Cardiovascular

I. Anatomy & Physiology of the Cardiovascular System

1. Structure of the Heart:

 Heart Wall Layers:

o Endocardium – innermost layer lining the chambers
 Chordae tendineae
o Myocardium – muscular middle layer responsible for contractions
o Epicardium – outermost layer
 Coronary Arteries
o Pericardium – protective sac enclosing the heart
 Chambers: Right atrium, right ventricle, left atrium, left ventricle
 Valves:
o Atrioventricular Valves:
 Tricuspid Valve: Between RA and RV
 Mitral (Bicuspid) Valve: Between LA and LV
o Semilunar Valves:
 Aortic Valve: Between LV and aorta
 Pulmonic Valve: Between RV and pulmonary artery

2. Blood Flow Through the Heart:

 Deoxygenated blood enters RA via superior/inferior vena cava → through tricuspid

valve → RV → through pulmonic valve → pulmonary artery → lungs
 Oxygenated blood returns via pulmonary veins → LA → through mitral valve → LV →
through aortic valve → aorta → right/left coronary arteries → systemic circulation

3. Heart Sounds:

 S1 ("Lub"): Closure of the mitral and tricuspid valves, heard best at the apex of the
heart.
 S2 ("Dub"): Closure of the aortic and pulmonic valves, heard best at the base of the
heart.
 S3: (“Kentucky”) Occurs after S2 during early diastole, caused by rapid ventricular
filling. It's often associated with heart failure or volume overload. Best heard at the apex
with the bell of the stethoscope. Can be normal in children and young people.
 S4: (“Tennessee”) Occurs just before S1 in late diastole, caused by atrial contraction
against stiff ventricle. It often indicates conditions like hypertension or myocardial
infarction. Best heard at the apex with the bell of the stethoscope.

4. Coronary Circulation:
  Supplies oxygenated blood to the myocardium
 Left Coronary Artery (LCA): branches into:
o Left Anterior Descending (LAD) artery – supplies anterior wall of LV and
septum
o Circumflex artery – supplies LA and lateral/posterior LV
 Right Coronary Artery (RCA): supplies RA, RV, inferior LV, and often the AV node
and SA node
 Blood drains from the myocardium into the coronary sinus → empties into the RA
o In general, the venous system parallels the arterial
system.
– The great cardiac vein follows the left anterior descending
artery, and the small cardiac vein follows the RCA.
– The veins meet to form the coronary sinus (the largest coronary
vein), which returns blood from the myocardium to the right
atrium.

5. Cardiac Conduction System:

 SA node (sinoatrial): Pacemaker of the heart, 60-100 bpm

o AV node (atrioventricular): Delays impulse, allows atria to contract
 Bundle of His /Right/Left bundle branches (Anterior and Posterior
fascicles)
 Purkinje fibers: Spread impulse through ventricles

* I remember the rates backwards so it’s:

SA node: 100-60

AV: 60-40

Bundle Branches 40-20

6. Cardiac Cycle:

 Systole: Ventricular contraction, blood ejection

 Diastole: Ventricular relaxation and filling
 Cardiac Output (CO): HR x Stroke Volume (SV)
o Key thing to know about this:
 Normal CO=4-8 L/min (its how much blood your heart pumps out in
a minute
 Normal heart rate = 60-100 anything over or under can affect CO
 Normal SV =60-100 mL/beat
 Ex: CO= (HR70)X (SV 70 mL) = (HR 70) x ( SV 0.7 L) = 4.9L
 Make sure to change mL to L. The CO must be in Liters!
 Cardiac output is determined by four major factors: Heart rate, Preload, Afterload, and
Contractility
  One key thing to remember throughout this entire section when talking about any issues
with the heart, the problem comes from either an issue with: pump, container, volume.
o What this means:
 Pump: you heart isn’t pumping good enough (too slow or too fast)
 Container: your blood vessels are too dilated, too constricted, too clogged
up with fat.
 Volume: you’re dehydrated, you’re overhydrated, you’re bleeding out,
etc..
 It all boils down to an issue with one of those three things.

7. Key Terms:

 Preload: Amount of blood in ventricles before contaction (preload= stretch)

o Affected by venous return; if blood volume is low (dehydration),
it falls
o The heart can only contract and stretch so much: think of it like a rubber band,
once it’s stretched so much it doesn’t go back to its original size or work right
anymore, right? The heart is the same way! It’s called Frank Starling Law.
 Technical definition: To a certain point, the greater the blood volume, the
greater the force with which the ventricle contracts. Beyond a certain
volume, however, the heart contracts less effectively. This is
called Starling’s law of the heart.
o Factors that increase preload include increased venous return to
heart and overhydration
o Factors that decrease preload include dehydration, hemorrhage,
and venous vasodilation

 Afterload: Resistance LV must overcome to circulate blood ( afterload= squeeze)

o RV into Lung = low pressure
o LV into Systemic system= arterial pressure= high pressure
 Contractility: Force of ventricular contraction
o the natural ability of the cardiac muscle fibers to shorten during systole.
 The heart has specialized cardiac cells that work together to generate
spontaneous impulse that allow your heart to beat in sync. This being in
sync and working together is called “cardiac automaticity” or
“autorhythmicity”
 HOW IT WORKS:
 SA NODE SAYS CONTRACTS: within milliseconds the
impulse is sent through the rest of the cells and the heart
contracts.
 A lot of irregular heart rhythms happen cause one of
these cells decides it wants to be the main topic of
discussion and starts sending impulses on its own.
Think like A-Fib, when people say they have a
 irregular heartbeat? One of those cells in their heart
is in there acting a fool and causing problems.
 These are called, Ectopic beats.
 Any impulse that doesn’t come from
the SA node is called a Ectopic beat/
 Ejection fraction
o – Normal is greater than 60% and is considered an indication of LV function.
 Mean arterial pressure (MAP)–
o the sum of the systolic blood pressure plus twice the diastolic blood pressure
divided by three. MAP= S+2D /3
 Ex: BP:120/80 MAP= 120+(2(80)) /3 MAP= 93.3 mmHg
o – Normal MAP is 80 to 100.
o – Measures the peripheral tissue perfusion.
 Pulse pressure
o Difference between systolic and diastolic pressures
o Noninvasive measure of cardiac output

Electrocardiography (EKG/ECG) Overview

Horizontal axis measures time
• Vertical axis measures voltage or amplitude
• Isoelectric Line
• Each small square represents 0.04 second on the horizontal axis and 1 mm on the
vertical axis.
• Each large square, bounded by heavy lines, is made up of 5 small squares and
represents 0.20 second and 5 mm.
– 5 large squares or boxes represent 1 full second
– 6 second strip = 30 Large squares

o Rate: Count the # of R waves in a 6 second strip and multiply by 10.

 R waves= ventricle rate
 P waves= atrial rate
 Regularity – measure the interval from one R wave to the next R wave, then
evaluate the rest of the R to R intervals for their regularity.
o Basically, see if there is an even, consistent pattern. When first I
started out learning how to read rhythms they taught us, it’s easy to do
this with an index card/paper. Pick two R waves, mark them on the
index card and then go along the strip and see if all the others line up
with your marks. If they do, then it’s regular, if it sometimes does
(pattern of inconsistency) = regularly irregularly, and if it doesn’t at
all its irregularly irregular.
 • Irregular rhythms may be irregularly irregular (if there is no pattern to the
irregularity) or regularly irregular (if a consistent pattern can be identified).

1. Wave Components:

 P wave: Atrial depolarization, 1st positive deflection

 PR interval: Time between atrial and ventricular depolarization (0.12–0.20 sec)
 QRS complex: Ventricular depolarization (0.06–0.10 sec), second positive deflection
 ST segment: Between depolarization and repolarization; elevation may indicate MI
 T wave: Ventricular repolarization, 3rd deflection
 QT interval: Total ventricular activity (should be < 0.44 sec)
 U-wave: 4th deflection if present – small, rounded, and
usually indicates electrolyte imbalance (hypokalemia)

2. Criteria have been established for interpreting an

ECG strip continued:

 Assess P waves – all the P waves should look alike in size and shape.
 Assess P and QRS complex – there should be one P wave before every QRS complex and one
QRS complex after every P wave.
 Measure PR INTERVAL and QRS COMPLEXES
 Identify abnormalities. – note any ectopic (abnormal) beats, deviation of the ST segment above
or below the baseline, and abnormalities in waveform shape and duration.
 PR Interval:
o is measured from the onset of
the P wave to the beginning of the QRS
complex.
– Normal range – 0.12 to 0.20 second
 QRS complex:
o Measured from the beginning of the QRS to the end of the QRS at the beginning of
the ST segment.
– Normal width falls within the 0.06 to 0.10 second range
 T waves:
o Are the T waves rounded and the same size and shape?
– Do the T waves follow the QRS complexes?
– The T wave represents ventricular relaxation.
– If the QRS complexes are close to the preceding T wave, the ventricles are
contracting prematurely.
– The closer the QRS is to the T wave, the greater the risk for serious ventricular
arrhythmia.– A change in ST segment may indicate myocardial damage.
3. Common Rhythms:

Supraventricular rhythms just mean the impulse that is telling your heart to beat is coming
from above the ventricles (AV node). Supra=above so, above the ventricles. If everything is
working right, it’s the SA node in your atria. That why we call most normal rhythms a
“normal sinus rhythm”.

 The other supraventricular rhythms are when that one or two cells in the heart start
trying to be bossy and sending the own impulses out of order, but they are still
above the ventricles (AV node) (A-Fib, A-Flutter, etc..)

Ventricular rhythms mean your SA node isn’t working right and it can be life threatening.
Your other pacemakers are trying to keep you alive the best they can. ( AV node, Bundle
Branches)

Assess patient before treating any suspected dysrhythmia Don’t just look at
the rhythm Remember: Treat the patient, not the monitor!!!!!!!!

Always check to see if the patient is symptomatic:

No symptoms = no treatment

Symptoms = Treatment

 Normal Sinus Rhythm: 60–100 bpm, regular, normal PQRST

 Sinus Arrhythmia:
o Definition: Normal variation in heart rate that occurs with the respiratory cycle;
HR increases with inspiration and decreases with expiration
 o EKG Features: Regular P waves, consistent PR intervals, varying R-R intervals.
(regular beat, regular beat, extra beat, small pause, regular beat, regular beat, extra
beat, small pause, regular beat, etc..) it still has a normal rhythm/pattern except
that small pause after the extra beat.
o Common in: Children, young adults, and during sleep
o Treatment: None required; considered a normal finding unless symptomatic
(rare). Have patient hold their breath and it will correct itself
 Bradycardia: <60 bpm; assess for symptoms
o HR < 60 bpm
o May cause dizziness, hypotension, syncope
o Treatment: If symptomatic — atropine, pacing, change medications
 Tachycardia: >100 bpm; assess underlying cause
o Usually asymptomatic, but if CO falls and compensatory
mechanisms fail then may have following symptoms:
– Dizziness; Lightheadedness; Fainting (syncope)
– Shortness of breath
– Rapid pulse rate
– Heart palpitations — a racing, uncomfortable or irregular heartbeat or
a sensation of "flopping" in the chest
– Chest pain
o Treatment: Treat underlying cause (e.g., fever, pain, dehydration)
o the treatment goals for tachycardias are to slow a fast heart rate
when it occurs, prevent future episodes and minimize complications.
– Treat cause
– Vagal maneuvers.
– Medications to slow heart rate – beta-adrenergic blockers, such as
metoprolol (Lopressor) and atenolol (Tenormin), and calcium channel
blockers such as verapamil (Isoptin)

 Premature Atrial Contractions (PACs):

o Early P wave, usually followed by normal QRS
o Often asymptomatic; may feel skipped beat
o Treatment: Usually not needed; treat underlying causes (stress, caffeine, etc.)
 BIG DIFFERENCE between PAC and PVC: a PAC the heat still send
blood out because both the atria and ventricles respond. SO this one isn’t
as serious.

 Atrial Fibrillation: Irregularly irregular rhythm, no identifiable P waves

o Irregularly irregular, no P waves can be acute or chronic
o Palpitations, fatigue, dizziness, decreased BP, weakness, confusion
o Treatment: Anticoagulants (e.g., warfarin), rate control (beta blockers, calcium
channel blockers), amiodarone, cardioversion, catheter ablation
o Main goals: rate control, clot prevention, stroke prevention, treat underlying
cause.
 Atrial Flutter:
o Sawtooth flutter waves, regular or irregular
  Usually regular with sawtooth appearance of P waves; Atrial rate
240+bpm; ventricular rate<150 bpm
o May feel palpitations, fatigue, weakness, anxiety, shortness of breath
o Treatment: Like Afib – rate control, anticoagulants, cardioversion
 Medication to slow ventricular response – digoxin and calcium channel
blockers

 Ventricular Tachycardia: Wide QRS, regular rhythm, no P waves

o Wide QRS, regular rhythm, no P waves
o May have pulse or be pulseless
o Treatment:
 With pulse — amiodarone, synchronized cardioversion.
 Without pulse — CPR, defibrillation
 Ventricular Fibrillation:
o No organized activity, no pulse
o Sudden Collapse
o Treatment: Immediate defibrillation, CPR, ACLS
 Asystole: Flatline, no electrical activity
o Unresponsive, no pulse
o Treatment: CPR, epinephrine, check leads (no defibrillation)
 Premature Ventricular Contractions (PVCs):
o Wide, bizarre QRS not preceded by P wave
o May feel palpitations or thump in chest
o Treatment: Monitor frequency; treat cause (electrolytes, ischemia); may use beta
blockers
 Bigeminy and Trigeminy:
 Bigeminy: A pattern in which every other beat is PVC
 EX: Normal Beat - PVC - normal beat - PVC.
 Trigeminy: A pattern in which every third beat is a PVC
 EX: normal - normal - PVC - normal - normal – PVC

Remember the heart isn’t pumping out blood with a PVC, so the more frequent the PVCs
occur, the more dangerous they are!

 Paced Rhythm:
o Visible pacer spikes before P and/or QRS depending on chamber paced
o Regular rhythm

Cardioversion vs. Defibrillation:

 Cardioversion:
o Used for: Unstable atrial fibrillation, atrial flutter, SVT, and VT with a pulse
o Delivery: Synchronized with the R wave to avoid shocking during T wave (risk
of R-on-T and VF) TURN ON THE MF’ING SYNC BUTTON!!!!!! Or you will
 literally kill your patient. Like dead. Be good at CPR if you forget to turn on the
sync button.
o Sedation: Usually required
o Elective procedure (supposedly)
o Energy levels: Lower (50–200 J depending on rhythm and machine)
 Defibrillation:
o Used for: Pulseless VT and ventricular fibrillation (VF)
 Delivers electrical shock to reset the heart’s rhythm
o Delivery: Unsynchronized (delivered immediately) they ain’t getting any deader!
 AED, Automatic Implantable Cardioverter-
Defibrillator (AICD)
o Sedation: Not required (used in cardiac arrest)
o Energy levels: Higher (200–360 J depending on machine)
o Emergency Procedure

** The only two shockable rhythms: Ventricular Fibrillation (V-Fib) and Pulseless
Ventricular Tachycardia (V-Tach)

4. Sudden Cardiac Death:

 Defined as death occurring within 1 hour of the onset of cardiac symptoms

– Usually caused by V-Fib and cardiac arrest
o CPR & Early Defib!
 Coronary heart disease is most common cause in U.S.
 Teach family about benefits of knowing CPR, Risk factors, and advanced directives.
 Causes: Coronary artery disease, previous MI, cardiomyopathy, electrolyte imbalances,
congenital heart defects, drug use/overdose
 Prevention (for high-risk patients):
o Implantable Cardioverter Defibrillator (ICD)
o Medication management (e.g., beta blockers, antiarrhythmics)
o Lifestyle modifications and cardiac rehab

5. Diagnostic Tests for the Heart:

 Electrocardiogram (ECG/EKG): Detects arrhythmias, ischemia, infarction, electrolyte

imbalances
 Echocardiogram: Ultrasound to visualize heart structure and function (valve function,
ejection fraction, wall motion)
 Chest X-ray: Shows heart size, shape, and pulmonary congestion
 Holter Monitor: Portable ECG monitoring over 24–48 hours to detect intermittent
arrhythmias
  Telemetry: Continuous ECG monitoring for real-time rhythm observation in hospitalized
patients
 Transesophageal Echocardiogram (TEE): Specialized echo using a probe in the
esophagus to view posterior heart structures more clearly
 Implantable Loop Recorder: Long-term ECG monitoring implanted
under the skin to detect sporadic arrhythmias, particularly useful for
unexplained syncope
 Cardiac Catheterization/Angiography: Invasive test to visualize
coronary arteries, assess blockages, measure pressures, obtain
biopsies
 MRI/CT Scan of the Heart: Detailed images for congenital
abnormalities, tumors, pericardial disease, or aortic dissection
 MUGA Scan (Multigated Acquisition Scan): Nuclear medicine test
that evaluates the function of the ventricles, especially ejection
fraction, using radioactive tracers and a gamma camera
 Stress Test (Exercise or Pharmacologic): Evaluates cardiac
response to increased workload; identifies ischemia
o For Pharm: Vasodilator drug is administered which may cause
ischemia in areas of the heart affected by CHD much like
exercise does.
 Drug: Dipyridamole (Persantine)
o It can produce false negatives and positive results:
 Negative results don’t always rule out heart disease
 Positive results don’t always mean heart disease.
 Alcohol will produce false positive, so don’t drink
before.

 Exercise Perfusion Imaging Stress Test: A nuclear medicine stress test using a
radiotracer (e.g., thallium or sestamibi) to assess blood flow to the heart muscle during
rest and exercise. It highlights areas of reduced perfusion (ischemia) or prior infarction.
o “Cold spots” found while reading results indicate lack of blood
flow to that area.
 Atherectomy: A catheter-based procedure used during cardiac
catheterization to remove atherosclerotic plaque from blood vessels.
Often used to treat peripheral artery disease or coronary artery disease
when plaque is calcified or difficult to stent.

6. Lab Tests:
Test Normal Peak Time Return to Clinical
Range Normal Relevance
Time
BNP (B-type <100 pg/mL 12-24 hours 3-5 days Elevated in
natriuretic (varies with after onset of (depending heart failure,
peptide) age and sex) heart failure on the cause) useful for
symptoms diagnosing
and
assessing
severity.
ANH (Atrial <50 pg/mL 1-2 hours 2-4 hours Released
natriuretic (varies by after atrial after from atria in
hormone) assay distension normalization response to
method) volume
expansion or
atrial stress.
LDH-1 13-22 U/L 12-48 hours 5-10 days Specific for
(Lactate after (slower myocardial
dehydrogena myocardial decline) infarction
se 1) injury (MI), often
used
alongside
other
markers.
LDH-2 12-22 U/L 12-48 hours 5-10 days Less specific
(Lactate after (slower than LDH-1,
dehydrogena myocardial decline) used to track
se 2) injury myocardial
damage.
CPK-MB 0-3 ng/mL 4-6 hours 1-3 days Specific for
(Creatine after myocardial
kinase MB) infarction injury, rises
quickly after
MI, and
returns to
normal in 48-
72 hours.
Troponin T <0.01 ng/mL 3-12 hours 5-14 days Highly
(cTnT) after (can be specific and
myocardial prolonged) sensitive for
injury myocardial
injury,
especially for
detecting
early MI.
Troponin I <0.03 ng/mL 3-12 hours 5-14 days Highly
(cTnI) after (can be specific for
myocardial prolonged) myocardial
injury injury, used
as a
definitive
marker for
MI.
Myoglobin 25-72 ng/mL 1-4 hours 24 hours Released
after early after
myocardial muscle
injury damage, not
specific to
cardiac injury
(also
elevated in
skeletal
muscle
injury).
C-reactive <3 mg/L 6-12 hours 1-2 weeks Indicates
protein (CRP) after acute (depending inflammation
inflammation on cause) , elevated in
cases of
acute
myocardial
injury or
infection.
Lipids:

Test Normal Range Clinical Relevance

Total Cholesterol <200 mg/dL Elevated total
cholesterol can
increase the risk of
atherosclerosis and
coronary artery disease
(CAD).
LDL (Low-Density <100 mg/dL (optimal), "Bad" cholesterol, high
Lipoprotein) 100-129 mg/dL (near levels increase the risk
optimal), 130-159 of plaque buildup in
mg/dL (borderline arteries and lead to
high), 160-189 mg/dL CAD.
(high), ≥190 mg/dL
(very high)
HDL (High-Density >40 mg/dL (men), >50 "Good" cholesterol,
Lipoprotein) mg/dL (women) helps remove LDL from
arteries. High levels are
protective against heart
disease.
Triglycerides <150 mg/dL Elevated triglycerides
can indicate metabolic
syndrome, diabetes,
and increase
cardiovascular risk.
VLDL (Very Low-Density 2-30 mg/dL (varies by Often calculated as 1/5
Lipoprotein) individual and lab) of the triglyceride level.
Elevated VLDL is
associated with
increased risk of
cardiovascular disease.
Total/HDL Ratio <5:1 A higher ratio suggests
an increased risk of
heart disease. Lower is
better.

Clinical Significance:

 Total Cholesterol: It’s a sum of all types of cholesterol, and while

total levels matter, the distribution (LDL, HDL) is more indicative of
cardiovascular health.

 LDL: A primary target for therapy in patients at risk for cardiovascular

disease.
 o Statins are commonly prescribed to lower LDL levels.

o LDL carry lipids towards arteries

o Lethal fats.

 HDL: Higher levels are protective and help in the reverse transport of
cholesterol from the arteries to the liver.

o HDLs carry lips away from arteries.

o Heathy fats.

 Triglycerides: Often elevated in patients with uncontrolled diabetes,

obesity, or excessive alcohol consumption, contributing to a higher risk
of heart disease.

 VLDL: Like LDL, contributes to plaque buildup in the arteries and is

linked with atherosclerosis.

 Total/HDL Ratio: A more comprehensive way of evaluating the

balance between total cholesterol and HDL levels.

Other Test:

 CBC – basic screening test

 Coagulation Baseline Study
 ABG (arterial blood gas)

7. Pacemakers:

Temporary Pacemakers

Temporary pacemakers are used for short-term treatment to restore a normal heart rhythm. They
are typically used in emergency situations or until the heart's rhythm stabilizes.

 Transvenous Pacemaker:
o Placement: The pacemaker lead is inserted through a vein (typically the
subclavian or femoral vein) into the heart's right ventricle.
o Use: Used when immediate pacing is needed due to arrhythmias like heart block,
bradycardia, or during post-operative recovery.
 Transcutaneous Pacemaker:
o Placement: Electrodes are placed on the chest wall, and electrical impulses are
delivered through the skin.
o Use: Often used as an emergency measure when there is a complete heart block or
other arrhythmias that require immediate pacing.
  Epicardial Pacemaker:
o Placement: Leads are placed directly on the surface of the heart, usually during
open heart surgery.
o Use: This pacemaker is temporary and used after certain types of heart surgeries
or during complications like post-cardiac surgery arrhythmias.

Permanent Pacemakers

Permanent pacemakers are implanted for long-term management of heart rhythm issues. These
pacemakers are intended to remain in place for the duration of the patient's life or until
replacement.

 Single-Chamber Pacemaker:
o Placement: One lead is inserted, typically into the right ventricle. The pacemaker
delivers impulses to either the atrium or ventricle, depending on the type.
o Use: Often used for patients with bradycardia or other conduction defects that
affect the heart’s rhythm.
 Dual-Chamber Pacemaker:
o Placement: Two leads are placed – one in the right atrium and one in the right
ventricle. This allows the pacemaker to coordinate the activity between the atrium
and ventricle.
o Use: Used for patients with atrioventricular (AV) block or other conduction
abnormalities that affect the synchrony between atrial and ventricular contraction.

Pacemaker Placement Considerations:

 Surgical Procedure: Permanent pacemakers are typically implanted under local

anesthesia in the upper chest. The leads are passed through veins and connected to the
pacemaker device.
 Battery Life: Permanent pacemakers can function for several years (typically 5-15
years), depending on usage.
 Infection Prevention: Care must be taken to avoid infection at the lead insertion site,
particularly in the case of permanent pacemaker placement.

Key Considerations:

 Indications for Use: Pacemakers are often indicated for bradyarrhythmias, AV blocks, or
other rhythm disturbances that are not responsive to medication or other interventions.
 Post-Procedure Care: After implantation, patients are monitored for any complications,
including infection, lead displacement, and proper device function.
 Precautions around:
– Cellular phones.
– Security systems.
– Medical equipment.
– Power-generating equipment.
8. Coronary Artery Disease (CAD)

 Pathophysiology: CAD is a condition where the coronary arteries (the blood vessels that
supply the heart muscle with oxygen-rich blood) become narrowed or blocked due to a
buildup of atherosclerotic plaques.
 Causes: Atherosclerosis, where plaques of fatty deposits, cholesterol, and other
substances narrow the coronary arteries.
 Signs and Symptoms:
o Chest pain (angina)
o Shortness of breath
o Fatigue
o Palpitations
o Dizziness or fainting
 Clinical Manifestations Reasons:
o Angina: Chest pain or discomfort that occurs when the heart muscle doesn't get
enough oxygenated blood. Can be stable or unstable (discussed later).
o Fatigue: Caused by reduced oxygen supply to the heart, making it harder for the
heart to pump efficiently.
o Shortness of breath: Often seen when the heart is unable to pump efficiently due
to inadequate blood flow.
o Palpitations and dizziness: Can occur due to arrhythmias triggered by ischemia.

9. Myocardial Infarction (MI)

 Pathophysiology:
o MI occurs when a coronary artery becomes acutely blocked by a thrombus (blood
clot), leading to the complete blockage of blood flow to a part of the myocardium.
This causes ischemia and necrosis of the heart muscle.
o STEMI: Involves a complete blockage of a coronary artery, leading to significant
myocardial injury. This is detected on an ECG by ST-segment elevation.
o NSTEMI: Involves partial blockage or transient blockage, causing less severe
myocardial damage. It is often associated with ST-segment depression or T-
wave inversion.
 Complications:
o Arrhythmias (e.g., ventricular fibrillation, ventricular tachycardia)
o Heart failure (due to loss of myocardial function)
o Cardiogenic shock (when the heart is unable to pump blood effectively)
o Pericarditis (inflammation of the pericardium)
o Thromboembolism (clot breaking off and traveling elsewhere)
 Management:
o Thrombolytics (e.g., alteplase) can dissolve the clot in STEMI patients if PCI
(Percutaneous Coronary Intervention) is not available.
o PCI: Preferred method in STEMI to reopen the blocked artery using angioplasty
or stenting.
 o Antiplatelets (aspirin, clopidogrel) to prevent clot reformation.
o Anticoagulants (heparin, enoxaparin) to reduce further clot formation.

10. Types of Angina

Cardiac cells are viable for 20 minutes before irreversible damage or infarction takes place

 Stable Angina:
o Pathophysiology: Caused by a fixed atherosclerotic plaque obstructing coronary
blood flow. It usually occurs during physical exertion, stress, or emotional
distress. GOES AWAY WITH REST AND/OR MEDS
o Management:
 Nitroglycerin: Sublingual or oral nitrate to relieve symptoms.
 Beta-blockers: Decrease heart rate and myocardial oxygen demand.
 Calcium channel blockers: Can be used for vasodilation.
 Aspirin: To prevent clot formation.
 Unstable Angina:
o Pathophysiology: Occurs when a plaque ruptures or when there is a temporary
reduction in blood flow due to a clot, causing worsening symptoms. DOES NOT
GO AWAY WITH REST AND/OR MEDS.
o Management:
 Immediate hospitalization: To rule out MI.
 MONA (Morphine, Oxygen, Nitroglycerin, Aspirin).
 Nitro: 0.4mg Sublingual every 5 mins for a Max of 3 doses
 AFTER 15 MINS UNRELIEVED CHEST PAIN CALL
911/ GO TO ER.
 Antiplatelet therapy and possibly thrombolytics or PCI for severe cases.
 Prinzmetal's Angina (Variant Angina):
o Pathophysiology: Caused by a spasm in the coronary artery, which leads to
temporary narrowing and ischemia. Can occur without atherosclerotic plaque. It
usually happens at night. It happens roughly around the same time every night.
o Management:
 Calcium channel blockers: Help relieve spasm and dilate the coronary
arteries.
 Nitrates: Can also be used to reduce coronary artery spasm.

11. Atherosclerosis

 Pathophysiology:
o It begins with endothelial injury from factors like hypertension, smoking, high
LDL cholesterol, or diabetes. This injury causes the attraction of inflammatory
cells that ingest lipids and form foam cells.
o A chronic inflammatory disease in which plaques of fatty substances, cholesterol,
and cellular waste accumulate on the inner walls of arteries.
 o Stages:
 Endothelial injury: Damage to the inner lining of the artery due to factors
like high blood pressure, smoking, and high cholesterol.
 Fatty streak: Accumulation of lipids in the artery wall.
 Plaque formation: The fatty streak forms a hard plaque, narrowing the
artery.
 Plaque rupture and clot formation: A ruptured plaque leads to clot
formation, which can completely block the artery.
 Prevention:
o Lifestyle modifications: Healthy diet, exercise, smoking cessation.
o Medications: Statins (to lower cholesterol), antihypertensives, and antidiabetic
agents.

12. Collateral Circulation

 Pathophysiology:
o Collateral circulation refers to the development of smaller, alternative blood
vessels (capillary vessels or microvessels) to bypass blocked or narrowed
coronary arteries.
o This development is typically gradual and occurs in response to chronic ischemia,
ensuring continued blood flow to the myocardium.
 Clinical Significance:
o Collateral circulation can help reduce the severity of MI and improve patient
outcomes by supplying blood to areas of the heart that might otherwise be
ischemic.
o Patients with longstanding CAD or those who have chronic ischemia may benefit
from better collateral circulation, which can improve prognosis.

13. Changeable and Unchangeable Risk Factors

 Changeable Risk Factors:

o High blood pressure: Causes damage to the endothelium, leading to
atherosclerosis. Management includes antihypertensive medications (e.g., ACE
inhibitors, diuretics).
 Dietary Approaches to Stop Hypertension (DASH)
o High cholesterol: Increases the likelihood of plaque formation in arteries. Statins
help lower LDL cholesterol.
o Smoking: Increases carbon monoxide levels, damages the endothelium, and
raises blood pressure. Smoking cessation significantly reduces CAD risk.
o Diabetes: Increases risk due to hyperglycemia's effect on vascular health. Tight
glucose control with insulin or oral agents is essential.
o Obesity/Sedentary Lifestyle: Routine physical activity can lower many CHD
risk factors, including LDL.
  Maintain a Healthy Weight - can lower your risk for CHD.
– A general goal to aim for is a body mass index
(BMI) of less than 25
o Metabolic syndrome: refers to a cluster of risk factors that increase the
likelihood of developing cardiovascular disease and type 2 diabetes. It's a
significant risk factor for atherosclerosis and CAD, contributing to the
progression of coronary artery blockages.
 Abdominal obesity: Central or visceral fat accumulation is a primary
characteristic, often measured by waist circumference (greater than 40
inches for men and 35 inches for women)
 Abdominal obesity is particularly dangerous because visceral fat (fat
around the organs) is metabolically active and contributes to
inflammation, increasing the risk of endothelial dysfunction and
atherosclerosis.
o Elevated homocysteine levels have been recognized as an independent risk factor
for cardiovascular disease, including CAD and MI.
 Elevated homocysteine can:
 Injure the endothelium of blood vessels, leading to increased
plaque formation and arterial stiffness.
 Enhance clot formation: Elevated homocysteine levels may
increase the risk of thrombosis (blood clots), which could result in
MI or stroke.
 Promote oxidative stress: High homocysteine levels increase
oxidative stress, which damages blood vessels and accelerates the
progression of atherosclerosis.

Change the way you eat:

Follow a Healthy Diet - Following a healthy diet can prevent or reduce high blood pressure and
high blood cholesterol and help you maintain a healthy weight.
• For patients with high blood cholesterol includes a healthy diet, physical activity, and weight
management.
– Diet with less than 7 percent of your daily calories should come from saturated fat.
– No more than 25 to 35 percent of your daily calories should come from all fats, including
saturated, trans, monounsaturated, and polyunsaturated fats.
– Should have less than 200 mg a day of cholesterol.
– Foods high in soluble fiber also are part of a healthy diet. They help prevent the digestive tract
from absorbing cholesterol.
– A diet rich in fruits and vegetables can increase important cholesterol-lowering compounds in
your diet.
– A healthy diet also includes some types of fish, such as salmon, tuna (canned or fresh), and
mackerel.
– Limit the amount of sodium
– Try to limit drinks that contain alcohol
  Unchangeable Risk Factors:
o Age: The risk increases with age, particularly after 45 years for men and 55 years
for women.
o Gender: Men are at higher risk earlier in life, but women’s risk increases post-
menopause.
o Family history: A family history of premature coronary artery disease (before 55
years in men or 65 years in women) significantly increases the risk.

14. Pharmacological Management of CAD and MI

 Antiplatelet Agents:
There are two classes of antiplatelet agents: glycoprotein
platelet inhibitors and platelet aggregation inhibitors.
– These drugs work by different mechanisms to inhibit platelet
function
o Platelet aggregation inhibitors –
 Mechanism: work in different places of the clotting cascade and prevent
platelet
adhesion, therefore no clot formation.
 Examples:
– Aspirin
– Pletal (cilostazol)
– Plavix (clopidogrel)
– Persantine (dipyridamole)
– Aggrenox (aspirin/dipyridamole)
– Ticlid (ticlopidine)
o Glycoprotein platelet inhibitors –
 Examples:
Generic Name: tirofiban; Brand Name: Aggrastat
– Generic Name: eptifibatide; Brand Names: Integrilin
– Generic Name: abciximab; Brand Names: ReoPro

 Heparin:
o given in acute phase of angina.
– Anticoagulant to prevent thrombus formation.

 Calcium Channel Blockers:

o Mechanism: to reduce coronary vasospasm and to depress the myocardium,
thereby reducing the oxygen consumption and workload of the heart
o Examples:
 Nifedipine (Procardia)
 Diltiazem (Cardizem)
 Verapamil (Calan)
 Amlodipine (Norvasc)
 Felodipine (Plendil)
 o Indications: Used to relieve angina by dilating coronary arteries and reducing
myocardial oxygen demand.
o Side effects: Hypotension, dizziness, edema, constipation.
 ACE Inhibitors:
o Mechanism: Reduces blood pressure by blocking the conversion of angiotensin I
to angiotensin II (which dilates blood vessels) so these meds reduce afterload
o Examples:
 Lisinopril, enalapril
o Indications: Used in heart failure and post-MI to prevent ventricular remodeling.
 Beta Blockers:
o Mechanism: Decrease heart rate and myocardial oxygen demand by blocking
beta-adrenergic receptors. (slow heart rate and decrease blood pressure)
o Examples: Metoprolol, atenolol.
o Indications: Used in stable angina, MI, and post-MI to prevent arrhythmias and
reduce mortality.
o Contraindicated: Asthma and COPD because it can cause bronchoconstriction.
 Nitroglycerin:
o Mechanism: Relaxes smooth muscle in coronary arteries, improving blood flow
and relieving chest pain. Vasodilator that opens the coronary arteries and
increases blood flow to the heart.
o Indications: Acute management of angina and MI.
o Sublingual tablets every 5 minutes max of 3 doses
 Longer acting nitroglycerin preparations include
oral tablets, ointment, transdermal patches and IV solutions.
o Side effects: flushing of the skin, increase in pulse and respirations, hypotension,
nausea, dizziness, and headache.
 Digoxin:
o Mechanism: Increases the force of myocardial contraction and decreases the
heart rate.
o Indications: Used in heart failure and atrial fibrillation.
o Signs of Toxicity: N/V, visual disturbances (yellow/green halos), arrhythmias.
 Therapeutic level: 0.8-2.0 ng/mL
 Toxic level: >2.0 ng/Ml
 Antidote: digoxin immune Fab (Digibind) is used in
extreme toxicity
 Advise client to eat foods high in potassium, such as
oranges, bananas, fruit juices, vegetables, and potatoes if taking
loop diuretics

o Check: Apical pulse before administering (hold if <60 bpm).

o
 Statins
o Action: reduce LDL by reducing cholesterol synthesis
o Examples: atorvastatin, simvastatin
o Use: Hyperlipidemia, CAD prevention.
 o Monitor: Liver function, CK levels (myopathy risk) myalgias (muscle aches) or
skin rashes may also develop
– Rhabdomyolysis – lethal breakdown of skeletal muscle
 Fibrates
o Examples: gemfibrozil, fenofibrate
oAction: lowers triglycerides and VLDL
oUse: Hypertriglyceridemia.
oCaution: Risk of myopathy with statins
 Combo Drugs:
o Examples:
 Antilipemic - ezetimibe (Zetia)
 ezetimibe +simvastatin (Vytorin)
– Acts on cells in the small intestine to block
cholesterol absorption, thereby reducing levels of
total cholesterol, LDL, and triglycerides

 Omega-3 Fatty Acids

o Source: Fish oil supplements or diet, Flax and flaxseed oil, walnuts,
canola oil, soybeans and soybean oil.
o Action: decrease triglycerides, anti-inflammatory properties.
o Use: Adjunct to diet in hypertriglyceridemia

15. Management and Care of Acute MI

 AMI or MI is when cells in an area of cardiac muscle infarct or necrose (die) due to lack
of blood and oxygen.
 Most deaths from AMI occur within the first hour after the onset of manifestations, often
before the patient reaches the hospital.
 The severity of the MI depends on several factors, including location, size, collateral
circulation, and time of onset to treatment.
 MI usually affects the left ventricle because it is the major “workhorse” of the heart; its
muscle mass is greater, and it needs more oxygen.
 Also classified as either transmural or subendocardial.
– Transmural infarction affects all layers of the heart
– Subendocardial infarction involves only the inner layer of the heart and does not
extend through the myocardium and epicardium.
Infarct Location Coronary Artery ECG Leads with
Involved Changes
Anterior wall Left Anterior Descending V1, V2, V3, V4
(LAD)
Septal wall Left Anterior Descending V1, V2
(LAD)
Lateral wall Left Circumflex (LCX) I, aVL, V5, V6
Inferior wall Right Coronary Artery II, III, aVF
(RCA)*
Posterior wall RCA or LCX V7–V9** (posterior
leads), reciprocal
changes in V1–V3
Right ventricle Proximal RCA V4R** (right-sided lead)

Remember: I See All Leads

Inferior : leads II, III, avF

Septal: leads v1-v2

Anterior: leads v3-v4

 Lateral: leads v5-v6 , lead 1, aVL

 Signs/Symptoms: Although chest pain or pressure is the most common

symptom of a heart attack, heart attack victims may
experience a variety of symptoms including:
o Pain, fullness, and/or squeezing sensation of the chest
o Jaw pain, toothache, headache
o Shortness of breath, dyspnea
o Nausea, vomiting, and/or general epigastric (upper middle abdomen) discomfort
o Sweating; cool, clammy skin
o Heartburn and/or indigestion
o Arm pain (more commonly the left arm, but may be either arm)
o Upper back pain
o General malaise (vague feeling of illness)
o No symptoms (Approximately one quarter of all heart attacks
are silent, without chest pain or new symptoms. Silent heart attacks are
especially common among patients with diabetes mellitus.)
 Tend to happen between 4:00 A.M. and 10:00 A.M. because of the higher blood
levels of adrenaline released from the adrenal glands during the morning hours

 Acute Care:
o Rapid evaluation of ABCs first
• Assess the pain
• Check for risk factors for CAD
• Quick examination of the heart and lungs.
 • Time is critical in limiting damage and preventing complications!!!! Time is
muscle. The more time wasted the more muscle dies.
o MONA for initial stabilization.
o Start 2 or 3 LARGE bore IVs.
o Thrombolytic therapy for patients who present early and meet criteria.
 Clot-Busting Medicines – Thrombolytic medicines, also called "clot
busters," or Fibrinolytic agents are used to dissolve blood clots that are
blocking the coronary arteries.
 Streptokinase (Streptase), anistreplase, and tissue plasminogen
activator (TPA) such as alteplase are currently used to attempt
reperfusion.
 Contraindications: Absolute:
 Active internal bleeding
 Trauma or surgery within past 2 weeks
 HTN that does not resolve with pain control
 Recent head trauma or known tumor
 Stroke within past 6 months
 Pregnancy
 Allergy to drug
 Contraindications: Relative:
 Trauma or surgery within past 2 months
 Chronic severe HTN
 Active peptic ulcer disease
 Hx of stroke, tumor, head injury
 Known bleeding problems
 Use of anticoagulants
 Exposure to agents made from Streptococcus bacteria
 Central IV lines
o PCI for immediate revascularization of the affected artery.
o Continuous ECG monitoring to detect arrhythmias.
o Pain management: Morphine for pain relief and anxiety reduction.
 Nursing Interventions:
o Monitor vital signs (heart rate, blood pressure, oxygen saturation) and pain
(level of chest pain).
o Administer prescribed medications (e.g., nitroglycerin, morphine).
o Patient education: On medications, lifestyle changes (diet, exercise, smoking
cessation), and recognizing symptoms of recurrent angina or MI.
 Post-MI Care:
o Cardiac rehabilitation: A structured program that includes physical activity, diet
changes, and education about heart disease management.
o Long-term medications: Continue antiplatelet therapy, beta-blockers, ACE
inhibitors, and statins to prevent further events.
 Heart attack complications are often related to the damage done to your heart during a
heart attack.
o This damage can lead to the following
conditions:
– Abnormal heart rhythms (arrhythmias).
 – Heart failure
– Heart rupture.
– Valve problems.
o Pericarditis (inflammation of the pericardium) may develop after an AMI, usually
within 2 to 3 days.
o Approx. 10% of clients experience extension or expansion of the MI within 10 to
14 days.

 Diagnostic Test:
o 12-lead ECG is completed and is the most important study to be done
– Characteristic changes in the ECG with an acute MI include:
 Inversion of the T wave
 Depression or Elevation of the ST segment
 Formation of a Q wave
o Serum creatine kinase (CK) and cardiac-specific troponins are most specific for
diagnosis of AMI
o CBC – an elevated WBC count of 12,000 to 15,000/mm3 is associated with
severe infarcts
o ESR – rises during the first week and may remain elevated for several weeks
o Chest X-ray
o Echocardiography
o Myocardial perfusion imaging scans
o Coronary angiogram: This test can show if your
coronary arteries are narrowed or blocked.

16. PTCA (Percutaneous Transluminal Coronary Angioplasty)

 Definition: A non-surgical procedure that uses a balloon-tipped catheter to open

narrowed or blocked coronary arteries.
 Purpose: Restore blood flow to myocardium during/after MI or in CAD.
 Procedure:
o Catheter inserted via femoral or radial artery → advanced to coronary arteries.
o Balloon inflated at site of occlusion → compresses plaque and widens artery.
 Nursing Care:
o Monitor for bleeding, hematoma at insertion site.
o Bedrest with leg straight (if femoral).
o Assess distal pulses and neurovascular status.
o Monitor for chest pain (could indicate re-occlusion).

17. Coronary Artery Stents

  Definition: Metal mesh tubes inserted into coronary arteries during PTCA to keep them
open.
 Types:
o Bare-metal stents
o Drug-eluting stents (release medication to prevent restenosis)
 Post-care:
o Antiplatelet therapy (e.g., aspirin + clopidogrel) to prevent stent thrombosis.
o Monitor for signs of restenosis (recurrent angina).
o Regular follow-ups and medication compliance are critical.

18. CABG (Coronary Artery Bypass Grafting)

 Definition: Surgical procedure that bypasses blocked coronary arteries using grafts (e.g.,
saphenous vein, internal mammary artery).
 Indications:
o Multiple vessel disease
o Left main coronary artery stenosis
o Failed medical or interventional therapy
 Procedure:
o Performed via median sternotomy, often using cardiopulmonary bypass (heart-
lung machine).
 Post-op Care:
o Monitor for arrhythmias, bleeding, infection.
o Respiratory support: IS, cough/deep breathing.
o Pain management and mobility encouragement.
o Cardiac rehab initiation.

19. MIDCAB (Minimally Invasive Direct Coronary Artery Bypass)

 Definition: A less invasive CABG done through small chest incisions without stopping
the heart.
 Used For: Single or double vessel disease (especially left anterior descending artery).
 Advantages:
o Less trauma, shorter hospital stay, quicker recovery.
 Limitations:
o Not suitable for multi-vessel disease.
 Nursing Considerations:
o Less intensive recovery, but similar monitoring for complications.
20. Intra-Aortic Balloon Pump (IABP)

 Definition: A mechanical device inserted into the aorta that inflates and deflates in sync
with the cardiac cycle.
 Purpose:
o Reduces afterload and improves coronary perfusion.
o Used temporarily in severe left ventricular dysfunction, cardiogenic shock, or
post-MI.
 Mechanism:
o Inflates during diastole (pushes blood into coronary arteries).
o Deflates before systole (reduces resistance to ejection).
 Nursing Care:
o Monitor for limb ischemia (check pulses).
o Maintain patient supine or with minimal HOB elevation.
o Strict aseptic technique; monitor for infection and bleeding.

21. Ventricular Assist Devices (VADs)

 Definition: Mechanical pumps that assist heart function and blood flow in patients with
severe heart failure.
 Types:
o LVAD: Assists the left ventricle.
o RVAD: Assists the right ventricle.
o BiVAD: Supports both ventricles.
 Indications:
o Bridge to transplant.
o Destination therapy (for non-transplant candidates).
 Nursing Care:
o Monitor for bleeding, infection, thromboembolism.
o Assess for proper functioning (device alarms, flow rates).
o Educate on battery management and driveline care.

22. Cardiac Rehabilitation

 Definition: A medically supervised program to help cardiac patients recover and improve
health/function after cardiac events.
 Phases:
1. Phase I (Inpatient): Begins during hospitalization; includes early mobility and
education.
2. Phase II (Outpatient): Supervised exercise, risk factor modification, nutritional
counseling.
 3. Phase III (Maintenance): Long-term maintenance, unsupervised exercise and
lifestyle changes.
 Goals:

o Improve cardiovascular fitness.

o Reduce recurrence of cardiac events.
o Promote psychological well-being.

 Components:

o Exercise training
o Nutritional guidance
o Stress management
o Smoking cessation
o Medication adherence education

23. Heart Failure

 Definition: Heart failure is a syndrome in which the heart is unable to pump enough
blood to meet the metabolic needs of the body. It results in inadequate tissue perfusion
and fluid volume overload.

 Causes (Etiology):

 Coronary artery disease (CAD) – most common

 Hypertension
 Myocardial infarction (MI)
 Cardiomyopathy
 Valve disorders
 Dysrhythmias
 Infections (e.g., myocarditis)
 Chronic lung disease
 Diabetes mellitus
 Substance abuse (alcohol, cocaine)

Type Definition Common Causes Symptoms

Failure of the left
Left-sided Dyspnea, orthopnea, crackles,
ventricle to pump CAD, MI, HTN
HF fatigue, cough, frothy sputum
effectively
Failure of the right
Right-sided Left-sided HF, COPD, Peripheral edema, ascites, JVD,
ventricle to pump
HF pulmonary hypertension hepatomegaly
effectively
Ventricles cannot contract
Systolic HF MI, dilated cardiomyopathy ↓Ejection fraction (<40%)
forcefully
Type Definition Common Causes Symptoms
Diastolic Ventricles cannot relax Aging, HTN, LV Normal EF but signs of HF
HF and fill hypertrophy present
Sudden onset, often due to Pulmonary edema, respiratory
Acute HF MI, acute valve rupture
MI or fluid overload distress
Chronic Long-term condition, Ongoing symptoms, frequent
HTN, CAD
HF typically progressive exacerbations

Left-sided HF

Left = Lungs

 Dyspnea on exertion (DOE)

 Orthopnea, paroxysmal nocturnal dyspnea (PND)
 Pulmonary crackles, wheezing
 S3 heart sound
 Fatigue, confusion, dizziness
 Cyanosis, cool extremities

Right-sided HF

Right = Body

 Peripheral edema
 Jugular vein distention (JVD)
 Ascites
 Hepatomegaly, RUQ tenderness
 Nausea, anorexia, weight gain

Pathophysiology

 ↓ Cardiac output → compensatory mechanisms:

o Sympathetic nervous system activation → ↑ HR, vasoconstriction
o RAAS activation → ↑ fluid retention → ↑ preload
o Ventricular hypertrophy → stiffening and remodeling
 These compensatory mechanisms worsen the problem over time.

Diagnostic Tests

 BNP (B-type natriuretic peptide): Elevated (>100 pg/mL) = HF

 Chest X-ray: Cardiomegaly, pulmonary congestion
  Echocardiogram: Measures EF, wall motion
 ECG: May show MI, arrhythmias
 Cardiac catheterization: Evaluate coronary arteries
 CBC, ABG, renal function, electrolytes: Assess organ function and complications

Pharmacologic Management
Drug Class Examples Purpose/Effect
ACE inhibitors Lisinopril, enalapril ↓ Afterload, BP,
progression of HF
ARBs Losartan, valsartan Alternative to ACEIs, ↓
preload/afterload
Beta blockers Metoprolol, carvedilol ↓ HR, ↓ BP, improve EF
Diuretics Furosemide, ↓ Fluid overload
spironolactone (preload)
Aldosterone Spironolactone K-sparing, prevents
antagonists remodeling
Digoxin Digoxin ↑ Contractility, slows
HR; narrow therapeutic
index
Nitrates Isosorbide, nitroglycerin ↓ Preload, vasodilation
Hydralazine + nitrates Used in Black patients ↓ Afterload and preload
as alternative to
ACE/ARBs
ARNI Sacubitril/valsartan Newer class, blocks
RAAS & enhances
natriuretic peptides
SGLT2 inhibitors Dapagliflozin, Originally diabetic
empagliflozin drugs, reduce HF
hospitalizations

It may be necessary to reduce the resistance the heart must pump against (afterload) :
• Angiotensin-Converting Enzyme (ACE) Inhibitors –used for vasodilation; also benefit by
preventing some structural cardiac changes that occur in heart failure
– Captopril (Capoten)
– Enalapril (Vasotec)
– Lisinopril (Prinivil, Zestril)
– Fosinopril (Monopril)
– Ramipril (Altace)
 o CRT (Cardiac Resynchronization Therapy)
 LVAD for end-stage HF
 Heart transplant (last resort)

Nursing Care

 Monitor I&O, weight, respiratory status

 Elevate HOB to ease breathing
 Administer meds as prescribed
 Assess for signs of fluid overload or hypoperfusion
 Patient education on diet, meds, activity, when to seek help
 Manage fatigue: Energy conservation techniques

Patient Education

 Daily weight monitoring

 Low-sodium diet
 Medication adherence (watch for side effects)
 Recognize signs of worsening HF:
o Increased SOB
o Edema
o Weight gain
o Fatigue
o Cough or orthopnea
 Smoking cessation, limit alcohol
 Vaccinations: flu and pneumonia

24.Cardiomyopathy
  Definition: Cardiomyopathy is a disease of the heart muscle that
affects its structure and function, potentially leading to heart failure,
arrhythmias, or sudden cardiac death.


Type Description Key Features Causes

Dilated (DCM) Most common. ↓ EF, S3, fatigue, Alcohol abuse,
Heart chambers edema, dyspnea viral infections,
enlarge and chemo,
weaken. pregnancy
Hypertrophic Thickened Dyspnea, chest Genetic
(HCM) ventricular wall pain, syncope, (autosomal
(esp. septum); sudden death dominant)
often genetic
Restrictive (RCM) Heart walls stiff, Fatigue, Amyloidosis,
restrict filling dyspnea, right- sarcoidosis,
sided HF signs radiation
Arrhythmogenic Muscle replaced Palpitations, VT, Genetic (rare)
Right Ventricular by fat/fibrous syncope
Cardiomyopathy tissue
(ARVC)
Takotsubo Transient LV Chest pain, ST Severe stress
(Stress-induced) dysfunction after elevation, normal (emotional or
emotional stress coronaries physical)

Nursing Care for Cardiomyopathy

 Monitor for signs of HF, arrhythmias, emboli

 Teach energy conservation techniques

 Emotional support

 Medication management:

o ACE inhibitors, beta blockers, diuretics, antiarrhythmics

o Avoid inotropes in HCM

 ICD or pacemaker may be indicated

 Little can be done to treat:
– Treatment is palliative and aimed at managing heart failure and the underlying cause if
known; also the dysrhythmias
• Hypertrophic cardiomyopathy – beta blockers or calcium channel blockers are used
 – Surgery to remove part of the ventricular septum (myectomy) is done to allow greater
outflow of blood

Diagnostic Testing:
 Cardiomegaly is visible on chest x-ray
 Echo – shows muscle thickness and chamber sizes to differentiate
between the types of cardiomyopathy
 ECG – shows dysrhythmias
 Cardiac catheterization and biopsy
 Blood tests to identify infections, elevated
levels of metal or iron

25. Heart Transplants

Indications

 End-stage heart failure unresponsive to medical/surgical therapy

 Cardiomyopathy, congenital heart disease, inoperable CAD

Contraindications

 Active infection

 Recent malignancy

 Severe pulmonary disease

 Noncompliance risk

 Irreversible organ damage (e.g., kidneys)

Post-Op Considerations

 Lifelong immunosuppressive therapy:

o Tacrolimus, cyclosporine, corticosteroids

 Rejection signs:

o Fatigue, low-grade fever, dyspnea, weight gain

 Infection risk:

o Strict aseptic technique, avoid sick contacts

 Routine biopsies to monitor for rejection

  Denervated heart = no angina sensation

Nursing Management

 Monitor for arrhythmias and rejection

 Support emotional/psychosocial adjustment

 Educate on medication adherence and infection prevention

26. Inflammatory Cardiac Disorders

Primary Key Nursing

Disorder Definition Diagnostics Treatment
Cause(s) Symptoms Care
Monitor for
Viral Chest pain,
ECG, arrhythmias,
Inflammation (Coxsackie, fatigue, Rest, treat cause,
↑ESR/CRP, reduce
of the heart adenovirus), palpitations, manage HF,
Myocarditis ↑troponin, activity,
muscle bacterial, dyspnea, avoid NSAIDs
echocardiogram, support
(myocardium) autoimmune, signs of HF, early
biopsy (rare) cardiac
toxins arrhythmias
function
Sharp
chest pain Assess pain,
NSAIDs,
Viral (most relieved by monitor for
Inflammation ECG (diffuse colchicine,
common), post- sitting up, tamponade
of the ST elevation), corticosteroids
Pericarditis MI (Dressler’s), friction rub, (Beck’s
pericardial echocardiogram, (autoimmune),
autoimmune, fever, triad),
sac chest X-ray pericardiocentesis
trauma, cancer possible position
if tamponade
pericardial upright
effusion
Fever, new
or
Monitor for
changing
emboli,
murmur,
Infection of the Bacterial (Strep, Blood cultures, Long-term IV teach
petechiae,
inner lining of Staph), IV drug echocardiogram antibiotics, antibiotic
Endocarditis Osler’s
the heart and use, prosthetic (TEE), possible valve prophylaxis
nodes,
valves valves ↑ESR/CRP surgery (e.g., dental
Janeway
work), oral
lesions,
hygiene
embolic
symptoms
Chronic valve Untreated/poorly Migratory ASO titer (anti- Antibiotics Emphasize
Rheumatic
damage from treated strep joint pain, strep), (penicillin), anti- completing
Heart
rheumatic throat → carditis, echocardiogram, inflammatories, strep
Disease
fever, an rheumatic fever valvular throat culture long-term treatments,
 Primary Key Nursing
Disorder Definition Diagnostics Treatment
Cause(s) Symptoms Care
monitor
valve
murmur
disease,
autoimmune (usually
→ heart prevent
reaction to mitral), prophylaxis
inflammation recurrence
Group A strep fever,
with
chorea
prophylactic
antibiotics

Myocarditis → Think muscle = arrhythmias, HF symptoms

Pericarditis → Think sac = positional chest pain, friction rub,

tamponade risk

Endocarditis → Think valves = murmurs, emboli, long IV antibiotics

Rheumatic Heart Disease → Think strep → immune → valve damage

(especially mitral valve)

27. Disorders of Cardiac Structure

Structural heart disorders affect the anatomy of the heart or great vessels,
interfering with blood flow, pressure gradients, and chamber efficiency. They
may be congenital or acquired.

Valvular Heart Diseases

Valves ensure one-way flow of blood. Dysfunction can cause:

 Stenosis: Valve doesn't open fully → obstruction

 Regurgitation (insufficiency): Valve doesn't close completely →

backflow
  Prolapse: Valve flaps bulge backward

Disorder Definition Causes Symptoms

Mitral Stenosis Narrowing of Rheumatic heart Dyspnea on
mitral valve disease exertion, fatigue,
orthopnea
Mitral Backflow into left MI, mitral Fatigue,
Regurgitation atrium prolapse, RHD palpitations,
crackles
Mitral Valve Valve leaflets Congenital, Often
Prolapse bulge into LA connective tissue asymptomatic;
during systole disorders may have
palpitations,
chest pain
Aortic Stenosis Narrowed aortic Age-related Angina, syncope,
valve → LV calcification, dyspnea,
overload congenital murmur
Aortic Blood leaks back Endocarditis, Water-hammer
Regurgitation into LV HTN, congenital pulse, fatigue,
dyspnea

Septal Defects (Atrial or Ventricular)

Usually congenital defects causing abnormal shunting of blood.

Defect Effect Symptoms Treatment

Atrial Septal Blood flows LA → Fatigue, murmur, May close
Defect (ASD) RA may be spontaneously;
asymptomatic in surgical or
childhood catheter closure
if large
Ventricular Blood flows LV → HF symptoms in Often closes
Septal Defect RV infants, murmur spontaneously in
(VSD) infancy; surgery
if not
What is a Heart Murmur?

 A murmur is an abnormal sound produced by turbulent blood

flow through the heart or great vessels.

 Heard as swooshing, blowing, or whooshing sounds with a

stethoscope during the cardiac cycle (systole or diastole).

Classification of Murmurs

Timing in Cardiac Cycle

Type Occurs During Examples

Aortic stenosis, Mitral

Systolic Between S1 and S2
regurgitation

Aortic regurgitation, Mitral

Diastolic Between S2 and S1
stenosis

Continuo Throughout systole and Patent ductus arteriosus

us diastole (PDA)

Causes

Cause Explanation

Valve Stenosis Narrowed valve → turbulent flow

Valve Regurgitation
Valve doesn't close properly → backflow
(Insufficiency)

Septal Defects Holes in the septum (ASD/VSD) → shunting

High Cardiac Output Fever, pregnancy, hyperthyroidism (may

States cause benign murmurs)

Congenital Heart
E.g., Tetralogy of Fallot, coarctation
Defects
 Grade Description

Grade Description
I Very faint, often missed
II Quiet, but clearly audible
III Moderately loud, no thrill

Patent Ductus Arteriosus (PDA)

 Definition: Persistence of fetal connection between aorta and
pulmonary artery

 S&S: Murmur (“machine-like”), bounding pulses, signs of HF

 Treatment: NSAIDs in infants (indomethacin), surgical ligation or device

closure

Coarctation of the Aorta

 Definition: Narrowing of the aorta (usually near ductus arteriosus)

 Symptoms:

o High BP in upper extremities

o Weak femoral pulses

o Headache, claudication

 Treatment: Surgical repair or balloon angioplasty

Aneurysms (Cardiac & Aortic)

 Definition: Localized dilation of the artery due to wall weakening

 Common Types:

o Aortic aneurysm (thoracic or abdominal)

o Ventricular aneurysm (post-MI complication)

S&S of Aortic Aneurysm:

 Often asymptomatic
  Pulsatile mass (AAA)

 Back/flank pain

 Bruit

 Rupture = severe pain, hypotension, shock

Treatment:

 Monitor if <5 cm (with imaging)

 Surgical repair or endovascular graft if >5.5 cm or symptomatic

 Strict BP control

Nursing Considerations
 Monitor for murmurs, arrhythmias, HF symptoms

 Pre-op and post-op education for surgical corrections

 Infective endocarditis prophylaxis for high-risk structural defects

 Encourage activity as tolerated, especially post-repair

 Psychosocial support for congenital conditions

 Regular follow-up imaging (e.g., echocardiography)

Diagnostic Tools
 Echocardiogram (TTE or TEE): visualizes valve function, chamber
size, septal defects

 Cardiac catheterization: pressure gradients, oxygen saturation

 MRI/CT angiography: vascular and aortic imaging

 Chest X-ray: enlarged heart, pulmonary congestion

 ECG: conduction issues, chamber enlargement