Peripheral Artery disease
intermittent claudication
Gradually increasing obstruction to the iliofemoral vessels and pain with ambulation
Description
§Atherosclerosis occludes the coronary arteries
§Diminishes blood supply
§Ischemia-temporarily deprived of blood supply
§Persistent ischemia or complete occlusion causes acute coronary syndromes
§Infarction-irreversible myocardial injury
myocardial cell ischemia
10 seconds
Unstable Angina
- Form of acute coronary syndrome (ACS) that results in reversible myocardial ischemia
- Fissuring or superficial erosion of plaque = transient episodes of thrombotic vessel occlusion and vasoconstriction at the site of plaque damage
- Occludes the vessel for no more than 10 to 20 minutes with return of perfusion before necrosis occurs
- Angina that is new onset, occurs at rest, increasing severity or frequency
Non-ST elevation MI (NSTEMI) or subendocardial infarction
Thrombus breaks up before complete distal tissue necrosis occurs
Involves only the myocardium directly beneath the endocardium (subendocardial)
ST wave depression or T-wave inversion
Name 3 things Myocardial remodeling causes
myocyte hypertrophy, scarring and loss of contractile function
Mediated by Ang II, aldosterone, catecholamines, adenosine oxidative stress, inflammatory cytokines
Can be limited or reversed- restore blood flow, sequential pacemakers, LVADs (left ventricular assist devices), ACE inhibitors and beta blockers
Evaluation
H&P
Ankle-brachial index
Risk factor reduction
Antiplatelet therapy
what is the number one cause of death in men and women
CAD
Stable angina
Stable Angina-recurrent predictable chest pain
- Caused by gradual luminal narrowing and hardening of arterial walls
- Blood flow is restored with rest– no necrosis of myocardial cells
- Substernal chest discomfort
- Caused by the buildup of lactic acid and abnormal stretching of the myocardium
- Afferent sympathetic fiber from C3-T4-variety of locations and radiation patterns of angina pain
- Pain is relieved by rest and nitrates
- Women and individuals with autonomic disorders (elderly, diabetics) my present with atypical symptoms
clinical manifestations
Individuals may experience dyspnea, diaphoresis and anxiety
ST elevation MI (STEMI) or transmural infarction
Thrombus lodges permanently in the vessel
Infarction extends from the endocardium to epicardium (transmural)
ST elevation
the result of scar tissue
necrotic area is replaced by scar tissue
Unable to contract and relax like healthy myocardial tissue
Acute Coronary Syndromes
Sudden coronary obstruction caused by thrombus formation over a ruptured or ulcerated atherosclerotic plaque
Prinzmetal angina
unpredictable chest pain
Also called variant angina: unpredictable and almost exclusively at rest
Often occurs at night during REM sleep
Pain is caused by vasospasm of 1 or more major coronary arteries
Can occur with or without atherosclerosis
May result from
Decreased vagal activity
Hyperactivity of the SNS
Decreased nitric oxide activity
ECC
ECG reveals ST segment depression and/or T-wave inversion
Resolves as the pain is relieved
Myocardial Infarction Pathway
After 8-10 seconds of decrease blood flow– myocardium becomes cool and cyanotic
Myocardial oxygen reserves deplete after ~8 seconds- anaerobic metabolism and decreased glycogen stores
Anaerobic glycolosis only supplies 65-70% of myocardial energy requirement and less ATP
Hydrogen ions and lactic acid accumulate
Oxygen deprivation- electrolyte disturbances (loss of K+, Ca++, Mg++)
Evaluation and Treatment
§Diagnosis:
§H&P
§ECG
§Helps localize the affected area through ST and T wave changes
§Serial cardiac biomarkers
§Cardiac troponin is the most specific indicator—obtain on admission
§CPK-MB
§LDH
Prinzmetal angina treatment
Ca++ channel blockers or long-acting nitrates should be continued even with remission
Serum cardiac biomarkers
normal
Oxygen and nutrient deprivation
decreased contractility
the most specific indicator—obtain on admission
Cardiac troponin
Silent ischemia
Silent Ischemia-no detectable symptoms
§Not associated with symptoms or may be associated with non-specific symptoms (fatigue, dyspnea, feeling of unease)
§Can occur in isolation or in individuals who also experience angina
§Global or regional abnormalities in the LV sympathetic afferent innervation
§DM
§Surgical denervation during CABG
§Following cardiac transplantation
§Local nerve injury by MI
§During mental stress or anger
§Release of catecholamines= increased HR, BP, vascular resistance, electrical instability
if symptoms persist despite medical treatment
Percutaneous intervention (PCI)
Ischemic cells release
catecholamines
Serious imbalance of sympathetic and parasympathetic function
Dysrhythmias
Heart failure
Left ventricular involvement
pulmonary congestion
Ang II is released during MI causing
vasoconstriction and fluid retention
Increases myocardial work exacerbating the effects of lost contractility
Local release
Growth factor for vascular smooth muscle cells, myocytes and cardiac fibroblasts
Promotes further catecholamine release and coronary vasospasm
Right ventricular involvement
increases in systemic venous pressures
the result of MI on myocardial tissue
Irreversible hypoxic injury cause cellular death and tissue necrosis at ~20 minutes of ischemia
Necrosis of myocardial tissue, release of troponin through damaged cell membranes
Lymphatics carry the troponin to the blood stream
Myocardial tissue is also destroyed by apoptosis and autophagy
NSTEMI and unstable angina are treated similarly
- antithrombotics
- anticoagulants
- PCI
overall STEMI treatment
Emergent PCI
Antithrombotics
Coronary artery bypass graft (CABG)