Lipp Vis Nursing ChaptLWBK1630_C02_p013-068

Chapter 2 • Cardiovascular Care  31

ACS Tissue Destruction

as arterial spasm, aortic stenosis, cardiomyopathy, or uncontrolled hypertension. Noncardiac causes include anemia, fever, thyrotoxicosis, and anxiety/panic attacks. Clinical Manifestations of Angina Pectoris • Chest pain or discomfort induced by physical exertion or emotional stress which is relieved by rest and nitroglycerin • Mild or severe pain which crescendos in discomfort and then decrescendos to relief • Substernal chest pain, pressure, heaviness, or discomfort such as a squeezing, aching, burning, choking, strangling, and/or cramping pain • Exertional shortness of breath • Nausea • Diaphoresis • Fatigue • Numbness or weakness in arms, wrists, or hands • Women are more likely to have “atypical” symptoms such as dyspnea and fatigue • Diabetics may have atypical, minimal or no symptoms Patterns of Angina Pectoris — are caused by varying combinations of increased myocardial demand, decreased myocardial perfusion, and coronary arterial pathology identified as: • Stable or Typical Angina —imbalance in coronary perfusion demand • Prinzmetal Variant Angina — coronary artery spasm • Unstable Angina (UA) —pattern of increasing pain, prolonged duration of pain, or pain occurring at rest

Superior vena cava

Arch of aorta

Pulmonary trunk

Right atrial auricle

Left atrial auricle

Right coronary artery

Circumflex branch of left coronary artery

Left anterior descending artery

ZONES OF MYOCARDIALINFARCTION

Papillary muscle

Damaged muscle from myocardial infarction

Reversible ischemia

Severe ischemia (recovery possible with revascularization)

Necrosis (damage irreversible)

Clinical Manifestations of Acute Coronary Syndrome • Chest pain • Pressure • Tightness or heaviness

• Nausea and/or vomiting associated with chest discomfort • Persistent shortness of breath

• Pain that radiates to neck, jaw, shoulders, back, or one or both arms • Indigestion or heartburn

• Weakness • Dizziness • Lightheadedness • Loss of consciousness

• Distal microvascular thromboembolism from plaque- associated thrombus • Thromboembolism from plaque erosion • Nonplaque-associated coronary thromboembolism • Dynamic obstruction (coronary spasm or vasoconstriction) obstruction to coronary flow • Coronary arterial inflammation • Secondary UA • Coronary artery dissection Treatment of UA/NSTEMI • Oxygen • Nitrates • Morphine • Beta blockers • Heparin of epicardial and/or microvascular vessels • Progressive mechanical

from underlying acute myocardial ischemia. ACS includes UA, non-ST elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI), depending on the degree of coronary artery occlusion. These conditions are characterized by differences in severity, risk, etiology, pathophysiology, presentation, and management. Angina is considered unstable when a patient experiences prolonged symptoms at rest. CAUSES OF UNSTABLE ANGINA OR NSTEMI • Thrombus or thromboembolism, usually arises from disrupted or eroded plaque • Occlusive thrombus, usually with collateral vessels • Subtotal occlusive thrombus on pre-existing plaque

TIP: Early recognition and treat- ment of UA is imperative to prevent complication such as sudden death.

ACUTE CORONARY SYNDROME

Acute coronary syndrome (ACS) is a term used to describe a group of clinical symptoms which result