CORONARY ARTERY

DISEASES
Disturbances in O2 Transport Mechanism
Infectious Disorders
◦ Pericarditis, Myocarditis, Endocarditis, RHD

Coronary Artery Disease

◦Atherosclerosis
◦Angina pectoris
◦Myocardial infarction
Congestive Heart Failure
Pulmonary edema
Arrythmias
HYPERTENSION
• A Raise in blood pressure 2x at least 2 weeks apart

.Primary or Essential Hypertension – no known cause /idiopathic

Risk Factors: Family History/familial
Faulty Diet, sedentary lifestyle, obesity , smoking, alcohol,
caffeine, stress
Secondary Hypertension – elevation of Blood pressure from a disease
process.
Risk Factors- DM,
Pheochromocytoma- tumor in adrenal medulla that releases
catecholamines

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5
 Risk Factors:
Non-Modifiable: Modifiable
•Race •Sedentary
•Heredity Lifestyle
•High Sodium
•Increase with Intake
Age
•Heavy Alcohol
•Male Gender consumption
•Diabetes and •Obesity
Renal Disease •Pregnancy
•Some Oral
Contraceptives 6
 Prevalence of Cardiovascular
Disease
32% of all deaths in 2008 contributed with
CVD.
no. 1 cause of Mortality in the Elderly.

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•CORONARY HEART DISEASE
•also known as Coronary Artery Disease (CAD) or
Ischemic Heart Disease.
•82% died with CHD are aged 65 years or over.
•Caused by hardening and narrowing of the blood
vessels of the heart. (Atherosclerosis
)

M.I
Main Cause: CAD

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Coronary Artery Disease/ Ischemic Heart Disease
/Atherosclerotic Cardiovascular Disease
Arteriosclerosis
• Thickening or hardening of
the arterial wall

Atherosclerosis
• A type of arteriosclerosis
caused by formation of
PLAQUE (chiefly composed
of cholesterol)
• Leading contributor to
coronary artery and
cerebrovascular disease
Coronary Artery Disease
Pathophysiology (atherosclerosis):
UNKNOWN
◦ Vascular damage (cause inflammation)

◦ Fatty streak development (intimal layer)

◦ Plaque (partial or complete occlusion of blood

flow)

◦ Complications
◦ Calcifications
◦ Ulceration
◦ Thrombosis
Coronary Artery Disease
Coronary Artery Disease
Assessment:
◦ BP (hypertension)
◦ Elevated cholesterol & triglycerides
◦ Elevated homocysteine (⭣risk if level >
15mmol/L)
◦ Blocks the production of nitric oxide on
the endothelium making cell wall less
elastic & permitting plaque to build up
◦ Diet: B-complex vitamin rich diet (folic
acid) - ⭣homocysteine
◦ Presence of abdominal obesity
◦ Elevated FBS
Coronary Artery Disease
Interventions:
◦Cholesterol screening
◦Diet
◦Smoking cessation
◦Exercise
◦Drug therapy
◦HMG-CoA reductase
inhibitors “Statins”
In combination with other substances,
LDLs can lead to plaque formation,
greatly increasing the chances
for myocardial infarction and stroke.
HDLs work to remove harmful LDLs
from the blood, thereby preventing
fatty buildup and formation
of plaque in arterial walls.
Coronary Artery Disease
The American Heart Association (AHA) now suggest the term ACUTE
CORONARY SYNDROME to describe any group of clinical
symptoms compatible with acute myocardial ischemia
◦ Ischemia –
◦ Atherosclerosis ⭣ ischemia

⭣O
insufficient blood supply
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ANGINA PECTORIS

Myocardial
Infarction
Coronary Artery Disease
Angina Pectoris
◦“Chest pain” of cardiac
origin
◦Most common clinical
manifestation of
myocardial ischemia
◦Myocardial ischemia
causes chemical and
mechanical stimulation of
sensory afferent nerve
endings in the coronary
vessels and myocardium
Types of Angina: CAUSE SYMPTOMS

Stable -75% coronary occlusion -Chest pain (15mins or

that accompanies less) and may radiate
exertion -Similar pain severity,
-Elevated HR or BP frequency & duration
-Eating a large meal with each episode
Unstable -Progressiveworsening - Chest pain of increased
of stable angina with frequency, severity &
>90% coronary duration poorly relieved
occlusion by rest or oral nitrates

Variant -Arterial
spasm in normal -chest pain that occurs
(Prinzmetal’s) or diseased coronary at rest (usually bet. 12 &
artery 8am), sporadic over 3-6
mos & diminishes over
time (ECG: ST –
elevation)
 S table Angina

R elieved -by rest & drugs

Occurs during exertion

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 UNstable Angina
Not relieved by rest & drug
Occurs on exertion emotion
-pre infarction angina

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 VARIANT /Prinzmetal’s Angina

•Cause: Arterial Spasm

may occur at rest-
between midnight and
early morning
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 Intractable/ refractory

Excruciating pain caused

by necrosis- MI

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 silent angina
asymptomatic

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LEVINE’S SIGN
 ANGINA:

Nitroglycerin- DOC of angina

-vasodilator- dilates 1 vein then arteries
st

- Preload , after load, BP

- SE: flushing, headache
- Store in dark container
- Refill q 6 mos
- 26
Myocardial Infarction
Etiology & Genetic Risk:
◦PRIMARY FACTOR: Atherosclerosis
◦Nonmodifiable risk factors
◦Modifiable risk factors
◦Elevated serum cholesterol levels
◦CIGARETTE SMOKING!!!
◦Hypertension
◦Impaired glucose tolerance
◦Obesity
◦Physical inactivity
◦Stress
Myocardial Infarction
Physical assessment/ Clinical Manifestations:
Myocardial Infarction
Interventions:
Pain management: MONA
◦Morphine
◦2- to 10-mg IV q 5-15 minutes
◦AE: respiratory depression, hypotension, bradycardia,
severe vomiting
◦Antidote: Naloxone (Narcan) 0.2 – 0.8 mg IV
◦Oxygen: 2-4L/min by nasal cannula
◦Nitroglycerin
◦Aspirin
Positioning – semi fowler’s
Provide a quiet & calm environment
 Medications
Nitrates
◦Nitroglycerine, Isosorbide dinitrate
(Isordil), Isosorbide mononitrate
(Imdur)
Beta Blockers
Calcium Channel Blockers
Thrombolytics/ Fibrinolytics
Coronary Artery Disease
 Angioplasty
also known as balloon angioplasty and
percutaneous transluminal angioplasty, is a
minimally invasive endovascular procedure used
to widen narrowed or obstructed arteries or
veins, typically to treat arterial atherosclerosis.

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Coronary Artery Disease
 Thrombolytic- Clot busting
agents
Dissolve thrombus/ clot in coronary arteries
T-PA (alteplase)
Streptokinase- bolus of 20,000 IU should
be followed by a maintenance infusion of
2,000 IU to 4,000 IU per minute over 30 to
90 minutes depending on the
achievement of coronary artery patency.
The administration of streptokinase may
be intravenous or intracoronary.
43
Disturbances in O2 Transport Mechanism
Infectious Disorders
◦Pericarditis, Myocarditis, Endocarditis, RHD
Coronary Artery Disease
◦Atherosclerosis
◦Angina pectoris
◦Myocardial infarction
Congestive Heart Failure
Pulmonary edema
Failure
“Pump failure”, inadequacy of the heart to pump
blood throughout the body
Congestive Heart Failure
◦accumulation of blood & fluid in organs & tissues
due to impaired circulation
Types:
◦Left-sided heart failure (LV fails)
◦Right-sided heart failure (RV fails)
Causes:
◦Damage to muscular wall (M.I.), Cardiomyopathy,
Hypertension, CAD, Valvular defects, Infections
1- No limitation of physical activity. Ordinary physical activity does not cause
undue fatigue, palpitation, dyspnea (shortness of breath).

2- Slight limitation of physical activity. Comfortable at rest. Ordinary physical

activity results in fatigue, palpitation, dyspnea (shortness of breath).

3- Marked limitation of physical activity. Comfortable at rest. Less than ordinary

activity causes fatigue, palpitation, or dyspnea.

4- Unable to carry on any physical activity without discomfort. Symptoms of heart

failure at rest. If any physical activity is undertaken, discomfort increases.

CLASS /PATIENT’S
SYMPTOMS
Failure
Left = Lungs
Failure
Diagnostic Findings:
◦Chest x-rays: reveals cardiomegaly
(hypertrophy)
◦Pleural effusions develops
◦ECG: abnormal findings (ventricular
hypertrophy, dysrhythmias)
◦Echocardiography – reveals cardiac
valvular changes, pericardial
effusions, chamber enlargement,
ventricular hypertrophy
◦Multigraded angiographic (MUGA)
scans – information about ejection
fraction
Medical Management:
Low-sodium diet, fluid restriction
Inotropic agents:
◦Digitalis: Digoxin (Lanoxin)
◦⭣ contractility, ⭣ HR, ⭣ conduction (AV node)
◦(-) sympa. activity, (+) parasympa Activity
◦Watch out for DIGITALIS toxicity: loss of appetite,
N&V, rapid, slow, irregular heart rate, disturbance in
color vision
◦Dopamine (Intropin), Dobutamine (Dobutrex)
Diuretics: Furosemide (Lasix), Chlorothiazide (Diuril)
Vasodilators (Nitroglycerin), ACE inhibitors (pril)