ARTERIAL BLOOD GAS (ABG)

PH: 7.35 7.45

PaCO2: 35 45 mmhg
PaO2: 80-100 mmgh
SaO2: 95-100%
HCO3: 22-26 meq/L

Step 1: check for perfect pH = 7.4
Acidotic less than 7.35
Alkalotic greater than 7.45
Acidosis = Extra acids are present or base is lost with pH less than 7.35
7.39
Cellular acidosis = cells are hypoxic or are processing proteins to yield
glucoses, there is an increase in lactic acid or ketoacid
Respiratory acidosis = if the function of the lungs is inadequate
(COPD/Asthma) the failure to effectively ventilate = inability to exhale
CO2 & that failure = Carbonic acid and pH
Renal Acidosis = kidney function is inadequate, the ability to break
carbonicacid from H2CO2 H & carbonic acid
Alkalosis = extra base is present or there is a loss of acid if pH is 7.41
7.45
Respiratory Alkalosis = hyperventilation is the primary problem, a
very rapid removal of CO2 causing carbonic acid to go (less acid) and
pH to go
Renal Alkalosis = Kidney function overstimulated (i.e. with
aggressive diuresis) may be excessive loss of hydration ions (H+)
causing carbonic acid to go down (less acid) & pH
Other Contributes = Gastric/Intestinal removal of acids may occur
w/diarrhea, vomiting, or excessive gastric drainage removes secretions
and influences Acid-Base balance i.e. NG tubes
Step 2 Check PaCO2
Check for perfect levels = 40mmHg; range (35 45mmHg)
Alkalosis
Acidotic
If PaCO2 is retained r/t hypotension, overly removed via hyperventilation
the change in pH will be opposite direction as PaCO2 = CO2 pH & Co2
pH
 STRUCTURE AND FUNCTION OF THE CARDIOVASCULAR SYSTEM
Heart
3 layers
Endocardium = thin inner lining
Myocardium layer of muscle
Epicardium = figrous outer layer
Heart is divided by the septum, creating:
Right atrium
Left atrium
Right ventricle
Left ventricle
Blood flow:
Inferior & Superior vena cava Tricuspid valve Right Atrium
Right Ventricle pulmonic value pulmonary artery lungs
left atrium pulmonary artery mitral valve left ventricles
aortic valve aorta high pressure circulation
Blood Supply
Myocardium has its own blood supply = coronary circulation
Left coronary artery arises from the aorta and divided in to 2:
Left anterior descending artery
Left circumflex artery
Both supply left atrium, left ventricle, interventricular
septum, and a portion of the right ventricle
Right coronary artery, also arises from the aorta
Right atrium
Right ventricle
A portion of the posterior wall of the left bundle of HIS part
of the cardiac conduction system
Due to this, obstruction of this artery often causes serious
defects in the cardiac conduction system
Conduction System
Action Potential = specialized nerve tissue responsible for creating
and transporting & transporting the electrical impulse
Initiating depolarization subsequently cardiac contraction
Electrical impulse initiated SA node (pacemaker of the heart)
muscle fibers of atria and cell-to-cell conduction
mechanical contraction of atria follows the depolarization of the
cells.
Electrical impulse travels from atria AV nose Bundle of HIS
Left & Right bundle branch branches both ventricles via
Purkinje fibers = synchronized ventricular contraction
Left bundle branch = 2 fascicles
Anterior
Posterior
Cardiac cycle starts with depolarization of the SA node.
Climax = ejection of blood into pulmonary and systemic
circulations
 Ends = repolarization when contractile fiber cells &
conduction pathways cells regain their resting polarized
conduction.

EKG
P-wave = firing of SA node & represents depolarization of fibers of the
atria
QRS complex = depolarization from the AV node throughout the ventricles
T-wave = repolarization of ventricles
U-wave (if seen) may represent repolarization of the Purkinje fibers or
may be assiociated with hypokalemia
Mechanical System
Depolarization, triggers mechanical activity
Systole, contaction of myocardium = ejection of blood from ventricles
Diastole, relaxation of the myocardium = filling of ventricles
CO = amount of blood pumped by each ventricle in 1 minute
Calculation = amount of blood ejected from venrion with each heart
beat = Stroke Volume (SV) x by the heart rate per min (HR)
CO = SV x HR
Normal adult at rest = 4 to 8 L/min
CI (cardiac Index) = CO divided by BMI
CI adjusts the CO to body size;
Normal = 2.8 to 4.2 L/min/m2
Factors affecting CO
HR regulated by autonomic nervous system
SV regulated by preload, contractility, and afterload
preload, contractility, and afterload = Workload of myocardium
= O2 demand
Preload
Frank Starlings law = the more myocardial fibers are stretched,
the greater their force of contraction
The volume of blood in ventricles @ end of diastole, before next
contraction = Preload
Preload determines amount of stretch placed on myocardial
fibers
Afterload
Afterload = peripheral resistance against which the left ventricle
must pump
Affected by size of ventricle, wall tension, and arterial blood
pressure
IF arterial BP , ventricles meet increased resistance to eject
blood. work demand; eventually = ventricular hypertrophy
(enlargement of the cardiac muscle tissure w/o in CO or
size of chambers)
Determine rate
Each small box = 0.04 seconds
Time = # of squares x 0.04 seconds
1500 small boxes = 1minute
Each large box = 0.2 seconds (5 small boxes)
 15 large boxes = 3 seconds
EKG paper is marks at 3 second intervals at top of vertical line
If regular = count the # of 0.04sec intervals between 2 R-waves,
divide by 1500
If Irregular = count the number or R-R intervals in 6 seconds, the
x10
Determine Rhythm
Presence/Absence of P-wave (SA node originated impulse)
Measure P-R interval (Normal = 0.12-0.20 seconds)
Measure QRS duration (Normal = 0.04-0.12 seconds)
Check P- wave, QRS Complex, ST segment, and T-wave
P - wave
Atrial contraction = atrial depolarization
Atrial muscle depolarization
Time it takes from the impulse to travel from the atria AV
node ventricles
Measure P-R interval (Normal = 0.12-0.20 seconds) or 3-5
small squares
QRS
Ventricular contraction/depolatizatoin
You do not see atrial repolarization r/t being obscured by QRS
complex
Measured from downward Q to return of S wave to baseline
Measure QRS duration (Normal = 0.04-0.12 seconds) or 3
small squares
T - wave
Ventricular repolarization
ST segment
Its noramally flat and on baseline
Represents time between ventricular contaction
(Depolarization) & ventricular repolarization
QT interval
Ventricular systole, represents depolarization and
repolarization of the ventricles
0.36 to 0.44 seconds OR 9-11 small squares
How to Calculate EKG
Calculate Cardiac rate
Count # of R waves in 6 sec interval then mult x10
More ACCURATE = 1500 divided (# of small squares in a minute)
between 2 R waves
Assess Rhythm
Regular? Use calipers to determine equal space between R
waves
Normal Sinus Rhythm
making sure a P wave is before every QRS at regular interval
measure PR interval
to see if impulses are conducted through the AV node at a
normal rate 0.12 0.20 seconds
 measure QRS
to see if impulses are conducted through the ventricles at a
normal rate being less than 0.12 seconds
determine if T waves follow every QRS & if they all look alike
Risk factors for dysrhythmias
Cardiovascular disease Electrolyte disturbances
Chronic renal failure Fear/anxiety
Hepatic/lung disease Fever
Pericarditis Pain
Drug use/abuse Hypoxia
Shock Infection
 Types of Dysrhythmias
Atrail
Nodal, Junctional (AV node)
Ventricular
Atrial Dysrhythmias
Sinus dysrhythmia/arrhythmia
Sinus Tachycardia
Sinus bradycardia
Sinus arrest
Asystole
Atrial Flutter
Atrial Fibrillation
Premature atrial contraction

Sinus dysrhythmia/arrhythmia
Rate = normal
Rhythm = slightly irregular
P wave = slight variation
PR Interval = normal
QRS = normal
T wave = normal
Sinus Tachycardia
Rate = greater than 100 bpm
Rhythm = regular
P wave = normal when visible, but not always r/t rapid rate
PR Interval = normal
QRS = normal
T wave = normal
Possible cause =: fever, exercise, dehydration, stress, caffeine
Significance = sustained cardiac workload and could lead to heart
failure in some pts
Tx = beta adrenergic blockers & underlying cause must be treated
Sinus bradycardia
Rate = less than 60bpm
Rhythm = regular
P wave = normal
PR Interval = normal
QRS = normal
T wave = normal
Causes =
Significance =excessive slowing reduces CO = dizziness, orthostatic
hypotension, dyspnea, disorientation
Treatment = tx underlying cause
Atropine will increase the rate if indicated; normal dose 0.5 1mg
For prolonged episodes, pacemaker would be the best option
Sinus arrest
Rate = variable (depending on the frequency of SA arrest)
Rhythm = irregular when SA nodes does not fire (no P wave),
otherwise regular
 P wave = usually normal. Except absent when SA node dose not fire
PR Interval = normal when P wave is present
QRS = normal except when the SA node fails to fire (no p wave)
T wave = normal when SA node fails to fire, QRS absent
Causes = myocardial disease, digitalis toxicity
Treatment = Occasional episodes are not treated, if frequent = require
pacemaker
Asystole
Rate = none
Rhythm = none
P wave = occasional to none
PR Interval = none
QRS = none
T wave = none
Significance = heartbeat has stopped and there is no blood circulating
Brain cells start to die in 4-5minutes
Treatment = CPR, ACLS
Adults = carotid pulse
Infants = bradial pulse
Children depends on size
Atrial Fibrillation
Rate
Atrial = 400+ bpm
Ventricular = 100-150bpm
Rhythm = Irregular
P wave = no clear waves, looks jagged Isoelectric line
PR Interval = cannot be measured
QRS = normal
T wave = not evident
Rapid rate increases cardiac workload,
Significance = associated with heart disease, COPD, hyperthyroidism,
can reduce cardiac output
Pt at risk for thrombus formation on atrial walls can become
arterial emboli
Treatment =
synchronized cardioversion
anti-dysrhythmic = amirodone, CA+ channel, beta adrenergic
blockers
antithrombolitic agents = heparin, warfarn
Atrial Flutter
Rate =
Atrial = 250-350bpm
Ventricular = 60-100 bpm
Rhythm = atrial regular, ventricular = regular or irregular
P wave = sawtooth appearance
PR Interval = cannot be measured
QRS = normal
T wave = not evident
Rapid rate cardiac workload & cardiac output
 Significance = caused by cardiac disease, valvular disease, or digitalsis
toxicity
Treatment =
Synchronized cardioversion
Anti-dysrhythmic = amiodrone, CA+2 channel, or beta adrenergic
blockers
Premature atrial contraction
Nodal/Junctional Dysrhythmias
1st degree AV Block
2nd Degree AV block
Wenckebach
Mobitz
3rd Degree AV Block

1st Degree Atriocentricular block
Rate = normal
Rhythm = regular
P wave = normal
PR Interval = longer than 0.20 sec
QRS = normal
T wave = normal
Significance = Aging, CAD, drug effects (dig toxicity)
Treatment = correct underlying problem
Check serum dig levels
2nd Degree Atrioventricular block (Wenckenbach)
Rate = normal atrial rate, slower ventricular rate
Rhythm = atrial regular, ventricular irregular
P wave = normal
PR Interval = progressively lengthen until QRS is dropped
QRS = some dropped/missing
T wave = dropped when QRS is dropped
Significance = impulses originate in the SA node but have increasingly
difficult time passing though the AV node
When impulses cannot reach the ventricles, a beat is dropped
Multiple dropped beats, cardiac output
Causes = possible MI ischemia, infarction, dig toxicity, electrolyte
imbalances
Treatment = correct underlying cause.
Admin atropine or isoproterinal? As prescribed
Possibly prep pt for pacemaker insertion
nd
2 Degree Atrioventricular block (Mobitz)
Rate = regular atrial rate; ventricular rate may be slower
Rhythm = irregular
P wave = normal evenly spaced
PR Interval = fixed; consistently normal or longer than normal
QRS = may be normal or wide; missing after some P waves
T wave = normal after QRS complexes
Significance = can follow after MI, or stem from conduction
abnormalities
 Frequent blocks reduce Cardiac output = hypotension &
bradycardia
Treatment =best for frequent block is usually pacemaker insertion
3rd Degree Atrioventricular Block
Rate = atrial rate exceeds ventricular rate; ventricular rate is below 45
bpm
Rhythm = irregular
P wave = normal
PR Interval = P waves and QRS unrelated
QRS = typically widened
T wave = normal when following a QRS
Significance = Passage of impulses through the AV node are
completely blocked
Atria beat at the usual SA rate and ventriculars beat independently
at an intrinsic rate of 30 45bpm
cardiac output, hypotension, bradycardia
Treatment = Atropine followed by pacemaker insertion
Ventricular Dysrhythmias
Premature ventricular contractions
Ventricular tachycardia
Ventricular fibrillation

Premature ventricular contractions (PVCs)
Rate = normal
Rhythm = irregular
P wave = normal except absent before PVC
PR Interval = normal except absent with PVC
QRS = bizarre with PVC, otherwise normal
T wave = opposite of PVC deflection, normal with other QRS
complexes
Significance = an impulse originating in the ventricle that causes a
contraction before an impulse is received through the AV node
Can be causes by myocardial ischemia, dig toxicity, electrolyte
imbalances, stress, and agents like dopamine
Frequent PVCs CO
Treatment =
Occasional PVCs require no tx
Frequent or symptomatic PVCs are treated with anti-dysrhythmic
drugs i.e. amiodrone, lidocaine, procainamide
Ventricular Tachycardia
Rate = ventricular rate 100-250 bpm
Rhythm = ventricular rhythm usually regular
P wave = cannot assess
PR Interval = none
QRS = wide, bizarre
T wave = deflected in the opposite direction from QRS
Significance = this pattern is ineffective in maintaining cardiac output
potentially life threating dysrhythmia
Possible causes = cardiac disease, hypokalemia, dig toxicity
 Cardiac output significantly and will progress to V-fib
Pt may report palpitations & could soon lose consciousness
Treatment = defibrillation
ACLS is required if pt has no pulse
If pt has pulse and BP dysrhythmia can be tx w/synchronized
cardioversion & anti-dysrhythmic drugs
Ventricular Fibrillation
Rate = cannot be counted
Rhythm = disorganized pattern
P wave = cannot assess
PR Interval = cannot assess
QRS = cannot assess
T wave = cannot assess
Significance = pattern is ineffective in maintaining cardiac output
Might stem from cardiac disease, electrolyte and acid-base
imbalance, hypothermia, or electrical shock
They will quickly lose consciousness & pulse and respirations
will stop
Survival depends on successful CPR, ACLS, and defibrillation
Management of Dysrhythmias
Anti-dysrhythmic Drugs T
These 4 categories all act by suppressing the origination and/or rate of
conduction of cardiac impulses
Common adverse Effects:
New dysrhythmias or Worsening existing dysrhythmias
Bradycardia
Hypotension
CHF
Contraindications:
Bradycardia, hypotension, CHF, and AV block
Sodium Channel blockers
Quinidine
Gi distress is common
Lidocaine
CNS depression/stimulation depending on dose
Only given IV and has a very short half-life
Most pts tolerate a repeated dose well
Flecainide acetate (Tambocor)
CNS: Visual disturbances possible not 1st choice r/t toxicity
VERY Toxic last choice
Beta adrenergic blockers
Propanolol (Inderal)
Can cause bradycardia
Can cause hypoglycemia and bronchospasm
Inhibit sympathetic response to stress, exercise, physiologic threats
I.e. physiologic symptoms to notify a DM pt that their BG is low
Used in caution w/those pts w/DM and Asthma
Potassium channel blockers
Amiodarone (cararone)
Highly toxic, can cause ARDS
 Increase Dig level causing a reduction in dose
Calcium channel blocker
Verapamil (Calan)
Can cause orthostatic hypotension, constipation, fluid retention
Due to fluid retention, pts are usually given a diuretic as well
Nursing Interventions
Administer at equal intervals to maintain therapeutic levels and
prevent changes
Monitor VS, ECG, Electrolytes
Assess for: CHF r/t excessive cardiac suppression: wt gain, edema,
SOA/dyspnea
Watch those with kidney and/or liver dysfunction
Teaching pts to take BP and Pulse & to never take OTC drugs without
first talking to their DR
Atropine (not classified as dysrhythmic)
Used to tx bradycardia & improve conduction through the AV node
Anticholinergic = s/e: dry mouth, constipation, blurred vision, urinary
retention, and tachycardia
Pacemaker
Long term management
Various types
Continuous Stimulation
Stimulate only when rhythm drops below a certain rate
Cardioversion
Synchronized electrical shock to stop electrical activity in the heart so that
it can resume a NSR
Its not always successful and can sometime create only temporary effects
Implantable cardioverter/defibrillator (ICD)
Implanted like a pacemaker
Delivers a shock to the heart when it detects V-tach or V-fib
Purpose is to restore a NSR

Cardiac Markers
CK-MB
Immunochemical process using monoclonal antibodies that measures this
cardio-specific process enzyme.
Concentration greater than 5% of total CK are highly indicative of MI
Serum levels increase within 4 6 hours of MI
Cardiac Specific Troponins
Contractile proteins that are released following an MI. Both Troponin T and
T-Iare highly specific to cardiac tissue
Normal Troponin-T = less than 0.1
Normal Troponin-I = less than 0.4
0.5 2.3 = inderterminate/suspicious of myocardial injury
Greater than 2.3 = + for myocardial injury

CRP
Marker of inflammation that can predict risk of cardiac disease and cardiac
events, even in pts with normal lipid values
 Normal = less than 1
Moderate Risk = 1 3
High Risk = greater than 3
BNP (b-type natriuretic peptide)
Peptide that causes natriureis
Elevation indicated presence of heart failure and distinguishes cardiac VS
respiratory causes of dyspnea
Optimal = less than 12
Moderate risk = 12 -15
High risk = greater than 15
TEE
Sends clear images of heart size, wall motion, valvular abonrms, and
possible source of thrombi without interference from lungs, or chest ribs.
Contrast may be injected in IV for evaluating direction of blood flow if
atrial/ventricle septal defect is suspected.
Doppler US and color flow imaging can also be used
MUGA (Multigated acquisition) scan
Dye mixed with small amount of pts blood, and reinjected. Images are
acquired at various points during cardiac cycle.
Indicated for pts w/MI, heart failure, valvular heart disease; can also be
used to eval the effect of various cardiac or cardiotoxic meds on the heart

DysrhythmiasAssessment
Dizziness, syncope
Chest pain, palpitations, abnormal heart sounds
N/V/D/C
Dyspnea
Abnormal pulse rates increased, decreased, irregular
Dx
Cause by interruption in normal conduction process
Can occur at any point in normal conduction process
Types of dysrhythmias
Sinus Dysrhythmias = originate in sinoatrial node and are
conducted along the normal conductive pathways
Tachycardia = sympathetic nervous system increases
automatically of SA node
HR above 100bpm
? causes = pain, exercise, hypoxia, PE, hemorrhage,
hyperthyroidism, fever
Bradycardia = parasympathetic nervous system (vagal
stimulation) causes automaticity of the SA node to bedepressed
HR decreased below 50bpm
? causes = MI, Valsalva maneuver, or vomiting,
arteriosclerosis in carotid sinus area, ischemia of SA node,
hypothermia, hyperkalemia, or drugs i.e. digitalis and
propranolol.
Treatment
Atropine
Isoproterenol
 Pacemaker
Atrial Dysrhythmias = abnormal electrical activity that results in
stimulation outside SA node but within the atria
PAC (premature atrial contractions)
Ectopic focus within one of the atria fires prematurely
\Normal phenomenon in some individuals, but may be caused
by emotional disturbances, fatigue, tobacco, or caffeine
May be early sign of abnormal electrical activity associated
with organic heart disease
Paroxysmal atrial tachycardia (PAT)
Rapid rhythmic discharge of impuses originating from an
ectipic focus within the atria followed by a normal ventricular
response at a rate of 160 250 bpm
If prolonged, the period of ventricular filling shortens, stroke
volume is reduces, and cardiac output is diminished, possibly
resulting in a pump failure, hypotension, and additional
dysrhythmias
Causes: atrial muscle ischemia, rheumatic heart disease,
acute MI, psychological factors (i.e. anxiety, stress, emotional
trauma)
Atrial Flutter
Arises from a ectopic focus in the atrial wall causing the atrium
to contact 250-400 bpm.
AV node blocks most of the impulses, protecting the ventricles
from receiving every impulse
Some patients are unaware of this, while others complaint of
palpitations/fainting
Causes = stress, hypoxia, drugs, disorders (chronic heart
disease, HTN)
Atrial Fibrillation
Most common atrial dysrhythmia arising from several ectopic
foic
Patients presents with a grossly irregular pulse rate,
Confusion, syncope, and dizziness may occur with severe
hypoxia; pump failure may result.
Causes = chronic lung disease, heart failure, and rheumatic
heart disease
Treatment
Amiodarone,
Adenosine
Verapamil
Synchronized Cardioversion
Ventricular Dysrhythmias = occur when one or more ectopic foci arise
within the ventricles
Premature ventricular contractions (PVCs)
One or more ectopic foci stimulate a premature ventricular
response
May decrease the efficiency of the hearts pumping actions
 Palpitations- a feeling of irregular heart beat or a lump in the
throat
Causes = ischemia r/t MI, infection, mechanical damage d/t
pump failure, deviations in concentrations of electrolytes (K, Ca,
Mg) Nicotine, caffeine, alcohol, drugs (i.e. digitalis, reserpine),
psychogenic factors (stress, anxiety, fatigue), and acute/chronic
lung disease
Ventricular Tachycardia
3 or more PVSc occurring in a row
Indicative of severe myocardial irritability
Physical effects include chest pain, dizziness, fainting,
occasional collapse
Treatment
Amiodarone
Lidocaine
Epinephrine
Defibrillation
Ventricular fibrillation
Most serious of ALL dysrhythmias because of potential cardiac
arrest death will occur IF NOT treated
Several ectopic foci within the ventricles are discharged at a
very rapid rate.
Causes = acute MI, HTN, rheumatic or arteriosclerotic heart
disturbances, or hypoxia
Unless blood flow is restored (CPR) and dysrhythmia is
interrupted (by defib), death will result within 90sec 5minutes
Heart Block = delay in conduction of impulses within the
atrioventricular system
Bundle Branch Block (BBB)
Right or Left branches of the bundle of His are blocked, causing
the impulses to change their path of conduction as they pass
through the myocardial tissue
Cause = MI or digitalis toxicity
Left BBB tends to be more serious and indicate more left sided
heart problems
st
1 degree = AV junction conducts all impulses, but a slower than
normal rate
2nd degree = AV junction conducts only some impulses arising in the
atria
Causes = infections, digitalis toxicity, CAD
Symptoms: slow heart rate, fainting, decreased blood pressure
Complete Heart Block
AV junction blocks all impulses to the ventricles, causing the
atria and the ventricles to dissociate and beat independently
each with its own pacemaker establishing a rate, ventricular rate
is low 20-40 bpm
Causes = congenital defects, vascular insufficient, fibrosis of the
myocardial tissue, or MI
Symptoms = palpitations, dizziness, syncope, dyspnea, confusion,
and cyanosis

Hemodynamic Monitoring
Pulmonary Artery Catheter
Multiple ports enable a variety of hemodynamic measurement, blood
collection, and infusions
Possible veins:
Internal jugular
Femoral
Subclavian
Brachial
Identification of lumens
Proximal can be used for arterial pressure/CVP, IVF, Lab draws
Distal measure pulmonary artery pressures (pulmonary artery
systolic PAS, pulmonary artery diastolic PAD, mean pulmonary artery
pressure, pulmonary artery wedge pressure) NOT used for IVF
Balloon inflation port intermittently used for PAWP
Normal Hemodynamic Values
CVP = 1 8 mmHg
PAS = 15 26 mmHg
PAD = 5 15 mmHg
CO = 4 6 L/min
Mixed venous gas saturation (SvO2) = 60 80%
Actions necessary for an accurate reading
Pt being in supine-position, HOB being no more than 30 degrees
Level transducer to phlebostatic axis
Zero transducer settings
Record settings
Compare to physical assessment
Monitoring Symptoms
Preload
Right Heart = CVP
Left Heart = PAWP
Elevated
Crackles in lungs
Jugular vein distention
Hepatomegaly
Peripheral edema
Taut skin turgor
Decreased
Poor skin turgor
Dry mucus membranes
Afterload
Right Heart = Peripheral Vascular Resistance (PVR)
Left Heart = Systemic Vascular Resistance (SVR)
Elevated
Cool extremities
Weak pulses1
Decreased
Warm extremities
Bounding pulses

Coronary Artery Disease (CAD)
CAD is leading cause of death in the US
Plaque = sludge made up of: fat, WBC, cholesterol, calcium, decaying tissue,
and other cellular garbage.
Arteriosclerosis = Thickening and loss of elasticity in walls of the arteries
that supply the myocardium
Pathologic process smooth muscle cells and collagen migrate into the
inner most layer of the artery = a narrow lumen & stiffened arterial walls
Lipids, calcium, and thrombi attach to the inner arterial walls resulting
in further loss of elasticity
Dx of CAD
Serum lipid profile
cholesterol & triglycerides
LDL and HDL
Abnorm LDL/HDL & TC/HDL ratios
Characteristic findings of ECG
Evidence of coronary artery occlusion of cardiac cath
Arthrosclerosis = fat and fibrin build up in the inner most arterial walls
Further thickening = narrowing of the lumen and loss of elasticity =
blood supply to affected tissues and resistance to blood flow
3 types of lesions can form:
Fatty streaks (1st one to appear)
Yellow streaks can show as early as teen years, but are believed to
be reversible
Fibrous plaque
Advanced atherosclerosis
Collagen, elastic fibers, and mucous matrix surround affected
muscle cells = raised lesions that protrude into the lumen
As they enlarge, they can block the lumen resulting in advanced
lesions.
Advanced lesions
Further damage
Can take form of: hemorrhage, calcification, cellular necrosis,
thrombi of intima
Collateral circulation form in efforts to create/maintain blood flow
Risk factors
Non-modifiable
Age
Gender
Race
Genetics
Modifiable (with improvements)
serum lipids: reduce fat intake, exercise, wt loss programs, &
anti-lipid drugs
HTN: life style changes, and anti-HTN drugs
Obesity: exercise, and wt reduction programs
Sedentary lifestyle: gradual increase in physical activity
DM: management of hyperglycemia
 If has central neuropathy may not feel much angina pain
Smoking: quitting
Excessive ETOH intake: reduce
Stress: relaxation and counseling
Prevention = identifying those at risk and modifying those risk factors
Signs/symptoms
Chest pain (Angina) = insufficient blood flow to the heart muscle from
narrowing of the coronary artery can cause CP
Angina described as burning/squeezing sternal pain that can radiate
to the arm, shoulder, jaw, neck. Epigastric pain is common.
Not all pts with CAD have pain,
Most common subjective manifestations are Fatigue and exercise
intolerance
Tachycardia, dyspnea, N/V, pallor, diaphoresis,
Types of Angina
Stable = onset when heart rate increases to meet oxygen
demands i.e. physical activity or emotional distress
Rest usually relieves the pain by decreasing oxygen demand
Pain does not improve with rest, Nitroglycerin usually helps.
Nitroglycerin =
Vasodilator that acts on coronary and peripheral vessels.
Sublingual tabs and spray are available for PRN use.
Can be taken shortly before strenuous activities to control
symptoms
Patches, ointments, and sustained-released tabs are used
to prevent angina episodes
Unstable = increased myocardial oxygen demand
It becomes progressively more severe and occurs more often
Intractable
Occurs despite rest and usually tx
Can be incapacitating
Variant (aka pringmetal or vasospastic angina)
Caused by CAD spasm
Longer duration vs stable angina
Cardiac arrest risk factors
MI
Heart failure
Electrical injury
Drowning
Drug OD
Hemorrhage
Fluid/electrolyte imbalance
Anaphylaxis
Asphyxiation
s/s of cardiac arrest
loss of consciousness
loss of pulse
no respirations
ECG changes
 Vtach
Vfib
Asystole
Initiate CPR
Dx of CAD
cholesterol and triglycerides
LDLs (lethal) and HDLs (helpful)
Characteristics on ECG
Evidence of coronary artery occlusion on cardiac cath
Medicaitons to help CAD
Anti-anginal agents
Anti-lipids may be prescribed for those who are unable to lower lipid
levels through diet, exercise, and wt loss

Bile acids sequestrate & Fibric acid derivatives should be used for short
term therapy only. And are contraindicated for pts who have renal or
liver disease, or have gall stones
Bile acids sequestrates
Cholestyramide (Questran)
Fibric acid derivatives (decrease triglyceride production)
Gemfibrozil (lopid)
HMG-COa reducatse inhibitors (statins)
Pravastatin (pravachol)
Can elevated liver enzymes and must be used with caution with
liver dysfunction
Can also cause muscle tenderness & CPK medication would be
d/c due to poss Rhabdomyolysis = disintegrate of striated
muscle fibers
Baby ASA
Prevent thrombus formation
NITRATES
Isorbid - SL and chewable tabs
Nitroglycerin
Vasodilator
CA CHANNEL BLOCKERS
Nifidipeime (Procardia)
Dilate coronary and peripheral arteries = myocardial blood flow
Peripheral vasodilation = cardiac workload by preload &
afterload
BETA BLOCKERS
Atenolol (tenerman)
heart rate and cardiac output = cardiac oxygen demands
Dilate peripheral blood vessels = BP, preload & afterload

Vasodilators side effects
Hypotension
Bradycardia
Rebound tachycardia (calcium channel blockers)
Fluid retention (calcium channel blockers)
 Congestive heart failure (beta blockers)
Nursing assessement for CAD
Pain nautres, location, precitipating factors, releaving mesures
Vitals bp, heart rate, RR
Med hx
Drugs
Beta blockers watch for s/s CHF (edema, dyspnea, wt gain)
Nursing dx for CAD
Activity intolerance
Teach: doing more when higher levels of energy, distribute tasks,
schedule periods of rest, prioritize
Anxiety/fear
Anxiety aggravates CAD symptoms
Be accepting of this
Teach them exacerbating factors and what can help
Relaxation techniques
CO
Myocardial contractility is affected by poor perfusion
Anti-anginal drugs can suppress myocardial contractility
May experience injury r/t orthostatic hypotension & circulation to
vital organs could be impaired
Acute pain
Protecting mechanism
When the myocardium lacks sufficient oxygen
Can scare the pt into restricting activity completely, teach angina
can be managed with modification of activities and drug therapy
Teach to keep nitrates tabs/spray with them at all times, protect
from heat, light, and moisture (i.e. do not keep next to body)
Nitro tabs should sting slightly underneath tongue if not obtain
fresh tabs
As soon as pain occurs stop what you are doing, place tablet or
spray under tongue, note time, avoid smoking, drinking, or eating
right after taking nitro
If pain persists after 5min place another tablet or spray under
tongue
Max 1 tablets in 5min intervals (total 3 tabs in 15min)
If pain persists after 3 doses call 911 due to poss heart attack
Headache and flushing are common s/e of nitrate
Nitrate patches apply on non-hairy part of body, might remove at
night to prevent hypotension at while sleeping, alternate site,
Self-care deficits
Encourage them to set priorities, doing what needs to be done first,
resting frequently, putting off what can be.
Home health might be needed
Deficient knowledge
Changing modifiable risks: smoking, obesity, HTN, lack of exercise