ADULTS I EXAM2 STUDY GUIDE

03/17/2015

Which cardiac risk factors are modifiable and which are

nonmodifiable?
Non-modifiable
o Age
o Over 50% of MIs occur in those over 65
o 80% of deaths from MI are in those over 65
o Gender
Males affected earlier than females
o Race African Americans have more HTN
o Genetic Factors Family history
Lifestyle Factors (Modifiable)
o Cigarette smoking**
o Physical Inactivity
o Diet
ISCHEMIA VS INFARCTION
Ischemia
o local or temporary lack of blood supply
Infarction
o irreversible damage and death to cells; necrosis of tissue

MYOCARDIAL INFARCTION (MI)

Obstruction of coronary artery by plaque causing lack of blood flow to
myocardium
Results in prolonged tissue ischemia and permanent cell damage
necrosis
Endocardium damage within 20 min
Epicardium damage 1-6 hours
Myocardium- last layer to sustain damage**
Transmural Infarction All 3 layers
Produces Q wave on ECG
MI LOCATION
LCA Entire left ventricle (most devastating)
LAD Anterior wall of left ventricle
LCx Lateral wall MI
RCA Right ventricle and inferior surface
AFFECTS WHO?
Women may experience atypical symptoms**
Indigestion, heartburn, nausea, vomiting, SOB, weakness
S/S MI
Chest pain substernal or precordial
May radiate to arm, neck, jaw or back
Tachycardia
Tachypnea, dyspnea

 Diaphoresis, cool, clammy skin

Hypotension
COMPLICATION OF MI
Dysrhythmias
Most frequent complication of MI**
Pump failure
Infarct extension
Structural defects
Pericarditis
Most specific lab test for MI is what?
Cardiac Markers
Cardiac Muscle Troponins** - most specific lab
CPK-MB
TREATMENTS
ACE Inhibitors **
o Decrease mortality rate and help prevent heart failure
Antidysrhythmics
Amiodarone
Procainamide
Calcium Channel Blockers
o Diltiazem, Cardizem

Beta Blockers
o Propanolol, Atenolol
MONA (TREATMENT OF MI)
Oxygen
Nitroglycerine
Aspirin
Morphine sulfate (drug of choice for cardiac pain)
o ***Remember MONA***
ANGINA
Stable
o (most common)
Know level of stress or activity that bring on pain
Unstable
o Changes in pattern of attacks
Intractable angina
o Severe incapacitating chest pain
Variant angina (Prinzmetals)
o Pain during times of rest
Silent ischemia
o Report no pain but have ECG changes with a stress test
Pain: Activity Pain Rest Relief**

o Described as Squeezing, tightness, heavy pressure or

constriction
o Begins beneath the sternum and may radiate to jaw, neck or
arm
o Usually last less than 15 min. and relieved by rest
o Associated Symptoms: dyspnea, pallor, tachycardia, fear
Lab tests to confirm presence of risk factors
o Lipids
o Glucose levels
*****What nursing dx would be a priority for a pt with unstable
angina?
Risk for decreased cardiac output
The most common cause of angina is atherosclerosis
Prolonged or severe angina attacks can lead to MI
HEART ANATOMY/SYSTEM
ELECTRICAL CONDUCTION SYSTEM
SA NodeBundle of HisAV Node (Junction)Bundle
branchesPurkinje FibersVentricles
ECG COMPONENTS
P Wave = Atrial depolarization
PR Interval = Time it takes impulse to travel from SA node to
Ventricles
QRS Complex = Ventricular depolarization
T wave = Ventricular repolarization

**HEART RATE CALCULATION (Six second strip method)**

Count number of R waves in 6 seconds
Multiply that number by 10 to determine HR/min
RHYTHM ANALYSIS
Determine Heart Rate (Inherent Rates)
Determine Rhythm
Analyze P waves
Analyze PR interval (PRI)
Analyze QRS Complex
Interpret Rhythm (give it a name!)
NORMAL SINUS RHYTHM
Rate: 60 100 bpm
Rhythm: Regular; 1:1 ratio with QRS
PR Interval: Less than .20 seconds
P waves: Peaked, upright; constant
QRS Complex: .04 - .12 seconds; same morphology
ST Segment: Isoelectric
T waves: Upright
*Sinus Bradycardia rate less than 60 bpm
*Sinus Tachycardia rate greater than 100 bpm
*Sinus Arrhythmia rhythm irregular (resp)

ATRIAL DYSRHYTHMIAS
Premature Atrial Contractions
Atrial Flutter
o Conduction defect in atrium
o Results in rapid atrial rate 250 400
o Ventricular response 75 - 150
o Not all impulses are conducted to the ventricles
o Atrial and ventricular rates are regular (if conduction ratio
consistent)
o Saw tooth atrial waves or F waves
o Tx: Catheter ablation is now the long-term treatment of
choice***
Atrial Fib
o Rapid, disorganized electrical activity in atria
o Atrial rate 300 600
o Ventricular response may be normal or accelerated
o Causes loss of atrial kick (20% 30% of CO)
o May be acute or chronic
o Patient at risk for blood clots in atrium due to pooling of
blood***
AV BLOCKS
1 AV Block (NO Treatment)
2 AV Block Type I (Mobitz I; Wenckebach) (NO TREATMENT)
2 AV Block Type II (Mobitz II)

3 AV Block Complete Heart Block

VENTRICULAR DYSRHYTHMIAS
V-Tach
If there is a pulse, treat with drugs first
If no pulse treat as if rhythm was Vfib
V-fib
Only definitive treatment is defibrillation
PACEMAKER CODES (5 letter system, usually first three letters used)
First letter = chamber being paced
A, V or D (dual)
Second letter = chamber being sensed
A, V, D, O (sensing function turned off)
Third letter = Type of response from pacemaker based on what is
sensed
I - Inhibited (controlled by patients heart)
T - Triggered (paces when it senses intrinsic heart activity)
D - Dual [inhibited and triggered]
O - None
CHOLESTEROL
HDL vs LDL; medication to treat with common side effects

MEDS: Statins (LDL removal)

SIDE EFFECTS: Muscle pain
NURSING: **Monitor hepatic function/LFTs**

POST-CARDIAC CATHETER ASSESSMENT

Post-Catheterization
VS Q 15m x 4, Q 30m X 4, Q 1H x2 then Q 4H
Monitor femoral artery site, pedal pulses; same as VS
normal saline
VALVE DISORDERS/MURMURS
Valves:
o Tricuspid, Mitral, Pulmonic, Aortic
Regurgitation
o Valves do not close
o Blood flows backwards
o Mitral regurgitation: systolic murmur
o Atrial regurgitation: L Ventricular hypertrophy,
increase BP
Stenosis
o Do not open completely
o Blood flow reduced

o Mitral stenosis: diastolic murmur; pulmonary

congestionR ventricular failure
o Aortic stenosis: L Ventricular failure and hypertrophy
Prolapse
o Stretching of the valve leaflet in systole
Arterial vasoconstriction increases afterload
RHEUMATIC HEART DISEASE
Mitral valve most frequent site
DIAGNOSIS
Throat culture: + for Group A beta hemolytic strep 25-40% of the
time
ENDOCARDITIS
Inflammation of endocardium
Infectious
Very uncommon
RISK FACTORS
Previous heart damange
Deformed valves
Prosthetic valves
HEART FAILURE

MEDS USED FOR HEART FAILURE

ACE inhibitors, ARBS, Hydralazine/isosorbide, Beta blockers,
Diuretics, Digitalis, Calcium channel blockers, IV infusion Natrecor
(nesiritide)
LAB TO TEST FOR HEART FAILURE
BNP
INFO

Systolic vs Diastolic
o S: more common; weakened heart muscle
o D: stiff and non compliant muscle, difficult ventricular filling
Stage A: high risk of developing left ventricular dysfunction
Stage B: Left ventricular dysfunction who have not developed
symptoms
Stage C: Left ventricular dysfunction with current or prior
symptoms
Stage D: with refractory end-stage heart failure
LEFT SIDED
Left ventricle cannot pump effectively
Results in increased left ventricular end diastolic pressure
o S/S
Dyspnea
Cough
Crackles
low SpO2
S3 sound

 Orthopnea
Pink frothy sputum
RIGHT SIDED
Right ventricle cannot pump blood effectively
Increased venous pressure = JVD
o S/S
Dependent edema
Hepatomegaly
Ascites
Anorexia/nausea
Weakness
Weight gain
TREATMENT HF
Upright position
Nitrates
Lasix
Oxygen
ACE inhibitors
Digoxin
o Fluids (decrease)
o Afterload (decrease)

o Sodium Restriction
o Test (Dig lvl, ABGs, K+ levels)
SHOCK
Secondary to dysrhythmias
Heart has impaired pumping ability = low supply to heart and
tissues
Systolic Arterial Pressure = <90mmHg or 30-60mmHg below
baseline
Urine Output <20ml/hr
Peripheral vasoconstriction
Cardiac index <2.1L/(min/m2)
IV agents to augment contractility
o positive inotropic medications
dobutamine and primacor
IV agents to reduce preload
o Lasix, NTG, Morphine
**Cautious use of IV arterial vasodilators or vasopressors
o nipride, or dopamine, epinephrine, levophed
Hypovolemic and ADH how related?
Nurse role in care of pt with septic shock
o Recognizing CNS, Cardiac, Respiratory, Renal and Skin
changes
STAGES OF SHOCK

 Vasodilation
Maldistribution of flow
Accelerated coagulation
Myocardial dysfunction
Pulmonary dysfunction
o Know that shock leads to anaerobic metabolism and cellular
death related to decrease oxygen to the tissues

Hypervolemic think diuretics

Most common type
Decrease in INTRAVASCULAR volume
o Direct loss: hemorrhage from chest, abs,retroperitoneum
o Indirect loss: third spacing (burns, ascites, edema)
o Tachycardia is the earliest SIGN
Early Signs:
o Thirst, change in LOC, restlessness, agitation
o Decrease in BP, Increase HR, Narrowing Pulse pressure,
Decrease Pulse rate & strength
o Decrease urine output dark urine
Late Signs:
o Low BP, Increase Pulse rate, Increase RR, Cyanosis, Cold,
pale, clammy skin, low urin output (30cc/hr), restlessness,
confusion
Positioning: TRENDELENBERG
Tx:

o Elevate legs
o O2
o 2 Large bore IV
o Large amt of fluid
o Watch for fluid overload
Pts s/p MI are at high risk
PULSE PRESSURE:
SYSTOLIC DIASTOLIC mmHg
MEAN ARTERIAL PRESSURE:
Diastolic + [1/3 (systolic diastolic)]

What EKG changes do we see with ischemia? Infarction?

ISCHEMIA- ST Depression
TPA criteria