Coronary Artery DiseaseAnginaAcute 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 – 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

– 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

Coronary Artery Disease

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”– 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

– 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

• 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

• 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

Questions ?

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