscosity

Pulmonary vascular resistance

The resistance the right ventricle must overcome to pump blood through pulmonary circulation, influenced by lung changes, pulmonary vascular obstruction and oxygenation

Causes of high systemic Vascular resistance

Hypertension, atherosclerosis, vasoconstriction leads to hypertrophy, then weakening and failure. Leading to left sided HF

Causes of high pulmonary vascular resistance

Pulmonary hypertension, chronic lung disease (COPD), pulmonary embolism, right ventricle struggles to push blood into pulmonary arteries, leading to right sided HF

positive inotrope

Drug that increases contractility (digoxin)

Negative chronotrope

Drugs that decrease HR

Venous return

Blood returning to heart influencing preload

Cardiac reserve

Ability of the heart to increase output in response to demand (exercise and stress)

Cardiotonic

A drug that improves the efficiency and strength of a hearts contraction, using calcium to lead to stronger myocardial contractions

How are hypertension, RAAS, and HF related?

HF leads to decreased cardiac output leading to RAAS Activation

RAAS leads to an increase in preload and afterload causing HTN and HF to worsen

What drugs interrupt the RAAS cycle?

ACE Inhibitors, ARBS and aldosterone antagonists

Cellular adaptation: what will happen to heart muscle if workload is increased?

hypertrophy

Atrial Natriuretic Peptide AMP

Released from atria of the heart, triggers atria stretch from increased volume/pressure, promotes natriuresis (sodium excretion), vasodilation, counteracts RAAS

Brain natriuretic peptide BMP

Released from ventricles, trigger’s ventricular stretch/overload in HF, Promotes vasodilation and sodium water retention, used to diagnose and monitor HF (HIGH LEVELS =WORSE HF SEVERITY)

Congested HF BMP

Measures severity of congested HF in patients

Why are most patients HF Patients on diuretics?

Helps reduce blood volume, lowered BP Decreases cardiac workload.

Frank starling law

Heart expanding due to increased pressure causes increased contraction

Class: Cardiac glycosides, anti arrhythmia agent, inotropic agent

Digoxin

Digoxin indications

HF, tachyarrhythmias (atrial fibrillation and atrial flutter)

Digoxin MOA

Positive inotropic effect, negative chronotropic effect

Digoxin adverse effects

Bradycardia, fatigue, headache, digoxin toxicity

Digoxin toxicity manifestations

Blurred vision, yellow/green halos, nausea and vomiting, anorexia

Digoxin RN Considerations

Check pulse prior, hold if below 60bpm, monitor digoxin levels

Digoxin PT teaching

Report signs of toxicity, regular follow up exams with serum digoxin levels, report signs of worsened HF

Digoxin antidote

Digoxin immune fab (digibind)

Class: inotropic agent, vasodilator/bipyrdines, PDE-3 inhibitior

Milrinone

Milrinone indications

Short term treatment for HF, Unresponsive to digoxin and other meds

MOA MILRINONE

PDE-3 leads to increase cAMP, increasing calcium leading to positive inotropic and vasodilation

Milrinone adverse effects

Arrhythmias, hypotension, headache, chest pain, thrombocytopenia

Milrinone RN Considerations

Monitor heart rhythm, and BP

Milrinone PT Teachings

Report palpations or dizziness

Cause of angina

Mostly due to atherosclerosis of coronary arteries, narrowing lumen leading to reduced blood flow

Types of angina

Stable, unstable, prinzmetal (variant)

Type of angina that occurs at rest or with minimal exertion

Unstable angina

Type of angina that occurs with exertion, predictable

Stable angina

Type of angina caused by coronary spasm, often at rest

Prinzmetal (variant) angina

Class: Nitrates/antiaginals

Nitroglycerin

Nitroglycerin indications

Angina

MOA of nitroglycerin

Vasodilation, decreased preload, decreased myocardial O2 demand

Nitroglycerin adverse effects

Orthostatic hypotension, headaches, reflex tachycardia

Nitroglycerin RN considerations

Interactions with ED MEDS

Nitroglycerin PT teaching

Sublingual: store in dark/cool place. Take up to 3 tablets. 1st dose: stop activity, place under tongue, wait 5 mins. If no relief-call 911. 2nd dose: wait 5mins, if not relief take 3rd dose: if last dose fails, PT is have a MI.

Transdermal: wear gloves, remove prior dose, rotate sites, remove hair if necessary

Class: calcium channel blockers

Diltiazem

Indications of diltiazem

Angina, hypertension, arrhythmias

MOA of diltiazem

Blocks calcium channels in heart and blood vessels, stopping excitations of muscles and vasodilation leading to decreased BP and HR

Diltiazem adverse effects

Peripheral edema, hypotension, bradycardia,constipation

Diltiazem RN considerations

Monitor BP and HR, Uusually comes with parameters, check vitals before administering meds

Diltiazem PT teaching

No grape fruit juice. Change positions slowly, report chest pain

Class: beta blockers

Metoprolol

Metoprolol indications

Hypertension, angina, HF, arrhythmias, MI

Metoprolol adverse actions

Bradycardia, hypotension, ED, ischemic heart disease is possible if stopped abruptly

MOA Of metoprolol

Decreased BP and HR by blocking beta1 blockers

metoprolol RN considerations

Monitor BP and HR, hold per providers parameters

Metoprolol PT teachings

Don not stop suddenly, taper off, change positions slowly

Cholesterol body functions

Cell membrane structure, vitamin D Production, bile acid formation, hormone precursor, myelin sheath production

Enzyme found in skeletal muscle, cardiac muscle and brain

Creatine kinase (ck)

Chlolestrol lowering meds can cause

Muscle injury/breakdown (myopathy, rhadomyolysis)

Elevated CK levels in blood suggests

Muscle breakdown

RN Considerations: if PT on cholesterol lowering medications reports muscle pain, tenderness or weakness

Check CK LEVELS

Class: bile acid sequestrants

Cholestyramine

Class: HMG-CoA reductase inhibitors

Atorvastatin

Class: cholesterol absorption inhibitors

Ezetimibe

Cholestyramine indications

Hypercholesterolemia

MOA of Cholestyramine

Binds to acid in GI tract, forms insolvable complex. Liver uses more cholesterol to make more bile acids leading to increase clearance of cholesterol and reduces LDLs.

RN Considerations of Cholestyramine

Interacts with many medications, including oral contraceptives

Pt teachings of Cholestyramine

Increase fiber and fluid to counteract constipation. Take with food, full glass of water, interferes with fat solvable vitamins (ADEK) take other meds 1 hour before or 4 hrs after taking Cholestyramine

Cholestyramine adverse effects

Constipation, GI upset

Atorvastatin indication

Hypercholesterolemia, prevents CAD

MOA of Atorvastatin

Decreases LDLs and increases HDLs

Atorvastatin adverse effects

Hepatotoxicity (malasie), muscle pain (myopathy), rhabdomyolysis (muscle breakdown, clogged kidneys)

RN considerations of Atorvastatin

Monitor liver function and CK levels, no pregnancy PTs

PT teaching of Atorvastatin

Avoid alcohol and grapefruit juice, report muscle pain, cola color urine (rhabdo). Take in evening, cholesterol is synthesized best at night.

Ezetimibe indication

Hypercholesterolemia

MOA of ezetimibe

Inhibits the absorption of cholesterol in small intestines

Ezetimibe adverse effects

Hepatotoxicity, muscle pain

RN considerations of Ezetimibe

Monitor liver and CK Function

Garlic RN considerations

Include in med rec, use caution with blood thinners

Garlic PT teaching

Report unusual bruising/bleeding

Omega 3 fatty acids indications

Hypertriglyceridemia, CV protection

Omega 3 fatty acids adverse effects

Fishy aftertaste, burps, GI upset, bleeding

Omega 3 fatty acids RN CONSIDERATIONS

Increased bleeding risks for patients, on blood thinners