ACUTE CORONARY SYNDROME

is a term used for any condition brought on by sudden, reduced blood flow to the heart. can describe chest pain you feel during a heart attack, or chest pain you feel while you're at rest or doing light physical activity (unstable angina). Acute coronary syndrome is often diagnosed in an emergency room or hospital.

 is caused primarily by atherosclerosis. Most cases of ACS occur from disruption of a previously non-severe lesion (an atherosclerotic lesion that was previously hemodynamically insignificant yet vulnerable to rupture). The vulnerable plaque is typified by a large lipid pool, numerous inflammatory cells, and a thin, fibrous cap.

RISK FACTORS
Gender Men are at higher risk at young age but risk increases with women during postmenopausal period Age People who are age 40 and above are at greater risk of having ACS. A family history of heart disease

 Major Independent Risk Factors for Coronary Heart Disease that can be controlled or modified Cigarette and Tobacco smoke Tobacco contains certain components that are known to damage vessel walls. The bodys response to this damage elicits the formation of atherosclerosis thereby increasing the risk of an acute MI.

 High blood cholesterol - An elevated total cholesterol level is major component of atherosclerotic plaque buildup which causes the development of an acute MI. High blood pressure - High blood pressure (squeezing of arteries and veins) has consistently been associated with an increased risk of developing an acute MI (both systolic and diastolic elevations).

 Physical inactivity exercise increase HDL (good cholesterol) and decreases LDL (bad cholesterol), triglycerides, and cholesterols. Diabetes - Patients with DM have a substantially greater risk of developing atherosclerotic vascular disease at an accelerated rate. This acceleration occurs regardless of whether the patient has DM Type 1 or DM Type 2.

SIGNS AND SYMPTOMS

Cardiovascular Chest pain occurs suddenly and continues despite rest and medication; usually described as pressure, squeezing, or a burning sensation across the precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm Heart sounds may include S3, S4 and a new onset of murmur (may reflect papillary muscle dysfunction) Increased jugular venous distention may be seen if the MI has caused heart failure

 Cardiovascular Hypertension - May precipitate angina or reflect elevated catecholamine levels d/t anxiety or to exogenous sympathomimetic stimulation Hypotension - indicates ventricular dysfunction due to myocardial ischemia, infarction, or acute valvular dysfunction Pulse deficit may indicate atrial fibrillation Palpitations

 Gastrointestinal Nausea Vomiting Genitourinary Decreased urinary output may indicate cardiogenic shock Skin Cool, clammy, diaphoretic and pale appearance d/t sympathetic stimulation may indicate cardiogenic shock

 Respiratory Shortness of breath Dyspnea (Exertional dyspnea that resolves with pain or rest), Tachypnea Crackles Pulmonary edema Neurologic Anxiety, restlessness and light-headedness may indicate sympathetic stimulation or a in contractility and cerebral oxygenation may also herald cardiogenic shock

ELECTROCARDIOGRAM
Classic ECG Changes: T-wave inversion, ST-segment elevation, and development of an abnormal Q wave. Myocardial injury causes the T-wave to become enlarged and symmetric. As the area of injury becomes ischemic, myocardial repolarization is altered and delayed, causing the T wave to invert.

 Myocardial injury also causes ST segment changes. The injured myocardial cells depolarize normally but repolarize more rapidly than normal cells causing the ST segment to rise at least 1mm above the isoelectric line when measured 0.08seconds after the end of the QRS. If the myocardial injury is on the endocardial surface, the ST segment is depressed 1mm or more for at least 0.08 seconds.

 MI is classified as a Q wave or non-Q wave infarction. With Q wave infarction, abnormal Q waves develops within 1-3 days because there is no depolarization current conducted from the necrotic tissue. An abnormal Q wave may be present w/o ST segment and T wave changes, which indicates an old MI. Patients with non-Q wave MIs dont develop a Q wave on the ECG after the ST segment and T wave changes, but symptoms and cardiac enzyme analysis confirm the Dx of an AMI.

LABORTORY TESTS
Creatine Kinase (CK or CPK) Released from damaged muscle, CK is an enzyme found in the heart, skeletal muscle and brain. It consists of 3 isoenzymes; mm (found in skeletal muscle, MB (found in cardiac muscle) and BB (found in brain tissue). Damage to any of these tissues causes the release of CK into the blood stream and hence an elevated level.

CKMB After cardiac injury, CK and the isoenzyme MB are released into the blood stream at a predictable rate. Within a 4 to 8 hour window (post injury), the CKMB level rises above normal and within 12 to 24 hours this level elevates to approximately 5 to 15 times normal. Within 2 to 3 days, the CKMB returns to normal. Because the MB isoenzyme is exclusive to cardiac muscle tissue, it is considered to be a very definitive test for diagnosing an acute MI.

Troponin Troponin is a protein that helps regulate heart muscle contraction and because it can be isolated in the blood, it is considered to be a sensitive indicator of an acute MI. Troponin consists of 3 separate proteins which are Troponin I, Troponin T and Troponin C. The function of each of these specific proteins is as follows:

 Troponin I and T these levels are not normally found in the blood stream so any detection of these protein in the blood indicates the infarction or death of cardiac muscle/tissue. Troponin C - binds to calcium ions and is not used to determine cell tissue/death.

Myoglobin heme protein that helps transport oxygen. Like CKMB enzyme, it is found in cardiac and skeletal muscle. The myoglobin level starts to increase w/in 1-3 hrs and peaks w/in 12 hrs after the onset of symptoms.

Cardiac Enzyme Normal Values

Enzyme/Protein Normal Values F: 30-135 units/L M: 55-170 units/L
0% of total CK 0.1 0.2 ng/ml 0 0.6 ng/ml

Creatine Kinase

CK-MB Troponin I Troponin T

ECHOCARDIOGRAM
It can assist with diagnosing which portion of the heart has been damaged and which coronary arteries have been affected. An echocardiogram can also help determine cardiac muscle movement/contraction and cardiac wall abnormalities.

DYSRHYTHMIAS
A dysrhythmia is the most common complication after an acute MI. Dysrhythmias after an acute MI are caused by the formation of re-entry circuits between the still healthy and necrotic myocardium.

EMBOLIC COMPLICATIONS
The most common time post acute MI for the development of embolism is within the first 10 days. Patients who suffer from the complication of embolism are at risk of developing limb ischemia, renal infarction, intestinal ischemia but the most common clinical presentation after an embolic event is a stroke.

PERICARDITIS
The cause of Pericarditis after acute MI is due to an inflammatory reaction that occurs secondary to the presence of necrotic tissue

CARDIOGENIC SHOCK (SECONDARY TO ACUTE MI)

occurs when the bodies needs for oxygen are not met for a prolonged period of time. When this occurs; the body attempts to compensate for the decreased oxygen supply by increasing heart rate, stroke volume and contractility. Unfortunately as this continues, the workload of the heart becomes too much and the result; total cardiac decompensation begins.

 When decompensation begins the patient shows signs of shock, low blood pressure, increased or decreased heart rate and decreased oxygen saturations. Other symptoms mimic those that are seen with congestive heart failure and/or pulmonary edema.

CONGESTIVE HEART FAILURE

blockage affects a large amount of heart muscle, the heart will not pump effectively. If the blockage shuts off blood flow to the electrical system of the heart, the heart rhythm may be affected.

PERCUTANEOUS TRANSMURAL CORONARY ANGIOPLASTY

PTCA is an effective revascularization procedure that is used to increase the diameter of an artery that has been stenosed due to coronary artery disease. With the use of fluoroscopy, a cardiologist can insert a catheter (through the femoral artery) and guide it through the arterial circulation through the ascending aorta and into the ostium of the right or left coronary artery.

 A balloon tipped catheter is then passed into the area of blockage and inflated (no more than 30 to 129 seconds) which in turns helps to compress plaque against the lumina of the artery. The balloon can also help to stretch the lumina itself which also improves blood flow. Of note: when the balloon is inflated, there is an occlusion of coronary blood supply, so patients often experience a degree of chest pain during balloon inflation.

 The degree of chest pain experienced and the difficulty in compression plaque may require that the physician inflate and deflate the balloon several times during the procedure.

MORPHINE
Because catecholamines are released in response to the anxiety and pain associated with suffering an acute MI (increasing the workload of the heart), Morphine can be used. Morphine is also beneficial in reducing the hemodynamic workload by increasing venous capacitance and reducing systemic vascular resistance (therefore decreasing myocardial oxygen demand).

NITROGLYCERIN
Nitrates such as Nitroglycerin cause vasodilation of the vessels and help to decrease cardiac oxygen demand, cardiac preload and afterload while increasing cardiac output.

ASPIRIN
The primary mechanism is believed to be related to irreversible inhibition of the cyclooxygenase pathway of platelets (blocking the formation of thromboxane A2 and thromboxane A2-induced platelet aggregation). It is strongly recommended that all patients who have suffered and acute MI be given a non-enteric coated aspirin (160mg to 325mg) to chew and swallow as soon as possible.

ANTICOAGULANTS (REOPRO)
ReoPro is a platelet glycoprotein II/b/IIIa receptor inhibitor that has been proven to be effective for the management of any coronary ischemic syndrome. It is starting during a PTCA procedure and in most cases is used as an adjunct for stent placement. ReoPro is given as an IV bolus of 0.25 mg/kg and followed by a continuous infusion rate of 10 mcg/min for the following 12 hours. The use of ReoPro is thought to reduce platelet aggregation by approximately 80%.

ANTICOAGULANTS (TICLID)
Ticlid is given in 250 mg doses BID and is also an Antiplatelet agent. Unlike aspirin, Ticlid does not block cyclooxygenase but instead interferes with the platelet activation mechanism that is mediated by adenosine diphosphate (ADP) which in turn interferes with the fibrinogen receptor glycoprotein IIb/IIIa. It takes approximately 2 weeks of therapy with Ticlid before the full benefit is achieved.

HEPARIN
Heparin is an anticoagulant that inhibits activated factors IS, S, SI and XII (which are all involved in the conversion of Prothrombin to thrombin). By inhibiting these activated factors, Heparin is thought to keep the blood thinner and prevents clotting. This is turns allows for easier blood travel through the vessels that are affected by narrowing and atherosclerosis.

BETA BLOCKERS
A Beta blocker acts by blocking the Badrenergic responses to catecholamine stimulation. Beta blockers decrease heart rate, blood pressure, contractility and myocardial oxygen demand. Being able to decrease the work load of the heart assists with improving cardiac output and lessens the severity of the damage caused by the acute MI. Beta blockers can actually interrupt an evolving MI, limit the infarct size and decrease the risk of ventricular arrhythmias by decreasing oxygen demand.

CALCIUM CHANNEL BLOCKERS

Calcium channel blockers prohibit the entry of calcium into smooth muscle. This assists with dilating coronary arteries and veins which in turn provides an increase in overall cardiac blood flow. Calcium channel blockers also decrease systemic blood pressure, total peripheral resistance and cardiac afterload.

ACE INHIBITORS
ACE inhibitors block to the conversion of Angiotensin I to Angiotensin II (which is a potent vasoconstrictor). The goal of and ACE inhibitor is to decrease blood pressure and afterload without increasing heart rate or the workload of the heart.

tPA (ATEPLASE)
tPA is a human protein that is manufactured by genetic engineering. Tissue plasminogen activator is one of several drugs not approved for use in certain patients who are suffering from and acute MI. tPA is designed to dissolve the blood clots (in the arteries) that are responsible for causing the majority of acute MIs. tPA is given in an initial 15 mg IV bolus then 0.75 mg/kg (maximum of 50 mg) over 30 minutes.

 This is then followed by 0.5 mg/kg (maximum 35 mg) over 60 minutes for a total of 100 mg over 90 minutes. Signs of reperfusion include pain relief; reperfusion arrhythmias (accelerated idioventricular rhythm, ventricular ectopy and bradycardia).

 Monitor for symptoms of heart failure/decreased cardiac output (VS, heart sounds, and S3 gallop). Observe for symptoms of cardiogenic shock (cool clammy skin, hypotension, decreased peripheral pulses, and pulmonary congestion). Titrate inotropic and vasoactive medication within defined parameters to maintain adequate contractility, pre/afterload and blood pressure.

 For complaints of chest pain, medicate and note severity, location, radiation, what were contributing factors (getting up, participating in ADLs for example) and report findings. Monitor intake and output (IV fluid, urine output, PO intake (fluid overload increases the workload of the heart and decreased cardiac output can cause a decrease in perfusion to the kidneys). Note results of diagnostic imaging studies (EKG, radionuclide imaging, and Dobutamine stress tests).

 Watch laboratory data closely (ABGs, serial enzymes, electrolytes, B-type natriuretic peptide, serum creatinine). Monitor oxygen saturation and provide O2 as ordered and necessary. Monitor blood pressure/pulse before and after the administration of cardiac medications. HOB should be at 30 degrees to decrease the work of breathing and decrease preload.

 Provide a proper rest/activity balance to assure that cardiac output is not compromised (gradually increase activity as condition warrants). Order small sodium restricted diet (sodium restriction helps to avoid fluid overload). Monitor bowel function (a stool softener should be ordered to avoid unnecessary pushing). Provide a peaceful environment that minimizes stressors to promote healing.

 Weigh patient daily (same time each day, same equipment). Assess for the presence of anxiety (keep environment free of unnecessary stressors, educate patient to the rationale for interventions and procedures). Assess for the presence of depression (depression is common after and acute MI and can result in increased mortality). Refer patient to cardiac outpatient program and support groups. Assist with organizing cardiac rehabilitation efforts post discharge.

 Educate patients about the dangers of cigarette smoking, a major risk factor for coronary artery disease (CAD). Bupropion increases the likelihood of successful smoking cessation. Emphasize low-cholesterol, low-salt diet. In addition, educate patients about AHA dietary guidelines regarding a low-fat, low-cholesterol diet. A cardiac rehabilitation program after discharge may reinforce education and enhance compliance.

 The following mnemonic may useful in educating patients with CAD regarding treatments and lifestyle changes necessitated by their condition: A = Aspirin and antianginals B = Beta blockers and blood pressure (BP) C = Cholesterol and cigarettes D = Diet and diabetes E = Exercise and education

 For patients being discharged home, emphasize the following: Timely follow-up with primary care provider Compliance with discharge medications, specifically aspirin and other medications used to control symptoms Need to return to the ED for any change in frequency or severity of symptoms

MORTALITY: TEN (10) LEADING CAUSES NUMBER AND RATE/100,000 POPULATION

5-yr. Ave

Causes
1. Heart Disease 2. Vascular Disease 3. Malignant Neoplasms 4. Accidents** 5. Pneumonia

(2001 2005)

2006* #
83,081 55,466

#
69,741 52,106

Rate
85.5 64.0

Rate
95.5 63.8

39,634
33,650 33,764

48.6
41.4 41.5

43,043
36,162 34,958

49.5
41.6 40.2

Note: Excludes ill-defined and unknown causes of mortality * reference year ** External causes of Mortality

5-yr. Ave

Causes
6. Tuberculosis, all forms
7. Chronic lower respiratory diseases

(2001 2005)

2006* # Rate

#
27,017 19,024

Rate

33.2 25,860 29.7 23.3 21,216 24.4 18.5 20,239 23.3

8. Diabetes Mellitus 15,123

9.Certain conditions originating in the perinatal period 10. Nephritis, nephrotic syndrome and nephrosis

13,931 9,785

17.2 12,334 14.2 12.0 11,981 13.8

MORBIDITY: 10 Leading Causes, Number and Rate*

5-yr. Ave

Diseases
1. Acute Lower Respiratory Tract Infection and Pneumonia**

(2000 2004)

2005 #
690,566 616,041 603,287 406,237 382,662

#
694,209 669,800 726,211 459,624 314,175
2. Bronchitis/Bronchiolitis 3. Acute watery diarrhea

Rate
884.6 854.7 928.3 587.0 400.5

Rate
809.9 722.5 707.6 476.5 448.8

4. Influenza 5. Hypertension

*per 100,000 population ** Does not include ALRI, Pneumonia cases only from 2000-2002

5-yr. Ave

Diseases
6. TB Respiratory 7. Heart Disease

(2000 2004)

2005 #
114,360 43,898

#
109,369 43,945

Rate
139.7 56.1

Rate
134.1 51.5

8. Malaria
9. Chicken Pox 10. Dengue fever

35,970
79,236 15,383

46.1
41.1 19.6

36,090
30,063 20,107

42.3
36.3 23.6