Chest Pain and Acute Coronary Syndromes _ACS_

Chest Pain and Acute Coronary Syndromes (ACS): Generate a differential diagnosis in a patient presenting with chest pain:  Cardiac: myocardial infarction, stable angina, unstable angina, tension pneumothorax, aortic dissection  Gastrointestinal, Boerhaave’s syndrome  Musculoskeletal  Psychiatric  Pulmonary embolus Outline the common causes of non-cardiac chest pain:  Gastrointestinal, GERD, esophageal spasm, peptic ulcer disease, biliary disease, musculoskeletal, cervical disk, hyperventilation, pulmonary, psychiatric Identify clinical presentation and manifestations of patients with Acute Coronary Syndromes: STEMI:  Symptoms similar to unstable angina, may have severe pain/pressure, shortness of breath, disphoresis, nausea  Caused by complete vessel occlusion with myocardial necrosis  Elevated cardiac enzymes NSTEMI:  Symptoms similar to unstable angina  Sufficient occlusion to cause tissue damage and mild myocardial necrosis  ST depression and/or T-wave inversion  Elevated cardiac enzymes Unstable Angina:  New onset angina, crescendo angina, or angina at rest  Caused by non-occlusive thrombus, may have non-specific EKG changes  Normal cardiac enzymes Differentiate between clinical presentation of five potentially life-threatening causes of chest pain: Acute Myocardial Infarction:  More discomfort than pain, “elephant sitting on my chest,” squeezing, crushing, not sharp, radiating Aortic Dissection:  Sharp, substernal, radiating to back, pulsatile/tearing  Blood pressure difference between the arms, nausea, vomiting, diaphoresis  Acute aortic regurgitation Pulmonary Embolism:  Stasis, hypercoagulability, vascular damage, severe, sharp, chest wall pain, worsened with inspiration, rapid pulse Tension Pneumothorax:  Tachycardia, chest tightness, sudden onset, low blood pressure, distended neck veins, shortness of breath  Primary Spontaneous: absence of underlying lung disease, smoking is risk, Marfan’s, homocystinuria, catamenial ptx  Secondary Spontaneous: complication of underlying disease, COPD, pneumocystis, CF, TB  Traumatic: broken rib, stabbing, etc. Cardiac Tamponade:  Discomfort, sometimes relieved by sitting upright or leaning forward; sharp, stabbing chest pain; palpitations, skin pale, or gray, or blue; difficulty breathing; pulse may be weak or absent Describe the diagnostic approach to a patient with chest pain:  Obtain history of CODIERS: chronology, onset, description/duration, intensity, exacerbating factors, remitting factors, social; identify risk factors     Blood pressure on both arms, auscultation, physical exam EKG, get repeat EKGs CxR MI Diagnosis: 2 of 3: clinical hx of ischemic like chest pain >20 minutes, changes in serial ECG tracings, rise and fall of serum cardiac enzymes Report the role of CK-MB and Troponin testing in ACS:  CK-MB is from the heart, peaks in less than 24 hours, gone by 36 hours  Troponin: peaks at 36 hours, present much longer, more specific for the heart Outline the initial therapeutic modalities available for the treatment of acute MI and angina:  Thrombolysis/angioplasty  Nitrates, beta-blockers, ASA, clopidigrel, heparin, ACE-I, statin, Ca antagonist, glycoprotein receptor blockers  CABG, stent, balloon Recognize prognostic indicators after MI: specifically ventricular systolic function (LVEF):  <40% EF results in a greatly increased mortality at 30 days Valvular Heart Disease Recognize the clinical presentation and manifestations of valvular heart disease, specifically: Aortic Stenosis:  Low to normal BP, carotid pulse: slow rising and narrow, neck veins flat chest: minimal basal crackles  Heart: apex impulse forceful, slow rising and falling  EKG: sinus rhythm, normal axis, normal ST segment and T waves, increased QRS voltage  CxR: normal cardiac size, lungs clear, prominent ascending aorta, no calcium in aortic root Aortic Insufficiency:  Systolic/diastolic spread; carotid pulse bounding and bisferriens; neck veins flat; chest: few crackles at bases  Heart: apex impulse at anterior axillary line, bounding and collapsing, quicke pulsations at nail beds, left parasternal area with slight lift  EKG: rhythm sinus, ST segments with S1 depression, T waves biphasic, QRS axis left  CxR: enlarged heart (primarily LV), lungs clear, ascending aorta dilated, no calcification, left atrium not enlarged Mitral Stenosis:  BP normal, carotid pulse normal, neck veins slightly prominent, chest crackles at bases  Heart: apex impulse normal, left parasternal area with prominent lift  EKG: irregularly irregular rhythm, ST segments isoelectric, T waves normal, QRS axis vertical, “m” shaped P wave  CxR: cardiac size normal, prominent pulmonary arteries and LA appendage, Kerley B lines, small aorta Mitral Insufficiency:  BP normal, carotid pulse normal, neck veins flat, chest clear to auscultation  Heart: apex impulse mid axillary, not forceful; left parasternal area with slight lift, S1 not heard, S2 soft  EKG: rhythm sinus, axis normal, ST segments and T waves normal, QRS wave normal  CxR: cardiac size slightly enlarged, LA appendage is visible, lungs without infiltrate, aorta normal, calcification possible in area of AV ring, LA slightly enlarged Know the ausculatory findings in each condition and the affects with positional changes: Aortic Stenosis:  S1 normal, ES present, S2 not audible, S3 not present, S4 present in LLSB  Murmur: crescendo decrescendo, systolic ejection Aortic Insufficiency:  S1 muffled, S2 soft, S3 and S4 not present  SEM and blowing decrescendo diastolic murmur at Erb’s area Mitral Stenosis:  S1 loud, S2 pul sound is loud, S3 and S4 absent, opening snap at base and LLSB  Murmur: mid diastolic rumble with pre-systolic accentuation Mitral Insufficiency:  S1 not heard, S2 soft, S3 and S4 absent  Holosystolic murmur, heard best at the base Congestive Heart Failure (CHF): Recognize the clinical presentation of CHF:  Asymptomatic LVD, congestive state, low output state, cardiogenic shock, combinations  Breathlessness, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, easy fatigue, cough State the common conditions that lead to the development of CHF:  Hypertension: systemic and pulmonary  Left ventricular disease: ischemic, infectious, metabolic, alcohol, infiltrative  Extracardic factors: anemia, salt intake, renal failure, toxic drugs Distinguish between systolic and diastolic heart failure:  Systolic: occurs when the heart muscle does not contract with enough force, so there is not enough oxygen-rich blood pumped throughout the body. An ejection fraction less than 40 percent indicates systolic heart failure  Diastolic: occurs when the heart contracts normally (a normal ejection fraction) but the ventricle does not relax or fill properly, so less blood enters the heart Differentiate between high-output and low-output heart failure:  High output: body’s need for blood is unusually high, as in anemia, hyperthyroidism, pregnancy. The heart might be working well otherwise, but it cannot produce a high enough cardiac output to keep up with this extra work.  Low output: secondary to ischemic heart disease, hypertension, dialted cardiomyopathy, and valvular and pericardial disease. Know the NYHA functional classifications:  Class 1: no limitation on physical activity  Class II: slight limitation of physical activity, ordinary activity results in fatigue, palpitation, dyspnea, or angina  Class III: marked limitation of physical activity, comfortable at rest, but less than ordinary physical activity causes problems  Class IV: unable to carry on any physical activity without discomfort, symptoms present at rest and increase with any activity Describe the diagnostic evaluation of patients presenting with CHF:  Recognize the syndrome  Determine the cause of the syndrome (ECG, xray, echo, MRI)  Clarify the factors precipitating congestion: salt restriction, afterload reduction  Stage the severity of the syndrome  Tailor the therapy to pathophysiologic observation Report the reasons for excessive morbidity and mortality associated with heart failure:  Increased risk for sudden cardiac death  Compliance problems Outline the optimal medical therapy in chronic heart failure:  Digitalis, loop diuretic, ACE-I, ARB, B-Blocker, ASA, smoking cessation, exercise, weight reduction, DM control Peripheral Artery Disease (PAD) and Claudication Recognize the clinical presentation of patients with PAD:  The majority are asymptomatic  May also present with chronic limb ischemia, acute limb ischemia, and stable claudication  Consider PAD in anyone with: exertional leg pain, >50 with risk factors, >70 without risk factors Summarize the prevalence, pathogenesis, and risk factors of PAD:  Incidence increases with age  Can result from atherosclerosis, thrombi, and emboli  Risk factors: smoking, DM, family hx, atherosclerosis, HTN, elderly Outline the diagnosis and assessment of disease severity:  Vascular history  Physical exam (assess pulses, inspect feet for ulcers and overall foot care)  Ankle-brachial index (ABI) measurement  Arteriography Demonstrate understanding of the functional descriptions of intermittent claudication:  Exertional aching pain, cramping, tightness, fatigue  Occur in muscle groups, not joints  Are reproducible from one day to the next on similar terrain and at same distance  Resolve completely with 2-5 minutes of rest Recall the arterial physical exam for PAD:  Femoral, popliteal, posterior tibial, and dorsli pedis pulses  Palpate for abdominal aortic aneurysm and auscultate for bruits Know the role of the ABI in the diagnosis of PAD:  ABI = (ankle systolic pressure)/(brachial artery systolic pressure).  95% sensitive and 99% specific for PAD Demonstrate ability to interpret ABI measurements:  Normal: 0.90 – 1.30  Mild: 0.70 – 0.89  Moderate: 0.40 – 0.69  Severe: < 0.40 Summarize the morbidity and mortality associated with PAD:  Stable claudication: 73%  Worsening claudication: 16%  Leg bypass surgery: 7%  Major amputation: 4%  Non-fatal CV events: 20%  Mortality: 30% Indicate the factors that may improve atherosclerosis/PAD:  Smoking cessation, lipid control, BP control, DM control, antiplatelet therapy, achieving ideal body weight, exercise Congenital Heart Disease Recognize the signs, symptoms and cardiac exam findings in the following non-cyanotic congenital heart diseases: Coarctation of the Aorta:  BP in arms > legs, absent femoral but palpable pedal pulses, thrills or bruits over the intercostals arteries  Rib notching is present on inferior edge of rib  Arteriography can be used to diagnose Atrial Septal Defect:  Ejection systolic murmur at 2nd LICS, fixed splitting of 2nd heart sound, Holt Oram Syndrome (thumb in same plane as fingers)  RV will be dilated  L  R shunt due to tone (compliance) of atria Ventricular Septal Defect:  Long systolic murmur heard at LLSB  CxR: shunt vascularity, prominent main pulmonary artery, left atrial enlargement, aorta is not enlarged Patent Ductus Arteriosus:  Continuous machinery murmur, in 2nd LICS  Heart is slightly enlarged, pulmonary artery is convex, aortic arch is prominent, increased pulmonary vascular markings (shunt vascularity) Pericardial Disease Identify the signs and symptoms associates with pericarditis:  Chest pain: severe, increased by changing position or deep inhalation; shortness of breath, fever List the potential causes of pericarditis:  Infection, MI, autoimmune disorders, chest trauma, cancer, kidney failure, drugs Know the drugs that cause pericarditis:  Procainamide, hydralazine, phenytoin, isoniazid Recognize the features of Dressler’s Syndrome:  A pericarditis that develops 2-10 weeks following an MI, believed to be a an autoimmune response to myocardial antigens  Symptoms include a low grade fever, chest pain, frictional cardiac rub, and, rarely, cardiac tamponade Outline the potential complications of pericarditis:  Tamponade  Constriction  Chronic pericarditis: occurs after a few weeks State the treatment approach for pericarditis:  Anti-inflammatory drugs, analgesics, pericardiocentesis for tamponade, pericardial window for chronic recurring pericarditis, pericardiectomy for constrictive pericarditis Hypertension Distinguish between essential and secondary hypertension  Secondary HTN: 15%, due to a primary cause, such as Cushings or coarctation of aorta  Essential: 85%, due to unknown cause List the causes of secondary hypertension:  Volume loading: too much water/salt intake      Excess rennin-angiotension II action: ex, ischemic kidneys Vasoconstriction: ex, pheochromocytoma Aldosteronism: ex, Conn’s syndrome Toxemia of pregnancy Renovascular: ex, renal artery stenosis State the stages of hypertension as defined by JNC VII:  Normal: S < 120 and D < 80  Prehypertension: S 120-139 or D 80-89  Stage 1: S 140-159 or D 90-99  Stage 2: S >160 or D > 100 Know the recommendations for initial drug therapy based on HTN stage (know the class of drugs):  Initially: lifestyle modifications; if inadequate, begin drug therapy  Stage 1, uncomplicated: diuretics  Stage 2, uncomplicated: diuretics + Ca blocker, ACE-I, or Beta-blocker Explain the compelling indications for individual drug classes:  High risk hypertension (HTN with heart failure, post-MI, coronary disease risk, DM, CKD, and recurrent strokes) respond best to different combinations of drugs, based on class  Classes are: diuretics, CCB, ACE-I, ARB, beta blocker, aldosterone antagonists Exhibit knowledge of abnormalities associated with the metabolic syndrome:  Obesity  Dyslipidemia  HTN  DM  Prothrombotic state, proinflammatory state Outline the recommendations for lifestyle modification for HTN prevention and treatment:  Lose weight if overweight  Limit EtOH intake, stop smoking  Reduce sodium to less than 2.4g per day, reduce fat and cholesterol  Exercise  DASH diet (dietary approaches to stop hypertension) Arrhythmias Demonstrate understanding of the common causes of arrhythmias: