Coronary artery disease (CAD) causes impaired blood flow in the arteries that supply blood to the heart. Also called coronary heart disease (CHD), CAD is the most common form of heart disease and affects approximately 16.5 million Americans over the age of 20. It’s also the leading cause of death for both men and women in the United States. It’s estimated that every 40 seconds, someone in the United States has a heart attack. The most common cause of CAD is vascular injury with cholesterol plaque buildup in the arteries, known as atherosclerosis. Reduced blood flow occurs when one or more of these arteries becomes partially or completely blocked. The four primary coronary arteries are located on the surface of the heart: Right main coronary artery Left main coronary artery Left circumflex artery Left anterior descending artery. When your heart doesn’t get enough arterial blood, you may experience a variety of symptoms. Angina (chest discomfort) is the most common symptom of CAD.

2. CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
AND MYOCARDIALAND MYOCARDIAL
INFARCTIONINFARCTION
PRESENTED BY
MR.B. KALYAN KUMAR Msc (N)
Dept Of MSN

5. CORONARY ARTERY DISEASE
 DEFINITION:
It is a broad term used to refer to the narrowing or occlusion
of the coronary arteries. It is the progressive narrowing of
one or more coronary arteries by atherosclerosis. CAD
results in ischemia when the internal diameter of the
coronary vessel is reduced by 50 % to 70%.

6. CORONARY ARTERY DISEASE
CAUSES
 Reduced coronary blood flow to the myocardium by
mechanical obstruction.
 Decrease in the flow of oxygenated blood to the
myocardium.
 Increased demand for oxygen may occur owing to an
increase in cardiac output.

8. CORONARY ARTERY DISEASE
NON MODIFIABLE RISK FACTORS
 Age
 Gender
 Family history
 Genetic factors

9. CORONARY ARTERY DISEASE
MODIFIABLE RISK FACTORS
 Cholesterol
 Lipoproteins
 Triglycerides
 Diabetes / hyperglycemia
 Hypertension
 Smoking
 Sedentary life styles.

10. OTHER RISK FACTORS OF CAD
1
• Coagulation factors
2
• Homocysteine
3
• C- Reactive Protein

11. CORONARY ARTERY DISEASE
 PATHO PHYSIOLOGY
Injury to the endothelial layer of the vessel
Lipo protein adhere to the endothelial wall
undergoing oxidative and chemical changes
Local inflammatory response ensues

12. Macrophages ingest lipid particles- foam cells
Formation of necrotic core within the plaque
Reduced blood flow due to atherosclerotic plaque
Plaque ruptures- platelet adhesion
Formation of thrombus

13. CORONARY ARTERY DISEASE
SIGNS & SYMPTOMS
 Silent CHD
 Angina- feel of pressure or squeezing , feel of
indigestion
 Pain worsens with activity & relieves with rest
 Shortness of breath

15. CORONARY ARTERY DISEASE
DIAGNOSTIC STUDIES
 History collection
 Physical examination
 Resting ECG
 Exercise ECG
 Echocardiography
 Coronary angiography

16. ACUTE MYOCARDIAL INFARCTION
 DEFINITION:
Myocardial infarction generally occurs when there is an
abrupt decrease in coronary blood flow following a
thrombotic occlusion of a coronary artery previously
narrowed by atherosclerosis. Infarction occurs when a
coronary artery thrombus develops rapidly at the site of
vascular injury.
- ELLIOTT M ANTMAN

17. ACUTE MYOCARDIAL INFARCTION
CAUSES
 Imbalance between myocardial oxygen supply and
demand due to atherosclerosis
 Coronary artery vasospasm
 Coronary artery thrombus
 Presence of dysrhythmia
 Coronary embolism
 Blunt trauma
 Cocaine use is associated with spasm.

18. ACUTE MYOCARDIAL INFARCTION
• Q- wave MI- ST segment
elevation &elevated cardiac
enzymes are seen
CLASSIFICATION
1
• Non Q- wave MI- ST segment
depression in 2 or more leads
along with elevated cardiac
enzymes
CLASSIFICATIO
N
2

19. MI BY SITE, ECG CHANGES &
COMPLICATION
LOCATION OF MI PRIMARY SITE OF
OCCLUSION
PRIMARY ECG
CHANGES
COMPLICATION
Inferior MI RCA(80-90%),
LCX(10-20%)
Leads II,III,avF First & second
degree heart block,
right ventricular
infarct
Infero lateral MI LCX II,III,Avf,v5,v6 Third degree heart
block, left HF,
cardiomyopathy,
left ventricular
rupture

20. LOCATION OF MI PRIMARY SITE OF
OCCLUSION
PRIMARY ECG
CHANGES
COMPLICATION
Posterior MI RCA or LCX No lead truly looks
at posterior surface.
Look for reciprocal
changes in v1 & v2-
tall broad R waves,
ST depression & tall
T waves
First, Second & third
degree heart blocks,
HF, Brady
dysrhythmia
Anterior MI LAD(Left anterior
descending)
v2- v4 Third degree heart
block, HF, Left
bundle branch block

21. LOCATION OF MI PRIMARY SITE OF
OCCLUSION
PRIMARY ECG
CHANGES
COMPLICATION
Anterior septal MI LAD V1-V3 Second & third
degree heart block
Lateral MI LAD or LCX V5, V6,I,Avl HF
Right ventricular RCA V4R Increased right
atrial pressure,
decreased cardiac
output , heart
block, hypotension

22. ACUTE MYOCARDIAL INFARCTION
 PATHOPHYSIOLOGY
Reduced blood flow to myocardium cause significant &
sustained oxygen deprivation to myocardial cells.
Normal functioning is disrupted as ischemia & injury lead
to eventual cellular death.
Myocardial dysfunction occurs as more cells become
involved.

23. ACUTE MYOCARDIAL INFARCTION
CLINICAL MANIFESTATION
 Severe chest pain- deep & visceral, sudden onset, occurring
at rest& persists fairly constantly for some hours.
 The sub sternal chest pain persisting for >30 min &
diaphoresis strongly suggests AMI.
 Weakness, sweating, nausea, vomiting, anxiety & a sense of
impending doom.
 Pericardial friction rub is heard with transmural MI.

24. ACUTE MYOCARDIAL INFARCTION
CLINICAL MANIFESTATION
 Systolic pressure declines by approximately 10- 15 mm hg
from the pre infarction state in the patients with transmural
infarction.
 Carotid pulse is often decreased in volume, reflecting
reduced stroke volume.
 Jugular venous distention with clear lung fields should raise
suspicion of right ventricular infarction.
 Temperature elevated up to 38 degree Celsius.

25. ACUTE MYOCARDIAL INFARCTION
LABORATORY STUDIES
 Electrocardiogram
 Serum cardiac markers- creatine kinase, cardiac specific
troponins, aspartate amino transferase.
 Lab tests- myoglobin, serum lipid measurements, serum
electrolytes, ABG.
 Imaging studies- two dimensional echocardiogram, trans
esophageal echocardiogram, chest radiograph, stress testing,
nuclear imaging studies, stress perfusion imaging, stress
echocardiography, MUGA, PET, MRI.
 Cardiac catheterization, angiography.

26. ACUTE MYOCARDIAL INFARCTION
COMPLICATIONS
 Ventricular extrasystoles
 Sustained ventricular tachycardia
 Ventricular fibrillation
 Atrial fibrillation
 Sinus bradycardia
 Sinus tachycardia
 Conduction disturbances
 Cardiac failure & cardiogenic shock
 Thrombo embolism.

27. ACUTE MYOCARDIAL INFARCTION
OTHER COMPLICATIONS
 Pericarditis
 Post myocardial infarction syndrome( dressler’s
syndrome).
 Left ventricular aneurysm.

28. ACUTE MYOCARDIAL INFARCTION
 ACUTE MANAGEMENT
 Thrombolytic therapy

29. ACUTE MYOCARDIAL INFARCTION
PHARMACOLOGICAL MANAGEMNT
 Beta- adrenergic blockers
 Calcium channel blockers
 ACE inhibitors
 Anti thrombotic therapy
 Aspirin

30. ACUTE MYOCARDIAL INFARCTION
PHARMACOLOGICAL MANAGEMNT
 Glycoprotein IIb / IIIa inhibitors
 Unfractionated heparin
 Low molecular weight heparin
 Direct thrombin inhibitors
 Warfarin sodium
 Statins

31. ACUTE MYOCARDIAL INFARCTION
SURGICAL MANAGEMENT:
 Percutaneous transluminal coronary angioplasty
 Directional atherectomy / rotational atherectomy
 Laser angioplasty
 Inter coronary stenting
 CABG

35. ACUTE MYOCARDIAL INFARCTION
ROLE OF CRITICAL CARE NURSE:
 Intervention for pain
 Interventions for impaired cardiac output
 Interventions for oxygenation
 Interventions for anxiety.