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DU PA CP Emergencies
Duke PA Chest Pain Emergencies
| Question | Answer |
|---|---|
| What are the possible etiologies of chest pain | Cardiac or vascular, pulmonary, GI, musculoskeletal, psychogenic |
| What is the assumption when it comes to chest pain | Always assume the worst until proven otherwise |
| Pleuritic chest pain is worse with __ | Deep inspiration |
| S&S of pulmonary embolus | Dyspnea, pleuritic and non-pleuritic chest pain, anxiety, cough and syncope |
| S&S of pneumothorax | Pleuritic pain, tracheal deviation, hyper resonance with decreased breath sounds unilaterally |
| S&S of pneumonia | Pleuritic pain with associated SOB, cough, fever, sputum production, rales and dullness |
| S&S of asthma/COPD | Dyspnea, chest tightness, wheezing, and cough |
| S&S of pulmonary edema | Severe respiratory distress, frothy pink or white sputum, rales, S3/S4, PND, orthopnea, edema |
| Inflammation of pleurae, usually caused by infection or connective tissue/inflammatory disease, friction rub with low grade fever | pleurisy |
| S&S of pulmonary hypertension | Pleuritic chest pain, loud P2, right ventricular lift |
| S&S for GERD/heartburn | Chest pain may be squeezing or pressure like, diaphoresis, radiation, N/V, post-prandial, postural changes, spasm, may be relieved with antacids/NTG |
| S&S of esophageal perforation | Acute, severe, unrelenting and diffuse pain in chest, neck or abdomen. May radiate to back or shoulder and swallowing may exacerbate pain |
| S&S of Mallory-Weiss tear | Hematemesis with or without prior vomiting episode |
| S&S of PUD | Burning epigastric pain, post-prandial sx, relieved with food, may present as N/V, wt loss, anorexia and bleeding |
| S&S of cholecystistis | Epigastric/RUQ visceral pain + fever/chills, N/V, anorexia, may radiate to back or scapular region |
| S&S of pancreatitis | Midepigastric, piercing pain, constant, radiates to back ,associated with N/V, abdominal distention and exacerbation in supine position, low grade fever, tachy and hypo |
| S&S of musculoskeletal cp | Sharp pain, worse with movement/palpation, true MS usually respondes to NSAIDS |
| S&S of anxiety/panic disorder cp | Fleeting chest pain, variable onset/duration, often reproducible on palpation (but not with exertion) |
| Time goal of obtaining an ECG | 10 minutes |
| What labs do you need to get for chest pain wu | Cardiac biomarkers, CMB, CBC, D-dimer, PT/PTT |
| What types of patients are put in the chest pain observation unit | Those with low probability for MI without ongoing chest pain or ischemic ECG changes |
| How do you r/o MI | serial ECG/s and cardiac biomarkers (CK/MB, troponin levels) |
| CK-MB peaks in __ hours | 24 |
| CK-MB is detected in __ hours | 3-12 |
| Ck-MB lasts for __ hours after event | 48-72 |
| Deep, pressure like pain in substernal region, may radiate, SOB, transient (2-30 min), precipitated by physical exertion or emotional stress, responsive to rest or NTG | Stable Angina Pectoris |
| Stable angina pectoris is strongly associated with what conduction abnormality | LBBB |
| What may show up on an ECG during angina | ST segment depression/possibly elevation, T wave inversion; btw episodes: 1/3 of pts have normal resting ECG |
| Treatment for stable angina pectoris | Risk factor modification, 81-325 ASA daily, beta blocker, ACEI, Nitrates, statins/lipid agents, consider revascularization |
| Treatment for patient with unstable angina | Admit/monitor/bed rest, MOAN (Morphine, O2, ASA, NTG) |
| Over 50% of deaths from acute STEMI occur within __ of event from __ | 1 hour, v-fib |
| How soon do T waves peak with an acute STEMI | 0-6 hours |
| How soon may you see ST segment elevations with an acute STEMI | 0-18 hours |
| How long does it take for an ECG to Q out following an acute STEMI | About 18 hours |
| What ECG finding is indicative of myocardial ischemia | ST elevation at the J point in 2 or more contiguous leads |
| What ECG findings are suggestive of myocardial ischemia that may progress to MI | ST depression, T wave abnormalities |
| The initial ECG is negative or non-diagnostic in up to __% of patients having an acute myocardial infarction | 40 |
| In an inferior MI ST changes will be seen in what leads | II, III, and aVF |
| In an anterior MI ST changes will be seen in what leads | V2-V5 or V1-V4 |
| In a lateral MI ST changes will be seen in what leads | I, aVL, V5-V6 |
| In an inferolateral MI ST changes will be seen in what leads | II, III, aVF, I, aVL |
| In an anterolateral MI ST changes will be seen in what leads | V4-V6, I, aVL |
| In a right ventricle MI, ST changes will be seen in what leads | R sided and V1R to V6R |
| ST elevation typically persists __ after onset of chest pain in a STEMI if no reperfusion therapy is done | 6-18 hours |
| What is the goal door to balloon time | <90 min |
| What are the absolute contraindications for lytics with acute STEMI | Prior intra-cranial hemorrhage, cerebral AVM, malignant neoplasm, active bleeding, suspected aortic dissection, ischemic CVA in past 3 months or closed head trauma, severe uncontrollable HTN |
| Unexpected non-traumatic death in clinically well or stable patients who die within 1 hour after onset of symptoms | Sudden cardiac death |
| What is the usual causative rhythm associated with sudden cardiac death | V-tach except in the setting of acute ischemia or infarction (then VF arrest) |
| When do most sudden cardiac deaths occur | In the early morning hours |
| List some conditions that can cause the following; chest pain, hypotension/shock, JVD | MI, arrhythmia, tamponade, massive PE, tension pneumo |
| List some conditions that can cause chest pain and hypovolemia | MI, Aortic dissection, leaking AAA |
| Name the valvular abnormality; mid-systolic click, inverted T waves on inferior leads | Mitral valve prolapse |
| Name the valvular abnormality; systolic ejection murmur transmitted to carotids, LVH on ECG | Aortic stenosis |
| Name the valvular abnormality; diastolic murmur transmitted to carotid arteries, wide arterial pulse pressure, ECG may show LVH | Aortic regurgitation |
| What are some factors that increase the risk of an aortic dissection | Male, 60-70 yo, pregnancy, connective tissue disorders (Marfan’s, Ehlers Danlos), hypertension, bicuspid aortic valve, coarctation of the aorta |
| Intimal tear in aorta that creates a false lumen between media and adventitia | Aortic dissection |
| Where do >95% of aortic dissections occur | Ascending aorta just distal to aortic valve or just distal to the left subclavian (fixed points) |
| What is a Stanford A aortic dissection | Any involvement of ascending aorta |
| What is a Stanford B arotic dissection | Not involving ascending aorta |
| What is a DeBakey I aortic dissection | Ascending aorta extending to distal (entire length) |
| What is a DeBakey II aortic dissection | Ascending aorta only (before left subclavian) |
| What is a DeBakey III aortic dissection | Descending aorta only (after left subclavian) |
| A Stanford A aortic dissection is the same as which DeBakey classifications | I and II |
| A Stanford B aortic dissection is the same as which DeBakey classification | III |
| Symptoms of aortic dissection | Sudden onset retrosternal and back pain, may see infarct patterns on ECG, neuro deficits/CVA, limb ischemia, syncope, shock, hypertensive, pulse discrepancies |
| What may a chest x-ray look like in a patient with an aortic dissection | Widened mediastinum, possibley left sided pleural effusion |
| When may an MRI be useful in an aortic dissection | For serial follow up |
| Treatment for an aortic dissection | Achieve relative hypotension and bradycardia (beta blocker first then nitroprusside to maintain SBP of 100-120 mmHg), contact cardiothoracic surgeon |
| What Stanford class of aortic dissection needs surgical repair | A |
| What Stanford class of aortic dissection can be treated medically | B (exceptions are rupture, limb or visceral ischemia, ongoing pain, saccular morphology, uncontrolled HTN, Marfan’s or AI |
| Clinical findings of an abdominal aortic aneurysm | Majority are asymptomatic, prominent aortic pulsation, pain (epigastric fullness or lower back and hypogastric region), gnawing, hours/days not positional |
| What change in symptoms indicates rupture of AAA | Severe back or abdominal pain and hypotension |
| What is the next step if diagnosis of AAA is clear on clinical grounds | Emergent vascular surgery consult |
| What is the next step if a patient with an AAA is hemodynamically stable | Bedside abdominal ultrasound (100% sensitive, unless rupture has already occurred) |
| Mass effect associated with thoracic AA | SVC syndrome, tracheal deviation, cough, hemoptysis, dysphagia, hoarseness |
| Symptoms of acute pericarditis | Pleuritic, sharp, stabbing chest pain that radiates to shoulders, back, neck that is worse on deep inspiration or movement, worse supine and relieved by sitting up and leaning forward. Low grade fever, dyspnea, friction rub LLSB |
| ECG changes in acute pericarditis | Diffuse upsloping ST segment elevations |
| Labs to get for evaluation of acute pericarditis | CBC with diff, BUN/creatinine, serologies (strep, ANA, viral), thyroid |
| Treatment of stable patient with acute pericarditis | Out patient with NSAIDS for 1-3 weeks |
| When should a patient with acute pericarditis be admitted | Myocarditis, uremic pericarditis, enlarged cardiac silhouette on CXR, or hemodynamic compromise |
| The most common patient population that gets tamponade has some type of __ | Malignancy |
| Occurs when pressure in the pericardial sac exceeds normal RV filling pressure, resulting in restricted filling and decreased cardiac output | Cardiac tamponade |
| What is beat to beat variability in the amplitude of the P and R waves unrelated to inspiratory cycle and is diagnostic of cardiac tamponade | Electrical alternans |
| S and S of cardiac tamponade | Shortness of breath, weakness (more likely than chest pain and tachycardia), JVD, pulsus paradoxus, electrical alternans, large cardiac silhouette on CXR |
| What is an exaggeration in the normal variation in the pulse during the inspiratory phase of respiration, in which the pulse becomes weaker as one inhales and stronger as one exhales | Pulsus paradoxus |
| What is Beck’s triad | Hypotension, elevated systemic venous pressures, small quiet heart |
| The presence of Beck’s triad is indicative of what condition | Cardiac tamponade |
| Treatment of cardiac tamponade | Volume resuscitation, pericardiocentesis, admit and consider pericardial window |
| Severe elevation of BP, no evidence of progressive TOD, absence of raised intracranial pressure | Hypertensive urgency |
| Hypertensive urgency benefits from BP lowering in __ | A few hours |
| Short term treatment for hypertensive urgency | Labetalol, clonidine or captopril, outpatient follow up within 72 hours |
| Acute, severe elevation in BP, evidence of rapidly progressive TOD (MI, pulmonary edema, stroke, renal failure) | Hypertensive emergency |
| Hypertensive emergency requires __ | Immediate, gradual reduction of BP( not to the normal range) |
| In a patient with hypertensive emergency rapid correction of BP to normal levels puts the patient at risk of what | Worsening cerebral, renal, or cardiac ischemia |
| What is the goal of treatment in hypertensive emergency | 10% decrease in first hour, 15% over next 3-12 hours to BP of no less than 160/110 |
| What must be present to kick hypertensive emergency up to the level of malignant hypertension | Papilledema |
| Do not ignore __ in patients with many low risk findings | A few high risk findings |
| cardiac enzymes: | normal in stable angina/USA; elevated in NSTEMI/STEMI |
| Thoracic AA: vascular sx | CHF, ischemia, thromboembolism |
| Conditions that may precipitate tamponade: | Malignancy induced pericarditis; Aortic dissection; MI with Ventricular rupture; Pacemaker perforation during implant |
Created by:
bwyche
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