1. Coronary Artery Disease Angina Acute Coronary Syndrome
J.O. Medina,RN,MSN,FNP,CCRN
Education Specialist
Nurse Practitioner
Critical Care & Emergency Services
California Hospital Medical Center

2. Coronary Artery Disease
Pathophysiology
Atherosclerosis : progressive, diffuse disease that narrows artery lumen by abnormal thickening, hardening of artery wall resulting in non-compliant vessels
CAD: characterized by development of atherosclerotic plaques, called atheromas or “lesions” that blocks coronary artery blood flow

3. Coronary Artery Disease
Development of lesions, starting in childhood, progress through phases, caused by injury to intima of artery
Progression of CAD
Phase I : fatty streaks – do not obstruct flow
Phase II: fibrous plaque- elevated lesion protruding into lumen obstructs flow to varying degrees
Phase III: complicated lesions – partially or totally occlude lumen
Occurs largely at points of artery bifurcation, usually more prominent at proximal end of artery
Process causes reduced supply of oxygen and nutrients to heart cells and inability to meet metabolic demands of the heart

4. Coronary Artery Disease
Process causes reduced supply of oxygen and nutrients to heart cells and inability to meet metabolic demands of the heart
MVO2 is dependent on
Preload
Afterload
Contractility
Heart rate
Myocardial oxygen supply is dependent on
Arterial oxygen content
Coronary artery perfusion
Imbalance between supply/demand ratio leads to myocardial ischemia

5. Coronary Artery Disease
Major effects of myocardial ischemia
Decreased contractility – pump failure
Electrical instability- arrythmias
Risk Factors
Non-modifiable risk factors
Age: death from CAD  with age
Sex
Family history
Race: afro-Americans have = 45% > hypertension than Caucasians

6. Coronary Artery Disease
Modifiable Risk Factors
Cigarette smoking: 2X increased risk for CAD
HTN: damages blood vessels leading to plaque formation and atherosclerosis
Hyperlipidemia: CAD and atherosclerosis by causing build up in artery walls
Physical Inactivity: risk of CAD 2X
Diabetes:  risk 2X in men; 3X in women
Obesity
Stress : increased catecholamine release;  sympathetic response

7. Plaque

8. Plaque With Thrombus

9. Angina
Chest discomfort caused by transient myocardial ischemia without cell death
Usually brought on by  physical or emotional stress
Precipitated by 4 “E’s”
Extreme emotion
Extreme temperature
Excessive eating
Exercise

10. Angina
Types
Angina Pectoris (classic angina): occurs at least 50-60% of one or more main coronary arteries
Stable – does not increase in severity or duration over months; promptly relieved by rest and/or NTG
Unstable Angina – (crescendo, preinfarction) progressively increases in severity, duration, quality, not relieved promptly by rest/NTG
Prinzmetal’s Angina – (variant) usually occurs at rest; due to coronary artery spasm
Silent Ischemia – no symptoms

11. Angina Clinical Presentation History – look for risk factors
Pain Profile
Onset: sudden
Location: precordial, substernal, diffuse, ache in arm (usually left)
Duration: 3-5 min; rarely longer than 20 minutes
Characteristics
P,Q,R,S,T
Associated Symptoms: weakness, dizziness, sweating, nausea, vomiting, dyspnea
Relief: rest
Treatment: NTG

12. Angina Physical Examination Diagnostics EKG : 3 “I’s” Echocardiogram
wall motion abnormalities
estimates ejection fraction
EF = EDV - ESV x 100
EDV
Normal EF 65% ( 10%)
measures cavity size and wall thickness of ventricles
may be used with EKG exercise tolerance test or Dobutamine to stress heart without exercise
Thallium Scans
radioisotope will be diminished in ischemic zones ; absent in infarcted zones referred as “cold spots”

13. Angina
Positron Emission Tomogaphy (PET) / Single Photon Emission Computed Tomography (SPECT)
differentiates normal, ischemic, infarcted tissue by assessing myocardial metabolism
Cardiac catheterization
“gold standard “ for diagnosing CAD
demonstrates location and degree of blockages
can identify type of blockage (i.e. calcium, clots, or spasm)
measure right and left heart pressure, EF, CO
demonstrates wall motion abnormalities
used to evaluate type of interventional therapies most suited: angioplasty, atherectomy, stenting, LASER) surgery, medication only

14. Angina Management  demands on heart Relieve Pain NTG Beta blockers
Calcium channel blockers
Relieve Pain
MONA
Demerol if bradycardia present

15. Angina  Coronary Artery supply Pharmacological agents PTCA
oxygen
NTG
calcium channel blocking agents
ASA
PTCA
increases inner diameter of coronary artery
achieved by advancing balloon catheter
Atherectomy - removal of plaque from the artery

16. Angina
Coronary artery stents - creates larger luminal diameter by physically compressing plaque against arterial wall
restenosis rate lower than PTCA
LASER - ablate plaque
Coronary artery bypass graft (CABG)
anastomosis of saphenous vein graft or internal mammary artery (IMA) bypassing blockage
selection criteria
angina not responsive to medical therapy
left main disease
failed PTCA

17. CABG

18. Acute Coronary Syndromes
Irreversible necrosis or death of myocardial tissue due to inadequate blood supply
1.5 million Americans suffer ACS annually
60% die prior to hospitalization; 15-25%
will die within next 4 weeks from complications
frequently occurs at rest, sleep or usual activities ; most common

19. Acute Coronary Syndromes
Pathophysiology
90% fatal transmural ACS associated with thrombosis ; 10% caused by vasospasm
irreversible cell death occurs within minutes of cessation of blood flow
subendocardium is first affected due to highest O2 demands and most tenuous blood supply
wavefront of cellular death - endo to epicardium

20. Acute Coronary Syndromes
Wavefront produces zones:
zone of necrosis - electrically and mechanically dead tissue
zone of injury- severe cellular injury; may be viable
zone of ischemia - reduced blood flow, but salvageable
amount of damage/necrosis depends on
duration of occlusion
artery blocked
degree of collateral blood flow

21. Acute Coronary Syndromes
Metabolic changes as cells convert to anerobic metabolism due to cellular ischemia
arrythmias
decreased contractility - pump failure
ANS response can be either
sympathetic nervous system response
 HR, contractility, SVR
parasympathetic nervous response
 HR, BP, CO, heart blocks

22. Acute Coronary Syndromes
Clinical Presentation
chest pain
80% experience chest pain ; 15-30% no chest pain
pain similar to angina, usually more severe, lasting
> 30 minutes, not relieved by NTG or rest
associated signs and symptoms
nausea / vomiting
weakness, cold perspiration, sense of doom
dizziness, palpitations, dyspnea

23. Acute Coronary Syndromes
Physical Examination
Precordial signs
heart sounds
Pulmonary assessment
Systemic signs
vital signs
LOC
JVD UO

24. Acute Coronary Syndromes
Diagnosis
12/13/15/18/21 Lead EKG
limitations
3 Is of ACS
zone of ischemia - T wave inversion
zone of injury - ST elevation
zone of infarction - Q wave
Cardiac Enzymes
ACS damages cell membranes, releasing enzymes into plasma within minutes
other myocardial injury defibrillation, CPR, CABG also release these enzymes

25. Acute Coronary Syndromes
CK (CPK) - creatine phosphokinase
rises in 3-6 hours post MI; peaks at 24 hours; returns to normal in 3-4 days
composed of 3 isoenzymes: MB (found in heart); MM (found in skeletal muscles); BB (found in brain)
CK-MB (CK#2) very sensitive to MI
rises within hours; peaks at hours; returns to normal in 3 days
must be >4% of total CK for definitive diagnosis of MI

26. Acute Coronary Syndromes
LDH - lactic dehydrogenase
consists of 5 isoenzymes; LDH 1most specific for myocardial damage
 LDH 1 occurs after CK elevation
helpful in delayed presentation
Other biochemical markers
myoglobin - found both in skeletal muscles and heart; rises within 2 hours; but not specific
Troponin I and T - more specific than CKMB; rise within 4 hours ; stay elevated 1-2 weeks

27. Cardiac Enzymes

28. Acute Coronary Syndromes
Management
Goals of therapy
re-establish supply and demand balance
salvage ischemic cells
relieve pain
prevent/treat complications
AHA ischemic chest pain algorithm

29. Acute Coronary Syndromes
Complications
arrythmia - most common complication
ventricular
PVC - 80%
VT %
VF %
bradycardias - common with inferior MI
AV block ( narrow Vs. wide QRS)
SVT
pump failure - common with anterior

30. Acute Coronary Syndromes
RVMI
Pericarditis
early within first week or up to 12 weeks post MI
dressler’s syndrome
Thromboemboli
from mural thrombi
atrial fibrillation
DVT
up to 30 %
due to immobility and hypercoagulable state

31. Acute Coronary Syndromes

32. Questions ?
Thank You!