HEART FAILURE - The heart is too weak to pump efficiently so it can’t provide proper cardiac output Diastolic: “left
c: “left ventricular diastolic dysfunction” remember diastole is the filling or resting phase of
to maintain the body’s metabolic needs.
 Results on the body: Organs and Tissues will suffer from the decreased blood flow,
pressure in the heart increases which over works the ventricles, body can become
congested with fluids (enter into congestive heart failure) that can cause life-
threatening complications.
Note: The left ventricle is the largest of all four chambers which allows for maximum pumping power.
CAUSES OF HEART FAILURE
Causes of Heart Failure:
Mainly due to the heart muscle (specifically the ventricles) becoming damaged or too stiff.
Remember the mnemonic: Failure
 Faulty heart valves: AV and SL valve problems (due to congenital issues or infection
(endocarditis) that causes blood to back flow (regurgitation) or stenosis (narrowing of the
valves that increases pressure of blood flow through the valves). This causes the heart to
work harder and become weak over time.
 Arrhythmias: Atrial fibrillation or tachycardia
 Infarction (myocardial) Coronary artery disease: part of the heart muscle dies due to a
blockage in the coronary arteries…muscle become ischemic and can die (main cause of left
ventricular systolic dysfunction)
 Lineage (congenital) family history
 Uncontrolled Hypertension: overtime this can lead to stiffening of the heart walls because
with untreated HTN the heart has to work harder and this causes the ventricles to become
stiff.
 Recreational Drug Use (cocaine) or alcohol abuse
Envaders (instead of Invaders): viruses or infections that attack the heart muscle
TYPES OF HEART FAILURE
Left-Sided Heart failure: the left side of the heart cannot pump blood out of the heart efficiently so
blood starts to back-up in the lungs.
 Most common type of heart failure.
 Left-sided heart failure is likely to lead to right-sided heart failure.
The left ventricle becomes too weak and doesn’t squeeze blood out properly. The heart failure can be
either SYSTOLIC OR DIASTOLIC.
Systolic: “Left ventricular systolic dysfunction” remember systolic is the contraction or
“squeezing” phase of the heart. In systolic dysfunction, there is an issue with the left ventricle being
able to eject blood properly out of the ventricle and the organs can’t get all that rich-oxygenated
blood it just received from the lungs. Patients will have a low ejection fraction.
 What is ejection fraction? Ejection fraction is a calculation used to determine the severity
of heart failure on the left side. A normal EF is 50% or greater meaning that more than half
of the blood that fills inside the ventricles is being pumped out. An EF can be measured
with an echocardiogram, heart cath, nuclear stress test. An EF of 40% or less is a diagnosis
for heart failure.
the heart. In diastolic dysfunction, the ventricle is too stiff to allow for normal filling of blood. Since
there isn’t an issue with contraction but filling the ejection fraction is usually normal.
Left-sided heart failure will present with PULMONARY Signs and Symptoms.
Right-Sided Heart Failure: the right side of the heart cannot pump the “used” blood it received from
the body efficiently so it can’t get the blood back to the lungs to get replenished with oxygen. The
causes the blood to back up peripherally (legs, hands, feet, abdomen).
 Right-sided heart failure causes congestion of blood in the heart and this increases the
pressure in the inferior vena cava (which normally brings “used” blood back to the heart
for re-oxygenation). This built-up pressure causes the hepatic veins to become very
congested with blood which leads to hepatomegaly and swelling peripherally.
 Right-sided heart failure is usually caused from left-sided heart failure because of the
increased fluid pressure backing up from the left side to the right. This causes the
right side of the heart to become overworked.
 Other causes: pulmonary heart disease “cor pulmonale” as a complication from
pulmonary hypertension or COPD.
Right-sided heart failure presents with PERPHIERAL SIGNS AND SYMPTOMS.
SIGNS AND SYMPTOMPS OF HEART FAILURE (know the difference S/S of left and right HF)
LEFT SIDED HEART FAILURE
DROWNING (these patients are literally drowning in their own fluid from the heart’s failure to pump
efficiently)
Difficulty breathing
Rales (crackles)
Orthopnea (cannot tolerate lying down…must sit-up to breath, especially while sleeping)
Weakness (extremely tired and fatigued due to shortness of breath and heart can’t compensate for
increased activity)
Nocturnal Paroxysmal dyspnea (awaking during sleep with extreme dyspnea)
Increased heart rate (due to fluid overload and the heart is trying to get the blood to organs but it
can’t because of muscle failure)
Nagging cough (can be frothy or blood-tinged sputum from fluid overload in the lungs…very bad sign)
Gaining weight from the body retaining fluid…2 to 3 lb in a day or 5 lbs in a week
RIGHT SIDED HEART FAILURE NURSING INTERVENTIONS FOR HEART FAILURE
Assessing:
SWELLING (fluid is backing up in the right side of the heart which causes fluid to back-up in the  Assess patient for worsening symptoms (right-sided failure…peripheral swelling vs left-sided
hepatic veins and peripheral veins) failure, pulmonary edema)
 Patient responsiveness to medication treatment:
Swelling of legs, hands, liver, abdomen  watch heart rate (Digoxin)
 respiratory status
Weight gain  blood pressure (vasodilators cause hypotension)
 diuretics (strict intake and output, daily weights, monitor electrolyte levels, especially K+)
Edema (pitting)
Monitoring:
Large neck veins (jugular venous distention)  Fluid status (may be ordered a Foley catheter, if on diuretics)
 Cardiac diet (low in salt and fats)
Lethargic (weak and very tired)  Fluid restriction (no more than 2 L per day)
 Lab values: watching BNP, kidney function BUN & creatinine, troponins levels, electrolytes
Irregular heart rate (atrial fibrillation) (especially potassium…if on Lasix: waste potassium and low potassium increases risk of digoxin
toxicity)
Nocturia (frequent urination at night) lying down elevates the legs and allows the extra fluid to enter  Edema in leg: Keep legs elevated and patient in high Fowler’s to help with breathing
into the vascular system which allows the kidneys to eliminate the extra fluid.  Safety (at risk for falls due to fluid status changes, swelling in legs and feet, and orthostatic
hypotension)
Girth of abdomen increased (from swelling of the liver and building up fluid in the abdomen)…can’t
breathe well and this causes nausea and anorexia. Educating:
 Early signs and symptoms heart failure exacerbation
TESTS USED TO DIAGNOSED HEART FAILURE  Shortness of breath
 BNP (b-type natriuretic peptide) blood test: a biomarker released by the ventricles when there is  Weight gain
excessive pressure in the heart due to heart failure.  Orthopnea
 <100 pg/mL no failure  Low salt (allowed 2-3 G sodium per day) and fluid restriction (no more than 2 L per day)
 100-300 pg/mL present  Vaccination to prevent illness, such as annual flu and to be up-to-date with pneumonia vaccine
 300 pg/mL mild  Exercise aerobic (as tolerated)
 600 pg/mL moderate  Daily weights (watch for no more than 2-3 lb per day and 5 lbs per week)
 900 pg/mL severe  Compliance with medications
 Source ClevelandClinic.org  Smoking cessation
 Chest x-ray  Limiting alcohol
 Echocardiogram
 Heart cath ADMINISTERING MEDICATIONS:
 Nuclear stress test Always Administer Drugs Before A Ventricle Dies!

HEART FAILURE CAN BE ACUTE OR CHRONIC AND CAN BE TRIGGERED/EXACERVATED WITH: Ace Inhibitors (angiotensin-converting-enzyme inhibitors):
 High salt intake or fluid (watch fluids)  First line of treatment for heart failure with beta blockers
 Infection  End in “pril” Lisinopril, Ramipril, Enalapril, Captopril
 Uncontrolled atrial fibrillation  Works by allowing more blood to get to the heart muscle which allows it to work easier. Also,
 Renal failure blocks the conversion of Angiotensin I or Angiotensin II (this causes vasodilation, lowers blood
pressure, allows kidneys to secrete sodium because it decreases aldosterone)
 Side effects: dry, nagging cough and can increase potassium (inhibiting angiotensin II which
decreases aldosterone in the body which causes the body to retain more potassium and excrete
sodium)
ARBs (Angiotensin II receptor blockers): Digoxin:
 End in “sartan” like Losartan, Valsartan  Positive inotropic effect that increases the heart’s ability to contract stronger and it has a
 Used in place of ACE inhibitors if patient can’t tolerate them negative chronotropic action that causes the heart to beat slower
 Blocks angiotensin II receptors which causes vasodilation. This lowers blood pressure and helps  So, the heart slows down and contracts stronger which allows the heart to pump more blood.
the kidneys to excrete sodium and water (due to the affects that blocking angiotensin II has on  Treatment for patients with left ventricular systolic dysfunction (however, not usually the first
the kidneys…decreases aldosterone). line of treatment due to side effects and toxicity risks), used alongside ACE/beta blockers, and
 Side effects: increases potassium levels, diuretics
NO dry nagging cough  Toxicity issues: monitor patient potassium level (hypokalemia <3.5 mEq/L) because
hypokalemia increases digoxin toxicity
Diuretics:  S & S of toxicity: nausea, vomiting, visual changes yellowish green halos
 Used along with ACE inhibitors or ARBs to decrease water and sodium retention which will  Normal Digoxin range 0.5 to 2 ng/mL
decrease edema in the body and lungs. This allows the heart to pump easier.  Not for patients with a second or third degree heart block
 Patients will urinate a lot! Monitor I&O  Check apical pulse before giving….>60 bpm
 Loop diuretics (most common) like Lasix or Furosemide (watch potassium level because they will  Antidote: Digibind
waste potassium)
 Potassium-sparing diuretics like “Aldactone” (can cause hyperkalemia, especially if taking with
ACE or ARBs)

Beta Blockers:
 Blocks norepinephrine and epinephrine effects on the heart muscle
 Given in stable heart failure with ACE inhibitors
 End in “lol” like Metoprolol, Carvedilol and Bisoprolol
 Not for acute heart failure because the negative inotropic effect on the heart. The negative
inotropic effect causes decrease myocardial contractility (slows heart) and decreases cardiac
work load.
 Used in stable heart failure in people with ventricular systolic dysfunction (there is a contraction
problem with the left ventricle) and to treat diastolic heart failure (remember there is a problem
with the heart filling in diastolic dysfunction). It will help the heart rest so the stiff ventricle can
fill properly and the volume of blood pumped out increases.
 Side effects: check pulse (bradycardia), no grape juice; mask hypoglycemic signs in diabetics,
respiratory issues in asthmatics and patients with COPD

Anticoagulants:
 Not used in all patients with heart failure
 Typically, used in patients with heart failure who are in a-fib because they are at risk for blood
clot formation or certain scenarios of left ventricular systolic heart failure when there is a low
ejection fraction of <35%.

Vasodilators:
 (arterial dilator) Hydralazine, Prescribed with a nitrate like Isordil (venous dilator)
 Sometimes used in place of an ACE or ARB, if patient can’t tolerate them
 This causes vasodilation in the arteries and veins to help decrease the amount of blood and fluid
going back which helps decrease the work load on the heart
 Side effects: low blood pressure, orthostatic hypotension
LEFT-SIDED VS. RIGHT-SIDED HEART FAILURE
In heart failure, the heart is FAILING to pump blood forward. Therefore, blood backs up and volume
overload occurs.
RIGHT SIDED HEART FAILURE
The right side of the heart receives deoxygenated blood from the systemic venous system.
When this side fails to pump blood properly it results in the congestion of blood in the right side of the heart
which goes into systemic venous circulation.
This increases the pressure in the inferior vena cava (which normally brings “used” blood back to the heart
for re-oxygenation). This built-up pressure causes the hepatic veins to become very congested with blood
and leads to hepatomegaly and systemic venous congestion. This will lead to swelling in the legs, abdomen,
and feet and weight gain.
What is ejection fraction? Ejection fraction is a calculation used to determine the severity of heart failure on
the left side.
A normal EF is 50% or greater meaning that more than half of the blood that fills inside the ventricles is
being pumped out. An EF can be measured with an echocardiogram, heart cath, nuclear stress test. An EF of
40% or less is a diagnosis for heart failure.
Diastolic heart failure (heart failure with preserved ejection fraction): also called “left ventricular diastolic
dysfunction”
Remember diastole is the filling or resting phase of the heart. In diastolic dysfunction, the ventricle is too
stiff to allow for normal filling of blood. Since there isn’t an issue with contraction but filling the ejection
fraction is usually normal.
Left-sided heart failure will present with PULMONARY Signs and Symptoms.

Right-sided heart failure is usually caused from left-sided heart failure because of the increased fluid DROWNING (these patients are literally drowning in their own fluid from the heart’s failure to pump
pressure backing up from the left side to the right. This causes the right side of the heart to become efficiently)
overworked.
Difficulty breathing
Right-sided heart failure presents with SWELLING and PERPHIERAL SIGNS AND SYMPTOMS
Rales (crackles)
Right-Sided Heart Failure Signs and Symptoms
To help you remember the signs and symptoms of right-sided heart failure, try to remember the Orthopnea (cannot tolerate lying down…must sit-up to breath, especially while sleeping)
mnemonic SWELLING (fluid is backing up in the right side of the heart which causes fluid to back-up in the
hepatic veins and peripheral veins). Weakness (extremely tired and fatigued due to shortness of breath and heart can’t compensate for
 Swelling of legs, hands, liver, abdomen (ascities) increased activity)
 Weight gain
 Edema (pitting) Nocturnal Paroxysmal dyspnea (awaking during sleep with extreme dyspnea)
 Large neck veins (jugular venous distention)
 Lethargic (weak and very tired) Increased heart rate (due to fluid overload and the heart is trying to get the blood to organs but it can’t
 Irregular heart rate (atrial fibrillation) because of muscle failure)
 Nausea (swelling of the abdomen and liver)
 Girth of abdomen increased (from swelling of the liver and building up fluid in the abdomen), can’t Nagging cough (can be frothy or blood-tinged sputum from fluid overload in the lungs…very bad sign)
breathe well and this causes nausea and anorexia.
Gaining weight from the body retaining fluid…2 to 3 lb in a day or 5 lbs in a week
Left-Sided Heart Failure Signs and Symptoms
The left side of the heart is responsible for pumping oxygenated blood it received from the lungs into
arterial circulation. However, when the left side of the heart fails it cannot pump blood out of this side
efficiently so blood starts to back up in the lungs, hence pulmonary circulation.

Most common type of heart failure.

Left-sided heart failure can be classified as SYSTOLIC OR DIASTOLIC.
Systolic heart failure (heart failure with reduced ejection fraction): also called “Left ventricular systolic
dysfunction”

Remember systole is the contraction or “squeezing” phase of the heart. In systolic dysfunction, there is an
issue with the left ventricle being able to eject blood properly out of the ventricle and the organs can’t get
all that rich-oxygenated blood it just received from the lungs. Patients will have a low ejection fraction.
MYOCARDIAL INFARCTION - The heart’s myocardial tissue layer dies from decreased blood flow due
to:
CAUSES
 Blockage in the coronary artery from coronary artery disease (most common)
 Coronary spasms from illicit drug usage drugs like cocaine or hypertension. This causes
constriction of the coronary artery and stops blood flowing to the heart muscle.
 Damage to the coronary artery due to coronary artery dissection. This is a tear in the inner layer
“tunica intima” of the artery which causes blood to leak in the “tunica media”. This restricts the
flow of blood through the coronary artery. It can happen spontaneously and occurs more likely
in young, active women.
PATHOPHYSIOLOGY OF MI:
The coronary arteries supply the heart with nutrients. They branch off from the aorta into the left and
right coronary artery.
Left Coronary Arteries:
Important to note: Blockages in the left coronary arteries can cause the worst damage from a
myocardial infarction. This is because blockages in the left coronary artery can cause anterior wall
death which affects the left ventricle. Anterior MIs affect the most myocardial tissue, especially if the
blockage occurs before it branches off and this can extend into the septum and lateral wall.
 Left anterior descending artery: supplies right and left ventricle and septum. This is the most
common site for blockages.
 Left circumflex: supplies the left atrium and ventricle
Right Coronary Arteries:
 Right coronary artery: supplies the right atrium and ventricle
 Right marginal artery: supplies the right ventricle and septum
What happens to the heart muscle after an MI?
When a coronary artery becomes 100% blocked the muscle cells die. Cell death is irreversible after
about 30 minute. The cells are gone forever and can never be replaced.
 Early signs of an MI…no physical changes to heart muscle yet (until about 6-8 hours), but when
the myocytes die cardiac enzymes are released: CK-MB (4 to 6 hours after MI), troponin (2-4
hours…most regarded) myoglobin (1 hours after injury…show injury but not too specific).
 Within 24-36 hours inflammation sets in and neutrophils come on the scene and congregate at
the damaged tissue site. This causes complication of possible pericarditis. In addition, within 24
hours the heart fails to pump efficiently (cardiogenic shock) and arrhythmias can develop (atrial
and ventricular dysrhythmia along with AV blocks).
 Within 10 days, granulation occurs when the macrophages come on the scene. They are WBCs
who’ve came to clean up the dead cells and other components. However, the new tissue formed
from granulation is not well formed and is weak. This increases the chance of cardiac rupture.
 Within 2 months scarring occurs, and the heart is affected in size and functionality due to
increased collagen.
Other Complications:
 Heart failure, depression, and ventricular aneurysm
SIGNS AND SYMPTOMS OF OF MYOCARDIAL INFRACTION:
Remember the mnemonic: CRUSHING
 Chest pain (intense, heavy)
 Radiating chest pain that goes to left arm, jaw, back
 Unrelieved by nitroglycerin or rest (chest pain)
 Sweating (cold)
 Hard to breathe (shortness of breath)
 Increased heart rate, blood pressure or irregular heart rate
 Nausea with vomiting
 Going to be anxious and scared
Note: Women can present differently by not having “heavy” chest pain. Their chest pain may be felt in
the lower part of the chest, experience shortness of breath, and feel extremely fatigued. They may
not seek immediate help because they think they are “just ill” with a sickness.
Silent MIs: this is where the patient has no symptoms of chest pain. Mainly occurs in diabetics due to
diabetic neuropathy where the nerves that feel pain are damaged in the heart.
DIAGNOSING WITH CARDIAC MARKERS & OTHER TOOLS
When the heart muscle is injured it releases cardiac markers overtime. This will help the health care
provider know that something is going on along with a 12-lead EKG (and other tools).
Blood Tests Cardiac markers:
 Troponins: gold standard now used by most hospitals in assessing for an MI. It is a protein
released from the heart when damage is present from a myocardial infarction. They are drawn
in a series (troponin levels will elevate 2-4 after injury). They are usually drawn every 6 hours for
3 sets. The nurse’s role is to collect levels and monitor them for an upward trend. If levels are
increasing, the physician will need to be notified.
 Myoglobin: an early cardiac marker released after heart injury (1 hour after injury). However,
not very cardiac specific…used in early detection..will need more blood tests to further evaluate.
 CK: protein released when there is muscle damage (not specific to just the heart)…so CK-MB
may be ordered to tell if it is the heart since CK-MB represents heart muscle (it elevates 4-6 hr
after injury).
Other tools used:
 Echocardiogram: ultrasound of the heart to look at the heart to see if there is damaged from an
MI.
 Heart Cath: a procedure where a special dye is injected into the coronary arteries and an X-Ray
is taken to see if there are any blockages, their locations, and if there is any muscle damage. If
there is a blockage, the cardiologist will assess the need for stent placement or other techniques
used to open the artery.
 Stress test with Myocardial Perfusion Imaging: assesses how the heart responses to stress and
evaluate the blood flow to the myocardial muscle.
 EKG:
 Shows ischemia, injury, and infarction.
 Nurses role: obtaining EKG (or delegating it to be done) looking for any EKG changes and
notifing md of them
 Compare newly obtained EKG to previous EKGs
What are you looking for on the EKG?
 ST-segment depression or elevation
 T-wave inversion or hyperacute
 Pathological Q-wave
Know the views of the heart based on an EKG reading:
 I, AVL, V5, V6: Lateral
 II, III, AVF: Inferior
 V 1, V2: Septal
 V 3, V4: Anterior
Nursing Interventions for Myocardial Infarction
 Monitoring & Assessing Cardiovascular system:
 Obtain a 12-lead EKG, have continuous bedside cardiac monitoring
 Monitoring blood pressure and heart rate
 Place on oxygen via nasal cannula per MD order 2-4 L
 Working IV access (multiple…may start drips and administer other IV medications)
 Monitor respiratory system: lung sounds “crackles”..represent heart failure
 Strict bedrest (activity puts strain on heart)
 Collect cardiac enzymes as ordered by the physician
Administering medications per MD order:
Mnemonic: Acute Angina Means Nasty Artery Blockages And Cardiac Complications
Antithrombotic agents: prevent formation of clot
 Lovenox (subq injection) monitor for bleeding (assess gums of mouth, stool (dark tarry), drop in
blood pressure and increase in heart rate, blood in urine)
 Heparin (drip usually or subq injection) monitor for bleeding just as with Lovenox, but watch
platelet count which may start to decrease after several days while being on Heparin. This could
represent Heparin-Induced Thrombocytopenia (<150,000 platelets)…. if this develops patient
may be be switched to Argatroban or Angiomax
 Monitor PTT (Partial thromboplastin time) normal 25-35 seconds
 60-80 therapeutic range (depends on facility)
Antiplatelets: decrease platelets aggregation and thrombus formation
 Aspirin: low dose (decrease the chances of a clot forming and decrease the chance of another
heart attack). Watch for signs and symptoms of GI bleeding, especially if patient has a history.
Plavix: taken if can’t take aspirin (may be prescribed short term for up to a year after the
myocardial infarction)
 Monitor for:
 Thrombotic Thrombocytopenic Purpura (TTP): clotting disorder where clots form in blood
vessels in the body which causes decreased blood flow to vital organs…low platelet count, neuro
changes, bruising, anemia, renal failure, fever
 Will need to discontinue medication for 5-7 days before a planned surgical procedure because
of the increase chance of hemorrhage while taking this drug. Patients need to let their surgeon
know they are taking Plavix because they will be switched to another antiplatelet prior to the
surgery. Plavix takes a while to clear in the body’s system.
Morphine: for chest pain relief (may find that morphine only relieves the chest pain rather than
nitro) hypotension, respiratory depression.
Nitrates: Nitroglycerin (ointment, sublingual, IV, patch, or oral “Imdur”): causes vasodilation and
increases blood flow to the heart, hence better blood flow to the area experiencing ischemia
 Monitor blood pressure, assess patient’s chest pain, monitor EKG and BP continuously if on drip.
 Side effects: headache, flushing, dizzy
Ace Inhibitors: end in “pril” Lisinopril, Ramipril, Enalapril, Captopril
 ACEI work by allowing more blood to get to the heart muscle and this allows it to work easier. It
does this by blocking the conversion of Angiotensin I or Angiotensin II (this causes vasodilation,
lowers blood pressure, and allows kidneys to secrete sodium because it decreases aldosterone)
 Side effects: dry, nagging cough and can increase potassium level (it does this by inhibiting
angiotensin II which decreases aldosterone in the body which causes the body to retain more
potassium and excrete sodium)
Beta blockers: “Coreg, Lopressor” decreases work load on the heart…slows heart rate and decreases
blood pressure
 Monitor for bradycardia, masking signs and symptoms of hypoglycemia in diabetics, breathing
problems in asthmatics and COPD…educate patient not to take beta blockers with grapefruit
juice because it slows the absorption of beta blockers
ARBS Angiotensin II receptor blockers:end in “sartan” like Losartan, Valsartan
 Used in place of ACE inhibitors if patient can’t tolerate them
 ARBs work by blocking angiotensin II receptors which causes vasodilation. This lowers blood
pressure and helps the kidneys to excrete sodium and water (due to the affects that blocking
angiotensin II has on the kidneys…decreases aldosterone).
 Side effects: increases potassium levels, NO dry nagging cough
Cholesterol lowering medication such as Statins: “Lipitor, Crestor, Zocor” (goal: LDL less than 100
mg/dL) helps lower LDL, total cholesterol, lower triglycerides, and increase HDL.
 Educate not to replace diet and exercise
 Notify doctor if they develop muscle pain or tenderness
 Monitor CPK (creatine kinase) levels…. which if elevated it can cause muscle problems
 Monitor liver function because statins act on the liver to block it from producing too much
cholesterol.
Calcium Channel Blockers: Norvasc, Cardizem
 This medications work by stopping the transport of calcium to the myocardium and into smooth
muscle which causes vasodilation on the coronary arteries.
 Monitoring heart rate, orthostatic hypotension, educate about good oral hygiene due to gum
enlargement.
ANGINA - Angina is a fancy term for chest pain. This is a type of chest pain that occurs when blood Mnemonic to remember: 4 S‘s for STABLE
flow to the heart muscle (hence the myocardium) is restricted by the coronary arteries.  Seeing it coming (predicable)
 Short (lasts less than 5 minutes)
Chest pain is a warning sign from the body that the heart is not receiving enough blood, and if it  Stops (relieved with nitroglycerin or rest)
doesn’t get this blood some sections of the heart are going to die.  Stiff or stenosed artery

How does the heart muscle receive blood? With stable angina, there is no damage to the heart muscle, troponin levels are normal, ECG is normal
 From a network of arteries known as the coronary arteries at rest or may have slight ST depression and inverted T waves with exertion.
 The coronary arteries originate from the aorta.
Unstable Angina
There are two main coronary arteries called:  Also called “pre-infarction angina”
 Left coronary artery  happens before a myocardial infarction
 right coronary artery  occurring due to decreased blood supply to heart muscle because a fatty plaque has ruptured
 These arteries feed the left and right side of the heart.  VERY serious and must be treated because it can progress to an MI
 A chain of events is set off with the aggregation of platelets and thrombus creation, which acts
Right side feeds: as a roadblock and partially or completely blocks blood flow through the artery. As the
 Left atrium: top chamber thrombus grows, it can cause muscle cells to die leading to an MI.
 Left ventricle: bottom chamber
 Interventricular septum: this is the wall that separates the right and left ventricle Mnemonic to remember: 4 UN‘s for UNSTABLE
 UNexpected (occurs with rest or little activity)
Left side feeds:  UNaltered by rest or nitroglycerin
 Right atrium: top chamber  UNrelenting (last more than 15 minutes, multiple episodes, and increases)
 Right ventricle: bottom chamber  UNsurvivable for muscle cells without treatment
 Bottom of left ventricle
 Electrical structures: SA & AV node NSTEMI
 Partial blockage of coronary artery
Types of Angina  No elevation of the ST segment
Stable Angina  ECG may show depressed ST segment or inverted T waves
 Also called “exertional angina”  Troponin levels will usually be elevated
 Happens when there is exertional stress
 This increases the oxygen demand by the heart Treatment:
 The blood flow within the arteries can’t keep up to allow blood to get to the heart muscle Heart cath to open up narrowed artery, nitro to vasodilate, heparin to prevent thrombus, antiplatelet
 Many cases are due to a fatty plaque within the coronary artery that causes stiffening and therapy (Clopidogrel)
Narrowing of the artery
 This leads to chest pain

Treatment includes:
 low fat and sodium diet
 smoking cessation
 managing glucose, if diabetic
 lowering cholesterol with statins
 Lowering blood pressure and increasing blood flow to the heart
 Beta blockers, nitrates, calcium channel blockers, ACEs, and ARBs
 Antiplatelets like aspirin
 Depending on the patient’s case heart catheterization may or may not be an option
STEMI
 Complete blockage of coronary artery
 ST segment elevated on the ECG, which tells us a huge area of the heart muscle is not getting
blood flow
 Troponins will be elevated
 Need to open up blood flow STAT to the heart muscle:
 Heart cath: percutaneous transluminal coronary angioplasty (PTCA) with stents to open artery
 Coronary artery bypass graft (CABG)

Variant Angina
 occurs due to a vasospasm of a coronary artery
 also called “prinzmetal angina”
 tends to happen during rest at night or in the morning
 short-lived ST segment elevation
 most common in patients who:
 use drugs that have a vasoconstriction effect on the arteries like smoking, cocaine,
marijuana
 high alcohol consumption
 exposure to cold
 vascular disorders
 Treatment: nitroglycerin
 Prevention: calcium channel blockers
CORONARY ARTERY DISEASE - the coronary arteries that deliver a constant supply of blood to the
heart muscle begin to develop fatty plaques that can lead to restriction of blood flow to the heart.
Patients who have coronary artery disease have developed fatty plaques due to atherosclerosis in the
arteries that provide the heart muscle with a vital blood supply. CAD can lead to heart muscle
damaged or death.
Fatty plaques are caused by a condition called ATHEROSCLEROSIS which creates fatty plaques in the
artery walls.
 Happens overtime
 Limits blood supply to the heart muscle and can rupture which can lead to thrombosis formation
(hence causing a myocardial infarction)
 Atherosclerosis can also lead to hypertension, chest pain, and heart failure.
Main Arteries that feed the heart muscle:
Left coronary artery which branches off to:
 Left circumflex artery: provides blood to left atrium & side and back of the left ventricle
 Left anterior descending artery: provides blood to the front and bottom of the left ventricle and
front of the septum
Right coronary artery provides blood to the right atrium and ventricle and to the bottom part of the
left ventricle and back of the septum and branches off to:
 Right marginal artery
 Posterior descending artery
These arteries can become atherosclerotic and factors that increase this include:
 Smoking
 Unhealthy: obese or overweight
 High cholesterol
 Sedentary lifestyle
 Diabetes
 Family history
Patho of Atherosclerosis Simplified:
Blood flows through the artery which contains the red blood cells and lipids (LDL). LDL (low-density
lipoproteins…the bad cholesterol) starts to adhere to the artery wall and grows overtime (risks factors
can increase the rate at which it grows).
As it grows the patient is usually asymptomatic until the plaque becomes so big the artery starts to
become narrow and blood flow to the heart becomes restricted. The patient can experience stable
angina when the artery is blocked enough to slightly impede blood flow (however, blood is still able to
get to the heart muscle), but the patient only has the chest pain during ACTIVITY. The activity
increases the heart rate and puts strain on the heart which already has compromised blood flow, but
when the activity STOPS the pain STOPS too.
Collateral circulation can develop if chronic ischemia is experienced. This is where more than one
artery forms to re-route blood to the heart muscle to make up for the decreased blood flow due to
the blockage.
Patients with fatty plaque buildup in the arteries are at risk for the plaques to rupture. This can lead to
coronary thrombosis where clotting material aggregates at the site of rupture and this leads to a
significant or complete blockage of the coronary artery. Patients will have acute coronary syndrome
with unstable angina or experience a myocardial infraction. This is a medical emergency.
Signs and Symptoms of Coronary Artery Disease:
 Many patients are asymptomatic during the early phases of CAD development.
 Chest pain during activity (stable angina…not a medical emergency but patients need to let their
doctor know about this chest pain so diagnostic testing can be performed). The pain may feel
like heaviness on chest….can progress to unstable angina where the patient will have pain at
rest and it is more intense…may not be relieved by Nitroglycerin.
 Shortness of breath: easily gets short of breath during activity because the blood supply is
impeded to the heart muscle.
 Very tired, feeling run down especially with activity
Diagnosed with:
 Blood tests: Lipoprotein profile: total cholesterol, LDL, HDL, triglycerides
 EKG: assesses if there are any changes in the ST segments or t-waves (shows if there is a heart
attack in the progress, previous heart attack, or compromised blood flow)
 A 24 or 48 hour Holter monitor may be ordered to watch the heart rhythm during the
patient’s regular activities of daily living.
 ST segment depression: demonstrates ischemia that is reversible
 ST segment elevation: infarction where there is injury to the heart muscle
 Stress test: monitor the heart rate and rhythm during exercise and see if there are any EKG
changes
 During activity, if blood flow is reduced ST segment depression will occur and patient may
have chest pain and then as activity stops the ST segment will return back to normal. A
patient will probably then be ordered a heart cath to assess where the potential blockage
is located.
 Also, a nuclear stress test may be ordered. This is where a tracer is injected and pictures of
the heart are taken to assess blood flow of the heart muscle during activity.
 Heart Cath: a special catheter is inserted into the femoral or radial artery to assess for blockages
in the artery. Dye is injected into the coronary arteries to assess if they are blocked (coronary
angiography)…moderate sedation is used and the patient breathes on their own.
Cardiac doctor makes the decision if the artery needs:
 PCI (also called angioplasty): Percutaneous Coronary Intervention
 Balloon angioplasty: inflates a balloon in the blocked artery to compress the plaque
against the artery wall and a stent is placed to allow blood to flow back through the artery.
 Atherectomy: removal of plaque from the artery
Sometimes, arteries cannot be stented and the patient will have to have surgery known as coronary
artery bypass graft.
Note: Patients with stable angina will complete a stress test to assess the need for a heart cath. The
most non-invasive testing is performed first to assess the need of more invasive procedures.
Nursing Interventions for CAD
Goal: prevent further progression of CAD
Cholesterol lowering medication:
 Statins “Lipitor, Crestor, Zocor” (goal: LDL less than 100 mg/dL) helps lower LDL, total
cholesterol, lower triglycerides, and increase HDL.
 Educate not to replace diet and exercise
 Notify doctor if they develop muscle pain or tenderness
 Monitor CPK (creatine kinase) levels…. which if elevated it can cause muscle problems
 Monitor liver function because statins act on the liver to block it from producing too much
cholesterol.

Educating patient about treatment, preventive measure, medications, and management Beta blockers:
 Educate the patient about the significance and complications of CAD (discussed in part 1 of this  end in “lol” Propranolol, Metoprolol
series)  lowers heart rate and blood pressure which reduces work load on the heart. This will help
 Modifying lifestyle: decrease episodes of chest pain
 How to manage with diet (low fat, low calorie)  side effects: mask hypoglycemia signs and symptoms like sweating and tachycardia in
 Exercise program diabetics, bradycardia, breathing problems in patients with COPD or asthma, don’t take
 Smoking cessation and why it is important with grapefruit juice
 Weight loss
 Monitoring heart rate and blood pressure ACE inhibitors:
 Signs and symptoms and when to seek help  end in “pril” Lisinopril
 Education about procedures: EKG, stress test, heart cath, lipid profile blood test  blocks the conversion of angiotensin I to angiotensin II which caused vasodilation….lowers blood
pressure…this decreases the workload on the heart.
MEDICATIONS FOR CAD  Side effect: nagging dry cough
Antiplatelet meds: prevent clots from forming or growing which decrease the chances of ischemia
 Aspirin: watching for GI bleeding.
 Plavix: for patients who can’t tolerate Aspirin or just had a stent placed
 Monitor for:
 Thrombotic Thrombocytopenic Purpura (TTP): clotting disorder where clots form in blood
vessels in the body which causes decreased blood flow to vital organs…low platelet count,
neuro changes, bruising, anemia, renal failure, fever
 Will need to discontinue medication for 5-7 days before a planned surgical procedure
because of the increase chance of hemorrhage while taking this drug. Patients need to let
their surgeon know they are taking Plavix because they will be switched to another blood
thinner prior to the surgery. Plavix takes a while to clear in the body’s system.

Nitrates:
 Nitroglycerin: dilates vessels to allow more blood to get the heart muscle
 Educate about how to take: sublingual (underneath the tongue)
 Take right when having chest pain
 Place one tab or one spray under the tongue
 Patient may feel dizzy or hot flushing after taking Nitro. As the nurse, you will need to
monitor their blood pressure because Nitro causes hypotension
 If not relieved in 5 minutes take another dose of Nitro a 2nd dose and
 If not relieved in 5 minutes take another one for a 3rd dose. The patient is NOT to take
more than 3 total doses. If not relieved with the 3rd dose of Nitro the patient needs to call
911.