Transcript Coronary Artery Disease Angina Acute Coronary Syndrome

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
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
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
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
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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
Coronary Artery Disease
– Major effects of myocardial ischemia
• Decreased contractility – pump failure
• Electrical instability- arrythmias
– Risk Factors
• Non-modifiable risk factors
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Age: death from CAD  with age
Sex
Family history
Race: afro-Americans have = 45% > hypertension than
Caucasians
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
Plaque
Plaque With Thrombus
Angina
 Chest discomfort caused by transient
myocardial ischemia without cell death
 Usually brought on by  physical or
emotional stress
 Precipitated by 4 “E’s”
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Extreme emotion
Extreme temperature
Excessive eating
Exercise
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
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
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”
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
Angina
 Management
–  demands on heart
• NTG
• Beta blockers
• Calcium channel blockers
– Relieve Pain
• MONA
• Demerol if bradycardia present
Angina
–  Coronary Artery supply
• Pharmacological agents
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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
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
CABG
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 0600-1200
Acute Coronary Syndromes
 Pathophysiology
– 90% fatal transmural ACS associated with
thrombosis ; 10% caused by vasospasm
– irreversible cell death occurs within 20-40
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
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
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
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
Acute Coronary Syndromes
 Physical Examination
– Precordial signs
• heart sounds
– Pulmonary assessment
– Systemic signs
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vital signs
LOC
JVD
UO
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 30-60 minutes
• other myocardial injury defibrillation, CPR, CABG
also release these enzymes
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 18-24 hours; returns to normal
in 3 days
– must be >4% of total CK for definitive diagnosis of MI
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
Cardiac Enzymes
Acute Coronary Syndromes
 Management
– Goals of therapy
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re-establish supply and demand balance
salvage ischemic cells
relieve pain
prevent/treat complications
– AHA ischemic chest pain algorithm
Acute Coronary Syndromes
 Complications
– arrythmia - most common complication
• ventricular
– PVC - 80%
– VT - 10%
– VF - 5-15%
• bradycardias - common with inferior MI
– AV block ( narrow Vs. wide QRS)
• SVT
– pump failure - common with anterior
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
Acute Coronary Syndromes
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