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 Definitions

Hyperkalemia QRS widens, P wave flattens, T wave peaks

Hypokalemia T wave flattens (or inverts), produces a U wave

Hypercalcemia QRS widens, QT shortens

Hypocalcemia Prolongs QT interval

Hypothermia ST elevates, slows rhythm

Digitalis ST depresses, T wave flattens (or inverts), QT shortens

Quinidine QT lengthens, T wave flattens (or inverts), QRS lengthens

Beta Blockers HR (pulse rate) decreases, blunts HR response to exercise;

Examples: Propranolol/Inderal

Nitrates Increases HR

Antirrhythmic Agents Prolongs QRS and QT intervals

Kalemia Potassium

Calcemia Calcium

Premature Ventricular

Contractions (PVC)

Abnormally wide, irregularly spaced QRS complexes, P wave

maybe absent

Terms Definitions

A single cycle = 2 stages

1st stage is diastole

1st stage which is diastole Represents ventricular filling and a brief period just prior to

filling at which time the ventricles are relaxing

2nd stage is systole

Stage 2 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 The AV valves close and the semilunar valves

open

Systole Step 3 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 Oxygenated blood is pumped into the aorta

Systole Step 8 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? S3 & S4 Heart Sounds

Phase 1 Atrial contraction,Atrial systole

Phase 2: Mitral valve closes "lub", S1,

Isovolumetric contraction Begins ventricular systole

Phase 3 Rapid ejection

Phase 4 Reduced ejection,

Aortic valve closes "dub", S2 Begins ventricular diastole

Phase 5 Isovolumetric relaxation

Phase 6 Rapid filling

Phase 7 Reduced filling

Stroke volume 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 normal

Ejection Fraction < 35% means 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 60-100

AV Node (AV Junction) Rate 40-60

Ventricles (Bundle Branches) Rate 20-40

Purkinje Fibers Rate <15

Reading an ECG 1 mm square equal 0.04 seconds

Reading an ECG 5 mm square equal 0.20 seconds (0.04 x 5 = .20)

Reading an ECG amplitude (voltage) is measured in millimeters

Reading an ECG duration (width) measured in seconds

Reading an ECG baseline is the isoelectric line, ECG Waveforms,

P Waves Atrial depolarization (activation)

P waves come before QRS

Duration of PR interval (PRI) 0.12-0.20 seconds

PRI Interval Rounded and upright deflection in I, II, aVF, V4,

V6,

PRI represents the time it takes for electrical

impulse to travel from

SA throughout atria

Reading an ECG Ask do you see a P wave?

Ask Is the P wave shaped normally?

Ask are all Ps similar

Ask is there one P wave for every Q wave, is there a 1:1 ration of P:QRS

Ask is the PRI normal

Ask are there any Abnormal P waves

Ask are there anyTall, Peaked P waves

Peaked P waves mean Right atrial hypertrophy, P pulmonale

Wide m-shaped P waves mean Left atrial hypertrophy ,P mitrale

QRS Complex Ventricular depolarization or activation

The Electrical conduction of the QRS down bundle to Purkinje Fibers

The Q wave is the 1st negative deflection

R wave 1st positive deflection

The S wave is a negative deflection after R

The QRS Complex duration is 0.06-0.12 seconds

Reading an ECG Ask is there a QRS for every P wave?

Ask is the R to R regular

Normal duration of the QT Interval ventricular excitation, contraction, recovery

beginning of QRS to end of T length depends on heart rate

faster HR The shorter QT interval

The slower HR The longer the QT interval

QT interval upper limits 0.39-0.43 seconds

Corrected QT (QTc) Normal HR: QT interval is < half the RR interval

QTc calculated by dividing the QT interval by the square root of the

RR cycle length

Normal QTc is <0.44sec

QT = Example .38, RR= .76, Square root of RR=

.87, .38 ÷ .87 = .44 ST Segment

Time of no electrical activity ST Segment

Ventricular depolarized and starting repolarization ST Segment

End of QRS to beginning of T When evaluating the ST segment do not measure

'length', only 'height' When evaluating the ST segment

Describe as isoelectric, elevated, or depressed T Wave

Ventricular repolarization The Peak of T

vulnerable period to hit and cause PVC T wave Do not

measure duration Describe T wave

Upright, round & smooth shape, inverted, peaked,

or depressed

U wave

Repolarization of Bundle of His and Purkinje fiber The U wave is

Normal in children The U wave can represents

hyperthyroidism or hypokalemia in adults Normal Sinus Rhythm

Regularity Regular Normal Sinus Rhythm Rate

60-100 Normal Sinus Rhythm

P wave Normal and upright: One P wave in front of each

QRS

PRI Rate .12 -.20 seconds & constant

QRS Rate < .12 seconds

Sinus Tachycardia Rate 101-150

Causes of Sinus Tachycardia Increased O2 demand ,fever, exercise,

Compensatory response to low Cardiac Output

(CO) Congestive heart Failure (CHF), dehydration,

hypovolemia

Hemodynamic effect of Sinus tachycardia Increased heart rate improves Cardiac Output

Sinus Tachycardia Management Correct cause

Sinus Bradycardia Rate <60 beats per minute

Causes for Sinus Bradycardia Increased parasympathetic tone: Athletes

SA nodal disease Sick Sinus Syndrome

SA Nodal disease or Sick Sinus Syndrome

Hemodynamic effects

Decreased Cardiac Output

Sick Sinus Syndrome Signs and Symptoms hypotension ,Orthostatic hypotension, syncope

Management for symptomatic bradycardia: Atropine, Pacemaker

Sinus Arrhythmia Regularity Irregular

Sinus Arrhythmia Rate 60-100

Sinus Arrhythmia P wave Normal and upright, one in front of each QRS

Sinus arrhythmia PRI Rate .12 - .20 seconds

Sinus Arrhythmia QRS Rate < .12 seconds

Sinus Arrhythmia Causes Heart Rate varies with respirations, due to

fluctuations in parasympathetic outflow

Sinus Arrhythmia Rate increases with inspirations, decreases with expiration

Atrial Rhythm 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 Irritable focus: sympathetic stimulation, caffeine

Hemodynamic effects of Atrial Rhythm None

Management of Atrial Rhythm None, reassurance

Premature Atrial Contractions (PAC) Single beat originates in atria and comes early in

cardiac cycle, Can occur in a cyclic pattern,

Bigeminy, trigeminy

Atrial Tachycardia Rate 150-250

Atrial Tachycardia P Wave Abnormal: coming

from different foci in heart

Atrial Tachycardia PRI

.12-.20 seconds Atrial Tachycardia QRS is

less than .12 seconds Cause for Atrial Tachycardia

Irritable SA or AV nodes Hemodynamic effect of Atrial Tachycardia

Depends on individual compensation abilities Management of Atrial Tachycardia:

Vagal stimulation cough, bear down, carotid

massage, Adenosine, Beta Blockers,Ca channel

Blockers, Amiodarone

ATRIAL Tachycardia ABC

A , Adensosine B, Beta Blockers, C, Calcium

Channel Blocker

Atrial Flutter

Area in atrium initiates impulse that is conducted

in repetitive, fast, cyclic pattern

Atrial Flutter Regularity

Can be regular or irregular Atrial Flutter Rate

250-350 Atrial Flutter P wave characteristics

"Saw Tooth" appearance Atrial Flutter PRI

Not measurable Atrial Flutter QRS is

Normal Atrial Fibrillation

Atrium very irritable: no longer beating in uniform

fashion, quivers

Atrial Fibrillation Regularity

Irregularly, irregular Atrial Fibrillation Regularity

Greater than 350 beats per minute Atrial Fibrillation P wave

Not measurable Atrial Fibrillation PRI

Not Measurable Atrial Fibrillation

QRS Normal Causes of Atrial fibrillation

Heart Dx, ischemia, rheumatic, mitral or tricuspid

valve disorders, overstretched atrium congestive

heart failure

Hemodynamic effects of Atrial Fibrillation

lose atrial kick, decreased stroke volume, Varying

ventricular response, decreased diastolic filling

time

Management of Atrial Defibrillation and Atrial

Flutter

Rhythm Control Convert to Normal Sinus Rhythm

Pharmacologica Management of Atrial Fibrillation

and Flutter

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 control the ventricular response

Pharmacologic Calcium channel blockers, beta blockers, digoxin

Complication Prevention Anticoagulate

Junctional Rhythms Also called junctional escape rhythm. AV node has

taken over when higher pacemaker fails to initiate

or conduct to AV node

Junctional Rhythm Regularity Regular

Junctional Rhythm Rate 40-60

Junctional Rhythm P wave Inverted before, during, or after QRS

Junctional Rhythm PRI Measurable only if before the QRS, then less

than .12

Junctional Rhythm QRS: Normal

Treat Junctional Rhythm if symptomatic with ATROPINE

Accelerated Junctional Rhythm Same as junctional rhythm, but faster rate

Accelerated Junctional Rhythm 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: Usually irregular because of PVC

Premature Junctional Contractions Rate Depends on the underlying rhythm

Premature Junctional Contractions P wave is Inverted before, during, or after QRS

Premature Junctional Contractions PRI is Measurable only if before the QRS, then less

than .12

Premature Junctional Contractions QRS is Normal

Premature Junctional Contractions Causes Irritable focus within AV junction, consider Digitalis

toxicity

Hemodynamic effects of Premature Junctional

Contractions is

None

Premature Junctional Contractions Management Observe

Junctional Tachycardia Rate 101-180 beats per minute

Hemodynamic effect more pronounced with 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 150-250

PSVT Paroxysmal Supraventricular Tachycardia

Paroxysmal Supraventricular Tachycardia

Treatment

Vagal Stimulation, Adenosine, Amiodarone,

Cardizem, Cardioversion, Ablation

Premature Ventricular Contraction Single beat originating from ventricle. Ventricle

depolarizes in abnormal fashion

Premature Ventricular Contraction Regularity Irregular

Premature Ventricular ContractionRate Depends on underlying rhythm

Premature Ventricular Contraction P wave PVC does not have P wave Premature Ventricular

Contraction PRI

PVC (no PRI)Underlying rhythm (PRI Normal) Premature Ventricular Contraction QRS

PVC wide bizarre, others normal, Can occur in a

cyclic pattern, Bigeminy, trigeminy

Premature Ventricular Contraction

Can occur together, Couplets, triplets 5-beat 'run',

May be unifocal or multifocal

Sinus tachycardia with PVCs in quadrigeminy

Multifocal PVCs, R on T Management: PVC

Assess for etiology, is it Drug induced, Caffeine,

alcohol, cocaine, sympathomimetic drugs

Causes of Premature ventricular contractions

Hypoxia,Cardiac disease, Acute coronary

syndrome, cardiomyopathy, ventricular aneurysm,

Metabolic imbalance, acidosis, Hypokalemia,

Irritation of the ventricle

Treat the

cause, Antidysrhythmic medication Ventricular Tachycardia

Ventricular impulse site speeds up and takes over

heart rhythm

Ventricular Tachycardia Regularity

Usually regular Ventricular Tachycardia Rate 150-250

Ventricular Tachycardia P wave None

Ventricular Tachycardia PRI None Ventricular TachycardiaQRS

QRS Wide bizarre, greater than .12 sec. VTach (Pulseless)

Defibrillate, CPR, Epinephrine VTach (With Pulse)

Amiodarone, Sotalol, Lidocaine Cardioversion Torsades de Pointe

Rapid unstable form of V-tach where QRS

appears to twist electrical orientation around the

isoelectric line

Torsades de Pointe Etiology

drugs that prolong QT interval (Quinidine,

Amiodarone, Tricyclic antidepressants),

hypomagnesemia, hypocalcemia, Congenital long

QT syndromes

Torsades de Pointe treatment

Correct cause and give IV Mg sulfate Idioventricular Rhythm Regularity

Usually regular Idioventricular Rhythm Rate

20-40 Idioventricular Rhythm P wave

None Idioventricular Rhythm PRI

None Idioventricular Rhythm QRS

Wide bizarre, greater than .12 seconds Idioventricular Rhythm Treatment4 Atropine, PPM

Ventricular Fibrillation 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),

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 Epinephrine 1 mg q 3-5 min, CPR, Correct cause

PEA Evaluate for cause

5 H"s 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 Hemophilia A - factor VIII deficiency

DISORDERS 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 (tPA—tissue 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 node—may occur with MI or CAD, rheumatic

heart disease, hyperthyroidism.

*Vagal stimulation.

*Electrolyte imbalances—hyperkalemia.

*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 regular—meaning, 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 diseases—usually a result of myocardial ischemia or infarction

(inferior wall); myocarditis.

*CAD—R 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

Ventricular Contractions

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

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 girls—and 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 Definitions

Acute pulmonary

edema

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

Cardiac output amount of blood pumped from the ventricles in 1 minute

Cardiac reserve ability of the heart to increase the cardiac output in response to metabolic

demand

Cardiac tamponade compression of the heart by blood or fluid in the pericardial sac

Cardiomyopathy disorder that affects the structure and function of the heart

Carditis inflammation of the heart

Endocarditis inflammation of the endocardium

Heart failure inability of the heart to function as a pump to meet the needs of the body

Hemodynamics the study of the pressures involved in blood circulation

Inotropic strengthening the contraction of the heart

Myocarditis inflammation of the heart muscle

Orthopnea difficulty breathing while lying down

Paroxysmal nocturnal

dyspnea

attacks of acute shortness of breath that occur at night, awakening the client

Pericardial effusion an abnormal collection of fluid between the pericardial layers

Pericardial friction rub leathery, grating sound produced by the inflamed pericardial layers rubbing

against the chest wall or pleura

Pericarditis inflammation of the pericardium

Regurgitation 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 narrowing of a valve opening, which obstructs forward blood flow

Valvular heart disease 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 Definitions

Acute coronary syndrome

(ACS)

a condition of severe cardiac ischemia

Acute myocardial

infarction

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

Angina pectoris 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 impaired tissue perfusion caused by pumping failure of the heart

Cardioversion restoration of a normal heart rhythm (normal sinus rhythm) using either

electric shock or medications

Diaphoresis profuse sweating

Ischemic inadequate blood and oxygen to meet a tissue's metabolic needs

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

Terms Definitions

Tachycardia abnormally rapid heartbeat (over 100 beats per minute)

Bradycardia slow heart rate, usually below 60 beats per minute

Flutter 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 Extra Beat (i.e. PAC, PJC, PVC)

Heart Block 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 Agent which alters the force of muscular contractions

Dromotrope a drug or substance that effects the conduction velocity of the heart

Chronotrope a drug or substance that effects the heart rate

What does an arrhythmia

result from?

Irregularitivity, contractilityies in automaticity, excitability, conduct

Arrhythmia 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

There are no contraindications to antiarrhythmics when needed to stop a

fatal arrhythmia

Class I Antiarrhythmics Membrane-stablizing agents, work on the fast sodium channels

Class Ia Antiarrhythmics Delays repolarization by blocking rapid sodium paths

Class Ib Antiarrhythmics Block sodium, but accelerates repolariztion

Class Ic Antiarrhythmics Massive blocking of sodium without much effect on repolarization

Class II Antiarrhythmics Beta blockers, block B receptors in the SNS

Class III Antiarrhythmics Prolong repolarization

Class IV Antiarrhythmics Inhibit the slow calcium channels

Prototype of Class Ia

Antiarrhythmics

Quinidine (Quinidex)

Action of Quinidine Blocks sodium pathways to cause delayed repolarization

Indication of Quinidine Atrial arrhythmias for long-term use (not typically given in a code

situation)

Side Effects of Quinidine 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

Lidocaine (Xylocaine)

Action of Lidocaine Decreases automaticity by decreasing the cells ability to accept/create

impulses.

Indications of Lidocaine Ventricular arrhythmias (lots of PVCs)

Side Effects of Lidocaine 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

Propafenone (Rythmol)

Action of Prophafenone Slows depolarization

Indications of

Prophafenone

Primarily severe long term ventricular arrhythmias. Given orally

Side Effects of

Propafenone

AV block, hypotension, decreased cardiac output, vertigo, metallic taste,

constipation, heart block

Implications for

Propafenone

Take with food

Monitor Vitals and EKG

Prototype for

Antiarrhythmic Class II

Propranolol (Inderal)

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 Hypotension, fatigue, vertigo, bradycardia, bronchospasm

Implications of Propranolol Monitor vitals, etc

Avoid in COPD and asthma patients

Prototype of Antiarrhymics

Class III

Amiodarone (Cordarone)

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

Verapamil (Calan)

Action of Verapamil Blocks the influx of calcium into cells

Indications of Verapamil SVT's (supraventricular tachycardia)

Also so slow ventricular rate in atrial fib and flutter

Hypertension

Side Effects of Verapamil Constipation, hypotension, bradycardia, heart block

Implications of Verapamil Discussed later with anti-anginal drugs

Prototype for Misc

Antiarrhythmic drugs

Adenosine (Adenocard)

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 Heart block, facial flushing, SOB, few seconds of asystole (flat-line)

Implications for Adenosine 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

_______?

High

Preload 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 The strength of the cardiac muscle

Increased contractility =

_______ blood going out.

Increased

How heart rate effects

cardiac output

To increase cardiac output, you could increase preload, afterload,

contractility or heart rate in a normal heart

Heart Failure 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?

Overstretch to counter hypertension

Poor muscle (e.g. MI with tissue necrosis)

Signs and Symptoms of

heart failure

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?

Positive inotropic drugs (Cardiac Glycosides-Digitalis)

Which drugs improve renal

sodium/water excretion?

Diuretics, Angiotensin Converting Enzyme Inhibitors (ACE Inhibitors)

Which drugs reduce blood

pressure?

Antihypertensives, diuretics, ACE Inhibitors

Which plant are cardiac

glyocsides obtained from?

The Foxglove

Prototype for Cardiac

Glycoside

Digoxin (Lanoxin)

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

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

Gradual digitalization--about 7 days to get po drug level to therapeutic

range

Acute Dosage of Digoxin Give large initial dose--digitalizing or loading dose followed by

maintenance doses

What is the typical oral

dose per day of Digoxin?

0.125 or 0.25mg (125-250mcg) daily

What is the typical loading

dose for Digoxin?

0.5mg (500mcg)

What are the GI side

effects of Digoxin?

Anorexia

Nausea

Vomiting

Diarrhea

What are the visual side

effects of Digoxin?

Green/yellow halos (chromatopsia)

What are the CNS side

effects of Digoxin?

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?

Commonly used in kids

Elderly need lover doses

Does Digoxin cross the

placenta and can it be

found in breast milk?

Yes

What is the interaction of

increase K+ and Digoxin?

Increased potassium=decreased dig finding

DECREASES EFFECT OF DIGOXIN

What is the effect of low

K+ levels and Digoxin?

Low levels of potassium=Increased dig binding

INCREASED EFFECT OF DIGOXIN

What is the effect of

potassium wasting

diuretics on Digoxin?

Increased effect of digoxin

What is the effect of

increased calcium on

digoxin?

Increased Ca+=Increased Dig binding

INCREASED EFFECT OF 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?

Take the apical pulse for 1 minute

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

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?

Ischemic Heart Disease

What are things that

increase myocardial

oxygen demand?

Exercise, hypertension (increase afterload), increased preload (CHF),

stress

What are things that

decrease myocardial

oxygen demand?

Lung disease, coronary artery disease, anemia

What is Chronic Stable

Angina?

Long term increase of oxygen demand with limited supply. Sharp pain

usually subsides 15 min after rest. Primarily caused by CAD.

What is Vasospastic

Angina?

Ischemia due to coronary vasospasm, often experience at the same time

everyday-often at night.

Organic Nitrates prototype: 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?

Dilates arteries, increases blood flow and oxygen

What effect does nitro

have on peripheral

vasculature?

Decreases afterload, allows the heart to work easier

What effect does nitro

have on afterload and

preload?

Decreases afterload and preload

What effect does nitro Decreases blood pressure (vasodilator)

have on blood pressure?

What effect does nitro

have on heart rate and

contractility?

Increase heart rate (only if on daily patch, common to use with beta-

blockers)

What are the indications of

Nitro?

Angina, sbulingual for prevention and treatment of attacks, acute MI,

CHF, intra-op or peri-op BP regulation (give IV).

What are the side effects

of Nitro?

Decreased BP, flusing of extermities, H/A (cerebral vasodilation), relex

tachycardia, contact dermatitis (from patch)

By what route do you

administer Nitro?

SL, buccal, IV, transdermal, traslingual spray

What are the interactions

of Nitro?

Potentiates antihypertensives, sedative, hypnotics, antidepresants, beta-

blockers.

IV Implications of Nitro: Must be on in infusion PUMP, monitor vitals

What drugs should you

caution patients about

while taking Nitro?

Viagra, Levitra and Cialis

Beta Blockers and Angina 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: Diltiazem (Cardiazem)

Examples of CCB's Diltiazem, verapamil, nifedipine, nicardipine

Indication of Verapamil: 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 Definitions

Adenosine is the generic name for

a. Nucleoside.

b. Adenocard.

c. Actidose.

d. Alupent.

B. Adenocard

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.

c. Narrow complex

supraventricular tachycardia.

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.

6 mg 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

a. Monitor the patient as the

asystole is transient.

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.

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.

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.

b. Hemodynamically stable

ventricular tachycardia

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.

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.

a. 300 mg IV push.

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.

b. Decrease platelet aggregation.

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.

c. 81 mg/kg IV drip.

d. 800 mg.

a. 160-325 mg orally.

Aspirin should be given as soon as possible to patients with:

a. Hemorrhagic stroke.

b. Gastrointestinal bleeding.

c. Unstable angina.

d. Active ulcer disease.

c. Unstable angina.

Atenolol is classified as a:

a. Calcium channel blocker.

b. ACE inhibitor.

c. Beta blocker.

d. Antipyretic.

c. Beta blocker.

Atenolol is indicated in the treatment of:

a. Cardiogenic shock.

b. Atrial fibrillation.

c. Third degree AV block.

d. Exacerbation of COPD.

b. Atrial fibrillation.

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.

a. 5 mg slow 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

non-labored. After maintaining adequate oxygenation, the most

appropriate drug of choice to elevate the man's blood pressure is:

Atenolol. Dobutamine

Adenosine. Dopamine

Dopamine

Which of the following best describes the actions of atropine d. Atropine is a

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.

parasympatholytic drug.

In which of the following conditions is atropine is indicated?

a. Symptomatic tachycardia.

b. Ventricular ectopy.

c. Organophosphate poisoning.

d. Atrial flutter of fibrillation.

c. Organophosphate poisoning.

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.

b. 0.5 mg rapid IV push.

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.

a. Decreased heart rate .

Calcium chloride is contraindicated in:

a. Hyperkalemia.

b. Digitalis toxicity.

c. Hypocalcemia.

d. Overdose of calcium channel blocker.

b. Digitalis toxicity.

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.

a. Calcium chloride, 20 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

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.

c. Calcium chloride.

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.

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.

b. Respiratory depression.

Digoxin is a cardiac glycoside derived from a plant known as:

a. Deadly nightshade.

b. Morning glory.

c. Foxglove.

d. Night blooming jasmine.

c. Foxglove.

Digoxin is used in the treatment of:

a. Atrial flutter or fibrillation.

a. Atrial flutter or fibrillation.

b. Ventricular tachycardia.

c. Ventricular fibrillation.

d. Atrioventricular block.

The adverse effects of digitalis toxicity include:

a. Hyperactivity.

b. Blurred, yellow, or green vision.

c. Ataxia.

d. Chest pain.

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.

b. May decrease the

effectiveness of her digitalis

preparation.

Diltiazem is in a class or medications known as:

a. Calcium channel blockers.

b. Beta blockers.

c. Beta sympathomimetics.

d. Cardiac glycosides.

a. Calcium channel blockers.

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.

a. Slowing conduction in the

atrioventricular node.

Diltiazem is indicated for the treatment of:

a. Sick sinus syndrome.

b. Cardiogenic shock.

c. Atrial fibrillation or flutter.

d. Ventricular tachycardia.

c. Atrial fibrillation or flutter.

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.

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.

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.

c. It is a synthetic catecholamine

that is primarily a beta1 agonist.

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.

a. Congestive heart failure

accompanied by hypotension.

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.

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.

b. Give via separate IV lines

since they are incompatible in the

same tubing.

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.

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.

c. Ventricular fibrillation.

d. Pheochromocytoma.

a. Hypotension from cardiogenic

shock.

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.

b. Labetalol may reduce the beta

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.

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.

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.

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.

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.

c. Epinephrine infusion, 2-10

mcg/minute.

Which of the following is not a typical adverse effect of

epinephrine?

a. Headache.

b. Dysrhythmias.

c. Chest pain.

d. Hypotension.

d. Hypotension

Racemic epinephrine is used in the emergency management of:

a. Ventricular fibrillation.

b. Hypovolemic shock.

c. Laryngotracheobronchitis.

d. Supraventricular tachycardia.

c. Laryngotracheobronchitis.

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.

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

B. Lorazepam, 1-4 mg IV over 2-

4 min... possibly Etomidate 0.2-

0.6 mg/kg IV over 30-60 seconds

The patient was sedated with etomidate prior to cardioversion and b. Monitor breathing and consider

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

intubation

The patient is a 29 year old woman complaining of heart

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.

b. Coffee (caffeine) antagonizes

the action of adenosine.

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.

c. Slowing or discontinuing of

amiodarone

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.

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

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

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

b. 1 mg/kg

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

b. glucagon

1 mg of glucagon is typically mixed with how much dilutent?

a. 1 mL

b. 5 mL

c. 10 mL

d. 20 mL

a. 1 mL

Which of the following is an indication of heparin administration?

a. acute myocardial infarction

b. allergic reaction

a. acute myocardial infarction

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

b. low platelet count

Heparin is given as an IV bolus of:

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

a. congestive heart failure

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

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

c. 5 mg/ hour

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

b. ibutilide

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

c. prolonging the action potential

duration

Ibutilide is indicated for which of the following dysrhythmias?

a. atrial fibrillation

b. asystole

c. ventricular fibrillation

d. ventricular tachycardia

a. atrial fibrillation

Inamrinone increases cardiac output without affecting:

a. alpha-adrenergic receptors

b. heart rate

c. myocardial contractility

d. vessel dilation

c. myocardial contractility

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

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

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

b. insulin

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

d. produces a reflex tachycardia

b. decreases peripheral

resistance

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

c. hypertensive crisis

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

c. 3 mg/ kg

Magnesium sulfate reduces muscle contractions by blocking:

a. Acetycholine

b. Dopamine

c. Epinephrine

d. Norepinephrine

a. Acetycholine

Which drug can be used as an antagonist to magnesium sulfate?

a. calcium gluconate

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.

b. Beta2 sympathomimetic.

Metoprolol is classified as a:

a. Beta sympathomimetic.

b. Alpha sympatholytic.

c. Cholinesterase inhibitor.

d. Beta sympatholytic.

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

b. Metoprolol.

While assessing an individual complaining of chest pain and

dyspnea, the patient reveals of history of COPD for which he self-

administers 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.

c. Is not indicated and should be

avoided.

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.

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.

b. Beta agonist.

c. Benzodiazepine.

d. Sedative hypnotic.

a. Narcotic analgesic.

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.

b. Decrease venous return to the

heart.

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.

a. Morphine decreases preload

and afterload.

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.

c. Chest pain from acute

myocardial infarction.

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.

d. Morphine is not indicated in

this patient.

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.

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.

b. Nitroglycerin may be given, but

monitor the blood pressure.

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.

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.

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.

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.

b. Hypotension.

Nitropaste is as absorbent paste containing:

a. 1% nitroglycerin.

b. 2% nitroglycerin.

c. 3% nitroglycerin.

d. 4% nitroglycerin.

b. 2% nitroglycerin.

The typical dosage of nitropaste for the adult with a suspected

acute myocardial infarction is:

a. ½ inch of paste

b. 1-2 inches of paste

c. 2-3 inches of paste

d. 3-4 inches of paste

a. ½ inch 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.

b. Nitropaste may be absorbed

by bare hands.

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

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.

c. Alpha and beta

sympathomimetic.

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.

c. 5-10 mcg/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

b. Extravasation may result in

tissue necrosis.

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.

b. Antidysrhythmic.

Procainamide is used in emergency care to:

a. Treat atrial fibrillation or flutter.

b. Induce sedation prior to and after cardioversion.

c. Treat ventricular tachycardia.

d. Treat hemodynamically stable junctional tachycardia.

c. Treat ventricular 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.

c. Procainamide, 20 mg/min IV.

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.

a. Is contraindicated in tricyclic

antidepressant toxicity.

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.

b. Torsades de pointes.

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-

Parkinson-White 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

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

a. Blood pressure is 104/76 mm

Hg

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

b. Lidocaine 1 mg/kg IVP until

PVCs are suppressed

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