CARDIAC NOTES

Anatomy and Physiology Heart

Three layers
o Endocardium (Inner layer) Ex (endocarditis is inflammation of
inner layer)
o Myocardium (middle layer /muscular lining)
o Epicardium/pericardium (outer layer/ sac)
Pericardium
The pericardium has 2 layers filled w/ fluid. When it gets inflamed and filled w/
more fluid there is Pericardial friction rub
In order to distinguish a pericardial friction rub (heart) from pleural
friction rub (lungs) need to ask pt to hold respiration for few seconds
Four chambers
Heart valves
o Atrioventricular (A-V) valves (S1/SYSTOLE)
o Semilunar valves (S2/DIASTOLE)
Coronary arteries (Feed the heart)
Cardiac conduction system
Cardiac hemodynamics (pressure of blood/ fluid volume status)
Overview of Anatomy and Physiology Heart
Cardiac Cycle
Systole (contraction)
Diastole (relaxation)
Cardiac Output= HR X SV
Anything that decrease cardiac output causes: dizziness, fatigue, LOC changes,
shortness of breath
HR
SV
Preload (diastole, relaxation, if there is a lot of fluid the preload will be increased
and vice)
Afterload (systole,
contraction)
Contractility
Autonomic Nervous System (ANS)
SNS (increase)
PSNS (decrease)
Terms - Cardiac Output
Stroke volume: amount of blood ejected with each heartbeat
Cardiac output: amount of blood pumped by ventricle in liters per minute
Preload: degree of stretch of cardiac muscle fibers at end of diastole
Contractility: ability of cardiac muscle to shorten in response to electrical
impulse
After load: resistance to ejection of blood from ventricle
Ejection fraction: percent of end diastolic volume ejected with each heart beat
CO = SV x HR
Control of heart rate
Autonomic nervous system, baroreceptors (located in aortic arch, righ
carotid, the monitor pressure throughout the body, when the pressure is low,
they send a signal to speed the HR)

Control of stroke volume

Preload: Frank-Starling Law (AMOUNT THE HEART CAN STRETCH WHEN
FILLING UP)
After load: affected by systemic vascular resistance, pulmonary vascular
resistance
Contractility increased by catecholamines, SNS, some medications
(Epinephrine, dopamine)
Decreased by hypoxemia, acidosis, some medications
Cardiac Conduction System
Properties of the conduction system:
Automaticity (ability of stimulate on its own)
Excitability
Conductivity
Sinoatrial (SA) node
Internodal pathways
Atrioventricular (AV) node
Bundle of His
Bundle Branches
Purkinje fibers

Terms - Cardiac Action Potential

Depolarization: electrical activation of cell caused by influx of sodium into cell
while potassium exits cell
Repolarization: return of cell to resting state caused by re-entry of potassium
into cell while sodium exits
Refractory periods
Effective refractory period: phase in which cells are incapable of depolarizing
Relative refractory period: phase in which cells require stronger-than-normal
stimulus to depolarize
Assessment
Health history
Demographic information
Family/genetic history
-CAD
-DM (bc glucose damages the vessels, makes them hard, decrease blood flow,
and perfusion)
- HTN
Cultural/social factors (smoking, drinking, drugs, food)
Risk factors
Modifiable (diet, weight, drugs, smoking, exercises, stress management)
Nonmodifiable (age, gender, race, genetics)
Most Common Clinical Manifestations (MI, ANGINA, HF)
Chest pain (due to lack of O2, hypovolemia or low BP, can also cause chest
pain)
Dyspnea (difficulty
breathing)

 Peripheral edema, weight gain (retention of H2O.)

Fatigue (not enough O2, pt
get tired)
Dizziness, syncope, changes in level of consciousness
Acute Coronary Syndrome (is prodromal, before, like S/S that there is a
cardiac problem.
-Shortness of breath
-Swell feet
- Tired
Experience prodromal symptoms for a month to more prior to acute event

Assessment
Medications
Nutrition (Low Na, low cholesterol)
Elimination (avoid straining, to avoid increase pressure)
Activity, exercise
Sleep, rest
Self-perception, self-concept
Roles, relationships
Sexuality, reproduction
Coping, stress tolerance
Prevention strategies
Laboratory Tests
Cardiac biomarkers
Serum Enzymes:
- Creatinine Kinase (CK), CK-MB
Whenever there is injury to the heart muscle
CK formerly known as (CPK)- elevation indicates muscle injury
CK-MB: specific to myocardial muscle, rises within 6 hours of injury and peaks at 18
hours post injury and returns to normal within 2-3 days.
Useful in DX of MI
- Lactic dehydrogenase (LDH)
After an MI, LDH is always elevated. THIS TEST IS DONE AFTER TROPONIN I, AND CK-MB
Found in many body tissues; elevation is detected within 24-72 hours after MI,
peaks in 3-4 days and returns to normal around 2 weeks.
Useful for delayed DX of MI
- Troponin T and I (First to be drawn, bc is more specific)
Is released when there is damaged to cardiac muscle (is the most important to detect
Heart attack, mainly Troponin I which is specific for heart muscle, troponin T is heart
muscle and skeletal muscle)
Onset is before CK-MB in MI; peaks at 24 hours and returns to normal around 2 weeks;
provides early sensitivity
More specific to cardiac injury for DX of MI
Laboratory Tests
Lipid profile: to determine risk factors of developing atherosclerosis (to
determine what build up of plaque)
Total serum lipids= 400-800 mg/dL
Triglycerides: lipids stored in fat tissue; normal 100-200 mg/dL
Cholesterol: main lipid associated with CAD; normal < 200mg/dL

Lipoproteins: proteins in the blood to transport cholesterol, triglycerides and other fats
HDL= 35-70 mg/dL (M); 35-85 mg/dL (F)
LDL= < 160 mg/dL
Laboratory Tests
Brain (B-type) natriuretic peptide (BNP)
BNP, is secreted from the ventricules, it indicates, INCREASED PRELOAD,
TOO MUCH FLUID. IS TO RULE OUT CHF. If BNP is elevated then I need to
look further for CHF.
A neurohormone that helps regulate BP and fluid volume.
Secreted from the ventricles in response to increased preload with elevated
ventricular pressure
Useful in the diagnosis of HF
Greater than 100 pg/mL
C-reactive protein (CRP)
A protein produced by the liver in response to inflammation. It is not specific
for heart. Anywhere where there is infection or injury to the body (Heart attack,
plaque to heart, cut in the toe anything that causes damage in the body elevates
this protein)
Elevated CRP is increased risk for CAD (Coronary Artery Disease)
High: 3.0 mg/dl or greater
Moderate: 1.0-3.0 mg/dL
Low: less than 1.0 mg/dL

Laboratory Tests
Homocysteine (not specific for heart attack)
An amino acid linked to the development of atherosclerosis (deposit of
plaque in arteries) because it can damage the endothelial lining of the arteries
and cause thrombus formation
A 12 hour fast is necessary before drawing a blood sample for an accurate
serum measurement
Optimal: less than 12 mol/L
Borderline: 12-15 mol/L
High risk: above 15 mol/L
Myoglobin (not a primary heart test)
O2 binding protein found in heart and skeletal muscle. Found in the blood when
released following muscle injury.
Laboratory Tests
Coagulation Studies
Partial thromboplastin time (PTT): 60-70 (Heparin)
Activated partial thromboplastin time (APTT): 20-39
Prothrombin time (PT): 9.5-12 (Coumadin)
International normalized ratio (INR); 2-3.5
Hematologic Studies
Complete blood count (CBC)
Hematocrit: M 42-52% F 35-47%

Hemoglobin M 13-18 g/dL F 12-16 g/dL

Platelets: 150,000-450,000/ mm
White Blood Cells (WBC)
Drug Levels
Digoxin: Therapeutic range is 0.5-2 ng/mL
Digoxin has a narrow therapeutic range. Drop blood levels routinely
Quinidine: Therapeutic range is 2-6 mcg/mL
Laboratory Tests
Electrolytes: normal levels are essential for proper cardiac function
Potassium (K): 3.5-5.0
Hypo: ventricular dysrhythmias, flattened T wave or presence of U wave
Hyper: ventricular dysrhythmias, tall peaked T waves and asystole
Sodium (Na): 135-145
Hypo: intracellular osmotic fluid shift= brain edema
Hyper: increased BP, abnormal HR, seizures, neurological impairment
Calcium (Ca):
Low Ca = low HR
Hight Ca= tachycardia
Hypo: ventricular dysrhythmias, prolonged QT interval, and cardiac arrest
Hyper: shorten the QT intervals and causes AV block, cardiac arrest
Magnesium (Mg):
High Mg=Bradycardia
Low Mg= Tachycardia
Hypo: ventricular tachycardia and fibrillation
Hyper: bradycardia, hypotension, prolonged PR and QRS intervals
Electrocardiography
12 lead ECG
Continuous monitoring: hardwire, telemetry
Signal-averaged electrocardiogram
Continuous ambulatory monitoring (HOLTER)
Transtelephonic monitoring
Wireless mobile monitoring
Cardiac stress testing
Exercise stress testing (how heart work in stress,
exercises)
Pharmacologic stress testing (how pt response under certain meds)
Diagnostic Tests
Radionuclide imaging
Myocardial perfusion imaging (if heart is perfussing well)
Test of ventricular function, wall motion
Computed tomography CT (Looking at structures)
Positron emission tomography
Magnetic resonance angiography
Diagnostic Tests
Echocardiography (ultrasound of the

heart)
US of heart to evaluate the structure and function of chambers and valves
Phonocardiography (recording w/ a simutaneos ECG)
Graphic recording of heart sounds with simultaneous ECG
Coronary Angiography/Arteriography
Invasive procedure where cardiologist injects dye into coronary arteries and
immediately takes a series of x-ray films to assess structure of arteries
Cardiac Catherization
Invasive procedure study used to measure cardiac chamber pressures, assess
patency of coronary arteries
Requires ECG, hemodynamic monitoring; emergency equipment must be
available
Assessment prior to test; allergies, blood work (PT, PTT)
Assessment of patient post-procedure; circulation, potential for bleeding,
potential for dysrhythmias
Activity restrictions
Patient education pre-, post-procedure
Hemodynamic Monitoring
Central Venous Pressure (CVP) (volume status)
High fluid or hypervolemia= Increased CVP and vice
CVP is looking at the right side of the heart
Appropriate for clients who require accurate monitoring of fluid volume status but
are not candidates for the more invasive pulmonary artery pressure monitoring
Done by a central catheter with the tip in the SVC to measure the R heart
filling pressure
Provides data about right ventricular preload. Not for left heart pressures
Normal CVP 2-8 cm H2O or 2-6 mm Hg
Decreased CVP= decreased circulating volume
Increased CVP= increased blood volume or right heart failure
Diagnostic Tests
Pulmonary artery pressure (PAP)
PAP = left side of heart
High PAP = TOO MUCH FLUID and vice
Appropriate for critically ill clients requiring more accurate assessments of
left heart pressures
Pulmonary artery catheter (Swan-Ganz) has the tip in the pulmonary artery
Pressure is obtained after the tip is wedged into a pulmonary capillary and
is called PCWP
Good indicator of left ventricular preload also called left ventricular end
diastolic pressure (LVEDP)

Normal Values of Hemodynamic Readings

Diagnostic Tests
Intra-Arterial Blood Pressure Monitoring
To obtain direct and continuous BP measurements in critically ill patients who
have sever hyper or hypertension
Arterial catheters are useful when ABGs are needed frequently
Allen test completed prior to insertion of catheter.
Allen test is to check for perfusion in the hand

-Ask pt to make a fist

- Occlude both (ulnar and radial arteries)
- Ask pt to open hand
- Release ulnar artery and check for return of blood to hand (red/pink hand)
Common Cardiovascular Medications
Ace Inhibitors prils
Angiotensin Receptor Blockers sartans
Beta Blockers: olols
Calcium Channel Blockers: dipine
Adrenergic Agonists (EPINEPHRINE, DOBUTAMINE)
Anticoagulants: Coumadin, Heparin
Cardiac Glycosides: Digoxin
Antidysrhythmics (Lidocaine, Quinidine) to correct fast
dysrhythmias

Diuretics (eliminate excess fluid)

Antihyperlipedemia (niacin, statin, Lipitor)
Thrombolytics (clot busters, but you have to have a clot to
give this)
Vasodilators (hydrolicine )
Nitrates (vasodilation, for chest pain. Too much could
aggravate angina due to decrease perfussion)
Analgesics
Morphine
Oxygen
Nytroglicerine
Aspirin
Physical Assessment-Cardiac
General appearance
Inspection of skin
Blood Pressure
Arterial pulses
Jugular venous pulsations
Heart inspection and palpation
Heart auscultation
Inspection of extremities
Assessment of other systems
Lungs
Abdomen
Cardiac Assessment- Auscultation
Normal Heart Sounds
S1: Tricuspid and mitral closure creates first sound
Heard the loudest at the apical
S2: closure of the pulmonic and aortic valves
Heard loudest over the aortic and pulmonic areas
Abnormal Heart Sounds
S3: heard after S2
Normal in children and adults up to 35 or 40 (physiological S3)

 Abnormally is due to overload of one or both ventricles (significant in HF)

S4: heard before S1
Generated during atrial CX as blood forcefully enters a noncompliant ventricle
Caused by ventricular hypertrophy: HTN, CAD, cardiomyopathy, etc.
Cardiac Assessment- Auscultation
Systolic clicks:
Caused by opening of rigid and calcified aortic or pulmonic valve during
ventricular CX
Murmurs: (due to valvular problems)
Created by turbulent blood flow
Causes of the turbulence may be a critically narrowed or malfunctioning valve
Friction Rub: (two layer of pericardium friction
together)
Harsh grating sound that can be heard in both systole and diastole.
Caused by abrasion or inflamed pericardial surfaces from pericarditis

Cardiovascular Conditions:
1. Coronary Atherosclerosis
Homocysteine is a test specific for atheroesclerosis
Atherosclerosis is the abnormal accumulation of lipid deposits and fibrous
tissue within arterial walls and lumen.
In coronary atherosclerosis, blockages and narrowing of the coronary
vessels reduce blood flow to the myocardium.
Cardiovascular disease is the leading cause of death in the United States for
men and women of all racial and ethnic groups.
CAD, coronary artery disease, is the most prevalent cardiovascular
disease in adults.
Pathophysiology of Atherosclerosis
Inflammation (red and swollen area)
Coagulation (stop bleeding)
Bradikinin, which causes the pain
-Anywhere there is a ischemia the goal is to reperfuse

Risk Factors
Non-Modifiable
Family Hx of CAD
Older than 45 years old
Gender (men earlier than women)

Race
Modifiable
Hyperlipidemia
Smoking

HTN
DM
Obesity
Physical inactivity
Laboratory Tests
Lipid profile: to determine risk of developing atheroclerosis
Total serum lipids= 400-800 mg/dL
Triglycerides: lipids stored in fat tissue; normal 100-200 mg/dL
Cholesterol: main lipid associated with CAD; normal < 200mg/dL
Lipoproteins: proteins in the blood to transport cholesterol, triglycerides and
other fats
HDL= 35-70 mg/dL (M); 35-85 mg/dL (F)
LDL= < 160 mg/dL
Medications
HMG-COA Reductase Inhibitors
Statins- Atorvastatin ( Lipitor)
Nicotinic Acids
Niacins (flushing, like a
tomato)
Fibric Acids
Gemfibrozil ( Lopid)
Bile Acid Sequestrants
Cholestyramine ( Questran)
Cholesterol Absorption Inhibitors
Ezetimibe (Zetia)
Omega-3-acid
Fish oils
The main goal of all this categories is to lower
cholesterol
The main side effect of this meds is
- Myalgia (muscle pain)
- GI bloating, constipation, dispepcia (GERD)
- Myositis (inflammation of muscle)
Clinical Manifestations
Symptoms are due to myocardial ischemia
Symptoms and complications are related to the location and degree of vessel
obstruction
Angina pectoris (Ischemia)
Myocardial infarction (if the ischemia wasnt corrected then MI
happens)
Heart failure
Sudden cardiac death (heart suddenly stops beating)

Clinical Manifestations
The most common symptom of myocardial ischemia is chest pain; however,
some individuals may be asymptomatic or have atypical symptoms such as

weakness, dyspnea, and nausea.

Atypical symptoms are more common in women and in persons who are older,
or who have a history of heart failure or diabetes. (nausea, weight gain)
2. Angina Pectoris
CAD (the buildup of plaque in the arteries lead to angina
pectoris)
A syndrome characterized by episodes or paroxysmal pain or pressure in the
anterior chest caused by insufficient coronary blood flow.
Physical exertion or emotional stress increases myocardial oxygen demand and
the coronary vessels are unable to supply sufficient blood flow to meet the
oxygen demand.
- 3 types of Angina
a) Stable angina: exertional
With stable angina, the pt take the nitro, and pain goes away.
b) Unstable angina:(preinfarction) exertional- with exercise or stress
This one happens right before the MI
It is not relieve with med and rest. Need to go to ER INMEDIATELY
c) Variant angina: (prinzmetals) spasms of coronary artery
Spasm means smaller (small blood vessel)
With angina the main med is nytroglicerin (1 SL) and if after 5 min still hurts, go to ER
COSTOCHONDRIATIS (MUSCLE PAIN) is often confused with chest pain
(GERD, PNEUMONIA, PANIC ATTACKS) can be confused with heart attack

For Angina the main thing is reperfuse !!!

Angina pain varies from mild to severe

May be described as tightness, choking, or a heavy sensation.
Frequently retrosternal and may radiate to neck, jaw, shoulders, back or arms
(usually left).
Anxiety frequently accompanies the pain.
Other symptoms may occur: dyspnea/shortness of breath, dizziness, nausea,
and vomiting.
The pain of typical angina subsides with rest or NTG.
Unstable angina is characterized by increased frequency and severity and is
not relieved by rest and NTG. Requires medical intervention!
Treatment
Treatment seeks to decrease myocardial oxygen demand and increase oxygen
supply
Medications
Oxygen
Reduce and control risk factors
Reperfusion therapy may also be done
Medications
Nitroglycerin
Beta-adrenergic blocking agents (to decrease the heart and the demand of O2)
Calcium channel blocking agents (to decrease the heart and the demand of O2)
Antiplatelet and anticoagulant medications
Aspirin
Clopidogrel and ticlopidine (Plavix)
Heparin
Glycoprotein IIB/IIIa agents
Treatment of Angina Pain
Treatment of angina pain is a priority nursing concern.
Patient is to stop all activity and sit or rest in bed.
Assess the patient while performing other necessary interventions.
Assessment includes VS, and observation for respiratory distress, and
assessment of pain. In the hospital setting, the ECG is assessed or obtained.
Administer oxygen.
Administer medications as ordered or by protocol, usually NTG.
Collaborative Problems
Acute pulmonary edema
Heart failure
Cardiogenic shock (shock is always related to lack of perfusion)
Dysrhythmias and cardiac arrest
Myocardial infarction
Patient Teaching
Lifestyle changes and reduction of risk factors
Explore, recognize, and adapt behaviors to avoid to reduce the incidence of
episodes of ischemia

Teaching regarding disease process

Medications
Stress reduction (bc stress
increase SNS)
When to seek emergency care
Angina Pectoris Review
Warning sign of impending MI
Women and older adults present atypically
3 types
Stable angina: exertional
Unstable angina:( preinfarction) exertional- with exercise or stress
Variant angina: (prinzmetals) spasms of coronary artery
Pain unrelieved by rest or nitro and lasting more than 15 min
differentiate angina from MI
Precipitated by exertion or stress
Relieved by rest or nitro
Symptoms last < 15 min
Angina Review
Client education:
Stop activity and rest
Place nitro under tongue
Should be a bite to the med
3 in 15 minutes if not go to ER
HEADACHE is most common s/e of nitro
Encourage patient to sit and lie down slowly
Encourage smoking cessation
Diet and lifestyle modification
Get cholesterol and B/P checked regularly
Remain physically active

Angina- Nursing Diagnosis

Risk or decreased cardiac tissue perfusion
Anxiety related to cardiac symptoms and possible death
Deficient knowledge

Noncompliance

Myocardial Infarction
An area of the myocardium is permanently destroyed. Usually caused by
reduced blood flow in a coronary artery due to rupture of an atherosclerotic
plaque and subsequent occlusion of the artery by a thrombus.
In unstable angina, the plaque ruptures but the artery is not completely
occluded. Unstable angina and acute myocardial infarction are considered the
same process but at different point on the continuum.
The term acute coronary syndrome includes unstable angina and myocardial
infarction.
MI

Blockage of one or more of the coronary arteries

Causes:
Arteriosclerosis, emboli, thrombus, shock, hemorrhage, hypoxia leading got
necrosis
Classic sign: substernal pain or feeling of heaviness on chest
Patients may report:
Substernal pain or pain over pericardium 15 min
Pain that is heavy and radiating down left arm
Spontaneous pain not relived by nitro or rest
Pain that radiates to jaw
Pain accompanied by SOB, pallor, diaphoresis, N/V
HR, B/P, temp, RR
Diagnosis
EKG
Angina= ST depression and/or T wave inversion (ischemia)
MI= T wave inversion (ischemia), ST elevation (injury), and abnormal Q wave
(necrosis)
When cardiac muscle suffers ischemic injury, cardiac enzymes are released into
the blood stream providing specific markers
Myoglobin
CK-MB
Troponin I
Troponin T

Thallium scans: shows absent

Cardiac Cath: evaluates blockage
Laboratory Tests
Cardiac biomarkers
Serum Enzymes:
Creatinine Kinase (CK), CK-MB
CK formerly known as (CPK)- elevation indicates muscle injury
CK-MB: specific to myocardial muscle, rises within 6 hours of injury and peaks
at 18 hours post injury and returns to normal within 2-3 days.
Useful in DX of MI
Lactic dehydrogenase (LDH)
Found in many body tissues; elevation is detected within 24-72 hours after MI,
peaks in 3-4 days and returns to normal around 2 weeks.
Useful for delayed DX of MI
Troponin T and I
Onset is before CK-MB in MI; peaks at 24 hours and returns to normal around 2
weeks; provides early sensitivity
More specific to cardiac injury for DX of MI
Management
Monitoring
V/S q15 until stable
EKG continuous monitoring (within 10 min in ER)
Location, severity, quality of pain
Hourly output
Labs
MONA

When B/P falls rapidly= dopamine

Thrombolytics= streptokinase, retavase
Promote energy conservation
Medications
Vasodilators
Nitroglycerin
Analgesics
Morphine
Beta-blockers/ Calcium Channel Blockers
Lopressor, Norvasc-Cardizem
Thrombolytic agents
Streptokinase
Antiplatelet
Aspirin, Plavix
Anticoagulants
Heparin, Lovenox
Glycoprotein inhibitors
Integrillin (blocks binding of fibrinogen=blocked platelet aggregation)
MI
Surgical Interventions
Percutaneous transluminal coronary angioplasty (PTCA)
Coronary artery bypass graft (CABG)
Complications
Heart failure and cardiogenic shock
Ischemic mitral regurgitation
Ventricular aneurysm/rupture
Dysrhythmias
Collaborative Problems
Acute pulmonary edema
Heart failure
Cardiogenic shock
Dysrhythmias and cardiac arrest
Pericardial effusion and cardiac tamponade
Invasive Coronary Artery Procedures
AKA: Percutaneous Coronary Interventions (PCI)
Percutaneous Transluminal Coronary Angioplasty
A balloon tipped catheter is used to open blocked coronary vessels and
resolve ischemia
Purpose is to improve blood flow within the coronary artery by compressing and
cracking the atheroma
Catheters are usually introduced into the femoral artery up to the aorta and
into the coronary arteries
Angiography is performed using dye to identify the blockage
Coronary Artery Stent

A metal mesh that provides structural support to a vessel at risk of acute

closure
Atherectomy
An invasive interventional procedure that involves the removal of the atheroma,
or plaque from the coronary artery by cutting, shaving or grinding
Brachytherapy
Reduces the recurrence of obstruction, preventing vessel restenosis by inhibiting
smooth muscle cell proliferation
Complications of PCI
Complications during a PCI procedure
Dissection
Perforation
Abrupt closure
Vasospasm of coronary artery
Acute MI
Acute dysrhythmias
Cardiac arrest
Complications after PCI procedure
Abrupt closure
Bleeding at insertion site
Retroperitoneal bleeding
Hematoma
Arterial occlusion
Acute renal failure
Coronary Artery Bypass Graft (CABG)
a blood vessel is grafted to an occluded coronary artery so that blood can
flow beyond the occlusion
Indications for CABG
Alleviation of angina that cannot be controlled with medication or PCI
Treatment of left main coronary artery stenosis or multivessel CAD
Prevention and treatment of MI, dysrhythmias or heart failure
Complications of CABG
Hemorrhage
Dysrhythmias
MI
Nursing Management-CABG
Pre-operative
Assessing the patient
Reducing the fear and anxiety
Monitoring and managing potential complications
Providing patient teaching
Postoperative
Assessing the patient
Monitoring for complications
Restoring cardiac output
Promoting adequate gas exchange
Maintaining fluid and electrolyte balance
Relieving pain
Maintaining adequate tissue perfusion
Maintaining normal body temperature

Potential Complications of Cardiac SX

Hypovolemia
Persistent bleeding
Cardiac tamponade
Fluid overload
HTN
Tachydysrhythmias
Bradycardia
Cardiac failure
MI
Hypothermia