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NURS 2220 Cardio 2

Exam 2 - cardio/disorders of perfusion and dysrhythmias

Disorders associated with alteration in perfusion CAD/PAD, Angina, ACS, MI, heart failure, cardiomyopathy, hypertention, sudden death, pulmonary embolus, pulmonary hypertension, endocarditis, percarditis, cardiac tamponade
Cardiac output heart rate x stroke volume. How much blood volume the heart pumps in one minute. expressed in L/min
components of stroke volume preload + afterload + contractility
preload degree of stretch of cardiac muscle at the end of diastole -- affects how much blood can enter the ventricles
afterload resistance to ejection of blood from the ventricle. Affects how much much blood can be ejected from the ventricles with contraction.
contractility ability of the cardiac muscle to shorten in response to electrical impulse
stroke volume the amount of blood ejected from the heart with each contraction
ejection fraction percent of end diastolic volume ejected with each heartbeat
medications used to correct too slow heart rate positive chronotropes
medications used to correct too fast heart rate negaitve chronotropes, antidysrhythmics
medications that increase preload volume expanders
medications that decrease preload diuretics, venous dilators
medications that increase afterload vasopressors
medications that decrease afterload vasodilators
medications that increase the strength of heart contraction positive inotropic agents
medications that decrease the strength of heart contraction negative inotropic agents (betablockers, calcium channel blockers)
adrenergic a drug that has effects on epinephrine as a neurotransmitter. Can be a stimulant or an inhibitor.
cholinergic a drug that has effects on acetylcholine. Can be a stimulant or an inhibitor
sympathomimetic a drug that has effects similar to epinephrine. Produces tachycardia.
sympatholytic a drug that blocks the effects of epinephrine
chronotropic a drug that alters the heart rate
inotropic drug that increases the force of myocardial contractility
dromotropic increases the velocity of electrical conduction in the heart
vasopressor drug that increases blood pressure by constricting blood vessels
vasodilator drug that dilates blood vessels. May or may not produce hypotension
catecholamine a drug with a chemical structure similar to epinephrine
alpha receptors found in the arterioles of the skin, mucosa, gut, and kidneys. causes arteriolar vasoconstriction when stimulated.
beta 1 receptors found in the myocardial muscle tissue and cardiac conduction system. Increase contractility and heart rate when stimulated.
beta 2 receptors found in vascular smooth muscle, bronchi and liver. cause coronary and peripheral vasodilation, bronchodilation when stimulated.
dopaminergic receptors found in the renal and mesenteric vasculature. Cause renal and mesenteric vasodilation when stimulated.
normal volume percentages 60% intracellular, 30% interstitial, 10% intravascular volume
primary volume issue intravascular volume. The circulating blood volume affects organ perfusion.
edema/swelling/fluid retention interstitial volume issue.
Crystalloid fluid therapy to increase preload Usually normal saline, Ringer's lactate. Hypotonic fluid (1/2 NS) or D5W are transient in intravascular space. Replacement of lost plasma volume requires 4x the volume of NS or LR.
Colloid fluid therapy to increase preload solutions containing starch or albumin. These hold fluid in the vascular bed.
Diuretic therapy to decrease preload Kidneys must be functional! osmotic diuretics (Mannitol, work in the proximal loop), loop diuretics (Lasix, work in the ascending loop, most potent agents), thiazide diuretics (work in the descending loop, often used in combination with loop agents).
Situations where vasodilators are used hypertension, heart failure (reduces preload and afterload), angina pectoris (coronary vasodilation, reduces O2 demand)
Effects of morphine on preload and afterload often used as a diuretic adjunct, helps reduce pulmonary edema, effects vasodilation of the pulmonary vascular bed, can give 1-3 mg IV, repeat q5 min. Administer cautiously to patients with asthma, head injury, ileus, or resp insufficiency
Nitroprusside affects preload and afterload. Rapid onset, used for hypertension crisis, acute CHF. Safe dosage 0.3-5 mcg/kg/min
Nitroglycerin affects preload, higher doses may decrease afterload. Rapid onset, used for post-op hypertension, unstable angina, CHF associated with MI. Safe dosage 10-100 mcg/min
Beta blockers have negative inotropic effects, used for hypertension, angina, chronic heart failure, control heart rate with Afib and other SVT. Can reduce risk of second MI, used perioperatively for non-cardiac surgery
Vasopressors cause vasoconstriction, used primarily when patient is still hypotensive in spite of fluids, often used in cases of sepsis, cadriogenic or post-op cardiac surgery.
Vasoconstrictors and afterload used for tachyarrhythmias, cardiac ischemia, vasopressin can cause tissue necrosis if it extravasates via IV.
Properties of cardiac cells automaticity, excitability, conductivity, contractility
Control of the heart ANS controls rate of impulse formation, speed of conduction, strength of contraction. pSNS controls the vagus nerve (decreases rate, slows impulse conduction, decreases force of contraction). SNS increases HR, force of contraction
depolarization electrical activatin of a cell caused by an influx of sodium into the cell while potassium exits the cell.
repolarization return of the cell to resting state when potassium re-enters the cell and sodium leaves
refractory period effective: phase in which cells are incapable of repolarizing relative: phase in which cells require stronger-than-normal stimulus to depolarize
normal pacemaker of the heart SA node
primary backup pacemaker of the heart AV node
secondary backup pacemaker of the heart ventricular cardiac cells
ECG electrocardiogram
P wave indicates the SA node is initiating an electrical impulse
PR interval amount of time it takes for the impulse to travel from the SA node through the atrium to the AV node
QRS complex amount of time it takes for the impulse to travel through the ventricles from the AV node to the bundle of His, through the bundle branches and the Perkinje fibers
ST segment early phase of ventricular repolarization
T wave bulk of the ventricles repolarizing
QT interval total amount of time it takes for the ventricles to depolarize and repolarize
Caring for patients with dyrhythmias assess CO and oxygenation, changes in LOC. ASsess rate, rhythm of apical and peripheral pulses, heart sounds, BP, pulse pressure, fluid retention, EKG.
normal sinus rhythm SA node fires 60 to 100 bpm. Follows a normal conduction pattern. can be bradycardia or tachycardia if HR is decreased or increased
sinus bradycardia SA node fires less than 60 bpm. Can be normal during sleep or for aerobically trained athletes
sinus tachycardia SA node fires more than 100 bpm. Can be normal during exercise.
clinical associations for bradycardia hypthermia, carotid sinus massage response, increased vagal tone, certain meds - parasympathomimetic drugs, hypothyroidism, increased ICP, obstructive jaundice, inferior wall MI
symptoms associated with bradycardia hypotension, pale/cool skin, weakness, angina, dizziness, confusion, disorientation, SOB
treatment of bradycardia atropine, pacemaker
clinical associations for tachycardia exercise, pain, hypovolemia, myocardial ischemia, heart failure, fever
symptoms associated with tachycardia dizziness, hypotension, angina
treatment of tachycardia determined by underlying cause, b-adrenergic blockers to reduce HR, antipyretics for fever, analgesics for pain
Common abnormal rhythms atrial flutter, atrial fibrillation, Junctional dysrhythmias, AV block (1st, 2nd and 3rd degree), premature ventricular contractions, v-tach, v-fib, asystole, pulseless electrical activity (PEA)
most common abnormal heart rhythm in the elderly population atrial fibrillation
atrial flutter tachydysrhymthmia. irritable site within the atrium that depolarizes rapidly. Not all impulses get through the AV node and cause ventricular contraction. Looks like jagged, sawtooth-shaped waves on the EKG. Originates from a single ectopic focus.
clinical conditions associated with atrial flutter CAD, hypertension, mitral valve disorders, pulmonary embolus, chronic lung disease, cardiomyopathy, hyperthryroidism, use of meds such as digoxin, quinidine, and epinephrine.
treatment of atrial flutter goal is to slow ventricular response by increasing AV block. First line treatment: anti-dysrhythmia drugs such as amiodarome or propafenone. Otherwise, radiofrequency catheter ablation can destroy the irritable area.
clinical significance of atrial flutter high ventricular rates and loss of atrial kick due to rapid, ineffective contractions can decrease cardiac output and precipitate heart failure, angina. Risk for stroke increases due to risk of thrombus formation in the atria
atrial kick contraction of the atria
atrial fibrillation disorganized atrial electrical activity due to multiple ectopic foci resulting in loss of atrial contraction. Prevalence increases with age, most common dysrhythmia in the elderly population.
Clinical conditions associated with atrial fibrillation underlying heart disease such as rheumatic heart disease, CAD. Cardiomyopathy, heart failure, pericarditis. May be caused by thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbance, cardiac surgery
clinical significance of atrial fibrillation decrease in cardiac output due to ineffective atrial contractions (loss of atrial kick) and rapid ventricular response. Thrombi may form in the atria as a result of blood stasis. If an embolus develops and travels to the brain, stroke may occur.
treatment of atrial fibrillation goal is to decrease ventricular response, prevent embolic stroke. Drugs used for rate control: b-andrenergic blockers (#1), calcium channel blockers (#2), digoxin. anticoagulation therapy (coumadin), anti-dysrhythmics, cardioversion, ablation, Maze
cardioversion electrical shock administered to "reset' the heart and hopefully convert to normal sinus rhythm. Delivered at a specific point in the cardiac cycle
junctional dysrhythmias originate in the AV node, usually because the SA node has failed to fire. Typically slower heart rates (40-60 bpm), normal QRS complex, no P-wave. Patiens may or may not be symptomatic. If not, lower ventricular rate is reason why patients can tolerate
clinical conditions associated with junctional dysrhythmias CAD, HF, cardiomyopathy, electrolyte imbalances, intferior MI, rheumatic heart disease, drugs such as digoxin, amphetamines, caffeine, nicotine.
clinical significance of junctional dysrhythmias servers as a safety mechanism when the SA node has not been effective, so we want to support these rhythms. Escape rhythms should not be suppressed. Rapid rhythms may result in reduction of cardiac output and heart failure
treatment of junctional dysrhythmias depends on whether patient is symptomatic. Drugs (atropine, b-adrenergic blockers, calcium channel blockers, and amiodarone). D/c digoxin if caused by digoxin toxicity. Pacemakers for patients who are symptomatic
AV Blocks First-Degree - not bad. Second-Degree Type I - sorta bad. Second-Degree Type II - quite bad. Third-Degree - very bad.
First-Degree AV block All impulses get through the AV node, but there is a delay in the impulse getting through. Normal conduction time is 0.2 seconds. First-Degree AV block is greater than 0.2 seconds, consistent for each beat
clinical conditions associated with first-degree AV block MI, CAD, rheumatic fever, hyperthyroidism, vagal stimulation, drugs such as digoxin, beta blockers, calcium channel blockers, flecainide
clinical significance of first-degree AV block usually asymptomatic. May be a precursor to higher degrees of AV block.
treatment for first-degree AV block monitor
Second-degree AV block type 1 (Mobitz I, Wenckebach gradual lengthening of the PR interval due to prolonged conduction time. Progressive delay until atrial impulse is nonconducted and a QRS complex is blocked. Block usually occurs at the AV node, but may occur in the His-Purkinje system
clinical conditions associated with Second-degree type 1 AV block drugs: digoxin, beta blockers. May be associated with CAD and other diseases that can slow AV conduction
clinical significance of second-degree type 1 AV block usually a result of myocardial ischemia or infarction. Almost always transient and well tolerated. May be a warning signal of more serious AV conduction disturbance
treatment for second-degree type 1 AV block observation if new onset. If patient is not tolerating it is usually because the ventricular rate is too slow. Permanent pacemakers for patients who do not tolerate. Symptomatic bradycardia is more likely with hypotension, HF and shock
Second-degree type 2 AV block (Mobitz II) The SA node fires normally, but some impulses are non-conducted. Usually occurs when a block in one of the bundle branches is present
clinical conditions associated with second-degree type 2 AV block rheumatic heart disease, CAD, anterior MI, digitalis toxicity
clinical significance of second-degree type 2 AV block often a result of heart disease. often progresses to third-degree AV block and is associated with a poor prognosis, reduced HR results in decreased CO, hypotension and myocardial ischemia
treatment of second-degree type 2 AV block if symptomatic, pacemaker.
third-degree AV heart block (complete heart block) no impulses from the atria are conducted to the ventricles. Atria are stimulated and contract independently from the ventricles. Ventricular rhythm is an escape rhythm. Very irregular PR interval.
clinical conditions associated with third-degree AV heart block severe heart disease (CAD, MI, myocarditis, cardiomyopathy), systemic diseases (amyloidosis, scleroderma), drugs (digoxin, beta blockers, calcium channel blockers)
clinical significance of third-degree AV block very symptomatic. decreased cardiac output with subsequent ischemia, heart failure and shock. Syncope may result from severe bradycardia or even periods of asystole. Low ventricular rate causes symptoms
treatment of third-degree AV block pacemaker, even if asymptomatic. Permanent pacemaker ASAP. Drug therapy rarely used.
escape rhythm usually occurs 2-3 seconds after failed conduction from the SA node. If it occurs several times, it is called an escape rhythm vs. an escape beat
Premature ventricular contractions (PVC) contraction originating in the ectopic focus of the ventricles. Results in a wide and distorted QRS complex. Can be multifocal, unifocal, ventricular bigeminy, ventricular trigeminy, couples, triplets, R on T phenomena
clinical conditions associated with PVC stimulant use: caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol. Digoxin. Electrolyte impabalances (esp. K+ and Mg2+), hypoxia, fever, diseases: MI, mitral valve prolapse, HF, CAD
clinical significance of PVC usually benign in a normal heart. May result in peripheral pulse defecit -- radial pulse cannot be felt due to insufficient ventricular contraction, ventricular irritability
treatment of PVC based on the cause. Oxygen therapy for hypoxia, electrolyte replacement (must replace both K+ and Mg2+), beta blockers, procainaminde, amiodarone**, lidocaine
ventricular tachycardia run of three or more PVCs. Monomorphic, polymorphic, sustained or nonsustained. Considered life-threatening because of decreased cardiac output and possibilty of deterioration ventricular fibrillation. No atrial kick, ventricles do not refill with blood
clinical conditions associated with v-tach MI, CAD, electrolyte imbalances, cardiomyopathy, mitral valve prolapse, long QT syndrome, digitalis toxicity, CNS disorders
clinical significance of v-tach patient can be stable (pulse) or unstable (no pulse). Sustained v-tach results in decrease in CO, hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest.
treatment of v-tach treat the cause if possible. For patients with a pulse, IV procainamide, sotalol, amiodarone, or lidocaine. For patients without a pulse, code, CPR, defibrillation. Epinephrine if defibrillation is unsuccesful.
ventricular fibrillation severe derangement of the heart rhythm characterized on the ECG by irregular undulations of varying contour and amplitude. (quivery). No effective contraction or cardiac output occurs
clinical conditions associated with v-fib acute MI, CAD, cardiomyopathy, may occur during cardiac procedures, accidental electric shock, hyperkalemia, hypoxia, acidosis, drug toxicity
clinical significance of v-fib patient will be unresponsive, pulseless and apneic. Death will result if not treated immediately.
treatment of v-fib CPR, ACLS, defibrillation and drug therapy
asystole total absence of ventricular electrical activity. No ventricular contraction or cardiac output occurs.
clinical conditions associated with asystole advanced cardiac disease, severe cardiac conduction system disturbance, end-stage HF
clinical significance of asystole patient will be unresponsive, pulseless, apneic. Prognosis is extremely poor.
treatment of asystole CPR, ACLS measures, transcutaneous pacing, IV therapy with epinephrine and atropine
Pulseless electrical activity (PEA) electrical activity that can be observed on the ECG, but no ventricular contractions
clinical conditions associated wtih PEA hypovolemia, hypoxia, metabolic acidosis, hyperkalemia or hypokalemia, hypothermia, drug overdose, cardiac tamponade, MI, tension pneumothorax, pulmonary embolus
treatment of PEA CPR, intubation, IV epinephrine. Atropine is used if the ventricular rate is slow. Treatment is directed toward correction of the underlying cause.
Sudden Cardiac Death death from a cardiac cause. Majority of sudden cardiac deaths result from ventricular dysrhythmias - vtach or vfib. Usually no warning signs
defibrillation most effective method of terminating vfib or pulseless vtach. Passage of DC electrical current through the heart to depolarize the cells of the myocardium to allow the SA node to resume the role of pacemaker. monophasic or biphasic waveform.
pacemakers implanted device that is used to pace the heart when the normal conduction pathway is damaged or diseased. Power source, one or more conducting leads and the myocardium. Myocardium (atria and ventricles) contract after stimulus from the pacemaker.
Created by: pinklrt98