This document provides information on the cardiovascular system and coronary artery disease. It discusses the pathophysiology of coronary artery disease where plaque builds up in the arteries leading to stenosis and reduced blood flow. This can cause chest pain called angina due to ischemia. The document outlines the symptoms, diagnosis, and management of coronary artery disease including medications, lifestyle changes, and possible surgical interventions. It also discusses related conditions like angina pectoris, myocardial infarction, and heart failure.

1. CARDIOVASCULAR
SYSTEM
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2. CORONARY ARTERY DISEASE
 Coronary artery disease is a progressive disease
leading to narrowing or occlusion of the coronary
arteries.
 As the vessel narrows, the patients may experience
symptoms of ischemia such as chest tightness and
angina.

3. PATHOPHYSIOLOGY
 Accumulation of fatty deposits and minerals in the coronary
arteries, called an atheroma or plaque, leads to stenosis and
eventually occlusion of the artery.
 In CAD, blood flow to the myocardium is reduced. The arteries are
unable to dilate to meet increased metabolic needs.

4. PATHOPHYSIOLOGY
 When myocardial oxygen demands are not met, ischemia results,
which can cause chest pain. The pain associated with CAD occurs
from a lack of oxygen to the myocardium from CAD and is called
angina pectoris.
 If coronary artery disease is not prevented or treated early, it can
progress to more serious cardiac disorders. These include angina,
myocardial infarction, heart failure, cardiac dysrhythmias, and
even sudden death.

5. S/S
 Asymptomatic.
 Chest pain (angina) because of decreased blood flow
to heart muscle and/or increase in myocardial oxygen
demand resulting from stress.
 Pain may radiate to the arms, back, and jaw.

6. MANAGEMENT
 Most risk factors for heart disease are related to lifestyle and
environmental factors.
 Encourage and educate the patient on cessation of smoking, dietary
changes, controlling hypertension, maintaining weight.
 Diet change: lower sodium, lower cholesterol and fat, decreased
calorie intake, increased dietary fiber

7. MANAGEMENT
 Administer low doses of aspirin.
 Administer beta-adrenergic blockers to reduce workload of heart:
metroprolol, propranolol, nadolol.
 Administer calcium channel blockers to reduce heart rate, blood
pressure, and muscle contractility; helps with coronary
vasodilation; slows AV node conduction.
 Administer nitrate if patient has symptomatic chest pains to reduce
discomfort and enhance blood flow to myocardium.

8. SURGICAL INTERVENTION
Coronary Atherectomy
 Coronary atherectomy is used to cut and remove plaque from
atherosclerotic coronary arteries. The catheter has a central
rotating blade that shaves off the plaque and contains it for removal
and pathological analysis.
Coronary Artery Stents
 Coronary artery stents are used to prevent closure of a coronary
artery from an atherosclerotic lesion. Stents are put in place during
an angioplasty.

9. NURSING MGT
 Monitor vital signs—signs of hypertension, irregular heart rate
 Monitor electrocardiogram
 Monitor labs—periodic lipid panel, liver function for patients on
statins
 Monitor for myalgias (muscle aches)

10. NURSING MGT
 Educate and encourage patients to
 Stop smoking
 Reduce alcohol consumption
 Change to a lower-fat, lower-cholesterol diet, as well as increased
dietary fiber intake
 Increase daily activity
 Weight reduction

11. ANGINA PECTORIS
 Angina pectoris is a clinical syndrome usually characterized by
episodes or paroxysms of pain or pressure in the anterior chest.
 The cause is usually insufficient coronary blood flow. The
insufficient flow results in a decreased oxygen supply to meet an
increased myocardial demand for oxygen in response to physical
exertion or emotional stress.

12. PATHOPHYSIOLOGY
 Angina pectoris (chest pain) is a symptom of ischemia and is the
primary symptom of coronary artery disease and heart attack.
 In the normal heart there is a balance between the oxygen supply
and demand of the myocardium.
 When an increased workload is placed on the heart, as in exercise or
strenuous activity, there is an increased demand for oxygen.

13. PATHOPHYSIOLOGY
 Normally, when the heart needs more oxygen, the coronary
arteries dilate to carry more blood.
 However, with CAD, the narrowed vessels are unable to dilate and
supply the heart with this extra blood and oxygen.
 This inability to supply more blood and oxygen causes
myocardial ischemia and chest pain. Chest pain results from the
ischemia but usually lasts only for a few minutes, especially if activity
is stopped.
 An episode of angina is typically precipitated by physical activity,
excitement, or emotional stress.

14. ANGINA PECTORIS
 There are three categories of angina.
Stable angina— Chest pain occurring during periods of
increased myocardial work because of reduced
coronary perfusion. The pain is predictable and can
usually be managed with nitroglycerin and rest.

15. ANGINA PECTORIS
 Unstable angina— The episodes of chest pain with unstable angina
increase in frequency and severity, placing the patient at risk for
myocardial damage or sudden death.
Rest does not decrease the chest pain of unstable angina. This pain
may even occur when the patient is at rest. ; is of increasing intensity,
force, or duration; isn't relieved by rest; and is slow to subside in
response to nitroglycerin.

16. ANGINA PECTORIS
 VARIANT ANGINA (PRINZMETAL’S ANGINA). The pain of variant
angina is similar to the pain in stable angina except it has a longer
duration and may occur at rest. The pattern of occurrence is often
cyclical, with the pain presenting about the same time each day. This
type of angina is often caused by coronary artery spasms and usually
does not cause damage to the myocardium

17. S/S
 Chest pain lasting 3 to 5 minutes—not all patients get substernal
pain (NB: Some pt. describe the pain as heaviness, tightness,
squeezing, or crushing pain in the center of the chest)
 Pain can occur at rest or after exertion, excitement, or exposure to
cold—due to increased oxygen demands or vasospasm.
 Pain may radiate to other parts of the body such as the jaw, back, or
arms—

18. S/S
 Sweating (diaphoresis)
 Tachycardia—heart pumping faster trying to meet oxygen needs as
anxiety increases.
 Difficulty breathing, shortness of breath (dyspnea)—increased
heart rate increases respiratory rate and increases oxygenation.

19. DIAGNOSIS
 Electrocardiogram during episode: T-wave inverted with initial
ischemia, which is reduced blood flow due to myocardium.
 Troponins, CK-MB, which is an enzyme released by damaged cardiac
tissue 2 to 6 hours following an infraction.
 Chest x-ray to determine signs of heart failure.

20. DIAGNOSIS
 Coronary arteriography to determine plaque build-
up in coronary arteries.
 Echocardiogram or stress-echo to determine any
abnormality of wall motion due to ischemia.

21. MANAGEMENT
 The treatment is directed at relieving and preventing anginal
episodes that could lead to a myocardial infarction. When
suspecting chest pain, always give oxygen as the first line of
defense.
 The risk factors identified for the patient determine the course of
treatment. Weight reduction; a low-fat, low cholesterol diet; and
stress reduction may help slow disease progression.
 The three major groups of medication used for angina are
vasodilators, calcium channel blockers, and beta blockers.

22. MANAGEMENT
 Administer nitrates— Nitrates dilate coronary arteries to
increase oxygen to the myocardium, and dilate peripheral vessels
so the heart does not have to work so hard to pump blood into
them.
Nitroglycerin—sublingual tablets or spray; timed-release tablets.
 Administer Calcium channel blockers: It relaxes vascular smooth
muscle, which leads to decreased peripheral vascular resistance
(afterload) and decreased myocardial oxygen demand. These drugs
dilate main coronary arteries, increasing the myocardial oxygen
supply. Nifedipine

23. MANAGEMENT
 Administer beta-adrenergic blocker—this class has a
cardioprotective effect, Beta blockers decrease heart rate, lower
blood pressure, and prevent release of rennin. This results in
decreased workload on the heart to help prevent anginal attacks
 Statins: Cholesterol and inflammation in artery walls are involved in
atherosclerosis development. Statins lower cholesterol levels by
reducing cholesterol production in the liver.

24. MANAGEMENT
 Aspirin for antiplatelet effect.
 Analgesic—typically morphine intravenously during
acute pain. The medicine is very fast-acting when
given this way and will decrease myocardial oxygen
demand as well as decrease pain.

25. NURSING MANAGEMENT
 Monitor vital signs—look for change in BP, P, R;
irregular pulse; pulse deficit;
 Monitor cardiac status using a 12-lead
electrocardiogram (EKG)
 Record fluid intake and output. Assess for renal
function.
 Assess chest pain each time the patient reports it.

26. NURSING MANAGEMENT
Remember PQRST (an acronym for a method of pain assessment)
Determine the
 Place,
 Quality (describe the pain—stabbing, squeezing, etc.),
 Radiation (does the pain travel anywhere else?),
 Severity (on a scale of 1 to 10),
 Timing (when it started and how long it lasts and what preceded the
pain).

27. NURSING MANAGEMENT
Educate and encourage the patient to
 Rest when pain begins to decrease oxygen demands.
 Avoid stress and activities that bring on an angina attack.
 Stop smoking. Smoking is associated with heart disease.
 Adhere to the prescribed diet and exercise plan.

28. MYOCARDIAL INFARCTION (MI)
 A myocardial infarction (MI), commonly known as a
heart attack, results in the death of heart muscle.
The affected myocardial cells in the heart are
permanently destroyed.

29. PATHO
 Myocardial infarction does not happen immediately.
Ischemic injury evolves over several hours before
complete necrosis and infarction take place.
 Blood supply to the myocardium is interrupted for
a prolonged time due to the blockage of coronary
arteries.
 The ability of the heart to contract, relax, and propel
blood throughout the body requires healthy cardiac
muscle

30. PATHO
 This results in insufficient oxygen reaching cardiac muscle,
causing cardiac muscles to die (necrosis).
 The body’s attempt to compensate for decreased cardiac
function triggers the sympathetic nervous system to increase heart
rate. The change in heart rate increases myocardial oxygen
demand, further depressing the myocardium.

31. PATHO
 The extent of the cardiac damage varies depending on the location
and amount of blockage in the coronary artery.
 Patients are typically (not always) symptomatic, but some patients
will not be aware of the event; they are said to have silent MI.

32. S/S
 Chest pain that is unrelieved by rest or nitroglycerin, unlike angina
 Pain that radiates to arms, jaw, back and/or neck
 Shortness of breath, especially in the elderly or women
 Nausea or vomiting
 Anxiety

33. S/S
 Restlessness
 Feeling of impending doom
 Pale, cool, clammy skin; sweating (diaphoresis)
 Sudden death due to arrhythmia usually occurs within first hour

34. DIAGNOSIS
 ECG: T-wave inversion—sign of ischemia.
ST-segment elevation
 Decreased pulse pressure because of diminished cardiac output.
 Elevated creatine kinase MB (CK-MB)—
 Elevated troponin I- and troponin T-proteins elevated within one
hour of myocardial damage.
 Less than 25 ml/hr of urine output due to lack of renal blood flow

35. MANAGEMENT
 The goal of medical management is to minimize myocardial
damage, preserve myocardial function, and prevent
complications.
 Medications are used to enhance blood flow to the heart muscle
while reducing the workload of the heart.
 OXYGEN: Supplemental oxygen is used to help meet myocardial
oxygen demand. Oxygen is administered immediately, usually at 2 L
per minute via nasal cannula.

36. MANAGEMENT
 Administer antiarrhythmics because arrhythmias are common as
are conduction disturbances.
Amiodarone.
 Administer thrombolytic therapy within 3 to 12 hours of onset
because it can re-establish blood flow in an occluded artery, reduce
mortality, and halt the size of the infarction.
Alteplase. Streptokinase.
 Administer beta-adrenergic blockers because they reduce the
duration of ischemic pain and the incidence of ventricular
fibrillation; decreases mortality.
Propranolol, Nadolol.

37. MANAGEMENT
 Administer analgesics to relieve pain, reduce pulmonary
congestion, and decrease myocardial oxygen consumption.
Morphine sulfate is the most commonly used narcotic for
several reasons
 Administer nitrates to reduce ischemic pain by dilation of blood
vessels; helps to lower BP. Nitroglycerin.
 Post-MI all patients should be commenced on a statin lipid
lowering drug.

38. NURSING MANAGEMENT
 Monitor Vital signs, look out for changes in pulse, heart sounds,
murmur.
 Continuous monitoring of ECG to detect arrhythmias
 Educate and encourage the patient on
low-fat, low-cholesterol, low-sodium diet.
Medication.
Smoking cessation.

39. NURSING MANAGEMENT
Patient should be encouraged to
 Limit activities.
 Reduce stress
 Adhere to lifestyle changes such as increase in exercise, diet changes.

40. HEART FAILURE
 Is a complication of other cardiovascular condition
rather than a disease in itself.
 HF occurs when the muscular layer of the heart
weakens causing it to fail as a pump and a circulator
of blood.

41. CAUSES
 Infection of the muscle
 Myocardial infraction
 Ageing
 Long standing HTN

42. PATHO
 Heart failure is a complex syndrome that can result from any cardiac
disorder (structural or functional) resulting in a failure to maintain
sufficient cardiac output to meet the demands of the body.
 The clinical syndrome of heart failure is characterised by
breathlessness, fatigue and fluid retention.

43. PATHO
 The mechanism by which the heart fails to deliver a sufficient cardiac
output is dependent on the underlying cause. The circulatory
system is exactly that: a system failure of one component affects
the entire system.
 HF may be classified as right sided HF or left sided HF.

44. LEFT SIDED HF
 It can be caused by Aortic Stenosis, Cardiomyopathy, Hypertension,
Heart Muscle Infections, Myocardial Infarction etc
 Normally, the ventricles of the heart contracts while the atria relax allowing
for filling and emptying.
 If the muscle of the left ventricle cannot contract effectively, some blood
is left in the left ventricle.

45. LEFT SIDED HF
 This prevent part of the blood in the left atrium from progressing
into the ventricle and in turn blood backs up into the pulmonary
vessel, pressure within those vessels increases and fluid leaks into
lung tissue producing congestion
 Alveolar edema is more serious because it reduces gas exchange
across the alveolar capillary membrane. Shortness of breath and
cyanosis may result from the decreased oxygenation of the blood
leaving the lungs and eventually pulmonary oedema.
 If not corrected, left sided heart failure will lead to failure of the
right side of the heart.

46. S/S LEFT-SIDED HEART FAILURE
 Dyspnea on exertion
 Dry hacky cough, especially supine
 Crackles, wheezing
 Orthopnea
 Paroxysmal nocturnal dyspnea
 Cyanosis
 Tachypnea, tachycardia
 Nocturia.

47. RIGHT SIDED HF
 It can be caused by chronic lung disease (cor pulmonale),
pulmonary embolism, pulmonary hypertension, Left-Sided Heart
Failure etc
 The major cause of right-sided heart failure is leftsided heart failure.
When the left side fails, fluid backs up into the lungs and
pulmonary pressure is increased. The right ventricle must
continually pump blood against this RESISTANCE.
 Right sided HF leads to backward build-up of blood in the
systemic blood vessels. As the blood backs up jugular neck veins
become distended

48. RIGHT SIDED HF
 Edema may occur in the peripheral tissues, and the abdominal
organs can become engorged.
 Congestion in the gastrointestinal tract causes anorexia, nausea, and
abdominal pain. The liver can becomes congested, known as
hepatomegaly.
 Congestion of the blood to and from the kidney may lead to
impaired renal function, preventing normal excretion of urine and
causing fluid accumulation.
 Inadequate circulation to and from the brain may cause mental
confusion and irritability which sometimes progresses to delirium
and coma.

49. S/S RIGHT-SIDED HEART FAILURE Jugular vein distention
 Dependent peripheral edema
 Ascites
 Weight gain
 GI pain, anorexia, nausea
 Fatigue, weakness
 Tachycardia
 Nocturia

50. DIAGNOSTIC EVALUATION
 Physical examination
 Electrocardiogram
 Chest x-ray examination
 Coronary angiography

51. MANAGEMENT
Treatment is aimed at the underlying disease and to improve the
heart’s pumping ability and decrease the heart’s oxygen demands.
 Oxygen therapy: Oxygen therapy assists in supplying the oxygen
needs of the tissue.
 Diuretics: It is usually administer for symptom control e.g
Furosemide, hydrochlorothiazide, spironolactone
 ACE inhibitors: it is administer to decrease afterload e.g Captopril,
enalapril, lisinopril.
 Beta blockers: It help to raise ejection fraction, and decrease
ventricular size.

52. MANAGEMENT
 Inotrope: It strengthen myocardial contractility: Digoxin.
 Vasodilator: It is given to reduce preload, relieve dyspnea: e.g
nitroprusside,
 Anticoagulants: it is given to a patients with severe heart failure, as
they have a propensity to develop thrombus and emboli
 Reduce fluids as fluid overload is a causative factor in CHF

53. NURSING MGT
 Monitor vital signs
 Record fluid intake and output—weigh daily to assess
for fluid overload.
 Position patient in semi-Fowler’s position to ease
breathing

54. NURSING MGT
 Administer oxygen as ordered because it helps to decrease
workload of heart.
 Raise legs when sitting to lessen dependent edema.
 Patients should be advised to stop smoking and reduce alcohol
and salt intake.
 Weight loss and regular aerobic exercise should be encouraged.
 Patients with evidence of fluid overload should restrict their fluid
intake