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Ischemic Heart Disease. Ana H. Corona, FNP-Student University of Phoenix May 2002. Myocardial Ischemia. Results when there is an imbalance between myocardial oxygen supply and demand Most occurs because of atherosclerotic plaque with in one or more coronary arteries

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ischemic heart disease

Ischemic Heart Disease

Ana H. Corona, FNP-Student

University of Phoenix

May 2002

myocardial ischemia
Myocardial Ischemia
  • Results when there is an imbalance between myocardial oxygen supply and demand
  • Most occurs because of atherosclerotic plaque with in one or more coronary arteries
  • Limits normal rise in coronary blood flow in response to increase in myocardial oxygen demand
oxygen carrying capacity
Oxygen Carrying Capacity
  • The oxygen carrying capacity relates to the content of hemoglobin and systemic oxygenation
  • When atherosclerotic disease is present, the artery lumen is narrowed and vasoconstriction is impaired
  • Coronary blood flow cannot increase in the face of increased demands and ischemia may result
angina
Angina
  • When ischemia results it is frequently accompanied by chest discomfort: Angina Pectoris
  • In the majority of patients with angina, development of myocardial ischemia results from a combination of fixed and vasospastic stenosis
chronic stable angina
Chronic Stable Angina
  • May develop sudden increase in frequency and duration of ischemic episodes occurring at lower workloads than previously or even at rest
  • Known as unstable angina: up to 70% patients sustain MI over the ensuing 3 months
angina cont
Angina: cont
  • Patients with mild obstruction coronary lesions can also experience unstable angina
  • >90% of Acute MI result from an acute thrombus obstructing a coronary artery with resultant prolonged ischemia and tissue necrosis
treatment of angina
Treatment of Angina
  • Treatment of Chronic Angina is directed at minimizing myocardial oxygen demand and increasing coronary flow
  • Where as in the acute syndromes of unstable angina or MI primary therapy is also directed against platelet aggregation and thrombosis
epidemiology
Epidemiology
  • Modifiable Factors: hyperlipidemia- ^ LDL (<130 normal) or low HDL (>60 normal), Hypertension, cigarette smoking and diabetes, obesity, BMI of >30
  • Non-Modifiable Factors: advanced age, male sex, family medical history: male <55 y/o, female <65 y/o
  • Other: sedentary lifestyle and stressful emotional stress
homocysteine
Homocysteine
  • Concentration of amino acid homocysteine is related to incidence of coronary, cerebral, and peripheral vascular disease
  • The risk of MI is 3x > in patients with high levels of homocysteine compared with those with the lowest levels
  • Supplement of diet with foliate and other B vitamins lower levels of homocysteine but not known where therapy improves coronary risk
fibrinogen
Fibrinogen
  • Elevated level of plasma fibrinogen is independent risk factor for CAD in males and females
  • Elevated levels of coagulation factor VII is risk factor X50 fold if with smoking or HTN
  • Careful HX taking: to evaluate s/s include: quality, location, radiation, precipitating factors, frequency
quality
Quality
  • Tightness, squeezing, heaviness, pressure, burning, indigestion or aching sensation
  • It is rarely “PAIN”
  • Never: sharp, stabbing, prickly, spasmodic, or pleuritic
  • Lasts a few seconds < 10 minutes
  • Relieved by NTG s/l
  • Levine Sign: clench fist to sternum
signs symptoms accompany angina
Signs & Symptoms accompany Angina
  • Dyspnea, nausea, diaphoresis resolve quickly after cessation of angina
  • Angina is a diffuse sensation rather than discrete
ischemic heart disease13
Ischemic Heart Disease
  • Imbalance between Myocardial oxygen supply and demand = Myocardial hypoxia and accumulation of waste metabolites due to atherosclerotic disease of coronary arteries
stable angina
Stable Angina
  • Stable Angina: chronic pattern of transient angina pectoris precipitated by physical activity or emotional upset, relieved by rest with in few minutes
  • Temporary depression of ST segment with no permanent myocardial damage
angina pectoris
Angina Pectoris
  • Angina Pectoris: uncomfortable sensation in the chest or neighboring anatomic structures produced by myocardial ischemia
variant angina
Variant Angina
  • Typical anginal discomfort usually at rest
  • Develops due to coronary artery spasm rather than increase myocardial oxygen demand
  • Transient shifts of ST segment – ST elevation
unstable angina
Unstable Angina
  • Increased frequency and duration of Angina episodes, produced by less exertion or at rest = high frequency of myocardial infarction if not treated
silent ischemia
Silent Ischemia
  • Asymptomatic episodes of myocardial ischemia
  • Detected by electrocardiogram and laboratory studies
myocardial infarction
Myocardial Infarction
  • Region of myocardial necrosis due to prolonged cessation of blood supply
  • Results from acute thrombus at side of coronary atherosclerotic stenosis
  • May be first clinical manifestation of ischemic heart disease or history of Angina Pectoris
precipitants
Precipitants
  • Exertion: walking, climbing stairs, vigorous work using arms, sexual activity
  • Vasoconstriction: extremities, increased systemic vascular resistance, increased in myocardial wall tension and oxygen requirements
  • Myocardial Ischemia displays a circadian rhythm threshold for Angina it is lower in morning hours.
physical examination
Physical Examination
  • Arcus senilis, xanthomas, funduscopic exam: AV nicking, exudates
  • Signs and symptoms: hyperthyroidism with increased myocardial oxygen demand, hypertension, palpitations
  • Auscultate carotid and peripheral arteries and abdomen: aortic aneurysm
  • Cardiac: S4 common in CAD, increased heart rate, increased blood pressure
ischemia
Ischemia
  • Myocardial ischemia may result in papillary muscle regurgitation
  • Ischemic induced left ventricular wall motion abnormalities may be detected as an abnormal precordial bulge on chest palpation
  • A transient S3 gallop and pulmonary rales = ischemic induced left ventricular dysfunction
diagnostic tests
Diagnostic Tests
  • Blood tests include serum lipids, fasting blood sugar, Hematocrit, thyroid (anemias and hyperthyroidism can exacerbate myocardial ischemia
  • Resting Electrocardiogram: CAD patients have normal baseline ECGs
    • pathologic Q waves = previous infarction
    • minor ST and T waves abnormalities not specific for CAD
electrocardiogram
Electrocardiogram
  • Electrocardiogram: is useful in diagnosis during cc: chest pain
  • When ischemia results in transient horizontal or downsloping ST segments or T wave inversions which normalize after pain resolution
  • ST elevation suggest severe transmural ischemia or coronary artery spasm which is less often
exercise stress test
Exercise Stress Test
  • Used to confirm diagnosis of angina
  • Terminate if hypotension, high grade ventricular disrrhythmias, 3 mm ST segment depression develop
  • (+): reproduction of chest pain, ST depression
  • Severe: chest pain, ST changes in 1st 3 minutes, >3 mm ST depression, persistent > 5 minutes after exercise stopped
  • Low systolic BP, multifocal ventricular ectopy or V- tach, ST changes, poor duration of exercise (<2 minutes) due to cardiopulmonary limitations
other diagnostic tests
Other Diagnostic Tests
  • Radionuclide studies
  • Myocardial perfusion scintigraphy
  • Exercise radionuclide ventriculography
  • Echocardiography
  • Ambulatory ECG monitoring
  • Coronary arteriography
management goals to reduce anginal symptoms
Management Goals to reduce Anginal Symptoms
  • Prevent complications – myocardial infarction, and to prolong life
  • No smoking, lower weight, control hypertension and diabetes
  • Patients with CAD – LDL cholesterol should achieve lower levels (<100)
  • HMG-COA reductase inhibitors are effective
pharmacologic therapy
Pharmacologic Therapy
  • Therapy is aimed in restoring balance between myocardial oxygen supply and demand
  • Useful Agents: nitrates, beta-blockers and calcium channel blockers
nitrates
Nitrates
  • Reduce myocardial oxygen demand
  • Relax vascular smooth muscle
  • Reduces venous return to heart
  • Arteriolar dilators decrease resistance against- which left ventricle contracts and reduces wall tension and oxygen demand
nitrates cont
Nitrates: cont
  • Dilate coronary arteries with augmentation of coronary blood flow
  • Side effects: generalized warmth, transient throbbing headache, or lightheadedness, hypotension
  • ER if no relief after X2 nitro's: unstable angina or MI
problems with nitrates
Problems with Nitrates
  • Drug tolerance
  • Continued administration of drug will decrease effectiveness
  • Prevented by allowing 8 – 10 hours nitrate free interval each day.
  • Elderly/inactive patients: long acting nitrates for chronic antianginal therapy is recommended
  • Physical active patients: additional drugs are required
beta blockers
Beta Blockers
  • Prevent effort induced angina
  • Decrease mortality after myocardial infarction
  • Reduce Myocardial oxygen demand by slowing heart rate, force of ventricular contraction and decrease blood pressure
beta 1
Beta -1
  • Block myocardial receptors with less effect on bronchial and vascular smooth muscle- patients with asthma, intermittent claudication
beta agonist blockers
Beta-Agonist blockers
  • With partial B-agonist activity:
  • Intrinsic sympathomimetic activity (ISA) have mild direct stimulation of the beta receptor while blocking receptor against circulating catecholamines
  • Agents with ISA are less desirable in patients with angina because higher heart rates during their use may exacerbate angina
  • not reduce mortality after AMI
beta blockers35
Beta-blockers
  • Duration of beta-blockers depends on lipid solubility
  • Accounts for different dosage schedules
esmolol
Esmolol
  • Short acting administered intravenously
  • Can be used to test tolerability of beta-blockage
  • Used for tachydysrhythmias and unstable angina
  • Primary prevention trials: beta blockers decrease incidence of first MIs with hypertensive patients
contraindications
Contraindications
  • Symptomatic CHF, history of bronchospasm, bradycardia or AV block, peripheral vascular disease with s/s of claudication
side effects
Side Effects
  • Bronchospasm (RAD), CHF, depression, sexual dysfunction, AV block, exacerbation of claudication, potential masking of hypoglycemia in IDDM patients
abrupt cessation
Abrupt Cessation
  • Tachycardia, angina or MI
  • Inhibit vasodilatory beta 2 receptors
  • Should be avoided in patients with predominant coronary artery vasospasm
beta blockers long term effects
Beta-Blockers: Long Term effects
  • Serum lipids: decrease of HDL cholesterol and increased triglycerides
  • Effects do not occur with beta-blockers with B-agonist activity or alpha-blocking properties
calcium channel blockers
Calcium Channel Blockers
  • Anti-anginal agents prevent angina
  • Helpful: episodes of coronary vasospasm
  • Decreases myocardial oxygen requirements and increase myocardial oxygen supply
  • Potent arterial vasodilators: decrease systemic vascular resistance, blood pressure, left ventricular wall stress with decrease myocardial oxygen consumption
nifedipine and other dihydropyridine calcium channel blockers
Nifedipine and other dihydropyridine calcium channel blockers
  • Fall in blood pressure, trigger increase heart rate
  • Undesirable effect associated with increased frequency of myocardial infarction and mortality
calcium channel blockers43
Calcium Channel Blockers
  • Secondary agents in management of stable angina
  • Are prescribed only after beta blockers and nitrate therapy has been considered
  • Potential to adversely decrease left ventricular contractility
  • Used cautiously in patients with left ventricular dysfunction
amlodipine and felodipine
amlodipine and felodipine
  • Are newer CCB
  • Decrease (-) inotropic effects
  • Amlodipine is tolerated in patients with advanced heart failure without causing increase mortality when added with ace inhibitor, diuretic, and digoxin
slide45
LDL
  • Undergoes oxidation in proximity of arterial wall = prone to atherosclerotic process
  • Vitamin E 200 – 400 IU daily may lower coronary death rates
drug selection
Drug Selection
  • Chronic Stable Angina: beta blocker and long acting nitrate or calcium channel blocker (not verapamil: bradycardia) or both.
  • If contraindication to BB a CCB is recommended (bronchospasm, IDDM, or claudication) any of CCB approved for angina are appropriate.
drugs
Drugs
  • Verapamil and Cardizem is preferred because of effect on slowing heart rate
  • Patients with resting bradycardia or AV block, a dihydropyridine calcium blocker is better choice
  • Patients with CHF: nitrates preferred amlodipine should be added if additional therapy is needed
drugs48
Drugs
  • Primary coronary vasospasm: no treatment with beta blockers, it could increase coronary constriction
  • Nitrates and CCB are preferred
  • Concomitant hypertension: BB or CCB are useful in treatment
  • Ischemic Heart Disease & Atrial Fibrillation: treatment with BB, verapamil or Cardizem can slow ventricular rate
combination therapy
Combination Therapy
  • If patients do not respond to initial antianginal therapy – a drug dosage increase is recommended unless side effects occur.
  • Combination therapy: successful use of lower dosages of each agent while minimizing individual drug side effects
combination therapy include
Combination Therapy Include:
  • Nitrate and beta blocker
  • Nitrate and verapamil or cardizem for similar reasons
  • Long acting dihydropyridine calcium channel blocker and beta blocker
  • A dihydropyridine and nitrate is often not tolerated without concomitant beta blockade because of marked vasodilatation with resultant head ache and increased heart rate
combinations
Combinations
  • Beta blockers should be combined only very cautiously with verapamil or cardizem because of potential of excessive bradycardia or CHF in patients with left ventricular dysfunction
other methods
Other methods
  • Patients with 1 – 2 vessel disease with normal left ventricular function are referred for catheter based procedures
  • Patients with 2 and 3 vessel disease with widespread ischemia, left ventricular dysfunction or DM and those with lesions are not amendable to catherization based procedures and are referred for CABG
unstable angina53
Unstable Angina
  • Ischemic episodes occur more frequently more intense, last longer.
  • Precipitated by less activity or even at rest
  • May progress to acute MI due to presence of complicated coronary lesions with ulceration, hemorrhage or thrombosis at side of atherosclerotic plaque
  • Lesions may heal: s/s return to more stable pattern
unstable angina cont
Unstable Angina: cont
  • It is a medical emergency
  • During episodes of angina, transient ST segment shifts or T wave flattening or inversion is likely
  • Signs of LV dysfunction (pulmonary rales, S3, Mitral regurgitation) may accompany ischemic episodes.
unstable angina cont55
Unstable Angina: cont
  • Therapy: reduce myocardial oxygen demand with increase coronary flow
  • Antiplatelet and anticoagulant agents
  • Aspirin and IV heparin: reduces incidence of myocardial infarction and cardiac death in unstable angina
  • Oral Antiplatelet drug: ticlopidine: used for ASA intolerance individuals
enoxaparin
Enoxaparin
  • Enoxaparin: low molecular weight heparin: effective in preventing ischemic events and death at 30 days and 1 year after administration than standardized IV heparin
silent ischemia57
Silent Ischemia
  • Silent or painless ischemia
  • Presence of ST shifts with absence of symptoms
  • Increased risk of myocardial infarction and cardiac death common in diabetic patients
  • Beta blockers or calcium channel blockers and aspirin, cardiac catheterization, if left main or 3 vessels disease with left ventricular dysfunction is demonstrated
acute myocardial infarction
Acute Myocardial Infarction
  • Is dreaded outcome in patients with ischemic heart disease
  • 1.5 million people sustain an MI in USA each year
  • Mortality rate of 25%
  • 60% of MI related deaths occur before medical facilities are reached
etiology
Etiology
  • MI: is due to prolonged myocardial ischemia - leads to irreversible necrosis of heart muscle
  • 90% due to acute thrombus at site of underlying coronary atherosclerosis
  • Non-atherosclerotic causes: cocaine use – due to ability of cocaine to increase myocardial 02 demand, induce coronary vasospasm & promote coronary thrombosis in association with platelet activation and endothelial cell dysfunction
clinical presentation
Clinical Presentation
  • Initial diagnosis: presenting history, PE, and ECG
  • Most common S/S: severe crushing chest pain
  • Lasts longer than Angina, more intense, nausea, diaphoresis, dyspnea and feeling of impending doom
symptoms
Symptoms
  • Circadian variability: occurring most commonly in morning hours, soon after awakening
  • Symptoms usually begin while at rest, and only occasionally are brought on by physical exertion
  • Some patients have less pronounced symptoms: generalized weakness, dyspnea, and indigestion.
  • 20% cases have no s/s: detected by ECG changes
slide62
MI
  • Common physical findings in MI relate to impaired left ventricular systolic and diastolic function, associated inflammatory responses and stimulation of the sympathetic and parasympathetic nervous system
other causes of substernal chest pain
Other causes of substernal chest pain
  • Aortic dissection or pulmonary emboli may be fatal if not quickly recognized
  • Inappropriate administration of thrombolytic therapy to patients with pericarditis or aortic dissection could result in severe complications or death
electrocardiogram64
Electrocardiogram
  • Q wave infarction, initial hyperacute T waves and ST elevation are present in the leads overlying involved myocardium
  • As cell death occurs, there is loss of the R wave and progressive Q wave development
  • The T wave begins to invert, followed by return of the ST segment over subsequent days
ecg cont
ECG: cont
  • T wave may remain inverted for weeks to months
  • The new Q wave persists permanently
  • Posterior wall infarctions: mirror image pattern in anterior chest leads
  • With initial ST segment depression
  • T wave inversion and development of tall R waves in leads VI and V2
ecg cont66
ECG: cont
  • Non Q wave infarction: new ST depression and/or T wave inversions persist for 48 hours or longer in leads overlying infarcting segments
  • BBB: diagnostic ECG evolution may not occur and diagnosis of Mi relies on presence of serum markers and laboratory modalities
serum markers of infarction
Serum Markers of Infarction
  • Certain proteins are released into circulation during an MI
  • Creatine kinase CK rises in plasma within 4 to 8 hours, peaks at 24 hours, returns to normal by 48 hours to 72 hours
  • Not specific for myocardial damage: skeletal muscle trauma and IM injection, and hypothyroidism
ck mb
CK-MB
  • CK-MB isoenzyme is more specific for diagnosis of AMI
  • Not influenced by skeletal muscle injuries
  • CK-MB rises and peaks slightly earlier than total CK and returns to normal within 36 – 72 hours
  • May be elevated in: myocarditis after surgery, hypothyroidism, repetitive cardioversion
enzymes
Enzymes
  • Acute MI: CK-MB is greater than 2.5% of total serum CK
  • Serum CK and CK-MB isoenzyme should be measured on admission, then 12 and 24 hours later in diagnostic evaluation of an acute MI
troponin
Troponin
  • Troponin I and T are sensitive and highly specific markers of acute MI
  • Levels begin to rise within 3 hours after onset of infarction and remain elevated for several days
  • Higher Troponin I levels or early (+) of Troponin T assay correlate with greater short-term mortality
myoglobin
Myoglobin
  • Myoglobin is released into circulation very early after myocardial injury and detected within 2 hours of infarction
  • Rapid renal clearance and low specificity limit it s diagnostic role
lactate dehydrogenase ldh
Lactate Dehydrogenase (LDH)
  • Rises within 24 to 48 hours of MI
  • Peaks at 3 – 5 days and returns to baseline by 7-10 days
  • Usefulness in patients who are admitted to hospital 2 – 3 days after onset of symptoms
  • Level of LDH-1 greater than LDH-2 = myocardial necrosis
thrombolytic therapy
Thrombolytic Therapy
  • Activates the natural fibrinolytic system to dissolve responsible thrombus
  • Reduces mortality and improves recovery of left ventricular function following AMI
  • Streptokinase SK, anisoylated plasminogen-SK activator (APSAC), tissue plasminogen activator (alteplase or t-PA), and modified plasminogen activator (reteplase or r-PA)
thrombolytics
Thrombolytics
  • Each of these drugs results in conversion of the proenzyme plasminogen to active plasmin which dissolves fibrin clots
  • Bleeding is the most important risk of each of these agents and their adjunctive therapies
  • Successful reperfusion: relief of chest pain and early peak of CK within 12 hrs
thrombolytics75
Thrombolytics
  • Reperfusion dysrhythmias are common: accelerated idioventricular rhythm, not require intervention
  • Antiplatelet and anticoagulant therapy used to maintain patency of coronary vessels following thrombolysis
thrombolytics76
Thrombolytics
  • Aspirin inhibits platelet function and reduces reocclusion following thrombolysis: 160 – 325 mg/day
  • Intravenous heparin needed to maintain vessel patency after initial thrombolytic therapy and is administered to achieve an activated PTT of 50 to 75 seconds for 48 hours