what does cardiac cycle consist of?

periods of atrial and ventricular systole (contraction and closed valves) and atrial and ventricular diastole (relaxation)

automaticity or autorythmicity

ability of cardiac muscle tissue to contract on its own, without neural or hormonal stimulation

nodal cells

establish rate of cardiac contraction; depolarize spontaneously and determine heart rate

conducting fibers

distribute the contractile stimulus to the general myocardium

in which node are pacemaker cells found?

in the sinoatrial (SA) node (cardiac pacemaker)

what is function of pacemaker cells?

to establish rate of contraction

where is the main pacemaker region of the heart?

in the wall of the right atrium

path of stimulus

from the SA node to internodal pathways to atrioventricular (AV) node to AV bundle, which divides into a right and left bundle branch. From here Purkinje cells convey the impulses to the ventricular myocardium.

what happens during diastole?

chambers of the heart fill up

during one cardiac cycle, where does the heart spend most of its time?

diastole

what happens during systole?

the inner volume of atrial chambers decreases

electrocardiogram (ECG,EKG)

recording of electrical activities in the heart

important landmarks of ECG

p wave, QRS complex, T wave

P wave

atrial depolarization

QRS complex

ventricular depolarization

T wave

ventricular repolarization

what does ECG analysis reveal and detect?

reveals the condition of the conducting system; detects cardiac arrythmias

cardiac arrythmias

abnormal patterns of cardiac activity

ST segment

time between ventricular contraction and relaxation

How does the ANS modify the heart rate?

norepinephrine produces an increase in heart rate and force of contraction, while acetylcholine produces a decrease in heart rate and contraction

cardioacceleratory center

located in the medulla oblongata; activates sympathetic neurons

cardioinhibitory center

governs the activities of the parasympathetic neurons

from what do cardiac centers receive inputs?

higher centers and receptors monitoring blood pressure and concentrations of dissolved gases in the blood

Terms
Hyperkalemia Hypokalemia Hypercalcemia Hypocalcemia Hypothermia

Definitions
QRS widens, P wave flattens, T wave peaks T wave flattens (or inverts), produces a U wave QRS widens, QT shortens Prolongs QT interval ST elevates, slows rhythm

Digitalis Quinidine Beta Blockers

ST depresses, T wave flattens (or inverts), QT shortens QT lengthens, T wave flattens (or inverts), QRS lengthens HR (pulse rate) decreases, blunts HR response to exercise; Examples: Propranolol/Inderal

Nitrates Antirrhythmic Agents Kalemia Calcemia Premature Ventricular Contractions (PVC)

Increases HR Prolongs QRS and QT intervals Potassium Calcium Abnormally wide, irregularly spaced QRS complexes, P wave maybe absent

Terms
A single cycle = 1st stage is 1st stage which is diastole Represents

Definitions
2 stages diastole ventricular filling and a brief period just prior to filling at which time the ventricles are relaxing

2nd stage is Stage 2 systole

systole Represents the time of contraction and ejection of blood from the ventricles

Diastole Step 1

Atria and ventricles are relaxed & the atrioventricular valves are open

Diastole Step 2

De-oxygenated blood from the superior and inferior vena cava flows into the right atrium

Diastole Step 3

The open AV valves allow blood to pass through to the ventricles

Diastole Step 4

The SA node contracts triggering the atria to

contract Diastole Step 5 The right atrium empties its contents into the right ventricle Diastole Step 6 The tricuspid valve prevents the blood from flowing back into the right atrium Diastole Step 7 In the next diastole period, the semilunar valves close and the AV valves open Diastole Step 8 Blood from the pulmonary veins fills the left atrium. Blood from the vena cava is also filling the right atrium Diastole Step 9 The SA node contracts again triggering the atria to contract Diastole Step 10 The left atrium empties its contents into the left ventricle Diastole Step 11 The mitral valve prevents the oxygenated blood from flowing back into the left atrium Systole Step 1 Right ventricle receives impulses from the Purkinje fibers and contracts Systole Step 2 Systole Step 3 The AV valves close and the semilunar valves open The de-oxygenated blood is pumped into the pulmonary artery Systole Step 4 The pulmonary valve prevents the blood from flowing back into the right ventricle Systole Step 5 The pulmonary artery carries the blood to the lungs. There the blood picks up oxygen and is returned to the left atrium of the heart by the pulmonary veins Systole Step 6 Left ventricle receives impulses from the Purkinje fibers and contracts

Systole Step 7 Systole Step 8

Oxygenated blood is pumped into the aorta The aortic valve prevents the oxygenated blood from flowing back into the left ventricle

Systole Step 9

The aorta branches out to provide oxygenated blood to all parts of the body. The oxygen depleted blood is returned to the heart via the vena cava

What heart sounds are found in systole? Phase 1 Phase 2: Isovolumetric contraction Phase 3 Phase 4 Aortic valve closes "dub", S2 Phase 5 Phase 6 Phase 7 Stroke volume

S3 & S4 Heart Sounds Atrial contraction,Atrial systole Mitral valve closes "lub", S1, Begins ventricular systole Rapid ejection Reduced ejection, Begins ventricular diastole Isovolumetric relaxation Rapid filling Reduced filling Amount of blood that is ejected from the ventricles with each beat

Ejection fraction

Ratio of the stroke volume ejected from the left ventricle with each beat to the volume of blood at the end of diastole Left Ventricular End Diastolic Volume

Ejection Fraction 50% is Ejection Fraction < 35% means

normal Poor ventricular function, Poor ventricular filling, Obstruction to outflow

Cardiac Conduction System consist of

SA Node, Intranodel Pathways, AV Nodes, Left and

Right Ventricle, Purkinje Fibers SA Node (Pacemaker) Rate AV Node (AV Junction) Rate Ventricles (Bundle Branches) Rate Purkinje Fibers Rate Reading an ECG 1 mm square equal Reading an ECG 5 mm square equal Reading an ECG amplitude (voltage) is Reading an ECG duration (width) Reading an ECG baseline is the P Waves P waves come before Duration of PR interval (PRI) PRI Interval PRI represents the time it takes for electrical impulse to travel from Reading an ECG Ask Ask Is the P wave Ask are all Ps Ask is there one P wave for every Ask is the PRI Ask are there any do you see a P wave? shaped normally? similar Q wave, is there a 1:1 ration of P:QRS normal Abnormal P waves 60-100 40-60 20-40 <15 0.04 seconds 0.20 seconds (0.04 x 5 = .20) measured in millimeters measured in seconds isoelectric line, ECG Waveforms, Atrial depolarization (activation) QRS 0.12-0.20 seconds Rounded and upright deflection in I, II, aVF, V4, V6, SA throughout atria

Ask are there anyTall, Peaked P waves mean Wide m-shaped P waves mean QRS Complex The Electrical conduction of the QRS The Q wave is the R wave The S wave is a The QRS Complex duration is Reading an ECG Ask is there a QRS for every Ask is the R to R Normal duration of the QT Interval beginning of QRS to end of T faster HR The slower HR QT interval upper limits Corrected QT (QTc) QTc calculated by

Peaked P waves Right atrial hypertrophy, P pulmonale Left atrial hypertrophy ,P mitrale Ventricular depolarization or activation down bundle to Purkinje Fibers 1st negative deflection 1st positive deflection negative deflection after R 0.06-0.12 seconds P wave? regular ventricular excitation, contraction, recovery length depends on heart rate The shorter QT interval The longer the QT interval 0.39-0.43 seconds Normal HR: QT interval is < half the RR interval dividing the QT interval by the square root of the RR cycle length

Normal QTc is QT = .87, .38 .87 = .44

<0.44sec Example .38, RR= .76, Square root of RR= ST Segment

Time of no electrical activity Ventricular depolarized and starting repolarization End of QRS to beginning of T 'length', only 'height' Describe as isoelectric, elevated, or depressed Ventricular repolarization vulnerable period to hit and cause PVC measure duration Upright, round & smooth shape, inverted, peaked, or depressed Repolarization of Bundle of His and Purkinje fiber Normal in children hyperthyroidism or hypokalemia in adults Regularity Regular 60-100 P wave

ST Segment ST Segment When evaluating the ST segment do not measure When evaluating the ST segment T Wave The Peak of T T wave Do not Describe T wave U wave

The U wave is The U wave can represents Normal Sinus Rhythm Normal Sinus Rhythm Rate Normal Sinus Rhythm Normal and upright: One P wave in front of each QRS

PRI Rate QRS Rate Sinus Tachycardia Rate Causes of Sinus Tachycardia

.12 -.20 seconds & constant < .12 seconds 101-150 Increased O2 demand ,fever, exercise, Compensatory response to low Cardiac Output (CO) Congestive heart Failure (CHF), dehydration, hypovolemia

Hemodynamic effect of Sinus tachycardia Sinus Tachycardia Management Sinus Bradycardia Rate Causes for Sinus Bradycardia SA nodal disease SA Nodal disease or Sick Sinus Syndrome Hemodynamic effects Sick Sinus Syndrome Signs and Symptoms Management for symptomatic bradycardia: Sinus Arrhythmia Regularity Sinus Arrhythmia Rate Sinus Arrhythmia P wave Sinus arrhythmia PRI Rate Sinus Arrhythmia QRS Rate Sinus Arrhythmia Causes

Increased heart rate improves Cardiac Output Correct cause <60 beats per minute Increased parasympathetic tone: Athletes Sick Sinus Syndrome Decreased Cardiac Output

hypotension ,Orthostatic hypotension, syncope Atropine, Pacemaker Irregular 60-100 Normal and upright, one in front of each QRS .12 - .20 seconds < .12 seconds Heart Rate varies with respirations, due to fluctuations in parasympathetic outflow

Sinus Arrhythmia Rate increases Atrial Rhythm

with inspirations, decreases with expiration P wave Abnormal: may be flattened, notched or lost in QRS, PRI rate is .12-.20 QRS< .12seconds, PRI, one in front of each QRS

Causes of Atrial Rhythm Hemodynamic effects of Atrial Rhythm Management of Atrial Rhythm Premature Atrial Contractions (PAC)

Irritable focus: sympathetic stimulation, caffeine None None, reassurance Single beat originates in atria and comes early in

cardiac cycle, Can occur in a cyclic pattern, Bigeminy, trigeminy Atrial Tachycardia Rate Atrial Tachycardia P Wave Abnormal: coming from different foci in heart .12-.20 seconds less than .12 seconds Irritable SA or AV nodes Depends on individual compensation abilities Vagal stimulation cough, bear down, carotid massage, Adenosine, Beta Blockers,Ca channel Blockers, Amiodarone A , Adensosine B, Beta Blockers, C, Calcium Channel Blocker Area in atrium initiates impulse that is conducted in repetitive, fast, cyclic pattern Can be regular or irregular 250-350 "Saw Tooth" appearance Not measurable Normal Atrium very irritable: no longer beating in uniform fashion, quivers Irregularly, irregular Greater than 350 beats per minute Atrial Fibrillation Regularity Atrial Fibrillation P wave Atrial Flutter Rate Atrial Flutter P wave characteristics Atrial Flutter PRI Atrial Flutter QRS is Atrial Fibrillation Atrial Fibrillation Regularity Atrial Flutter Regularity Atrial Flutter Atrial Tachycardia QRS is Cause for Atrial Tachycardia Hemodynamic effect of Atrial Tachycardia Management of Atrial Tachycardia: ATRIAL Tachycardia ABC 150-250 Atrial Tachycardia PRI

Not measurable Not Measurable QRS Normal Heart Dx, ischemia, rheumatic, mitral or tricuspid valve disorders, overstretched atrium congestive heart failure lose atrial kick, decreased stroke volume, Varying ventricular response, decreased diastolic filling time Rhythm Control Pharmacologica Management of Atrial Fibrillation and Flutter

Atrial Fibrillation PRI Atrial Fibrillation Causes of Atrial fibrillation Hemodynamic effects of Atrial Fibrillation

Management of Atrial Defibrillation and Atrial Flutter

Convert to Normal Sinus Rhythm Amiodarone, disopyramide, flecainide, dofetilde, sotalol , Electrical cardioversion , only if less than 48 hours!

Surgical Management of Atrial Fibrillation

MAZE procedure, requires open heart surgery, Ablation procedure

Rate Control Pharmacologic Complication Prevention Junctional Rhythms

control the ventricular response Calcium channel blockers, beta blockers, digoxin Anticoagulate Also called junctional escape rhythm. AV node has taken over when higher pacemaker fails to initiate or conduct to AV node

Junctional Rhythm Regularity Junctional Rhythm Rate Junctional Rhythm P wave Junctional Rhythm PRI

Regular 40-60 Inverted before, during, or after QRS Measurable only if before the QRS, then less than .12

Junctional Rhythm QRS:

Normal

Treat Junctional Rhythm if symptomatic with Accelerated Junctional Rhythm Accelerated Junctional Rhythm Rate

ATROPINE Same as junctional rhythm, but faster rate 61-100, Usually well tolerated by patient, No treatment necessary

Premature Junctional Contractions

Single beat originating within AV junction. Atria depolarize by retrograde conduction (backwards). Causes the P wave to be inverted and occur before, during, or after QRS

Premature Junctional Contractions Regularity: Premature Junctional Contractions Rate Premature Junctional Contractions P wave is Premature Junctional Contractions PRI is

Usually irregular because of PVC Depends on the underlying rhythm Inverted before, during, or after QRS Measurable only if before the QRS, then less than .12

Premature Junctional Contractions QRS is Premature Junctional Contractions Causes

Normal Irritable focus within AV junction, consider Digitalis toxicity

Hemodynamic effects of Premature Junctional Contractions is Premature Junctional Contractions Management Junctional Tachycardia Rate Hemodynamic effect more pronounced with

None

Observe 101-180 beats per minute junctional tachycardia. Leads to decreased cardiac output, due to abnormal atrial kick and rapid rate

Managementof Junctional Tachycardia

Control rapid rate with Calcium channel blocker, Beta blocker, or Amiodarone

AV nodal ablation with PM for severe

symptomatic patients,Narrow Complex Tachycardias

Supraventricular Tachycardia (SVT)

a broad term for a group of rhythms originating

above the ventricle Supraventricular Tachycardia Sinus tachycardia, Atrial tachycardia, Atrial flutter, Atrial fibrillation, Junctional tachycardia Supraventricular Tachycardia Rate PSVT Paroxysmal Supraventricular Tachycardia Treatment Premature Ventricular Contraction 150-250 Paroxysmal Supraventricular Tachycardia Vagal Stimulation, Adenosine, Amiodarone, Cardizem, Cardioversion, Ablation Single beat originating from ventricle. Ventricle depolarizes in abnormal fashion Premature Ventricular Contraction Regularity Premature Ventricular ContractionRate Premature Ventricular Contraction P wave Irregular Depends on underlying rhythm PVC does not have P wave Premature Ventricular Contraction PRI PVC (no PRI)Underlying rhythm (PRI Normal) PVC wide bizarre, others normal, Can occur in a cyclic pattern, Bigeminy, trigeminy Can occur together, Couplets, triplets 5-beat 'run', May be unifocal or multifocal Multifocal PVCs, R on T Assess for etiology, is it Drug induced, Caffeine, alcohol, cocaine, sympathomimetic drugs Hypoxia,Cardiac disease, Acute coronary syndrome, cardiomyopathy, ventricular aneurysm, Metabolic imbalance, acidosis, Hypokalemia, Irritation of the ventricle cause, Antidysrhythmic medication Ventricular impulse site speeds up and takes over Ventricular Tachycardia Ventricular Tachycardia Regularity Treat the Management: PVC Causes of Premature ventricular contractions Sinus tachycardia with PVCs in quadrigeminy Premature Ventricular Contraction QRS Premature Ventricular Contraction

heart rhythm Usually regular Ventricular Tachycardia Rate Ventricular Tachycardia P wave Ventricular Tachycardia PRI QRS Wide bizarre, greater than .12 sec. Defibrillate, CPR, Epinephrine Amiodarone, Sotalol, Lidocaine Cardioversion Rapid unstable form of V-tach where QRS appears to twist electrical orientation around the isoelectric line drugs that prolong QT interval (Quinidine, Amiodarone, Tricyclic antidepressants), hypomagnesemia, hypocalcemia, Congenital long QT syndromes Correct cause and give IV Mg sulfate Usually regular 20-40 None None Wide bizarre, greater than .12 seconds Ventricular Fibrillation Idioventricular Rhythm Regularity Idioventricular Rhythm Rate Idioventricular Rhythm P wave Idioventricular Rhythm PRI Idioventricular Rhythm QRS Idioventricular Rhythm Treatment4 Atropine, PPM Extremely irritable heart. Totally chaotic with no discernable waves or complexes Ventricular Fibrillation Hemodynamic effects No contraction: no forward blood flow, no cardiac output Management: Vfib + pulseless Vtach CHECK for a PULSE, no pulse, then, SHOCK at (150-200j for biphasic) or (360j for monophasic), Torsades de Pointe treatment 150-250 None None Ventricular TachycardiaQRS VTach (Pulseless) VTach (With Pulse) Torsades de Pointe Torsades de Pointe Etiology

CPR for 5 cycles (about 2 minutes), CHECK for a PULSE. Asystole No electrical activity, Results in flat line on ECG monitor Asystole Management: Check in different lead, CPR, Epinephrine every 3-5 minutes PEA Pulseless electrical activity Electrical activity without mechanical contraction. Rhythm on monitor without detectable puls Asystole Management PEA 5 H"s Epinephrine 1 mg q 3-5 min, CPR, Correct cause Evaluate for cause Hypovolemia, Hypoxia, Hydrogen ions (acidosis), Hyper or hypokalemia ,hypothermia Five, T's Tables, Drug overdose, Tamponade, Tension pneumothorax, Thrombosis , coronary, Thrombosis

Management for Bradycardia

Meds - Atropine and isoproterenol Electrical Mgmt. - Pacemaker

Management for Atrial fibrillation, supraventricular tachycardia (SVT), or ventricular tachycardia with pulse

Meds - Amiodarone, adenosine, verapamil Electrical Mgmt. - Synchronized cardioversion

Management for Ventricular tachycardia without pulse or ventricular fibrillation

Meds - Amiodarone, lidocaine,and epinephrine Electrical Mgmt. - Defibrillation

Cardioversion

Delivery of a synchronized, direct countershock to the heart, used "shock" the heart back to normal sinus rhythm.

Defibrillation

Delivery of an unsynchronized, direct countershock to the heart, used during v-fib or pulseless v-tach.

Pacemaker

A battery-operated device that electrically stimulates the heart when the natural pacemaker of the heart fails to maintain an acceptable rhythm.

Stable angina

Occurs with exercise or emotional stress and is relieved by rest or nitroglycerin (Nitrostat).

Unstable angina

Occurs with exercise or emotional stress, but it increases in occurrence, severity, and duration over time.

Variant angina

is due to a coronary artery spasm, often occurring during periods of rest.

ANGINA

*Precipitated by exertion or stress *Relieved by rest or nitroglycerin *Symptoms last < 15 min *Not associated with nausea, epigastric distress, dyspnea, anxiety, diaphoresis

MYOCARDIAL INFARCTION

*Can occur without cause, often in the morning after rest *Relieved only by opioids *Symptoms last > 30 min *Associated with nausea, epigastric distress, dyspnea, anxiety, diaphoresis

Asystole

no cardiac electrical activity, no contractions of the myocardium and no cardiac output or blood flow.

Disseminated Intravascular Coagulation (DIC)

Abnormal excessive clotting depleting clotting factors & trigger diffuse hemorrhage. *Risk factors include:

Blood transfusion reaction Cancer, especially certain types of leukemia Infection in the blood by bacteria or fungus Liver disease Pregnancy complications (such as placenta that is left behind after delivery) Recent surgery or anesthesia Sepsis (a serious infection) Severe tissue injury (as in burns and head injury) *Symptoms Bleeding, possibly from multiple sites in the body Blood clots Bruising Drop in blood pressure

Prothrombin time (PT)

performance indicator measuring the efficacy of the "extrinsic" coagulation pathways (damaged tissue). 12-15 sec. Level 1.5-2.5 x's normal Standard Lab for Coumadin

Activated partial thromboplastin time (APTT)

performance indicator measuring the efficacy of the "intrinsic" coagulation pathways (damaged vessel linings & Factors). 30-45 sec. Level should be 1.5-2.5 x's normal & activated clotting time (ACT) - Lab for heparin

Platelet count norms

150,000-400,000/ul

Activated partial thromboplastin time (APTT) Values

30-45 sec. (Intrinsic)

Prothrombin time (PT) Normal Value

12-15 sec. (Extrinsic)

International normalized ratio (INR) Norms

< 2.0

APPT & PT value for Anticoagulant Therapy

1.5-2.5 x's normal

FSP (Fibrin split products) Norms

< 10mg/L

D-dimer assay

< 250ng/mL (specific to DIC, pulmonary embolus)

COAGULATION DISORDERS

Hemophilia A - factor VIII deficiency Hemophilia B - factor IX deficiency von Willebrand's disease - platelet dysfunction ITP Immune Thrombocytopenic Purpura - Autoimmune platelet destruction DIC - Abnormal excessive clotting depleting clotting factors

Normal Platelet Count

150,000 - 400,000 platelets per microliter (mcL).

Hemoglobin norms

12-18 g/dL

Hematocrit Norms

37-52%

Potassium Norms

3.5 - 5

Blood glucose norms

70 - 110

ITP Immune Thrombocytopenic Purpura

Autoimmune platelet destruction, children after viral illness, Chronic ITP women 20-40 yrs, D. *Platelets have short lifespan of 1-3 days (normal 8-10 days) *S & S: petechiae, ecchymoses, purpura, prolonged bleeding, menses, nose or gums *low plts < 150,000, anemia,

ITP treatment

A. Platelets (< 20,000 = life threatening for cerebral hemorrhage) B. Corticosteroids C. Splenectomy D. Immunosuppressive agents E. plt transfusions F. IV immunoglobulin (attach to the antibodies on the platelets to help the platelets live longer) G. Eltrombopag (Promacta)--thrombopoietin receptor agonist

DIC Lab Values

1. PT---prolonged 2. APTT---prolonged 3. Fibrinogen level---decreased 4. Platelets---decreased 5. **FSP's---increased (specific to the breakdown of fibrin) 6. **D-dimers---increased (specific to the breakdown of fibrin)

DIC Tx

1. *Treat underlying cause 2. Reverse clotting/control bleeding 3. Transfusion therapy--platelets, FFP, packed RBCs, Factor replacement 4. Antithrombin III 5. Drotrecogin alfa (Xigris)

DVT symptoms

*S&S - Calf. Groin pain or tenderness, Leg area reddened and warm, Possibly cyanosis, Measure circumference of both legs, Mild fever

Pulmonary Embolism symptoms

S&S - Sudden, pleuritic chest pain, Dyspnea, tachypnea, Anxiety, Tachycardia, Hemoptysis, Fever, cough, Lung crackles, Cyanosis, hypoxemia, *Fat emboli often have petechiae on chest

DVT - ns care & Tx

*Tx - Warm moist packs, Elevate extremity, Bedrest (or not), Anticoagulation therapy: Heparin, Lovenox, Coumadin, Analgesics (NSAIDs), Wraps or TED hose after resolved

DVT prevention

ROM exercises, SCDs (sequential compression devices) - augment leg muscle pump, Early ambulation, Avoid pillows under knees, Change position often, Prophylactic Anticoagulant therapy

Pulmonary Embolism - ns care & Tx

O2 Therapy, IV Heparin gtt then later Coumadin, Lovenox subq used more now, Narcotics for pain, Thrombolytics (tPAtissue plasminogen activator), Bedrest, Surgery: a) Pulmonary embolectomy b) Inferior vena cava filter (Greenfield filter) inserted prevent further PE

HEMOPHILIA

hereditary coagulation disorder that has deficiency or absence of a coag. factor

Hemophilia A (Classic hemophilia)

X-linked recessive, Factor VIII deficiency (intrinsic pathway)

Hemophilia B (Christmas disease)

X-linked recessive, Factor IX deficiency

von Willebrand's disease

autosomal dominant, vWF and plt dysfunction

HEMOPHILIA S&S

Prolonged, persistent or delayed bleeding after minor trauma,Prolonged bleeding after circumcision, Bleeding form gums, nose, GI Ulcers, Hematuria, Hematomas, Nerve compression, Hemarthrosis

HEMOPHILIA Tx:

Stop the bleeding, Infuse deficient clotting factors, Freeze-dried concentrates of factors, Genetically engineered recombinant factor VIII or IX (will not have anything like HIV or Hepatitis since it does not come from a human)

Coumadin

Blocks synthesis of Vitamin K dependent clotting factors in liver,

First-degree heart block, or first-degree AV block

the electrical impulse moves through the AV node slower than normal, but every impulse is conducted to the ventricles, but duration of AV conduction is prolonged (prolonged PR interval)

PR interval

Reflects the the time it takes for the impulse to get from the atria to the ventricles. P wave + PR segment = the beginning of the P wave to the beginning of the QRS complex.

A normal PR interval

0.12 to 0.20 seconds this corresponds to 3 to 5 small boxes.

1st-degree block

Conduction is slowed without skipped beats (regular rhythm). All normal P waves are followed by QRS complexes, but the PR interval is longer than normal (> 0.20 sec).

1st degree AV Block Tx:

Usually no treatment required. Identify and correct electrolyte imbalances. Withhold any offending medications. May require hospital admission if there is an associated underlying cardiac

condition (MI, Myocarditis).

Causes of 1st degree AV Block

*Ischemia or injury to AV nodemay occur with MI or CAD, rheumatic heart disease, hyperthyroidism. *Vagal stimulation. *Electrolyte imbalanceshyperkalemia. *Drugs: digoxin, amiodarone, beta blockers, calcium channel blockers,

Other names for 2nd Degree AV Block, Type 1

Mobitz I, Wenckebach

2nd Degree AV Block

The PR interval progressively lengthens with each beat until the atrial impulse is not conducted and the QRS complex is dropped. Atrial rhythm is regularmeaning, when measuring the P-to-P interval, it is continuously equal). Ventricular rhythm is irregular (R-to-R interval NOT equal).

Causes of 2nd degree AV Block

*Occurs normally in people with high vagal tone (as in young children or athletes during sleep). *AV nodal diseasesusually a result of myocardial ischemia or infarction (inferior wall); myocarditis. *CADR coronary artery supplies the AV node... atherosclerosis or blockage of this artery leads to 2nd degree, type I AV block and slowed AV conduction *Drugs like digoxin, beta blockers, Ca++ channel blockers.

2nd degree AV Block Tx:

*Almost always transient and well tolerated...therefore requiring no treatment. *Any drugs that might be responsible for impairing AV conduction may need to be d in dosage or discontinued

Normal PR Interval

0.12 - 0.20 sec.

QRS Measurements

<0.12 normal, if > Bundle Branch Block

Treatment for Bradycardia

Atropine or Pacemaker may be required.

Causes of Sinus Tachycardia

Associated with physiologic stressors Exercise Pain Hypovolemia Myocardial ischemia Heart failure (HF) Fever

Causes of Sinus Bradycardia

Occurs in disease states i.e. , Hypothyroidism, Increased intracranial pressure, Obstructive jaundice, Inferior wall MI

Treatment for Tachycardia

Treat underlying cause Beta blockers to reduce HR and myocardial oxygen consumption Antipyretics to treat fever Analgesics to treat pain

Atrial Flutter

Atrial rate is 200 to 350 beats/minute. Atrial rhythm is regular, and ventricular rhythm is usually regular.

Causes of Atrial Flutter

CAD Hypertension Mitral valve disorders Pulmonary embolus Chronic lung disease Cardiomyopathy Hyperthyroidism

Treatment for Atrial Flutter

Drugs to slow HR: Calcium channel blockers, -adrenergic blockers Electrical cardioversion may be used to convert the atrial flutter to sinus rhythm emergently and electively

Atrial Fibrillation

Total disorganization of atrial electrical activity. P waves are replaced by chaotic, fibrillatory waves. Ventricular rate varies, and the rhythm is usually irregular. Most common dysrhythmia, Prevalence increases with age.

Causes of Atrial Fibrillation

Usually occurs with underlying heart disease Rheumatic heart disease

CAD Cardiomyopathy HF Pericarditis

Treatment for Atrial Fibrillation

-adrenergicDrugs for rate control: Digoxin, blockers, calcium channel blockers Long-term anticoagulation: Coumadin Antidysrhythmic drugs used for conversion: Amiodarone, propafenone

First-Degree AV Block

Every impulse is conducted to the ventricles, but duration of AV conduction is prolonged.

Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)

Atrial rate is normal, but ventricular rate may be slower because of nonconducted or blocked QRS complexes resulting in bradycardia. Once a ventricular beat is blocked, the cycle repeats itself with progressive lengthening of the PR intervals until another QRS complex is blocked. The rhythm appears on the ECG in a pattern of grouped beats. Ventricular rhythm is irregular. The P wave has a normal shape. The QRS complex has a normal shape and duration.

Second-Degree AV Block, Type 2 (Mobitz II)

Atrial rate is usually normal. Ventricular rate depends on the intrinsic rate and the degree of AV block. Atrial rhythm is regular, but ventricular rhythm may be irregular. The P wave has a normal shape. The PR interval may be normal or prolonged in duration and remains constant on conducted beats

Third-Degree AV Heart Block (Complete Heart Block)

The atrial rate is usually a sinus rate of 60 to 100 beats/minute. The ventricular rate depends on the site of the block. If it is in the AV node, the rate is 40 to 60 beats/minute, and if it is in the His-Purkinje system, it is 20 to 40 beats/minute

Premature Ventricular Contractions

Rhythm is irregular because of premature beats. The P wave is rarely visible and is usually lost in the QRS complex of the PVC. The QRS complex is wide and distorted in shape, lasting longer than 0.12 second. The T wave is generally large and opposite in direction to the major direction of the QRS complex.

Causes Premature

Stimulants: Caffeine, alcohol, nicotine, aminophylline, epinephrine,

Ventricular Contractions

isoproterenol Digoxin Electrolyte imbalances Hypoxia Fever Disease states: MI, mitral valve prolapse, HF, CAD

Treatment for PVC

Based on cause of PVCs Oxygen therapy for hypoxia Electrolyte replacement -adrenergic blockers,Drugs: procainamide, amiodarone, lidocaine

Ventricular Tachycardia

Ventricular rate is 150 to 250 beats/minute. Rhythm may be regular or irregular. . The P wave is usually buried in the QRS complex, and the PR interval is not measurable.

Causes for Ventricular Tachycardia

MI CAD Electrolyte imbalances Cardiomyopathy Mitral valve prolapse Long QT syndrome Digitalis toxicity Central nervous system disorders

Treatment for Ventricular Tachycardia

Precipitating causes must be identified and treated (e.g., hypoxia). Medication (Oxygen, Corderone, Lidocaine, Procainamide, Magnesium).

Cardioversion with a pulse Defibrillation and CPR without a pulse.

ITP (idiopathic thromboycytopenic purpura) S&S

Petechiae, purpura, ecchymoses, bleeding, mucous membrane bleeding. life threatening if platelets <20,000 or cerebral hemorrhage

ITP (idiopathic thromboycytopenic purpura)

platelets bellow 150,000 The two types of ITP are acute and chronic Acute ITP generally lasts less than 6 months. It mainly occurs in children

both boys and girlsand is the most common type of ITP. Acute ITP often occurs after a viral infection.

Chronic ITP lasts 6 months or longer and mostly affects adults. However, some teenagers and children do get this type of ITP. Chronic ITP affects women two to three times more often than men

Terms
Acute pulmonary edema Cardiac output Cardiac reserve

Definitions
Accumulation of fluid in the interstitial spaces and alveoli of the lungs; may be classified as either cardiogenic (due to acute heart failure) or noncardiogenic amount of blood pumped from the ventricles in 1 minute ability of the heart to increase the cardiac output in response to metabolic demand

Cardiac tamponade Cardiomyopathy Carditis Endocarditis Heart failure Hemodynamics Inotropic Myocarditis Orthopnea Paroxysmal nocturnal dyspnea

compression of the heart by blood or fluid in the pericardial sac disorder that affects the structure and function of the heart inflammation of the heart inflammation of the endocardium inability of the heart to function as a pump to meet the needs of the body the study of the pressures involved in blood circulation strengthening the contraction of the heart inflammation of the heart muscle difficulty breathing while lying down attacks of acute shortness of breath that occur at night, awakening the client

Pericardial effusion Pericardial friction rub

an abnormal collection of fluid between the pericardial layers leathery, grating sound produced by the inflamed pericardial layers rubbing against the chest wall or pleura

Pericarditis Regurgitation

inflammation of the pericardium failure of a valve to close properly, allowing substances (e.g., blood) to flow back through it

Rheumatic fever

a systemic inflammatory disease caused by an abnormal immune response to infection with group A beta-hemolytic streptococci

Stenosis Valvular heart disease

narrowing of a valve opening, which obstructs forward blood flow deformity of one or more of the heart valves affecting blood flow through the chambers of the heart and/or to the pulmonary or systemic circulation

Terms
Acute coronary syndrome (ACS) Acute myocardial infarction Angina pectoris

Definitions
a condition of severe cardiac ischemia

myocardial cell necrosis (death) due to lack of blood and oxygen

chest pain that occurs when there is a temporary imbalance between myocardial blood supply and demand

Atherosclerosis

disease in which the lining of medium and large arteries is affected by lesions called atheromas or plaque

Cardiac arrest

cessation of effective heart contractions and blood circulation; usually caused by ventricular fibrillation

Cardiac dysrhythmia

disturbance or irregularity in the electrical system of the heart

Cardiogenic shock Cardioversion

impaired tissue perfusion caused by pumping failure of the heart restoration of a normal heart rhythm (normal sinus rhythm) using either electric shock or medications

Diaphoresis Ischemic Myocardial infarction (MI)

profuse sweating inadequate blood and oxygen to meet a tissue's metabolic needs myocardial cell necrosis (death) due to lack of blood and oxygen

Terms
Tachycardia Bradycardia Flutter

Definitions
abnormally rapid heartbeat (over 100 beats per minute) slow heart rate, usually below 60 beats per minute abnormally rapid beating of the auricles of the heart (especially in a regular rhythm)

Fibrillation

extremely rapid contractions of the heart that lack the power needed to pump blood around the body

Premature Arrhythmia Heart Block

Extra Beat (i.e. PAC, PJC, PVC) an interference with the normal electrical conduction of the heart defined by the location of the block (1st degree-slow, 2nd degree-most signals will get through, but slowly, 3rd degree-"road block" nothing gets through)

What are some things that enhance automaticity?

Lack of oxygen (MI, anemia, etc) Chemical toxicity (Dig, electrolytes, acid-base imbalance, stress) Stretch on fibers (CHF, aneurysm)

Automaticity

The ability of the heart to generate and conduct electrical impulses on its own.

Inotrope Dromotrope Chronotrope What does an arrhythmia result from? Arrhythmia

Agent which alters the force of muscular contractions a drug or substance that effects the conduction velocity of the heart a drug or substance that effects the heart rate Irregularitivity, contractilityies in automaticity, excitability, conduct

Loss/lack of rhythm; any deviation from the normal (sinus) rhythm of the heart; an irregularity of the heartbeat

How do antiarrhythmics act?

Depress automaticity, slowing condction rates, increasing refractoriness to premature stimulation, combination of these mechanisms. This is accomplished by altering the movement of one or more ions (Na, K, Ca) across the heart membranes

What are the indications for antiarrhythmics?

Antiarrhythmics are selected according to the type of abnormal rhythm determined by the EKG. Most affect automaticity but and may also have an effect on contractility (may be wanted or unwanted) may cause actions outside of the heart (mostly undesirable).

Contraindication for antiarrhythmics Class I Antiarrhythmics Class Ia Antiarrhythmics Class Ib Antiarrhythmics Class Ic Antiarrhythmics Class II Antiarrhythmics Class III Antiarrhythmics Class IV Antiarrhythmics Prototype of Class Ia Antiarrhythmics Action of Quinidine

There are no contraindications to antiarrhythmics when needed to stop a fatal arrhythmia Membrane-stablizing agents, work on the fast sodium channels Delays repolarization by blocking rapid sodium paths Block sodium, but accelerates repolariztion Massive blocking of sodium without much effect on repolarization Beta blockers, block B receptors in the SNS Prolong repolarization Inhibit the slow calcium channels Quinidine (Quinidex)

Blocks sodium pathways to cause delayed repolarization

Indication of Quinidine Side Effects of Quinidine

Atrial arrhythmias for long-term use (not typically given in a code situation) AV block, hypotension, decrease cardiac output, widened QRS, low platelets, GI upset, cinchonism

Cinchonism

side effect of quinine use includes tinnitis, headache, blurred vision, confusion, abdominal pain, nausea, vomiting, diarrhea, vertigo, rashes, dizziness, dysphoria

Implications of Quinidine

Give 1 or 2 hours after meals. Monitor EKG with IV dose. Check levles *Cannot be given to anyone toxic to dig*

Prototype of Antiarrhythmic Class Ib Action of Lidocaine

Lidocaine (Xylocaine)

Decreases automaticity by decreasing the cells ability to accept/create impulses.

Indications of Lidocaine Side Effects of Lidocaine

Ventricular arrhythmias (lots of PVCs) AV block, hypotension, decreased cardiac output, CNS sedation, seizures (seen in longer term use and in patient's with kidney problems (can cause toxicity))

Implications of Lidocaine

Monitor EKG with IV dose...must be on a pump. Watch for toxicity

Prototype of Antiarrhythmics Class Ic Action of Prophafenone Indications of Prophafenone Side Effects of Propafenone Implications for Propafenone Prototype for Antiarrhythmic

Propafenone (Rythmol)

Slows depolarization Primarily severe long term ventricular arrhythmias. Given orally

AV block, hypotension, decreased cardiac output, vertigo, metallic taste, constipation, heart block Take with food Monitor Vitals and EKG Propranolol (Inderal)

Class II Action of Propranolol Non-selective beta blocker. Blocks the B1 and B2 Decreases conduction velocity and slows heart rate Indication of Propranolol Tachycardia, atrial dysrhythmia ventricular arrhythmias (PVCs) Side Effects of Propranolol Implications of Propranolol Hypotension, fatigue, vertigo, bradycardia, bronchospasm Monitor vitals, etc Avoid in COPD and asthma patients Prototype of Antiarrhymics Class III Action of Amiodarone Prolongs repolarization Long 1/2 life (about 50 days) Indications of Amiodarone Atrial arrhythmias in CHF Recurrent life threatening arrhythmias Side Effects of Amiodarone Halo vision, pulmonary fibrosis (blue-gray skin), hepatic necrosis, hyper or hypothyroid *Grapefruit juice is a NO NO!!* Prototype for Antiarrhytmic Class IV Action of Verapamil Indications of Verapamil Blocks the influx of calcium into cells SVT's (supraventricular tachycardia) Also so slow ventricular rate in atrial fib and flutter Hypertension Side Effects of Verapamil Implications of Verapamil Prototype for Misc Antiarrhythmic drugs Constipation, hypotension, bradycardia, heart block Discussed later with anti-anginal drugs Adenosine (Adenocard) Verapamil (Calan) Amiodarone (Cordarone)

Action of Adenosine

Inhibits SA and AV node impulse conduction Stops the heart-chemical defibrillant

Indications for Adenosine

SVT, works as a chemical defibrillant short 1/2 life- 10 sec, clears body in less than 1 min

Side Effects of Adenosine Implications for Adenosine

Heart block, facial flushing, SOB, few seconds of asystole (flat-line) MD MUST BE PRESENT Patient must be on an EKG Have resuscitation equipment nearby

Cardiac Output

The amount of blood ejected by the ventricles in one min (SVxHR), or who well the heart meets its obligations to provide an adequate blood supply to the body

Hypovolemic

cool, clammy skin, low BP, rapid thready pulse, rapid shallow RR, decrease LOC

If stroke volume is low, heart rate should be _______? Preload

High

The degree of ventricular stretch that occurs just before, Volume of blood that fills the heart and stretches the heart muscle fibers during its resting phase (volume of blood in ventricles at end of diastole, just prior to contraction)

Afterload

The amount of tension or pressure needed to eject the blood or the amount of pressure the heart must press against

Contractility Increased contractility = _______ blood going out. How heart rate effects cardiac output Heart Failure

The strength of the cardiac muscle Increased

To increase cardiac output, you could increase preload, afterload, contractility or heart rate in a normal heart This is the inability of the heart to maintain adequate cardiac output to meet the metabolic needs of the body due to impaired pumping ability. Results in inadequate peripheral tissue perfusion, congestion of lungs and pulmonary

edema. Most begins with L ventricular failure & progress to failure of both ventricles. What are the causes of heart failure? Signs and Symptoms of heart failure Overstretch to counter hypertension Poor muscle (e.g. MI with tissue necrosis) Respiratory rales/wet, SOB (LHF) Peripheral fluid accumulation, edema, ascites (RHF) Tachycardia Low urine output Treatment for heart failure Decreased fluid intake Decreased salt intake Decreased activity-O2 need Medications Which drugs improve contractility to improve cardiac output? Which drugs improve renal sodium/water excretion? Which drugs reduce blood pressure? Which plant are cardiac glyocsides obtained from? Prototype for Cardiac Glycoside What are the + Inotropic actions of Digoxin? Binds to receptors, allows more sodium influx into the cell which allows more free calcium to activate contractile proteins during contraction. Overall effect is better/stronger contraction What are the - Chronotropic actions of Digoxin? DECREASES SNS stimulus and INCREASES PSNS stimulation to the heart Overall effect is more filling time and better stretch What are the - Dromotropic actions of Digoxin? Increases heart conduction system sensitivity to PSNS influence Digoxin (Lanoxin) The Foxglove Antihypertensives, diuretics, ACE Inhibitors Diuretics, Angiotensin Converting Enzyme Inhibitors (ACE Inhibitors) Positive inotropic drugs (Cardiac Glycosides-Digitalis)

Vasculature of Digoxin

Constriction of arterioles and subsequent reflex vasodilation which outweighs the vasoconstriciton Constriction of the veins helps to decrease organ engorgement

Indications of Digoxin

CHF Artial Arrhythmias Nodal Arrhythmias

Nonacute Dosage of Digoxin Acute Dosage of Digoxin

Gradual digitalization--about 7 days to get po drug level to therapeutic range Give large initial dose--digitalizing or loading dose followed by maintenance doses

What is the typical oral dose per day of Digoxin? What is the typical loading dose for Digoxin? What are the GI side effects of Digoxin?

0.125 or 0.25mg (125-250mcg) daily

0.5mg (500mcg)

Anorexia Nausea Vomiting Diarrhea

What are the visual side effects of Digoxin? What are the CNS side effects of Digoxin?

Green/yellow halos (chromatopsia)

Bradycardia Heart Block Arrhythmias

What are the signs of Digoxin toxicity?

Cardiac Arrhythmias A/N/V Chromatopsia Weakness Fatigue Level /1.8ng/ml

What do you look for to prevent Digoxin toxicity?

Note visual changes Correct dosage Routine blood levels

Monitor K+ levels Good patient teaching What is the treatment for Digoxin toxicity? Stop dig Treat arrhythmias Monitor K+ Monitor EKG If life threatening use Digibind (not give unless very toxic) May need K+ therapy What population receives Digoxin? Does Digoxin cross the placenta and can it be found in breast milk? What is the interaction of increase K+ and Digoxin? What is the effect of low K+ levels and Digoxin? What is the effect of potassium wasting diuretics on Digoxin? What is the effect of increased calcium on digoxin? What are some examples of drugs that effect Digoxin? ANS drugs, antacids, gut motility drugs, corticosteroids, glucose, calcium salts, quinidine, verapamil, beta blockers, diuretics, cholestyramin, neomycin, Phenobarbital, and many more What should you always do before you administer Digoxin? What are the implications for Digoxin? Baseline EKG, labs, history. Observe for relief of CHF symptoms, take at same time each day, asses for toxicity, monitor apical for regularity and rate. Consider holding med if HR less than 60 or greater than 120. Monitor Take the apical pulse for 1 minute Increased Ca+=Increased Dig binding INCREASED EFFECT OF DIGOXIN Increased potassium=decreased dig finding DECREASES EFFECT OF DIGOXIN Low levels of potassium=Increased dig binding INCREASED EFFECT OF DIGOXIN Increased effect of digoxin Commonly used in kids Elderly need lover doses Yes

dig levels (want 0.1 to 1ng/ml). IV push dig over at least 5 minutes What is angina? Chest pain related to an imblanace between teh needs of the heart and the supply of oxygen. This leads to cardiac ischemia. What is the #1 killer in the US primarily resulting from coronary artery disease? What are things that increase myocardial oxygen demand? What are things that decrease myocardial oxygen demand? What is Chronic Stable Angina? What is Vasospastic Angina? Organic Nitrates prototype: Long term increase of oxygen demand with limited supply. Sharp pain usually subsides 15 min after rest. Primarily caused by CAD. Ischemia due to coronary vasospasm, often experience at the same time everyday-often at night. Nitroclygerin (Nitrobid, Nitrostat, Nitrong) Also includes: rapid acting Amylnitrate & long acting Isosorbide dinitrate and mononitrate Kinetics of Nitroglycerin Absorbed from mucus membranes and skin-not effective orally (due to first pass metabolism) What effects does nitro have on coronary arteries? What effect does nitro have on peripheral vasculature? What effect does nitro have on afterload and preload? What effect does nitro have on blood pressure? Decreases blood pressure (vasodilator) Decreases afterload and preload Decreases afterload, allows the heart to work easier Dilates arteries, increases blood flow and oxygen Lung disease, coronary artery disease, anemia Exercise, hypertension (increase afterload), increased preload (CHF), stress Ischemic Heart Disease

What effect does nitro have on heart rate and contractility? What are the indications of Nitro? What are the side effects of Nitro? By what route do you administer Nitro? What are the interactions of Nitro? IV Implications of Nitro: What drugs should you caution patients about while taking Nitro? Beta Blockers and Angina

Increase heart rate (only if on daily patch, common to use with betablockers)

Angina, sbulingual for prevention and treatment of attacks, acute MI, CHF, intra-op or peri-op BP regulation (give IV). Decreased BP, flusing of extermities, H/A (cerebral vasodilation), relex tachycardia, contact dermatitis (from patch) SL, buccal, IV, transdermal, traslingual spray

Potentiates antihypertensives, sedative, hypnotics, antidepresants, betablockers. Must be on in infusion PUMP, monitor vitals Viagra, Levitra and Cialis

Slow HR so filling time increases and oxygen supply to heart is maximized. Conserve energy or decrease demand. Also block catecholamines, suppress rennin, and increase urine output. The only beta blockers approved for angina are atenolol, metoprolol, nadolol and propranolol.

Calcium Channel Blockers and Angina

Work to decrease myocaridal oxygen demand by causing arterial potent vasodilation and by negative inotropic action. Depress automaticity and conduction throught the SA and AV nodes. Prevent Ca+ from entereing into and interacting in the contraction process leading to muscle relaxation.

Prototype of CCB: Examples of CCB's Indication of Verapamil:

Diltiazem (Cardiazem) Diltiazem, verapamil, nifedipine, nicardipine VAsospastic angina, chronic stable angina, essential hypertension, migraines, rapid atrial arrhythmias

Side Effects of Verapamil:

Constipation, decreased BP, decreased CO, AV block, arrhythmias, dermatitis, male fertility decreases

Implications of Verapamil:

Monitor for arrhythmias, CHF, decreased BP, constipation. Increase intake of water and bulk forming foods if consitpated. Take SR on empty stomach, take every day at same time. Limit caffeine intake.

Emergency cardiac drugs

Terms
Adenosine is the generic name for a. Nucleoside. b. Adenocard. c. Actidose. d. Alupent. Adenosine is primarily used in the treatment of a. Wide complex junctional dysrhythmia. b. Narrow complex pulseless bradycardia. c. Narrow complex supraventricular tachycardia. d. Wide complex ventricular tachycardia with pulses. The typical initial dose of adenosine in the adult patient is: a. 60 mg slow IV push followed by a saline flush and elevation of the extremity. b. 6 mg rapid IV bolus followed by a saline flush and elevation of the extremity. c. 12 mg rapid IV bolus followed by a saline flush and elevation of the extremity. d. 3 mg/kg rapid IV bolus followed by a saline flush and elevation of the extremity. The patient is a 39 year-old woman complaining of chest pain and slight dyspnea. She states that her heart suddenly started racing. The ECG shows sinus tachycardia at a rate of 140 per minute. After giving adenosine, the patient develops a 'strange look' and the monitor shows asystole. The best immediate response is: a. Monitor the patient as the asystole is transient.

Definitions
B. Adenocard

c. Narrow complex supraventricular tachycardia.

6 mg rapid IV bolus followed by a saline flush and elevation of the extremity.

a. Monitor the patient as the asystole is transient.

b. Immediately start chest compressions and ventilation. c. Administer 1 mg of epinephrine IV and begin CPR. d. Administer 1 mg of atropine and begin CPR. Which of the following is not an adverse effect of adenosine? a. Paresthesias. b. Headache. c. Palpitations. d. Hypertension. Amiodarone is used in the treatment of: a. Ventricular fibrillation. b. Hemodynamically stable ventricular tachycardia. c. Pulmonary edema secondary to congestive heart failure. d. Sinus tachycardia accompanied by hypotension. The patient has a history of hypertension and has been treated with labetalol. If you give amiodarone to treat a paroxysm of supraventricular tachycardia that is refractory to adenosine, it may precipitate a. Severe hypertension and worsen the tachycardia. b. Hypotension accompanied by bradycardia. c. Atrial fibrillation with pulmonary edema. d. Bradycardia with prolongation of the P-R interval. The typical dose of amiodarone in persistent ventricular fibrillation is: a. 300 mg IV push. b. 150 mg IV drip. c. 1.5 mg/kg IV push. d. 30 mg IV drip. In an acute myocardial infarction, aspirin is used to: a. Dilate the coronary arteries. b. Decrease platelet aggregation. c. Relieve the patient's anxiety. d. Control nausea and vomiting. The typical dose of aspirin for an adult patient with an acute myocardial infarction is: a. 160-325 mg orally. b. 40-100 mg orally. a. 160-325 mg orally. b. Decrease platelet aggregation. a. 300 mg IV push. d. Bradycardia with prolongation of the P-R interval. b. Hemodynamically stable ventricular tachycardia d. Hypertension.

c. 81 mg/kg IV drip. d. 800 mg. Aspirin should be given as soon as possible to patients with: a. Hemorrhagic stroke. b. Gastrointestinal bleeding. c. Unstable angina. d. Active ulcer disease. Atenolol is classified as a: a. Calcium channel blocker. b. ACE inhibitor. c. Beta blocker. d. Antipyretic. Atenolol is indicated in the treatment of: a. Cardiogenic shock. b. Atrial fibrillation. c. Third degree AV block. d. Exacerbation of COPD. The patient has been diagnosed with an acute myocardial infarction. The typical dose of atenolol for the patient is: a. 5 mg slow IV. b. 15 mg rapid IV. c. 20 mg slow IV d. 25 mg rapid IV. The patient is a 56-year-old man with an acute anterior wall myocardial infarction. The ECG indicates sinus tachycardia at with no ectopy and his vital signs are BP - 82/64, P - 108, R - 22 and nonlabored. After maintaining adequate oxygenation, the most appropriate drug of choice to elevate the man's blood pressure is: Atenolol. Dobutamine Adenosine. Dopamine Which of the following best describes the actions of atropine sulfate? a. Atropine is a sympathomimetic drug. b. Atropine is a parasympathomimetic drug. c. Atropine is a sympatholytic drug. d. Atropine is a parasympatholytic drug. d. Atropine is a parasympatholytic drug. Dopamine a. 5 mg slow IV. b. Atrial fibrillation. c. Beta blocker. c. Unstable angina.

In which of the following conditions is atropine is indicated? a. Symptomatic tachycardia. b. Ventricular ectopy. c. Organophosphate poisoning. d. Atrial flutter of fibrillation. The patient is a 62 year-old male complaining of chest pain and shortness of breath. His ECG shows sinus bradycardia at 50 beats per minute that is accompanied by a blood pressure of 88/50. Upon further examination, the patient reveals that he is being treated for urinary retention. Because this patient is hemodynamically unstable, the dose of atropine is: a. 1 mg slow IV push. b. 0.5 mg rapid IV push. c. 0.5 mg/kg slow IV push. d. not indicated in this patient. Which of the following may occur if atropine is given too slowly? a. Decreased heart rate . b. Overcorrection of the blood pressure. c. Tachycardia and palpitations. d. Flushed, hot, dry skin. Calcium chloride is contraindicated in: a. Hyperkalemia. b. Digitalis toxicity. c. Hypocalcemia. d. Overdose of calcium channel blocker. A 6 y/o child who accidentally ingested his mother's verapamil is found unresponsive and profoundly hypotensive. Emergency management of this child consists of: a. Calcium chloride, 20 mg/kg slowly IV or IO. b. Dopamine, 2-20 mcg/kg/min. c. Epinephrine, 0.5-1.0 mg/kg slowly IV or IO. d. Atropine, 0.5 mg slowly IV or IO. The patient is a 58 year-old woman with end stage renal disease who been on dialysis for nearly 4 years. She became ill during her last dialysis treatment two days earlier and was unable to complete it. This morning, her husband found her unresponsive. Initial

c. Organophosphate poisoning.

b. 0.5 mg rapid IV push.

a. Decreased heart rate .

b. Digitalis toxicity.

a. Calcium chloride, 20 mg/kg slowly IV or IO.

c. Calcium chloride.

examination reveals hypotension, bilateral rales in the lung bases, and what appears to be ventricular tachycardia on the ECG. The widened QRS complexes appear to be sine waves and no P waves are noted. Pharmacologic treatment for this patient includes: a. Lidocaine hydrochloride.. b. Amiodarone. c. Calcium chloride. d. Atenolol. It is important to flush the IV tubing between the administration of calcium chloride and sodium bicarbonate because: a. Sodium bicarbonate inactivates calcium chloride. b. Calcium chloride inactivates sodium bicarbonate. c. Calcium chloride binds with the IV tubing rendering it inactive. d. Calcium chloride and sodium bicarbonate cause precipitation. The patient is a 60 year-old male complaining of severe chest discomfort. His ECG shows ventricular tachycardia; however, he is conscious, alert, and stable with a blood pressure of 104/60. Antiarrythmic treatment has been ineffective and the patient will undergo synchronized cardioversion. A major concern with giving diazepam to the patient is: a. Reflex bradycardia. b. Respiratory depression. c. Status seizures. d. Confusion and ataxia. Digoxin is a cardiac glycoside derived from a plant known as: a. Deadly nightshade. b. Morning glory. c. Foxglove. d. Night blooming jasmine. Digoxin is used in the treatment of: a. Atrial flutter or fibrillation. b. Ventricular tachycardia. c. Ventricular fibrillation. d. Atrioventricular block. The adverse effects of digitalis toxicity include: a. Hyperactivity. d. Chest pain. a. Atrial flutter or fibrillation. c. Foxglove. b. Respiratory depression. d. Calcium chloride and sodium bicarbonate cause precipitation.

b. Blurred, yellow, or green vision. c. Ataxia. d. Chest pain. The patient is a 72 year-old woman with a history of atrial fibrillation and congestive heart failure. She is being treated with digoxin to control her ventricular response. She has recently been diagnosed with hypertension and was prescribed the calcium channel blocker, verapamil. This combination of medications: a. Is of little concern as they have no significant interaction. b. May decrease the effectiveness of her digitalis preparation. c. Reduces the absorption of digitalis from the GI tract. d. May lead to an increased serum concentration of digitalis. Diltiazem is in a class or medications known as: a. Calcium channel blockers. b. Beta blockers. c. Beta sympathomimetics. d. Cardiac glycosides. Diltiazem acts by: a. Slowing conduction in the atrioventricular node. b. Reducing the inotropic state of the heart. c. Increasing the heart rate and contractility. d. Stimulates tone of the vagus nerve. Diltiazem is indicated for the treatment of: a. Sick sinus syndrome. b. Cardiogenic shock. c. Atrial fibrillation or flutter. d. Ventricular tachycardia. The typical initial dose of diltiazem for the adult patient is: a. 25 mg/kg IV over 2 minutes. b. 25 mg IV over 2 minutes. c. 0.25 mg/kg IV over 2 minutes. d. 0.25 mg rapid IV push. Choose the correct statement about dobutamine. a. It is related to epinephrine and is an alpha, beta1 and beta2 specific agonist. c. It is a synthetic catecholamine that is primarily a beta1 agonist. c. 0.25 mg/kg IV over 2 minutes. c. Atrial fibrillation or flutter. a. Slowing conduction in the atrioventricular node. a. Calcium channel blockers. b. May decrease the effectiveness of her digitalis preparation.

b. It is an alpha-specific agonist used to elevate blood pressure in shock. c. It is a synthetic catecholamine that is primarily a beta1 agonist. d. It increases both the chronotropic and inotropic states of the heart. The indications for dobutamine include: a. Congestive heart failure accompanied by hypotension. b. Symptomatic bradycardia with pulmonary hypertension. c. Bronchial asthma accompanied by hypotension. d. Hypotension caused by systemic vasodilation. The typical dose range of dobutamine for adult and pediatric patients is: a. 1-5 mcg/kg/minute. b. 10-20 mcg/kg/minute. c. 5-10 mcg/kg/minute. d. 2-20 mcg/kg/minute. You are preparing to give dobutamine and furosemide to treat a patient with congestive heart failure. What special considerations may be needed to administer these two drugs at the same time? a. Give both medications concurrently to enhance the effects of each drug. b. Give via separate IV lines since they are incompatible in the same tubing. c. Give furosemide just after starting dobutamine to potentiate furosemide. d. There are no special considerations pertaining to dobutamine and furosemide. Choose the correct statement about dopamine. a. It is related to epinephrine and is an alpha1 and beta1 agonist. b. It is an alpha-specific agonist used to elevate blood pressure in shock. c. It is a synthetic catecholamine that is primarily a beta1 agonist. d. It decreases both the chronotropic and inotropic states of the heart. Which of the following is an indication for dopamine? a. Hypotension from cardiogenic shock. b. Hypotension caused by hypovolemia. a. Hypotension from cardiogenic shock. b. It is an alpha-specific agonist used to elevate blood pressure in shock. b. Give via separate IV lines since they are incompatible in the same tubing. d. 2-20 mcg/kg/minute. a. Congestive heart failure accompanied by hypotension.

c. Ventricular fibrillation. d. Pheochromocytoma. The patient is a 60 year-old man with hypotension secondary to an acute myocardial infarction. Past medical history indicates that he has been taking labetalol for hypertension. Which of the following statements is correct regarding the interactions between labetalol and dopamine? a. There are no significant interactions between the two drugs. b. Labetalol may reduce the beta effects of dopamine. c. Dopamine may enhance the effects of labetalol. d. Labetalol may enhance the effects of dopamine. The patient is a 70 year-old woman in cardiogenic shock following an acute myocardial infarction. In assessing the woman, she states that she has a history of depression and has been taking Nardil for the past several years. To correct this patient's hypotension, dopamine may be indicated. Care must be taken when giving dopamine to this patient, because: a. MAO inhibitors such as Nardil potentiate catecholamines. b. Dopamine inhibits Nardil and depression can worsen. c. Dopamine will have no effect on increasing her blood pressure. d. Nardil and dopamine have no significant interactions. Epinephrine is best described as a. An endogenous catecholamine and is an alpha and beta agonist. b. An alpha-specific agonist used to elevate blood pressure in shock. c. A synthetic catecholamine that is primarily a beta1 agonist. d. A drug that decreases the chronotropic and inotropic states of the heart. Epinephrine is used in the emergency management of: a. Hypovolemic shock. b. Ventricular fibrillation. c. Ventricular tachycardia. d. Premature ventricular contractions. A 60 year-old male patient with symptomatic bradycardia has not responded to the maximum dose of atropine or higher dose levels of dopamine. The treatment options at this time include: a. Amiodarone, 300 mg IV push. c. Epinephrine infusion, 2-10 mcg/minute. b. Ventricular fibrillation. d. A drug that decreases the chronotropic and inotropic states of the heart. d. Nardil and dopamine have no significant interactions. b. Labetalol may reduce the beta effects of dopamine.

b. Propranolol, 1-3 mg over 2-5 minutes IV. c. Epinephrine infusion, 2-10 mcg/minute. d. Inamrinone, 0.75 mg/kg over 10-15 minutes. Which of the following is not a typical adverse effect of epinephrine? a. Headache. b. Dysrhythmias. c. Chest pain. d. Hypotension. Racemic epinephrine is used in the emergency management of: a. Ventricular fibrillation. b. Hypovolemic shock. c. Laryngotracheobronchitis. d. Supraventricular tachycardia. The dose of racemic epinephrine in the treatment of croup is: a. 5 ml drug in 5ml of saline then given slowly IV b. 5ml drug in 5ml sailine administered by nebulizer. c. 0.25-0.5 ml drug in 2.5 ml sailine given slowly IV. d. 0.25-0.5 ml drug in 2.5 ml saline given by nebulizer. The pateint is a conscious adult male in stable ventricular tachycardia that is unresponsive to lidocaine or other pharmacologic therapy. In preparation for synchronized cardioversion, the patient should be given: a. Diazepam, 25 mg IV push b. Lorazepam, 1-4 mg IV over 2-4 min c. Etomidate, 0.2-0.6 mg/kg IV over 30-60 seconds d. Fentanyl, 0.2 mg over 15 seconds The patient was sedated with etomidate prior to cardioversion and tolerated the procedure well. He is now in normal sinus rhythm, but his ventilatory rate is 4-6 breaths per minute. At this time, emergency treatment includes: a. Naloxone, 0.4-2.0 mg IV push b. Monitor breathing and consider intubation c. Epinephrine, 0.5 mg slowly IV d. Diphenhydramine, 25 mg IV push The patient is a 29 year old woman complaining of heart b. Coffee (caffeine) antagonizes b. Monitor breathing and consider intubation B. Lorazepam, 1-4 mg IV over 2-4 min... possibly Etomidate 0.2-0.6 mg/kg IV over 30-60 seconds D. 0.25-0.5 ml drug in 2.5 ml saline given by nebulizer c. Laryngotracheobronchitis. d. Hypotension

palpatations. She says that her pulse "feels like it is racing." She also states she was drinking coffee when her "heart took off." The woman's ECG reveals supraventricular tachycardia at a rate of 160. After treating the patient with an intial and repeat dose of adenosine, there is no change in her ECG. The lack of response to adenosine is most likely because: a. The ECG is a rapid AV junctional rhythm and not PSVT. b. Coffee (caffeine) antagonizes the action of adenosine. c. The woman is allergic to adenosine d. Adenosine is ineffective in treating PSVT. A 56 year old male had hemodynamically stable ventricular tachycardia. He was given amiodarone including a maintenance amiodarone infusion. Then, he received daizepam followed by synchronized cardioversion. Following the cardioversion, the patient's ECG displayed normal sinus rhythm that gradually slowed to sinus bradycardia. At this point, treatment would include: a. Adminstration of atropine b. Infusion of dopamine or dobutamine c. Slowing or discontinuing of amiodarone d. Administration of atenolol or lebatolol. The patient has retrosternal chest discomfort with referred pain to the left arm and fingers. After placing the patient into a semi-fowler's position, administering supplemental oxygen, the patient is given nitroglycerin 0.4 mg SL. He states that his chest discomfort is less severe, but he feels weak and very dizzy. Assessing the patient's vital signs reveals a blood pressure of 76 by palpation, pulse of 120, ventilatory rate of 22. Urgent treatment at this time includes: a. Adenosine to slow the heart rate and increase blood pressure b. Placing the patient in a supine position and reassessing vitals. c. Initiating a dopamine drip at the lowest dose possible. d. Labetalol and dopamine to stabalize the blood pressure and pulse Furosemide works by inhibiting reabsorption of sodium and chloride in the: a. bloodstream b. distal renule tubules c. liver d. loop of Henle

the action of adenosine.

c. Slowing or discontinuing of amiodarone

b. Placing the patient in a supine position and reassessing vitals

d. loop of Henle

IV doses if furosemide can reduce cardiac preload by: a. altering potassium regulation b. decreasing capillary sphincter tone c. increasing creatinine clearance d. increasing venous capacitance Which of the following is a correct dose of furosemide for a pediatric patient? a. 0.6 mg/kg b. 1 mg/kg c. 6 mg d. 10 mg You are treating a patient with calcium channel blocker cardiotoxicity who does not respond to conventional therapy. Another drug to consider is: a. furosemide b. glucagon c. insulin d. romazicon 1 mg of glucagon is typically mixed with how much dilutent? a. 1 mL b. 5 mL c. 10 mL d. 20 mL Which of the following is an indication of heparin administration? a. acute myocardial infarction b. allergic reaction c. hypotension d. severe thrombocytopenia Before administering heparin with fibrinolytic therapy, a blood sample should be obtained for control of: a. decrease red blood cells b. low platelet count c. partial thromboplastin time d. thrombocytopenia Heparin is given as an IV bolus of:

d. increasing venous capacitance

b. 1 mg/kg

b. glucagon

a. 1 mL

a. acute myocardial infarction

b. low platelet count

...

a. 30 IU/ kg b. 60 IU/ kg c. 90 IU/ kg d. 120 IU/ kg Hydralazine is used almost exclusively for the treatment of: a. congestive heart failure b. increased intracranial pressure c. preeclampsia and eclampsia d. seizure disorder Your patient is prescribed diazoxide and you have received an order for hydralazine. Which side effect would you expect? a. CNS depression b. muscle fatigue c. respiratory depression d. severe hypotension After an initial dose of 10 mg of hydralazine, you begin an infusion at a rate of: a. 0.5 mg/ hour b. 0.5 mg/ min c. 5 mg/ hour d. 5 mg/ min Which of the following drugs would act as an adjunct to electrical cardioversion for a patient in atrial flutter? a. adenosine b. ibutilide c. isoproterenol d. verapamil Ibutilide aids in treatment of dysrhythmias by: a. decreases the refractory period of cardiac tissue b. increasing the Q-T interval c. prolonging the action potential duration d. temporarily halting the transmission of impulses through the AV junction Ibutilide is indicated for which of the following dysrhythmias? a. atrial fibrillation a. atrial fibrillation c. prolonging the action potential duration b. ibutilide c. 5 mg/ hour d. severe hypotension a. congestive heart failure

b. asystole c. ventricular fibrillation d. ventricular tachycardia Inamrinone increases cardiac output without affecting: a. alpha-adrenergic receptors b. heart rate c. myocardial contractility d. vessel dilation You are treating a 50-year-old man in severe congestive heart failure that is refractory to diuretics, vasodilators and other inotropic agents. A drug to consider administering is: a. amiodarone b. atenolol c. diltiazem d. inamrinone Which of the following is a contraindication to inamrinone? a. hypotension b. prior administration of dopamine c. severe congestive heart failure d. tachycardia In cases of hyperkalemia, 50% dextrose is administered with what drug to lower potassium levels? a. digoxin b. insulin c. magnesium sulfate d. verapamil Which of the following is true of the mechanism of action of labetalol? a. labetalol is a beta blocker only b. labetalol is a beta2 selective blocker c. labetalol is an alpha blocker only d. labetalol is a more potent beta-blocker than alpha-blocker To lower blood pressure in hypertensive crisis, labetalol: a. decreases cardiac output b. decreases peripheral resistance c. increases preload b. decreases peripheral resistance ... b. insulin d. tachycardia d. inamrinone c. myocardial contractility

d. produces a reflex tachycardia Which of the following patient conditions would be an indication for labetalol? a. cardiogenic shock b. congestive heart failure c. hypertensive crisis d. second and third-degree heart block If you administer lidocaine to a patient with liver dysfunction, you would expect: a. decreased metabolic clearance b. decreased ventricular fibrillation threshold c. lessened dysrhythmic effects d. reflex tachycardia The maximum total dose of lidocaine is: a. 1 mg/ kg b. 2 mg/ kg c. 3 mg/ kg d. 4 mg/ kg Magnesium sulfate reduces muscle contractions by blocking: a. Acetycholine b. Dopamine c. Epinephrine d. Norepinephrine Which drug can be used as an antagonist to magnesium sulfate? a. calcium gluconate b. dexamethasone c. procainamide d. sodium bicarbonate Which of the following best describes metaproterenol? It is a(n): a. Parasympatholytic medication. b. Beta2 sympathomimetic. c. Alpha2-adrenergic sympathomimetic. d. Parasympathomimetic medication. Metoprolol is classified as a: d. Beta sympatholytic. b. Beta2 sympathomimetic. a. calcium gluconate a. Acetycholine c. 3 mg/ kg ... c. hypertensive crisis

a. Beta sympathomimetic. b. Alpha sympatholytic. c. Cholinesterase inhibitor. d. Beta sympatholytic. The patient is a 48 year-old male complaining of severe pressure in the chest. The ECG indicates a suspected acute myocardial infarction. In order to reduce the area of ischemia as well as reduce the work load and oxygen demand of the heart, urgent care of the patient may include: a. Naloxone. b. Metoprolol. c. Metaproterenol. d. Dobutamine While assessing an individual complaining of chest pain and dyspnea, the patient reveals of history of COPD for which he selfadministers albuterol. In this case, treating the patient with metoprolol: a. Should be followed by an infusion of dobutamine. b. Is indicated at half the typical dose. c. Is not indicated and should be avoided. d. Should be followed by an infusion of lidocaine. The patient is experiencing a paroxysm of supraventricular tachycardia that has been unresponsive to other, non-pharmacologic interventions. The dose of metoprolol for the patient is: a. 1-3 mg slowly IV to a total of 0.1 mg/kg. b. 5 mg slowly IV to a total of 15 mg. c. 0.25-0.50 mg/kg slow IV push. d. 10-25 mg slowly IV to a total of 100 mg. Choose the correct statement pertaining to the concurrent administration of metoprolol and verapamil? a. The combination may cause severe hypotension. b. The combination has no interaction and is safe. c. Administer half of the typical dose for each drug. d. Administer twice the typical dose for each drug. Morphine sulfate is classified as a: a. Narcotic analgesic. a. Narcotic analgesic. ... b. 5 mg slowly IV to a total of 15 mg. c. Is not indicated and should be avoided. b. Metoprolol.

b. Beta agonist. c. Benzodiazepine. d. Sedative hypnotic. Morphine acts to reduce pain as well as: a. Decrease seizure activity. b. Decrease venous return to the heart. c. Dilate bronchi and bronchioles. d. Block beta receptors and slow the heart rate. Which of the following best describes the effect that morphine has on reducing the myocardial oxygen demand? a. Morphine decreases preload and afterload. b. Morphine dilates the coronary arteries. c. Morphine increases the ventricular response rate. d. Morphine increases the inotropic state of the heart. For which of the following is morphine sulfate indicated? a. Symptomatic bradycardia from acute myocardial infarction. b. Headache from significant head injury. c. Chest pain from acute myocardial infarction. d. To lower blood pressure in hypertensive crisis. A 48 year-old male is complaining of severe chest pain and shortness of breath. His ECG shows first degree heart block at 46 beats per minute that is accompanied by a blood pressure of . Which of the following is correct regarding the treatment of the patient's chest pain? a. Give 1 mg morphine slow IV push. b. Morphine should be given at a normal dose. c. Monitor the patient's rate and depth of breathing. d. Morphine is not indicated in this patient. After receiving 5 mg morphine to alleviate his chest pain, the patient's rate and depth of breathing slows dramatically. Even though the patient is receiving supplemental oxygen, there is slight cyanosis around the patient's lips. The pulse oximetry reveals a SpO2 of 80% with supplemental oxygen being delivered. The appropriate emergency management of this patient includes: a. Immediately intubate the patient. b. Increase the oxygen being delivered. ... d. Morphine is not indicated in this patient. c. Chest pain from acute myocardial infarction. a. Morphine decreases preload and afterload. b. Decrease venous return to the heart.

c. Administer naloxone and monitor. d. Give etomidate and intubate. A 60 year-old male complains of severe chest pain and dyspnea. His skin is pale, cool, and clammy. The 12-lead ECG shows ST-segment elevation in leads V3 and V4. Vital signs indicate Pulse - 88 bpm and regular, BP - 92/56 , and Respiration 22. Choose the correct statement about administering nitroglycerin to the patient. a. Nitroglycerin is contraindicated for the patient due to hypotension. b. Nitroglycerin may be given, but monitor the blood pressure. c. Nitroglycerin may only be given after increasing the blood pressure. d. Nitroglycerin may be given concurrently with an infusion of dopamine. The patient is a 55 year-old male with a suspected acute myocardial infarction. During the examination the man admits to using tadalafil (Cialis) approximately 12 hours earlier. In treating this patient, nitroglycerin: a. Is permissible since tadalafil was taken more than 8 hours earlier. b. Can be given and one-half the typical adult dose. c. Should be avoided to prevent severe hypotension. d. May be given along with dopamine to maintain blood pressure. In small doses, nitroglycerin acts to reduce chest pain due to myocardial ischemia by: a. Reducing preload and myocardial oxygen demand. b. Dilating the coronary arteries and providing addition flow. c. Increasing afterload to ensure adequate myocardial perfusion. d. Providing analgesia of the ischemic myocardium. Nitroglycerin should not be used in suspected: a. Ischemia chest pain. b. Congestive heart failure. c. Pulmonary hypertension. d. Intracranial hemorrhage. The patient is a 56 year-old male who will be receiving an IV infusion of nitroglycerin to control refractory chest pain. IV therapy should be initiated using tubing that is free of polyvinyl chloride (PVC) because: a. The tubing can absorb up to 80% of the nitroglycerin. ... d. Intracranial hemorrhage. a. Reducing preload and myocardial oxygen demand. ... b. Nitroglycerin may be given, but monitor the blood pressure.

b. Nitroglycerin reacts with the tubing to form a precipitate. c. Nitroglycerin mixes with the tubing and becomes toxic. d. There is no concern regarding the type of IV tubing used. A 59 year-old male is complaining of severe chest discomfort. His ECG shows normal sinus rhythm with ST-segment elevation in leads II, III and aVF. He is conscious, alert, and stable with a blood pressure of . Nitroglycerin is administered to help alleviate the chest pain. A major concern with giving nitroglycerin to this patient is: a. Reflex bradycardia. b. Hypotension. c. Headache. d. Nystagmus. Nitropaste is as absorbent paste containing: a. 1% nitroglycerin. b. 2% nitroglycerin. c. 3% nitroglycerin. d. 4% nitroglycerin. The typical dosage of nitropaste for the adult with a suspected acute myocardial infarction is: a. inch of paste b. 1-2 inches of paste c. 2-3 inches of paste d. 3-4 inches of paste Wear gloves when applying nitropaste to a patient because: a. It is easier to spread over the patient's skin. b. Nitropaste may be absorbed by bare hands. c. Gloves ensure even distribution of the paste. d. Nitropaste can be effectively massaged into the skin. After applying nitropaste to a patient's chest, cover the application with a transparent wrap and secure with tape. This procedure is performed to: a. Ensure transfer of the paste to another person while moving the patient. b. Enhance absorption of the paste and ensures potency of the delivered drug. c. Slow degradation of the medication after the nitroglycerin is ... b. Nitropaste may be absorbed by bare hands. a. inch of paste b. 2% nitroglycerin. b. Hypotension.

exposed to air. d. Allow the site to be visible in the event of a skin reaction to nitropaste. Norepinephrine is classified as a: a. Alpha sympathomimetic. b. Beta sympathomimetic. c. Alpha and beta sympathomimetic. d. Alpha and beta parasympathomimetic. The use of norepinephrine should be considered: a. After other catecholamines have been tried. b. As a first line drug in cardiogenic shock. c. Immediately after atropine in unstable bradycardia. d. In cardiac arrest prior to giving vasopressin. When used to treat hemodynamically significant hypotension from cardiogenic shock in an adult who has not responded to sympathomimetics, norepinephrine can be administered at: a. 0.5-1 mcg/minute initially. b. 2-5 mcg/kg/minute initially. c. 5-10 mcg/minute initially. d. 0.1-2 mcg/kg/minute initially. The patient is a 60 year-old woman post-acute myocardial infarction in cardiogenic shock. She is to receive norepinephrine infusion to stabilize her blood pressure. A large stable vein should be used for the infusion because: a. A large quantity of fluid must be given rapidly. b. Extravasation may result in tissue necrosis. c. The large vein ensures an inotropic response. d. An IV infusion pump requires a large stable vein. Procainamide is classified as a: a. Narcotic analgesic. b. Antidysrhythmic. c. Benzodiazepine. d. Beta blocker. Procainamide is used in emergency care to: a. Treat atrial fibrillation or flutter. c. Treat ventricular tachycardia. b. Antidysrhythmic. b. Extravasation may result in tissue necrosis. c. 5-10 mcg/minute initially. ... c. Alpha and beta sympathomimetic.

b. Induce sedation prior to and after cardioversion. c. Treat ventricular tachycardia. d. Treat hemodynamically stable junctional tachycardia. A conscious adult male is in stable ventricular tachycardia that is unresponsive to lidocaine or other pharmacologic therapy. In lieu of synchronized cardioversion, the patient may be given: a. Dobutamine, 2-5 mcg/minute IV infusion. b. Lorazepam, 1-4 mg IV over 2-4 minutes. c. Procainamide, 20 mg/min IV. d. Etomidate, 0.2-0.6 mg/kg over 15 seconds. The patient is a 62 year-old male complaining of chest pain. The initial impression of his ECG is ventricular tachycardia. Careful assessment of the patient reveals a history of depression treated with Elavil. The patient admits to taking four times the average dose of Elavil. Management of the dysrhythmia with procainamide: a. Is contraindicated in tricyclic antidepressant toxicity. b. Should immediately resolve the ventricular tachycardia. c. Is followed by lidocaine and a lidocaine infusion. d. May be followed by atropine for post-treatment bradycardia. Contraindications to the administration of procainamide include: a. Ventricular tachycardia with normal QT interval. b. Torsades de pointes. c. PSVT refractory to other measures. d. Atrial fibrillation with rapid rate in WPW. A 76-year-old female calls 9-1-1 because her heart is "skipping." Her vital signs are BP 128/76 mmHg, P 152 bpm, R 20/min. and SaO2 93%. She denies chest pain but admits she has trouble catching her breath if she walks across the room. Her lungs are clear to auscultation. She tells you that she has a history of Wolff-ParkinsonWhite syndrome. Her ECG shows a narrow QRS complex tachycardia that is irregularly irregular. You are unable to identify any P waves. Which of the following drug treatments would be appropriate for this patient? a. Adenosine 6 mg rapid IVP b. Diltiazem 15-20 mg IV over 2 minutes c. Procainamide 20 mg/min IV infusion d. Verapamil 20 mg slow IV a. Adenosine 6 mg rapid IVP b. Torsades de pointes. a. Is contraindicated in tricyclic antidepressant toxicity. c. Procainamide, 20 mg/min IV.

When should you stop the infusion of procainamide in a 70 kg patient? a. Blood pressure is 104/76 mm Hg b. Sinus tachycardia with PACs is seen c. QRS is 0.08 seconds d. Total dose of 700 mg has been given Your patient was diagnosed with a myocardial infarction. His vital signs are stable and his ECG shows a normal sinus rhythm with frequent multifocal PVCs. You have given aspirin and nitroglycerin and he is pain free. Which of the following drugs would be appropriate to administer at this time? a. Amiodarone 150 mg IV infusion over 10 minutes b. Lidocaine 1 mg/kg IVP until PVCs are suppressed c. Procainamide 20 mg/minute until blood pressure drops d. Propranolol 0.1 mg/kg divided into 3 doses Which of the following post-myocardial infarct patients would be a candidate for administration of propranolol a. Auscultation of the lungs reveals bilateral rales audible to the scapulae. b. Blood pressure is 106/74 mmHg c. Heart rate is 48 bpm and irregular d. Home medicine includes albuterol and maxair

a. Blood pressure is 104/76 mm Hg

b. Lidocaine 1 mg/kg IVP until PVCs are suppressed