NURS 301 Cardiovascular Unit Part Test 2 Study Guide.pdf

NURS 301 Test 2 Study Guide

Ch. 32-38: Cardiovascular Unit Part 1

Anatomy and Physiology Review

The Heart

oEndocardium- thin inner lining of the heart

oMyocardium- Middle muscular layer

oEpicardium- Outer fibrous membrane

oPericardium- 2 layered “sac” that surrounds the heart; consists of Visceral layer (inner) and

Parietal layer (outer)

Pericardial sac contains 10-30 mL of pericardial fluid that prevents a friction rub

Increased pericardial fluid= cardiac tamponade

Decreased pericardial fluid= Friction rub

Systemic Circulation: Blood Flow through the Heart

1. Right atrium receives blood from the superior and inferior vena cava and coronary sinus

2. Blood passes from right atrium through the tricuspid valve to the right ventricle

3. Blood passes from the right ventricle through the pulmonic valve into the pulmary artery and to the

lungs for oxygenation

4. Pulmonary vein returns freshly oxygenated blood back to the left atrium

5. Blood passes from left atrium to the left ventricle through the mitral valve

6. Blood exits the left ventricle through the aortic valve out into the aorta and to the body

oA/V valves: Tricuspid and Bicuspid (mitral)

oSemilunar valves: Pulmonic and aortic

oException: Arteries normally always carry oxygenated blood, but the pulmonary artery is the exception!

It carries deoxygenated blood to the lungs, and the pulmonary vein carries oxygenated blood back to

the heart from the lungs

oRemember: Tissue Paper My Assets! (Valves right to left in order of blood flow)

Coronary Circulation: Myocardial Blood Supply

oThe heart has its own circulatory system

oRight above the cusps of the aortic valve are the Sinuses of Valsalva which open into the right and

left coronary artery

oBlood flows to the heart muscle during diastole

Myocardium receives blood during diastole!

oRight coronary artery supplies the right atrium and the right ventricle (part of the posterior left

ventricle)

oLeft coronary artery branches into the left anterior descending and the left circumflex artery that

supply the left atrium and left ventricle

oDefinitions:

A. Ischemia= Tissue Hypoxia; Inadequate blood flow to meet the myocardial oxygen needs

Reversible lack of oxygen to tissues causing hypoxia

The pain that goes along with myocardial ischemia is called angina pectoris

B. Infarction= Result of permanent loss of blood supply and cellular death; Irreversible tissue

death

C. Perfusion= Measure of blood flow and oxygen delivery to tissues.

No perfusion can lead to MI, stroke, or acute renal failure!

Check bowel sounds, pedal pulses

Check kidney perfusion by measuring urinary output. A patient should produce at least

30 mL/hr

Conduction System

a) SA Node- specialized nerve tissue (the heart’s pacemaker).

The SA node is located at the top of the right atrium

If a patient has a “sinus rhythm,” it means the bat originated from the SA node. However,

“sinus” can include brady, normal, or tachy rates

b) Action Potential- Electrical impulse travels through the heart and leads to contraction

c) Contraction- Occurs when calcium flows into cardiac cells after depolarization

d) AV Node- allows time for atria to fill by providing a break in the contraction

Mid way point; a pause to allow the atria to fill

e) Bundle of His- Picks up the impulse and spreads it over the ventricles by way of the Purkinje Fibers

f) Repolarization- cells return to former state

g) Systole- absolute refractory period during which the cardiac muscle gradually recovers and is excitable

again. During contraction, the heart briefly loses its self excitability

oAuscultation:

S1= Closing of AV valves (lub)

S2= Closing of SL valves (dub)

S3= Ventricular gallop (“KenTUCKy”)- d/t fluid overload, CHF, or murmur; common in peds

S4= Atrial Kick (TENessee)

EKG

1) P-Wave= Depolarization (contraction) of the atrium

2) PR Interval= Measure of the time required for the impulse to spread from the SA node to the

ventricle (from top to bottom of heart)

3) QRS Interval= Depolarization (contraction) of ventricles

4) T-Wave= Repolarization of ventricles

5) U-Wave= If present, may mean hypokalemia or repolarization abnormalities

Three Electrolyes that Influence the Heart:

oPotassium

oCalcium

oMagnesium

ST elevation of 1 mm off baseline indicates ischemia and/or infarction!

“STEMI”= tombstone on EKG!

EKG Strip: (Know the times! Assume each strip is 6 seconds, so multiply “R’s” by 10 to get HR)

oEach small box is 0.04 seconds, each large box is 0.20 seconds

oP wave= 0.06-0.12 seconds

oPR Interval= 0.12-0.20 seconds

oQRS Complex= 0.04-0.12 seconds

Cardiac Output

CO= amount of blood pumped per minute.

CO= HR (heart rate) x SV (blood ejected per beat in mL)

oCardiac Output: WNL= 4-8 L/min (LITERS)

oStroke Volume: WNL 60-70 mL/beat (MILILITERS)

Ex. CO= HR x SV

= 70 bmp x 70 mL

= 490 mL/min 4.9 L/min

Normal Blood Volume: (since CO=4-8 L/min, you pump entire blood volume within 1 minute!)

oFemale: 4-6 L

oMale: 4-8 L

Generally, if heart rate goes up, cardiac output will go up. But this is only true to a certain point. If

HR is greater than 120 bpm sustained, CO would decrease b/c chambers don’t have time to fill

causing the stroke volume to decrease!

oIt is ok to have a HR >120 bmp acutely, but just don’t discharge the patient until it is

managed

Three Components of SV: (Cardiac meds will affect one of these)

1) Preload= Volume!

The volume of blood in the ventricles at the end of diastole, before the next

contraction

End diastolic volume (EDV) determines the amount of “stretch” placed on the

myocardial fibers

Ex. An ejection fraction of 70% means 30% of blood remains in ventricle after

contraction

Causes of increased preload: (too much blood left in the heart)

Hypervolemia/fluid overload

Cardiac valve regurgitation (murmurs allow for back up)

Pump failure/CHF

Multiple blood transfusions

Salt tablet

Causes of decreased preload: (not enough blood return to the heart)

Hypovolemia/Low circulatory blood volume

 Hemorrhagic shock/Bleeding

Lasix

Dehydration

Diabetes insipidus (no ADH)

Anaphylaxis (vasodilation)

2) Afterload= Resistance!

Reflects the vascular resistance against which the left ventricle pumps

Affected by size of ventricle, vascular wall tension, and arterial blood pressure

Causes of increased afterload:

 Vasoconstriction or meds that vasoconstrict

Hypertension

Fight or flight

Smoking

Stress

Causes of decreased afterload:

 Calcium channel blockers or other vasodilators

Hypotension

Distributive shock

3) Contractility= Squeeze!

Speaks to how “in shape” the muscle is

When contractility rises, the SV rises by increasing the emptying of the ventricles

Causes of increased contractility:

 Epinephrine/norepinephrine SNS

Stress

Positive inotropes such as Digoxin

Causes of decreased contractility:

 Increased aging

o* Increasing preload, afterload, or contractility increases the workload of the heart and

increases the need for oxygen. We need to manage our stress and hypertension!

oStarling’s Law: To a point, the more the fibers are stretched, the greater their force of

contraction. The more fluid/stretch, the greater the contraction. But if the fibers are

overstretched, they will break!

Regulation of Cardiovascular System

Autonomic Nervous System regulates the SNS (excitatory) and the PNS (inhibitory)

oSympathetic (beta 1 receptors) increase heart rate and contractility

oParasympathetic (vagus nerve) decreases heart rate

oExercise, temperature, and medications exert their effects on the heart through the ANS!

oExample of Negative Feedback System!

Baroreceptors (“Baro”= pressure)

oLocation: Aortic arch, carotid sinus, vena cava, atria, and pulmonary arteries

oSense pressure changes within the arterial system

oSend messages to the vasomotor center (brain stem)

oIncreased blood pressure inhibits the sympathetic beta 1 receptors and enhances the

parasympathetic system to decrease HR and cause peripheral vasodilation

oMake sure you check HR and BP before giving vasodilators such as ACE inhibitors or CCB’s!

Blood Pressure

The pressure exerted by blood against the walls of the arterial system

Systolic is the peak pressure against the arteries when the heart contracts

Diastolic is the residual pressure during ventricular relaxation

BP= CO x SVR (systemic vascular resistance)

Can be measured invasively through arterial pressures. A catheter is inserted into an artery (an

“art line”) for continuous monitoring

Can be measured non-invasively through a manual cuff

Korotkoff Sounds

oAuscultate first tapping- spurt of blood into constricted artery (systolic BP)

oDisappearance of the tap is the diastolic pressure

Pulse Pressure= Difference between SBP and DBP

oEx. If a patient has a BP of 120/80, their pulse pressure is 40

oMonitor the pulse pressure of a fresh post op patient! A narrowing pulse pressure means

bleeding or hypovolemia! (120/60…120/70…110/70)

oWidening PP means neuro problem! (120/80…130/70…140/60)

oA stable PP but decreasing BP means dehydration (120/80…110/70…100/60)

oIsolated systolic hypertension can cause a widened PP at baseline, this is a normal effect

of aging (120/80…150/80…180/80)

**Mean Arterial Pressure (MAP)= Average pressure within the arterial system that is felt by

organs in the body; a “perfusion measure”

oMAP= DBP + 1/3 PP

Ex. Patient has a BP of 120/60

MAP= 60 + 1/3 (120-60)

= 60 + 20

= 80

oNormal value for MAP= 70-100

oYou need a MAP ≥60-70 to perfuse the vital organs!

Effects of Aging on CV System

Increased collagen in the heart muscle leads to a stiffer heart and decreased contractility

Valves acquire lipids and collagen accumulation

Decreased response of the heart to exercise

Decreased # of pacemaker cells in the SA node

Decreased # of beta receptors

Decreased # of elastin in arterial walls causing walls to stiffen

Despite these change, under normal circumstances, the heat functions well

*Hypertension is NOT considered a normal consequence of aging! Heart rate does not markedly

drop, but it may decrease slightly

Cardiovascular Assessment

Read in book

Subjective and objective data

Listen to heart valves APE To Man

Listen for 1 full minute apically for pulse rate

Check JVD; Edema= Right sided CHF

Pulses:

o0= Absent

o1= Decreased

o2= Normal

o3= Increased

o4= Bounding

Non-Invasive Studies (Read in book)

Chest X-Ray- Structural changes and size of heart

EKG= At rest, stress test or continuous monitoring

ECHO= Ultrasound of heart

oLVEF= % left ventricular ejection fraction. 60-70% is normal, <40% means heart failure

Nuclear Cardiology= Radioactive isotope injected; blocks show up as different colored “cold

spots”

Cardiac Markers

An EKG may appear normal during an MI! Therefore, it is important to draw cardiac mrkers

Three Enzymes- found in all cells and released into circulation when cells are injured

1) C-Reactive Protein (CRP)- Normal <1.0 mg/dL

oGeneral inflammatory marker in the body but also released when MI occurs

oAny inflammatory conditions such as RA, MI, or Inflammatory Bowel Disease can increase

CRP

2) Creatinine Phosphokinase (CPK or CK)-Normal male= 15-105 U/L; Female= 10-80 U/L

oFailure of CPK to normalize may mean ongoing damage; Increased CPK= Cellular Injury!

oCK-MB (CK-2)- found primarily in cardiac muscle and cardiac nerve cells; can rise within

4-6 hours of MI, peak in 18 hours, return to normal in 2-3 days (if concentrations of CK-

MB make up >5% total CK, it is indicative of MI)

oThere is also Skeletal CK and Neuro CK

3) Troponin- Normal <0.4 ng/mL

oGold Standard! Biomarker of choice in diagnosis of MI!

oHighly specific to cardiac muscle!

oRises in 4-6 hr, peaks 10-24 hours, returns to normal in 4 days

This is why if you come into the ED really early, you may not see an increase in

troponin…yet!

Draw troponin levels every 4 hours until they’re stable

There is significant cardiac damage if troponin reaches a whole number

Lipids- Total cholesterol should be <200 mg/dL

oLDL (Bad cholesterol; makes you feel Lousy)

Carries cholesterol TO the heart

Should be <130 mg/dL

oHDL (Good cholesterol; makes you feel Healthy)

Carries cholesterol AWAY from the heart

Should be 33-70 mg/dL for men and 40-88 mg/dL for women

Cardiac Catheterization

Right Sided= Venous Approach

oThrough a vein into the right atrium/ventricle

oMeasures right chamber pressures and pulmonary artery wedge pressures (PAWP)

Left Sided= Arterial Approach

oAccessed through an artery to the left ventricle

oEvaluate the chamber pressure and oxygen content

oCoronary angiography- dye into vessels to visualize arteries on the screen during the cath

o*Patient is more likely to bleed with an arterial approach!

“cold spots” indicate areas with a lack of blood flow

Read about risky complications!

oPulmonary embolism, infection, bleeding, hematoma, allergic reaction, looping kinking or

breaking of catheter, aortic dissection, dysrhythmia, MI, stroke

oShell fish allergy often is accompanied by dye allergy

Nursing Responsibilities:

oPre-Cath:

Teaching: Procedure takes about 2-3 hours and you must be awake so that you can

cough and take deep breaths. Your heart will flutter, but you will be on continuous

ECG

Permission

Patient should be NPO 6-18 hours prior ideally (may not happen during emergency!)

oPost-Cath:

Check peripheral pulses, assess warmth and color of extremeties evey 15 minutes for

1 hour, then decreasing as ordered

Assess for bleeding from the site, especially if a left sided arterial approach was

used!

Assess respiratory status for pulmonary embolism! A plaque may lodge in the lungs

to cause a pulmonary embolism

Assess for cardiac arrhythmias

Coronary Artery Disease

Definition: Type of blood vessel disorder in the general category of atherosclerosis

Alcohol is now considered a major risk factor!

Derives from 2 Greek words: Ather (fatty mush) and Skleros (hard)

Plaques may occur anywhere, but they have an affinity for:

oCoronary artery (causing MI)- CAD is the leading cause of MI!

oCarotid artery (causing stroke)

Stages of CAD

1) Early Stage- Silent and goes undetected

2) Fatty Streaks- Lipid filled smooth muscle cells

Appear in coronary artery by age 15

Increase in surface area as patient ages

Considered reversible at this stage because they have not become hardened or

calcified

3) Raised Fibrous Plaque- Begin progressive changes in endothelium of arterial wall!

Appear in the coronary artery by age 30

Multi-factor causes

After injury- plaque develops

Entrapped lipids become calcified

Vessels become narrowed; smoking causes vasoconstriction and would worsen the

problem

4) Complicated Lesion

Most dangerous phase of the disease

Hemorrhages occur when the walls stretch

Layers develop that consist of calcification, lipids, thrombus, dead, necrotic tissue

Necrotic tissue becomes hard and causes rigidity and narrowing

Modifiable v. Non-modifiable Risk Factors

Non-Modifiable:

oAge, gender, race, family history

o*CAD is most common in white, middle aged men!

oDiabetes Mellitus- tenency to connective tissue degeneration and

endothelial dysfunction; issues with lipid metabolism. Lay down fat in

the vessels

Modifiable:

oSerum cholesterol >200 mg/dL

oHypertension; Smoking

oObesity (contributes to both hypertension and hyperlipidemia)

oSedentary lifestyle; stress and behavior patterns

Health Promotion and Maintenance

Identify those at risk and eliminate their risk factors!

Health education and nutrition

**Meds- Chart on Page 770 (Know cholesterol lowering meds!)

oFour Classes of Cholesterol Lowering Meds:

1. Bile Acid Sequestrants- Drugs that bind with bile acids in the

intestine, forming insoluble complexes and resulting in removal

of LDL and cholesterol

2. Lopid- Resists lipoprotein production

3. Lipitor- Inhibits cholesterol synthesis

4. Zetia- Inhibits absorption of cholesterol in intestine

Angina Pectoris (pg 772)

Pathophysiology:

oDemand for oxygen exceeds supply

oMay be d/t atherosclerosis

oCan occur with arrhythmias

Precipitating Factors:

Physical exertion

Strong emotions (ex. Fight with wife)

Extreme temperatures (ex. Shoveling snow in extreme cold)

Heavy meals

Sexual activities

Stimulants such as caffeine

Typse of angina

1) Stable (Classic)

Transient chest pain alleviated when precipitating factor is removed

Stage 3 CAD; can be managed with rest and Nitro; patterned and predictable

Ex. “My chest pain goes away when I stop shoveling snow”

2) Unstable (Progressive)

Stage 4 CAD; conventional methods of control don’t work

Ex. “My chest pain did not go away after I stopped shoveling the snow… I even took

Nitro!”

3) Printzmetal’s Variant (coronary vasospasm)

Rare

Seen often in patients with history of migraines or Reynaud’s

May occur in patient without CAD

Usually follows period of high physical demand

May follow epinephrine, histamine, prostaglandins

Has nothing to do with CAD! Vessels are clean; it is STRESS induced!

Common in stressed females!

Ex. Mrs. Clarke gets chest pain when she’s stressed

Clinical Manifestations of Angina:

oChest pain

oVague, strange feelings, pressure or ache in the chest

oMay c/o indigestion or burning

oOther sites in the body

oGo right to cardiac work up! Atypical pain should lead you to think cardiac etiology

oMales feel elephant on chest with pain radiating down left arm

oFemales feel high anxiety, and weird pains in their teeth, ear, neck, or abdomen

oDiabetics may not feel any pain d/t neuropathy! They have silent ischemia

Complications of Angina

oArrhythmia

oMI

Diagnostic Tests for Angina

oHistory

oLipid panel

oTread mill

oNuclear imaging

oAngiography

Drug Therapy for Chronic Stable Angina

oNitrates- Nitroglycerin; dilate coronary and peripheral vessels

oBeta Blockers- block beta 2 receptors to decrease heart rate, slow flow through AV node

oCalcium Channel Blockers- decrease heart rate; decrease afterload

oACE Inbibitors- Block conversion of angiotensin I to II (RAAS causes kidneys to sense the

low volume. Aldosterone makes sodium and fluids be retained. We need to prevent this!)

oAntiplatelet Aggretages- Aspirin

oCholesterol Lowering Meds- watch for patient complaints of muscle pain with statins (ex.

Lipitor)

oIf patient complains of muscle pain, discontinue the med and try a different one

Management of CAD

a) Nitrates- Dilate coronary arteries and peripheral vessels

oSub Lingual: Relief of pain in 3 min. and lasts for 45 min; may take 3 each 5 minutes apart. If

no relief, seek medical assistance. (“5-5-5, then 911”)

oOintment (nurse should wear gloves so her BP doesn’t drop!)

oTransdermal (the Nitro patch)

oLong acting (pills)

oIntravenous (drip)

b) Anti-platelet Aggregate

c) Beta Blockers (slow the HR)

d) Calcium Channel Blockers (Vasodilate and decrease afterload)

e) Percutaneous Transluminal Coronary Angioplasty (PICA)- Balloon

f) Atherectomy- Shave plaque off from vessel, sucked out in vacuum

g) Laser atherectomy- shave plaque, sucked out in vacuum

Nursing Management of Acute Condition

a) Assess the etiology of the discomfort

b) Oxygen and nitrates administration

c) Narcotics

d) Vital signs

e) Comfortable positioning

If a patient comes into the ED with chest pain, give them MONA! (Morphine, Oxygen, Nitrates,

Aspirin)

**TEST** The #1 Way to determine of they’re having an infarct or ischemia is to hook them up to an

EKG! So hook them up BEFORE you even give them MONA!

Nursing Management of Chronic Condition

Teaching

Identify precipitating factors

oRisk factor modification

oNitroglycerin teaching

Ch. 36: Dysrhythmias

EKG Strip Review

Rate: Count each 6 second strip for number of complexes, then multiply by 10 for 60 second

total (“rule of 10’s.” Rate is the first thing you calculate!

o<60 bpm= Bradycardia

CO compromised

o60-100 bpm= “Normal Rate”

o>100 bmp= Tachycardia

If HR goes up a little, CO goes up with it. But, if HR goes above 120 bpm sustained,

SV goes down, so CO goes down too because the ventricles don’t have time to fill

Rhythm: Regular or Irregular?

oMeasure P-P Interval with calipers for atrial rate

If P-P interval is the same, the patient has a “regular atrial rhythm”

oMeasure R-R Interval with calipers for ventricular rate

If the R-R interval is the same, the patient has a “regular ventricular rhythm”

oEKG Readings

P= Atrial depolarization (contraction)

QRS= Ventricular depolarization (contraction)

T= Ventricular repolarization

o“Sinus Rhythm” means the beat originated in the SA node, it can still be an abnormal rate

“Normal Sinus Rhythm”

oRate= 60-100 bpm

oRhythm= Regular

oSA node is initiating the beats

Sinus Tachycardia

oNormal complexes, but at an accelerated rate

oSA node still originates the beat

oRate= >100 bpm

oRhythm= Regular (check P-P and R-R intervals)

oCauses: Patient may be dehydrated, experiencing a SNS response, or in pain

Sinus Bradycardia

oPoor cardiac output

oPatient may go into circulatory arrest d/t poor perfusion

oIf acute, may be managed with medicine. If chronic, may need a pacemaker

oAthletes may have this naturally

oRate: <60 bpm

oRhythm: Reglar (P-P and R-R intervals are equal)

Atrial Flutter (A-Flutter)

oAtrial dysrhythmia with multiple P-Waves for every one QRS complex

oAtria are contracting several times for every one ventricular contraction

oAppearance of “saw tooth” waves.

oRate: The atria fire and contract 250-400 times per minute (result of irritable atrial focus)

oRhythm: Can be regular OR irregular!

oCauses: Severe electrolyte imbalance (Mg, K, or Na)

Atrial Fibrillation (A-Fib)

oThat atria are essentially “quivering,” not contracting. The result is CHAOS!

oNo discernable P-Wave! (no atrial depolarization)

oAs we age, we lose the natural pacemaker cells; loss of “atrial kick”

oAtrial contraction contributes 20-30% of CO normally, but here we have stasis of blood which

can lead to increased risk for blood clotting. The patient needs to be on Warfarin or other

anticoagulant

oChronic, stable A-fib can allow for good perfusion and CO, but if it becomes rapid A-fib with

V-tach, your CO is SEVERELY impaired! Patient needs a CCB quick!

oControlled A-Fib- Ventricular response rate is <100 bpm; we are okay with this.

oUncontrolled A-Fib (“Rapid A-Fib”)- Ventricular response rate is >100 bpm…BAD!!!

Rapid A-Fib is an emergency! We need to put the patient on a Calcium Channel

Blocker drip in the ICU

We need to slow down their ventricles so we can get that 70% of CO emptied!

(Ventricles are responsible for 70% of CO, atriums are only responsible for 30%)

oRate: Multiple foci or pacemakers fire in the atria at the same time resulting in chaotic

impulses at a rate of 400 or more per minute!

oRhythm: Irregular; R-R is wide, then narrow, then wide…

Ventricular Tachycardia (V-Tach)

oNo consistent P waves associated with QRS

oNo PR interval

oWide and bizarre QRS complex (>0.12 seconds)

One wide and bizarre QRS= “Premature Ventricular Contraction (PVC)”

Two wide and bizarre QRS= “Couplet”

oVery little CO! Patient will flat line soon… we need to hang meds quickly!

oRate:

Atrial rate is not usually countable; Ventricular rate is between 100-250 bpm

oRhythm: Usually regular

oCauses: Magnesium or potassium imbalance; try to reverse this electrolyte imbalance!

Ventricular Fibrilation (V-Fib)

oMultiple areas within the ventricles fire at random, asynchronous times producing a chaotic

and completely disorganized rhythm

oThe ventricles are “quivering,” not contracting

oAbsent P waves and the PR interval is unobtainable! Followed by flatline

oNo cardiac output, no pulse, and no BP! Your patient is essentially DEAD!

No cardiac output means organs will infarct!

Call the code team!

oRate: Too fast to count

oRhythm: Irregular

Ch. 34: Coronary Artery Disease and Acute Coronary Syndrome

Myocardial Infarction

Introduction to Myocardial Infarction

Ischemic changes become irreversible and necrosis/infarction results

Heart Attack Mortality:

oIf you have MI out of hospital, mortality rate is 30-50%

oIf you have MI in hospital, mortality rate is only 5-10%

Heart can withstand ischemia for 20 minutes by switching from aerobic to anaerobic metabolism

It is possible to have a small MI and never know it until years later when you are hooked up to an

EKG and they see a ST segment elevation

ED with Chest Pain: Rule Out MI!

Treatment: MONA

oMorphine- reduces pain, SNS response, and anxiety. Acts as a vasodilator to reduce

afterload

oOxygen

oNitroglycerin- Vadodilator opens coronary arteries

oAspirin- Anti-Platelet aggregate you need to chew!

EKG- See ST segment elevation, we know it was either a myocardial infarct or ischemia. Gives us

the best indicator of infarct. If the ST elevation is > 1 mm off baseline, infarct has occurred!

Cardiac Enzymes- look for CK-MB and Troponin!

Diagnostic Cath Lab/Interventional Cath- Open occluded vessel. Place stent or balloon

Patho of MI

Cardiac cells can withstand ischemia for approximately 20 min before cell death occurs

Earliest tissue to become ischemic is the sub-endocardium (the innermost layer)

Takes 4-6 hours for entire thickness of heart muscle to become necrosed

80-90% of MI’s are thrombus related

STEMI- Diseased vessel is totally occluded by thrombus. Send pt straight to the cath lab!

Non-STEMI- Diseased vessel is partially occluded by a thrombus

oEKG looks normal. The patient may still have chest pain, and cells are still dying

oNeed to resort to cardiac markers to diagnose

oLook at blood work… they may need to go to the cath lab!

Contractile function stops in the area of cardiac cellular death

Degree of altered function depends on size and location of infarct (most MI’s involve left ventricle)

Infarctions described by area which correlates with circulation (anterior, inferior, lateral, septal,

posterior… MI)

Healing Timeline after an MI

First 24 hours:

oInflammatory response and enzymes (serum cardiac markers) are leaded from the dead

cardiac cells

oCollateral circulation develops around infracted area

10-14 days post MI:

oScar tissue still weak; myocardium especially vulnerable to stress

6 Weeks post MI:

oScar tissue is said to be healed

oDecrease in scarred muscle compliance leads to:

Uncoordinated wall motion

Ventricular dysfunction

Pump failure can result (CHF)

Clinical Manifestations of MI

Pain- substernal or atypical

Nausea and vomiting- vomiting center and vasovagal reflexes stimulated

Sympathetic stimulation- Release Epi, NorEpi, and glycogen. Causes diaphoresis, peripheral

vasoconstriction. Skin is ashy, clammy, and cool. Patient experiences anxiety. Serum glucose will be

elevated

Low Grade Fever- Due to inflammatory process caused by cell death

Cardiovascular- HR and BP go up initially, then CO drops off. The blood is shunted to the brain,

lungs and heart

oAssessment

Listen: Hear S3 “KenTUCKy” d/t fluid back up. Also hear crackles in the lungs

Feel weak pulses, decreased urinary output

Complications of MI

Dysrhythmias- most common complication after MI.

Murmurs and dysrhythmias can be a permanent complication

CHF (heart is failing pump)

Cardiogenic shock- loss of 40% of ventricle

Papillary muscle rupture- causes mitral valve regurgitation

Ventricular aneurysm- Myocardial walls bulge during contraction. They can harbor thrombi

Pericarditis- inflammation of visceral or parietal pericardium around the heart

o2-3 days after the MI, you really start to see the inflammatory cascade. The patient’s chest

pain will increase with inhalation, coughing, and movement of the upper body. This pain is

what characterizes pericarditis

oPericardial Effusion- Too much fluid

oPericardial Friction Rub- No enough pericardial fluid

oTo differentiate between cardiac or pleural friction rub, have the patient hold their breath

oPatient may run a low fever

Diagnosis of MI

History of pain, risk factors

12- lead EKG is primary tool!

oIf ST is elevated greater than 1 mm in two continuous leads, MI has occurred

oSTEMI- More extensive MI; prolonged, complete coronary occlusion. May see pathologic Q-

wave

oNon-STEMI- Transient thrombosis; incomplete coronary occlusion. No pathologic Q wave

o50% of MI’s have a normal EKG!

Enzymes are released into the blood from necrotic heart tissue after an MI. Levels will rise

during/after MI

oCK-MB (CK2)

oTroponin- Cardiac specific; may not appear immediately

Management of MI

CCU (Coronary ICU)

Vital signs- look for MAP to be above 70

Bedrest (need to reduce their oxygen demand!)

Arterial catheter- invasive or non-invasive “Art line”

Cardiac catheter

Reperfusion Therapy- Goal is to salvage as much myocardial muscle as possible

oPercutaneous Coronary Intervention (PCI) or Fibrinolytic Therapy

oPTCA (PCI)- balloon and/or stent; PCI is the first line of treatment for a patient with a

confirmed MI. The goal is to try to open the effected artery. This is different than a CABG!

Fibrinolytic Therapy (“clot busting”) (KNOW for test!)

oGoal is to stop the infarction by dissolving the thrombus in the coronary artery and

reperfusing the myocardium

orPA reteplase, tPA alteplase

oUsed to treat an MI or stroke

oFibrin holds the clot together. Plasminogen and plasmid break down fibrin

oMajor concern with fibrinolytic therapy is reocclusion of the artery.

oThe major complication with fibrinolytic therapy is bleeding!

oContraindications against Fibrinolytic Therapy: (see page 783 figure 34-14)

a) Active internal bleeding

b) History of cerebral aneurysm in Circle of Willis or AV (arteriovenous) malformation

c) Intracranial hemorrhage

d) Recent stroke

e) Significant closed head injury or facial trauma

f) Suspected aortic dissection

g) **If MI is greater than 6 hours past, the patient is NOT a candidate!

IV Heparin Drips- Can also be used to prevent reocclusion of the artery

oAfter balloon/stent has opened the vessel, this keeps it open

oDraw PTT when giving Heparin. PTT should be 1-2x greater than WNL when pt is on Heparin

Nursing Management of MI Patients

Acute Care

oCardiac monitor- rest, comfort, O2 therapy

oPain control- anxiety control

Chronic Care

oCardiac rehabilitation

oPatient education

oResumption of sexual activity, exercise

By day 2, patient can ambulate in hallway and begin limited stair climbing

Tell patient to monitor heart rate!

oBuild up stamina

Coronary Artery Bypass Grafting (CABG)

Coronary Surgical Revascularization: What is it?

Constriction of new conduits for blood transport between aorta and other major coronary arteries

Allows for blood flow to continue beyond the stenosis

An artery is stenotic if its diameter is narrowed by more than 75-80%

Requires sternotomy (opening of chest cavity) and use of cardiopulmonary bypass machine

(CPB)

May be triple or quadruple bypass, so graft can be from internal mammary artery, saphenous vein,

radial artery, gastroepilotic artery, and/or inferior epigastric artery. Use veins or arteries!

CABG Graft Illustration

Surgeon anastamoses (connects) saphenous vein to aorta (upper left) and to the coronary artery

(lower right)

Surgeon pulls a graft from leg, flips it, and puts it in an aorta

CABG is a palliative treatment, not a cure! Grafted vessel is anastamosed (connected with sutures)

to coronary artery distal to the stenosis

How is it done?

Graph from saphenous vein (commonly used because it doesn’t disrupt peripheral circulation)

Vessel is reversed (because veins have valves, arteries don’t)

Anastamosed (attached/sewn) proximally to aorta and distally to the blockage

Re-occlusion can occur

Venous grafts tend to develop hyperplasia

Life expectancy of a venous graft is 5-10 years

Aspirin and statins for life!

Internal Mammary Artery (IMA)

IMA is most common artery used for CABG

Left IMA is left attached to its point of origin from the left subclavian artery

Mobilized from chest wall and attached to the coronary artery distal to the stenosis

Right IMA can be used in a similar way

Patency Rate is 85-95% at 10 year post procedure

Triple Bypass

Use:

1. Saphenous vein

2. Radial artery

3. Internal mammary artery

**Patient would not have a radial pulse!!!

Repeat CABG (Gastroepiploic artery or epigastric artery)

Requires a laparotomy or sternotomy (two huge incisions!)

Wound complications increase (most patients are diabetic; increased infection risk d/t

hyperglycemia)

Other arteries tend to be more delicate

Morbidity and mortality

Nursing Care: Two surgical sites, assess for cardiac distress through pain, arrhythmias, and

complications such as fever or drop in BP, urinary output, change in pulses

Q: What concerns would you have for a patient post-CABG?

A: Increasd HR, increased WBC, drop in H&H, decreased BP, decreased pedal pulses, decreased

urine output, muffled heart sounds, JVD

MID-CABG

Minimally invasive direct coronary artery bypass graft

Uses a thoracotomy approach to mobilize the LIMA or the RIMA using beta blockers to slow the

heart

oAnything requiring a thoracotomy disrupts the phrenic nerve pathway and can cause chronic

pain

Before closure, meds are stopped; Shorter recovery period

Does not require a sternotomy or CPB!

Few are candidates! Cannot be used in obese patients because you need good visualization

Management of Cardiopulmonary Bypass

Need a CPB to act as the patient’s heart and lungs because the surgeon needs the heart completely

still for the CABG. Allows work on a still heart

Cardiopulmonary Bypass Machine pumps oxygenated blood

Machine receives blood from catheters in the vena cava or right atrium, oxygenates it, and returns

it via pump to aorta to perfuse organs during surgery

**Permissive Hypothermia is created

oCold fluids infused

oLower the oxygen demand of the heart so the surgeon can work on a stilled heart

oLike hibernation. Cool them down, then warm them up slowly

Preop IV, prophylactic antibiotics

Procedures- crack chest and spread the ribs, CPB, graft, closure, chest tube and sterna drains

placed

Post Op Complications: (KNOW for test!)

a) Hypovolemia

b) Cardiac tamponade

c) Arrhythmia

d) Emboli

e) Fever

f) MI or CVA

g) Wound infection- sterna wound infection common in diabetics d/t hyperglycemia impairing

the neutrophil function

h) Hemorrhage

Inflammatory Cascade

oFluid in pericardial sac may cause cardiac tamponade

oDo a pericardial centesis to allow heart to beat.

Clinical Manifestations

oPatient will feel like they can’t breathe

oSee JVD, increased HR, muffled heart sounds, and S3

Ch. 35: Heart Failure

Definition of Heart Failure

A cardiovascular state in which the heart is unable to pump an adequate amount of blood to meet

the metabolic need of the tissues

Heart failure is a condition, not a disease

Perfusion problem! Normally Bi-Ventricular. The heart is a failing pump

Statistsics of Heart Failure

According to American Heart Association (AHA), about 5 million Americans with HF and about

470,000 cases diagnosed each year

Risk Factors for HF

CAD/MI

Advancing Age- lose contractility

HTN/Hypertensive crisis- wears the heart out!

Diabetes Mellitus

Smoking

Obesity

*CAD and advancing age are primary risk factors!

Systolic HF vs. Diastolic HF

Systolic HF- heart can’t pump effectively (normal ejection fraction 60-70%)

oLowered EF with systolic failure

oDecrease in left ventricular ejection fraction is the hallmark of systolic dysfunction!

Diastolic HF- impaired ability of ventricle to relax and fill during diastole.

oEF may be normal but still have HF symptoms

oStiffened ventricle

Can see mixed systolic and diastolic dysfunction

Left-Sided Failure

Patho:

oBlood backs up through the left atrium to the lungs

oIncreased pressure causes fluid to leak out of the vessels leading to pulmonary congestion

and impaired gas exchange

Most Common Causes: CAD and HTN

Clinical Manifestations: increased HR, crackles, S3, altered mental status, rerstless, confused,

weakness, dyspnea, frothy pink tinged sputum

o Pleural effusion (fluid back up in 2 layers of pleura. Need to do a thoracentesis to pull

fluids off lungs)

oParoxysmal Nocturnal Dyspnea- When supine, fluid pools and patient feels like they’re

drowning

Right-Sided Failure

Patho: Weakened right ventricle

Primary Cause: Left sided failure leads to right failure, then you have “biventricular failure”

Clinical Manifestations: Increased HR, JVD, weight gain, ascites, hepatomegaly, splenomegaly,

dependent edema, anorexia

oAnasarca- gross gerneralized edema with pitting

Compensatory Mechanism for HF

A. Sympathetic nervous system- beta receptors increase HR, but this does not help CO

B. Dilation- Blood continues to back up, increased wall tension, increased work load (Starling’s Law)

C. Renal Response (RAAS)- kidneys sense decreased blood flow, vasoconstriction, sodium and

water retention increases fluid overload

D. Hypertrophy

All these compensatory mechanisms worsen the clinical presentation by increasing the oxygen

demand on the heart! None of them work!

Complications of HF

1. Pulmonary Edema- refers to acute, life threatening condition where lung alveoli fill with fluid

which increases pulmonary pressures

a. Patient may be agitated, pale, cyanotic, severe dyspnea, wheezing, coughing, frothy,

blood-tinged sputum d/t irritation in lungs

b. Crackles- fluid needs to be pulled off with a thoracocentesis

2. Pleural Effusion- Fluid between visceral and parietal pleura; need a thoracocentesis

3. Left Ventricle Thrombus- Stasis of blood leads to MI or stroke if thrombus becomes an emboli

4. Hepatomegaly- liver engorged; right sided CHF, leads to cirrhosis and fibrosis

5. Weight Changes- rapid weight gain during acute HF. May gain 10 lbs in one week d/t fluid wt!

Diagnostic Factors for HF

Physical exam

ABG’s

X-Ray

ECG

Hemodynamics

ECHO- ultrasound of heart; look at left ventricular ejection fraction.

oIf left ventricular EF < 40%, this means systolic failure!

Cardiac cath, nuclear imaging

Beta Natriuretic Peptide (BNP) is a dieresis peptide released from ventricle in response to fluid

overload

oBNP greater than 100 pg/mL means heart failure!

Management of HF

Treat the underlying cause! (see pg. 804 table 35-6)

oOxygen therapy and rest- bed rest to decrease the demand for oxygen

oDaily weights- mobilizing fluid to become normovolemic; monitor I&O

oSodium restricted diet

oPharmacology

Pharmacology of HF

1. Diuretics (Lasix)

oReduce preload

oMobilize edematuous fluids with loop diuretics… watch potassium levels!!!

Trying to get rid of intravascular fluids to reduce pulmonary venous pressure

Never push IV potassium!

2. ACE Inhibitors

oReduce afterload by preventing the retention of sodium and water

oEx. Capoten, Vasotec, Lotensin

3. Beta Blockers

oBlock the negative effects of the SNS on the failing heart

oSlow the HR, lower conduction to decrease the workload on the heart (balance supply and

demand)

oGive a small dose to treat HF, big dose would be to treat HTN

oEx. Coreg 3.25 mg PO will not effect BP, it is okay to give if HR is 60

4. Positive Inotrope (Digoxin; “Lenoxin”)

oPositive Inotrope= Increases contractility of heart

oNegative Chronotrope= Decrease heart rate

oNarrow therapeutic range (1-2 ng/dL)

oWatch for dig toxicity! (anorexia, nausea, vomiting, arrhythmia)

Hypokalemia caused by loop diuretics is common cause of toxicity because

hypokalemia enhances the action of Digoxin.

Patient may have dangerous heart rhythms!

Nutritional Considerations

Sodium restrictions because water follows salt! Less than 2 grams of sodium per day to treat

edema!

Dietary Approach to Stop Hypertension (DASH) Diet- low in fat

Health promotion- control sodium and teach compliance with meds. There is an issue with non

complicance; for example beta blockers cause lethargy and lasix makes you urinate a lot!

Acute interventions

oDecrease intravascular volume- give Lasix!

oDecrease venous return- give ACE inhibitor

oImprove gas exchange- give O2 therapy; bed rest

oImprove cardiac function- Positive inotrope digoxin or a tiny beta blocker

oReduce anxiety- patient may feel drowning; keep SNS at bay

Chronic Management

oDiet and weight- Daily weights to monitor fluid retention

oDrug therapy- compliance!

oRest- Pace yourself!

Ch. 33: Hypertension

Definition of Hypertension

Hypertension is the persistent elevation of systolic BP ≥ 140 mmHg OR diastolic BP ≥ 90 mmHg

NOT a one time reading!

65 million American adults have HTN (nearly 1/3)

Hypertension Classifications

1. Essential HTN- aka Primary or Idiopathic HTN

oAccounts for 90-95% of all HTN

oContributing Factors: (Multi-Factorial with genetic component)

Increased sympathetic nervous system stimulation

Overproduction of sodium retaining hormones and vasoconstrictors

Increased sodium intake

Greater than ideal body weight

DM

Excessive alcohol intake

Stress

2. Secondary Hypertension

oAccounts for 5-10% of all HTN

oOccurs with a specific cause that can be identified and corrected

oTreat the underlying cause!

Coarctation of the aorta (congenital narrowing)

Renal disease (renal artery stenosis)

Endocrine disorders (pheochromocytoma)

Remove the pheo to allow BP to go down to normal

Meds such as oral contraceptives and NSAIDS; cocaine use

Categories of Hypertension (KNOW!)

A. Optimal: Systolic <120 and Diastolc <80

B. Prehypertension: Systolic 120-139 OR Diastolic 80-89

C. Stage 1: Systolic 140-159 OR Diastolic 90-99

D. Stage 2: Systolic ≥160; Diastolic ≥ 100 (Concern with MI or stroke!)

Clinical Manifestations of HTN

Headache, epistaxis (nose bleed)

Easily fatigued

Dizziness, blurred vision

Hypertension is often called the “Silent Killer” because it is often asymptomatic!

Complications of HTN

Most common complications of HTN are target organ diseases!

A. Heart- CHF

B. Brain- Cerebral vascular disease (atherosclerosis= most common cause)

C. Peripheral vasculature- CAD (d/t stress in endothelium and fatty streaks)

D. Kidneys- Nephrosclerosis

E. Eyes- Retinal damage (blurred vision)

Diagnostics of HTN

BP measurements in both arms, 2 measurements 5 minutes apart

Labs: BUN, creatinine, urinalysis electrolytes, glucose

oScreen for renal involvement and provide a baseline

Chest x-ray and ECG

**Hypertension is not diagnosed on a single office visit! Come back for checks… 3 consecutive high

reading visits confirm the diagnosis!

Management of HTN

Regular exercise

Stress reduction

No smoking

Medications in a stepwise approach

Nutrition- DASH diet

Drug Therapy for HTN (KNOW med table on pg. 748-751)

1. Diuretics- Thiazide, “diur’s” first line

oDecrease preload/intravascular volume

oWatch potassium levels unless you are using a potassium-sparing diuretic

oMonitor pt for orthostatic hypotension, hylokalemia, and alkalosis

2. Beta Blockers- “lol’s” block beta receptors

oDecrease HR and cardiac output, reduce sympathetic vasoconstructive tone and afterload

oWatch HR, use cardioselective (beta 1) as indicated

oBlock Beta 1 Lower HR, lower conduction through AV node

oActive Beta 2  Bronchodilator; never give a beta 2 blocker to an asthmatic!

3. Calcium Channel Blockers- Cardiazem, Verapamil, and the “pines”)

oPrevent Calcium entry into vascular smooth muscle and cardiac cell

oVasodilate, decrease HR and contractility.

oMonitor HR

4. ACE Inhibitors- “prils”

oBlock conversion of angiotensin I to II

oPrevent RAAS mediated vasoconstriction

oDecreased endothelial dysfunction; used in HF, tachycardia, MI, HTN, DM, and chronic

kidneys disease

oWatch for dry, hacking cough (20-30% of patients)

Stepwise Plan of Meds

Step 1- Non-pharmacological

Step 2- Thiazide diuretic, beta blocker, calcium channel blocker, or ACE inhibitor

Step 3- Add a second drug of a different class, increase 1st drug dose, or substitute

Step 4- Add a third drug or substitute

Step 5- Further evaluate, refer, or add a third or fourth drug

The goal is to go through multiple classes before going high on one dose

Nutritional Management of HTN

Sodium restriction (2 grams per day)

Caloric restriction

Lower fats; obesity exacerbates HTN

Modify alcohol consumption

Ch 37: Inflammatory and Valvular Heart Disease

A. Infective Endocarditis

oInfection of the endocardial valve surface with microorganism (usually bacterial)

oOccurs when turbulence within the heart allows organisms to infect (ie strep infection moves

to the valves)

Endocardium is continuous with heart valves

Blood flow spreads the bacteria to the valves

oNon-specific clinical findings

oTreat with antibiotics

oProphylactic antibiotics- use before surgery or dental procedures

B. Acute Pericarditis

oInflammation of the pericardial sac

oMay be infectious cause, uremia, acute MI

oSymptoms include pleuritic rub, SOB

Hallmark finding= pericardial friction rub!

oPericardial effusion- excess fluid in pericardium. Treatment is pericardiocentesis

oTamponade Complications- accumulation of fluid compresses heart

C. Mitral Stenosis

oMost result from rheumatic fever (acute inflammatory disease affecting all layers of the

heart; leads to scarring and deformity of heart valves)

oObstruction of flow out of left atrium

oSOB, fatigue, palpitations, loud first heart sound, low pitched diastolic murmur

Primary symptom= Exertional Dyspnea

D. Mitral Regurgitation

oBackflow of blood to left atrium from left ventricle d/t incomplete mitral valve closure during

systole

oEx. Mitral prolapse

oAsymptomatic for years!

E. Aortic Stenosis

oObstruction of blood flow from left ventricle to aorta

oResult of age, rheumatic fever, CAD, or calcification

F. Aortic Regurgitation

oRetrograde blood flow from aorta into left ventricle during diastole

oLeaf abnormality (ie 2 leafs present instead of 3)

oEndocarditis

G. Prosthetic Valves

oMechanical Valves- patient on anticoagulant for life d/t increased risk of

thromboembolism

More durable than biological valves

oBiological Valves- From pigs-porcine or cows-bovine or homograft- human valve

Do not need anticoagulant therapy

Ch. 38: Vascular Disorders

Chronic Arterial Occlusive Disease (Aortoilliac Disease/Leriche’s Syndrome)

Definition- Atherosclerotic occlusive disease involving abdominal aorta and or both iliac arteries

Pain in hip, buttocks, or thighs

Intermittent claudication

Pulses absent or diminished in lower extremeties

Surgery (aortofemoral graft)

Lower Extremity Disease (PAD)

Progressive narrowing

Femoral, popliteal, tibial, or peritoneal vessels (femoral and popliteal are most common)

Occurs in 60’s or 80’s

Leading cause is atherosclerosis

Smoking, HTN, hyperlipidemia, family history, DM, obesity, sedentary lifestyle

Classic Symptom= Intermittent Claudication

Pain as disease progresses; (starts as intermittent claudication, then becomes continuous)

Diagnosis of Vascular Disease

Doppler ultrasound- sound waves toward vessels

Duplex imaging- like an arteriogram; ultrasound of the vessels. Color maps blood flow through

arterial region

Management of Vascular Disease

Protect the extremity- protect from trauma, decrease ischemic pain, prevent infection, maximize

perfusion. Don’t soak their feet!!

Slowing the progression; first treatment goal is to modify CVD risk factors

Decreasing the vasospasm

Improving collateral circulation

Surgery:

a) Endarterectomy- opening of artery and removing obstructing plaque

b) Patch Graft Angioplasty- Open artery, remove plaque, and sew patch to opening to widen

lumen

c) Vascular Bypass Surgery- Most common, use native vein or synthetic graft to bypass

blood around lesion

Thrombophlebitis

Formation of a clot in association with inflammation of the vein

Classified as superficial or deep

Virchow’s Triad: (high risk for DVT)

1. Venous stasis (i.e. immobile patient, obese, traveling)

2. Damage to the endothelium stimulates platelet activation (i.e. HTN, chemicals,

hyperlipidemia, smoking, etc)

3. Hypercoagulability (i.e. oral contraceptives, or other coagulotherapy)

Clinical Manifestations of Thrombophlebitis:

oSuperficial- palpable, firm cordlike vein which is tender, red and warm; may have fever and

leukocytosis

oDeep- may have no symptoms or have unilateral leg edema, pain, warm skin, and a

temperature greater than 38 Celsius

oPain on flexion of foot (Homan’s Sign) is classic, but unreliable

oDVT Prophylaxis for all inpatients who are immobile (ie TEDS, foot pumps, leg sleves,

Heparin, or Lovenox SubQ)

Complications of Thrombophlebitis:

oPulmonary embolus

oChronic venous insufficiency- results from valvular destruction allowing retrograde

venous blood flow. Causes pooling of blood in legs and swelling. Can lead to venous leg

ulcers!

Treatment of Thrombophlebitis:

oBed rest; Elevation of extremity

oWarm, moist heat to relieve pain and inflammation

oAnticoagulation therapy ; Surgery (rare)

oUse of Greenfield Filter is inserted (IVC filter)

Review Questions:

Ch. 32

1. Patient with tricuspid valve disorder will have impaired blood flow between

a. Right atrium and right ventricle

2. Patient with severe blockage in right coronary artery. What affected?

a. AV node

3. If purkinje system is damaged, conduction of electrical impuse impaired through

a. Ventricles

4. Portion of vascular system responsible for hemostasis

a. Endothelial layer of arteries

5. When BP rises, the homeostatic mechanism to compensate involves

a. Baroreceptors that inhibit SNS causing vasodilation

6. P wave represents impuse

a. Arising at SA node and depolarizing the atria

7. Auscultate left MCL at 5th ICS

a. Mitral area

8. Pulse deficit of 23 beats may be caused by

a. Dysrhythmias

9. When assessing cardiovascular system of 79 y/o

a. Difficulty isolating apical pulse

10. When caring for pt returning from cardiac cath

a. Monitor Vital signs, ECG, check catheter insertion site and distal pulses

11. The blood pressure of a 71-year-old patient admitted with pneumonia is 160/70 mm Hg. Which of the

following is an age-related change that contributes to this finding?

a. Loss of elasticity in arterial vessels

12. While assessing the cardiovascular status of a patient, the nurse performs auscultation. Which of the

following practices should the nurse implement into the assessment during auscultation?

a. Palpate the radial pulse while auscultating the apical pulse.

13. A 59-year-old man has presented to the emergency department with chest pain. Which of the following

components of his subsequent blood work is most clearly indicative of a myocardial infarction (MI)?

a. Troponin

Ch. 33

1. Modifiable risk factor for HTN

a. Excessive alcohol consumption

2. Major consideration in management of older adult with HTN

a. Use careful technique in assessing BP of patient because of possible ausculatory gap

3. Pt with newly diagnosed HTN has BP of 158/98 after 6 months of exercise and diet

a. Medication will be required because BP is not at goal

4. The nurse teaches a patient with hypertension that uncontrolled hypertension may damage organs in the

body primarily by which of the following mechanisms?

a. Hypertension promotes atherosclerosis and damage to the walls of the arteries.

5. When teaching a patient about dietary management of stage 1 hypertension, which of the following

instructions is most appropriate?

a. Restrict sodium intake

6. In caring for a patient admitted with poorly controlled hypertension, the nurse would understand that

which of the following laboratory test results would indicate the presence of target organ damage

secondary to the primary diagnosis?

a. Serum creatinine of 2.6 mg/dl (WNL= 0.6-1.2)

7. In reviewing medication instructions with a patient being discharged on antihypertensive medications,

which of the following statements would be most appropriate for the nurse to make when discussing

atenolol (Tenormin)?

a. Make position changes slowly, especially when going from a lying down to a standing position

8. The nurse is caring for a patient admitted with emphysema, angina, and hypertension. Before

administering the prescribed daily dose of atenolol 100 mg PO, the nurse assesses the patient carefully.

Which of the following adverse effects is this patient at risk for given the patient’s health history?

a. Bronchospasm

9. The nurse is caring for a patient with hypertension who is scheduled to receive a dose of atenolol

(Tenormin). The nurse should withhold the dose and consult the prescribing physician for which of the

following vital signs taken just before administration

a. HR= 48

Ch. 34

1. Person with CAD should not

a. Add weight lifting to his exercise program

2. Ischemia

a. Will be relieved by rest, nitroglycerin, or both

3. Patient two days post MI experiences chest pain “It hurts when take deep breath”

a. Obtain vital signs and auscultate for pericardial friction rub

4. Unstable angina meds

a. Antiplatelet, Beta blockers, nitro

5. Patient recovering from uncomplicated MI should

a. Begin exercise program with at least five 30 min sessions per week

6. Most common finding in pt at risk for sudden cardiac death is

a. Left ventricular dysfunction

7. The community health nurse is planning health promotion teaching targeted at preventing coronary

artery disease (CAD). Which of the following ethnic groups would the nurse select as the highest

priority for this intervention?

a. White male

8. Which of the following individuals would the nurse identify as having the highest risk for CAD?

a. A 45-year-old depressed male with a high-stress job

9. For which of the following antilipemic medications would the nurse question an order in a patient with

cirrhosis of the liver?

a. Atorvastatin (Lipitor) may cause liver damage

10. After teaching a patient with chronic stable angina about nitroglycerin, the nurse recognizes the need for

further teaching when the patient states

a. I can take up to five tablets every 3 minutes for relief of my chest pain.”

11. When planning emergent care for a patient with a suspected MI, the nurse will anticipate administration

a. Oxygen, nitroglycerin, aspirin, and morphine.

12. The nurse is providing teaching to a patient recovering from an MI. Discussion regarding resumption of

sexual activity should be

a. Discussed along with other physical activities.

13. Postoperative care of a patient undergoing coronary artery bypass graft (CABG) surgery includes

monitoring for which of the following common complications?

a. Atrial dysrhythmias

14. A patient was admitted to the emergency department 24 hours earlier with complaints of chest pain that

were subsequently attributed to ST-segment-elevation myocardial infarction (STEMI). Which of the

following complications of MI should the nurse anticipate

a. Cardiac dysrhythmia

15. The nurse is examining the ECG of a patient who has just been admitted with a suspected MI. Which of

the following ECG changes is most indicative of prolonged or complete coronary occlusion?

a. Pathologic Q wave

16. For which of the following is percutaneous coronary intervention (PCI) most clearly indicated

a. Acute MI

Ch. 35

1. Systolic failure

a. Decreased EF and increased PAWP

2. Compensatory mechanism with HF that leads to fluid retention and additional workload on heart

a. Neurohormonal response

3. Med that will decrease preload and afterload and relieve anxiety

a. Morphine sulfate

4. Pt with chronic HF and A-fib treated with digitalis and loop diuretic. Nurse should

a. Monitor serum potassium levels

5. The nurse is administering a dose of digoxin (Lanoxin) to a patient with heart failure (HF). The nurse

would become concerned with the possibility of digitalis toxicity if the patient reported which of the

following symptoms?

a. Anorexia and nausea

6. The nurse is preparing to administer digoxin to a patient with HF. In preparation, lab results are

reviewed with the following findings: sodium 139 mEq/L, potassium 3.0 mEq/L, chloride 103 mEq/L,

and glucose 106 mg/dl. The nurse should do which of the following at this time?

a. Hold drug and report K

7. The nurse would recognize that indications for the use of dopamine (Intropin) in the care of a patient

with heart failure include

a. Hypotension and tachycardia

8. A patient with a recent diagnosis of HF has been prescribed furosemide (Lasix) in an effort to

a. Reduce preload

Ch. 36

1. Infective endocarditis sign and symptoms

a. Retinal hemorrhage, splinter hemorrhage, osler’s nodes, erythematuous macules on palms

and soles

2. Chronic constrictive pericarditis complication

a. JVD

3. Myocarditis

a. Angina, pleuritic chest pain, pericardial friction rub

4. Myocarditis priorities

a. Oxygenation and ventilation

5. Long term consequence of rheumatic fever

a. Valvular heart disease

6. Priority for patient during acute rheumatic fever

a. Administer antibiotics as ordered

7. Indicator of decreased cardiac output in patient with aortic valve regurgitation

a. SOB on minimal exertion and diastolic murmur

8. Dianostic study differentiates the types of cardiomyopathy

a. Echocardiography

9. Patient with HF secondary to dilated cardiomyopathy. Priority:

a. Monitor patient’s response to prescribed meds

10. Upon admission assessment, the nurse notes clubbing of the patient’s fingers. Based on this finding, the

nurse will question the patient about which of the following disease processes?

a. Endocarditis

11. While admitting a patient with pericarditis, the nurse will assess for which of the following signs,

symptoms, and complications of this disorder?

a. Pulsus paradoxus

12. The nurse conducts a complete physical assessment on a patient admitted with infective endocarditis.

Which of the following findings are significant?

a. Regurgitant murmur at the mitral valve area

13. Which of the following nursing actions should the nurse prioritize during the care of a patient who has

recently recovered from rheumatic fever?

a. Teach the patient about his or her need for continuous antibiotic prophylaxis.

Ch. 38

1. Suggests abdominal aorta has ruptured

a. Sudden severe low back pain, bruising along flank

2. AAA repair

a. Administer IV fluids and monitor kidney function

3. Rest pain is manifestation of PAD that occurs d/t

a. Decrease in arterial blood flow to nerves of feet

4. Pt with infective endocarditis develops sudden left leg pain with pallor, paresthesia, and loss of

peripheral pulses

a. Notify physician of change in peripheral perfusion

5. High risk for venous thromboembolism

a. 32 y/o woman who smokes, takes oral contraceptives, and planning trip to Europe

6. S/S acute venous thromboembolism

a. Mild to moderate calf pain and tenderness; unilateral edema and induration of thigh

7. Pt teaching for anticoagulant therapy

a. Watch for signs of bleeding

8. Pt with venous leg ulcers, intervention

a. Apply graduated compression stockings

9. The nurse is admitting a 68-year-old preoperative patient with a suspected abdominal aortic aneurysm

(AAA). The medication history reveals that the patient has been taking warfarin (Coumadin) on a daily

basis. Based on this history and the patient’s admission diagnosis, the nurse should prepare to administer

which of the following medications?

a. Vitamin K

10. The nurse is caring for a patient who has been receiving warfarin (Coumadin) and digoxin (Lanoxin) as

treatment for atrial fibrillation. Because the warfarin has been discontinued before surgery, the nurse

should diligently assess the patient for which complication early in the postoperative period until the

medication is resumed?

a. Cerebral or pulmonary emboli

11. The nurse is reviewing the laboratory test results for a 68-year-old patient whose warfarin (Coumadin)

therapy was terminated during the preoperative period. The nurse concludes that the patient is in the

most stable condition for surgery after noting which of the following INR (international normalized

ratio) results?

a. 1.0

12. The nurse would determine that a postoperative patient is not receiving the beneficial effects of

enoxaparin (Lovenox) after noting which of the following during a routine shift assessment?

a. Pain/swelling in lower extremety

13. A postoperative patient asks the nurse why the physician ordered daily administration of enoxaparin

(Lovenox). Which of the following replies by the nurse is most appropriate?

a. This medication will help prevent blood clots from forming in your legs until your level of

activity, such as walking, returns to normal.”

14. The nurse is caring for a newly admitted patient with vascular insufficiency. The patient has a new order

for enoxaparin (Lovenox) 30 mg subcutaneously. Which of the following should the nurse do to

correctly administer this medication?

a. Leave the air bubble in the prefilled syringe.

15. Which of the following is a priority nursing intervention in the care of a patient with a diagnosis of

chronic venous insufficiency (CVI)?

a. Teaching the patient the correct use of compression stockings

16. A patient with varicose veins has been prescribed compression stockings. How should the nurse teach

the patient to use these?

a. While you’re still lying in bed in the morning, put on your stockings

17. Assessment of a patient’s peripheral intravenous site reveals that phlebitis has developed over the past

several hours. Which of the following interventions should the nurse implement first?

a. Remove the patient’s IV catheter.

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