Pharmacology: Cardiac Exam (copy)

How many chambers in the heart

4

two types of valves

AV and semilunar

SA node conduction rate

60-100

AV node conduction rate

40-60

ventricular rate

30-40

cardiac cycle

events that occur in the heart from the beginning of one heartbeat until the next

3 major events in cardiac cycle

diastole, atrial systole, ventricular systole

cardiac output

total amount of blood ejected by one ventricle in liters/min

cardiac output is calculated

stroke volume X heart rate

stroke volume

amount of blood ejected from one of ventricles per heartbeat

stroke volume is determined by what

preload, afterload, contractility

preload

end-diastolic volume, amount of blood left in the ventricle at the end of diastole

afterload

resistance to left ventricular ejection, work the heart must overcome to eject blood

contractility

force generated by the contracting myocardium

blood flow through the heart

from body into the SVC/IVC to the RA, through tricuspid valve into RV, into pulmonary valve to pulmonary artery to lungs

from lungs into LA, through mitral valve into LV, through aortic valve into aorta and out to the body

coronary arteries are perfused

during diastole

L coronary artery has 3 branches

left main CA, L anterior descending (widow maker), circumflex

electrophysiology pathway of heart

SA node - AV node - bundle of His - R/L bundle branches - Purkinje fibers

P wave

depolarization of R/L atria

PR interval

tracks atrial impulse through AV node, bundle of His, and R/L bundle branches

QRS complex

depolarization of the ventricles

ST segment

end of ventricular conduction/depolarization; beginning of ventricular repolarization

T wave

ventricular recovery (repolarization)

pulse pressure (PP)

a reflection of stroke volume, ejection velocity, and systemic vascular resistance (SBP-DBP = PP)

baroreceptors

located in aortic arch, respond to blood pressure changes

chemoreceptors

respond to oxygen and carbon dioxide and blood pH

blood pressure regulator hormones

antidiuretic hormone (ADH) and Renin-Angiotensin-Aldosterone System (RAAS)

factors affecting BP

blood volume, artery diameter, cardiac output

autoregulation

the ability of the body tissues to regulate their own blood flow

tissue factors affecting blood flow

histamine, bradykinin, serotonin, prostaglandines

essential (primary) hypertension

hypertension with no known cause

secondary hypertension

hypertension resulting from some other condition

body response to hypotension

stimulate SNS, release NE/Epi, kidneys retain fluid, increase BP, vasoconstriction, activation of RAAS

body response to hypertension

kidneys excrete more fluid, decrease cardiac output, vasodilation

DASH

dietary approaches to stop hypertension

thiazide

antihypertensive, first line of treatment

Angiotensin Converting Enzyme inhibitors (ACEi)

Captopril

blocks conversion of Angiotensin I to Angiotensin II

Uses of ACEi

treats HTN, reduces proteinuria/slows renal impairment in diabetics, treats heart failure

ACEi adverse effects

angioedema, persistent cough, hyperkalemia

ACEi BBW

injury/death to fetus

ACEi nursing implications

increased risk of hyperkalemia, administer 1 hr before or 2 hrs after meals, can crush, monitor BP/HR, watch for persistent cough

Angiotensin II Receptor Blockers (ARBs)

Losartan

blocks vasoconstricting and aldosterone-secreting effects of angiotensin II receptors

ARBs not affective for what treatment

monotherapy in AA

ARB adverse effects

angioedema

BBW for ARBs

injury/death to fetus

ARB contraindications

P/L

ARB nursing implications

interaction with fluconazole (hypotension), assess BP/HR, electrolytes (K+), angioedema, hyperkalemia, monitor renal function

Calcium channel blockers (CCBs)

amlodipine, diltiazem, verapamil

first line of treatment for AA, inhibit influx of calcium ions

CCB use

hypertension, Afib

CCB adverse effects

headache, fatigue, dizziness, edema, flushing, N/V

CCB nursing implications

interacts with fluconazole/itraconazole-increases effects of CCBs, no grapefruit juice (toxicity), do not crush ER form, DO NOT stop abruptly - may result in rebound tachycardia

Direct Renin Inhibitors

aliskiren

inhibit conversion of angiotensinogen to angiotensin I

Direct Renin Inhibitors contraindications

do not take with a high fat meal, P/L

Direct Renin Inhibitors nursing implications

teach S&S of hyperkalemia, ensure pt not pregnant

Alpha1-adrenergic blocker

doxazosin, tamsulosin (BPH)

Beta-adrenergic blocker (olol)

metoprolol (selective)

propranolol (non-selective)

timolol (glaucoma)

alpha-beta-adrenergic blocker

carvedilol

Antiadrenergic agents

endocrine: hypoglycemia treatment

uses: HTN, MI prevention, BPH tx, glaucoma tx, tachycardia, angina pectoris, LV hypertrophy

Antiadrenergic agents BBW

must wean off, may cause reinfarction if stopped abruptly

Alpha1-adrenergic blockers (doxazosin)

used for BPH (tamsulosin)

give at bedtime

Alpha 2 agonists (clonidine)

decreased sympathetic outflow

used for children with ADHD

beta-adrenergic blockers BBW

DO NOT stop abruptly - may result in re-infarction, exacerbated angina, MI, death (CAD)

alpha-beta-adrenergic blockers how delivered

pushed over 5 min

carvedilol -take with food

NS should not be used with variant angina (ineffective)

other alpha blocker

phentolamine - given as antidote for infiltration of many cardiac drugs to prevent extravasation

Vasodilators

nitroprusside and hydralazine

nitroprusside

given IV, protect from light!

what happens if nitroprusside not placed under dark brown bag

metabolizes into cyanide

symptoms of cyanide toxicity

N/V, muscle twitching, spams, seizures

hydralazine

limited effect on HTN, give with adrenergic blocker and diuretic for fluid retention

diuretics

hydrochlorothiazide

monitor electrolytes (K+)

first line of treatment for HTN

furosemide

loop diuretic, monitor K+

spironolactone

potassium-sparing diuretic, still monitor labs

3 properties of cardiac cells

automaticity, excitability, conductivity

Na+ channel blockers: Class IA

cardiac effects: heart block/hypotension

Na+ channel blockers class 1A BBW

high risk for prodysrhythmic properties - save for life-threatening Ventricular arrhythmias

contraindications of Na+ channel blockers class 1A

heart block, prolonged QT syndrome

nursing implications of Na+ channel blockers class 1A

ECG, liver/renal fn, prevent interactions (avoid grapefruit juice)

IV form not compatible with furosemide

do not crush/chew

watch blood counts

Na+ channel blockers class 1C

flecainide

slow conduction velocity and refractory period

may cause new dysrhythmias

where should Na+ channel blockers class 1C be initiated

in the hospital under constant cardiac monitoring

use for Na+ channel blockers class 1C

life threatening ventricular arrhythmias

BBW for Na+ channel blockers class 1C

nonfatal cardiac arrest and death in patients with recent MI or chronic Afib

potentially fatal prodysrhythmic effects

class 2 beta-adrenergic blockers

NS: propranolol (B1-2) given PO/IV

action of class 2 beta-adrenergic blockers

slows stimulation of beta receptors

slows SA/AV nodal conductions

decreases influence of SNS

decreases excitability of heart, cardiac workload, and O2 consumption

uses for class 2 beta-adrenergic blockers

supraventricular tachycardia (SVT)

HTN

adverse effects of class 2 beta-adrenergic blockers

laryngospasms, bronchospasms, SA/AV blocks, pulmonary edema

contraindications for class 2 beta-adrenergic blockers

sinus bradycardia

2/3 degree block

HF

bronchial asthma

bronchospasm

nursing implications for class 2 beta-adrenergic blockers

interactions with drugs that increase QT interval (verapamil)

take with meals, do not discontinue abruptly

may mask signs of hypoglycemia

BBW for class 2 beta-adrenergic blockers

can exacerbate cardiac ischemia increasing risk of chest pain and MI if stopped suddenly, must wean off over 2 week period

class 3 potassium channel blocker

amiodarone

metabolites accumulate in liver, lungs, fat, skin and other tissues

need loading doses

action of class 3 potassium channel blockers

vasodilating effects and decreases SVR

prolongs conduction- duration of action potential

block cardiac potassium channels

uses for class 3 potassium channel blockers

various life threatening tachyarrhythmias, ventricular/atrial

IV for acute refractory of Vtach/Vfib

adverse effects of class 3 potassium channel blockers

cardiac arrhythmias, hepatotoxicity, thyroid dysfunction

BBW for class 3 potassium channel blockers

risk of fatal pulmonary toxicity

contraindications for class 3 potassium channel blockers

severe bradycardia, hypokalemia, thyroid dysfunction

nursing implications for class 3 potassium channel blockers

administration should begin in hospital with continuous monitoring and emergency equipment on standby

monitor HR, BP, ECG, watch for ectopy

patient teaching

class iv calcium channel blockers adverse effects

dizziness, brady cardia, hypotension, AV blocker, asystole

contraindications for class iv calcium channel blockers

impaired hepatic function

heart block

cardiogenic shock

nursing implications for class iv calcium channel blockers

interactions with amiodarone: increases risk of sinus arrest

do not give w/ grapefruit juice: increases toxicity

administer IV, titrate dose then start on oral

do not crush ER

unclassified antidysrhythmic: adenosine

used for paroxysmal SVT

how is adenosine given

rapid IV push/rapid flush