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Assessment Primary survey/ resuscitation Secondary survey Factors For Consideration Unmodifiable • Age • Sex • Heredity • Race Modifiable • B/P • Obesity • Dyslipidemia • Smoking • Sedentary life style • Stress • Diabetes Subjective data Chief complaint History of present illness • • • • • • • Onset: OPQRST Pain: PQRST Provocation Quality Region/radiation Severity Time Duration Development over time Periodicity (? Comes/goes) Focused Survey Focused Survey (Continued) Dyspnea • SOB Dyspnea on exertion Positional dyspnea • Paroxysmal nocturnal dyspnea • Orthopnea Cough Dry, “cardiac” cough Hemoptysis Syncope Palpitations Fatigue Nausea and Vomiting Headache Behavioral change Activity limitations Injury: mechanism and time Medical History Coronary Heart Disease • • • • Angina Previous MI Hypertension CHF Pulmonary Disease Diabetes Renal Disease Previous Cardiac Surgery Congenital Anomalies Allergies Current/Past Medication Use Nitrates Beta Blockers Calcium Channel Blockers Antihypertensives Digitalis Diuretics Antidysrhythmics Anticoagulants Steroids Specific Pulmonary Drugs Illicit Drugs OVC Medications Physical Exam General Survey • LOC • Respiratory status Rate, regularity, effort, breath sounds • Skin Color, temperature, moisture, capillary refill • Edema Dependent, extremities, sacrum, pleural effusion, ascitis, cardiac (pitting) Physical Exam Cyanosis • Central • Peripheral Clubbing B/P Measurement • Both arms • Orthostatic (supine, sitting, standing) 0 = absent 1 = thready 2 = normal 3 = bounding Apical heart rate • Regular, irregular, regularly irregular, irregular irregular Peripheral pulses Pupils • Size, equality, reactive Physical Exam Inspection Tracheal position Neck veins Thorax • Configuration Deformities, anterior, posterior, A-P diameter, symmetrical movement Injuries, penetrating, blunt (ecchymosis, contusions) evidence of scars, surgery Abnormal chest movement, asymmetrical, paradoxical Physical Exam (Inspection) Precordium • Apical pulse • Abnormal precordial movements, heaves, lifts, pulsations, retractions • Epigastrium, pulsations Physical Exam: Palpation Areas tender, or crepitus Epigastrium Physical Exam: Auscultation Auscultatory sites • Murmurs: systolic/diastolic • Variations in rhythm • Extra sounds Pericardial friction rub Venous hum Arterial bruits • Clicks Physical Exam: Diagnostic Procedures ECG, 12 lead • Rate, rhythm • Presence of cardiac dysrhythmias • Evidence of myocardial ischemia, injury • Presence of intraventricular conduction defect • Evidence of previous MI CBC Serum electrolytes Cardiac serum markers • Troponin • Basic metabolic profile • Coagulation studies • Digoxin level • Serum creatinine, BUN • T& C • ABGs • Routine urinalysis Physical Exam: Diagnostic Procedures Comparison of Diagnostic Markers Marker Time from Obstruction Appears CK-MB Specifi c to Cardiac Specific to AMI Disappears 6 hours 36 hours Yes Yes Myoglobin 2 hours 24 hours No No Troponin I 2 hours 1 week Yes No Diagnostic Procedures Pulse oximetry Radiography • Chest x-ray Heart size and location Presence of edema Pulmonary infiltrates Pleural effusions Air and fluid levels in trauma patients Mediastinal width Bony structure integrity Cardiac catheterization Echocardiogram Interventions Determine priorities • Airway, vital signs, cardiac rhythm, ABGs, Pulse oximetry, • Control pain • Relieve anxiety • Education patient/other • Prevent complications Establish care plan Emergency equipment Initiate appropriate interventions Document data Monitor responses and adjust Pediatrics Growth & Development • R/T congenital heart disease (heart defects) • Acquired heart disease (rheumatic fever) • Endocrine (diabetes) • Other Drug ingestions, ex: tricyclics, digoxin Trauma (falls, MVCs) Suffocation (plastic bags, drowning, accidental hanging) Pediatric Pearls: • Cardiac arrest usually d/t progressive deterioration in respiratory and heart function • CHF, cardiogenic shock, dysrhythmias are unusual. If occur congenital. • Immature conduction system and autonomic innervation may contribute to dysrhythmias Geriatric Presence of chronic diseases Altered drug metabolism Multiple physiological differences and changes in lab values must be considered when assessing the older patient Psychological and social changes: patient may have different goals for their treatment, discuss with patient Geriatric patients can adapt to disease so well that symptoms are not obvious Arteriosclerotic changes in aorta and peripheral pulses may pose a difficulty in palpating Rhythm abnormalities are so common that they may be “normal” Pearls “Go slow, stay low” with medications Concurrent use of other medications cause problems, • Easy to use meds are helpful (transdermals) • One time or two time doses daily • Evaluate medications on a frequent basis Angina Stable • Symptom of ischemia • “pain or discomfort” • Poorly localized • Flow/Demand imbalance • May be chronic, acute, or unstable Angina (continued) Unstable angina • New symptoms of angina • Increasing symptoms that occur at rest or with on exertion • Usually due to platelet aggregation • Leads to atypical chest pain Angina (Continued) Unstable angina diagnosis • Angina is at rest, as well as minimal exertion (usually 20 minutes or longer) • Angina of new onset (several weeks), starting with physical exertion, and markedly limits activity • Previously diagnosed stable angina Normal ECG Abnormal ECG Same Patient, Inverted T Waves Angina cont’d Variant Angina • May or may not be due to atherotic changes • Thought to be due to coronary spasm • Prinzmetal’s angina • May occur at the same time, daily • Usually not associated with exertion or stress • Occurs at younger ages • ST elevation seen during pain, then disappears Angina: Curveballs GERDs Biliary Colic Chest Wall Pain Pericarditis PE Aortic Dissection Dysrhythmias Diagnostic Procedures: ECG ST depression may accompany pain with stable angina Transient ST-segment deviations (depression or elevation), and T wave inversion occur commonly with unstable angina Variant angina: ST elevation occurs with pain, subsides when pain does May see LV hypertrophy, old MI, nonspecific ST and T-wave abnormalities and AV defects Diagnostic Procedures (Continued) CBC Cardiac serum markers…no elevation should occur unless cell damage Chest X-ray ( CHF, cardiomegaly) Interventions Continuous monitoring O2 IV, Draw labs 12 Lead ECG Rest Decrease anxiety SL NTG, B/P 100 mm HG followed by a drip • Assess for H/A • Reflex tachycardia • Cautious with elderly Interventions (continued) Beta blockers • If clinical situation deteriorates after B Blocker, consider coronary artery spasm • Assess for signs of heart failure • Adverse effects of blockers are considered more common and severe in geriatric Interventions (continued) Administer antiplatelet agents • ASA (4-5 baby aspirin) • Administer ASAP • Decreases platelet activation and thrombus formation TEACH/EDUCATION Acute Myocardial Infarction Myocardial Infarction (MI)Coronary Occlusion Heart Attack MI: Data Physical exam General appearance: Anxious, restless, clenched fist against chest (Levine sign) Look of doom Heart rate: may be ok, tachycardia (most common), bradycardia (inferior and RV), Regular or irregular PVCs common Data (continued) Arterial BP • Majority of patients with uncomplicated MI are normotensive • May be elevated due to SNS stimulation Pain and anxiety • Decreased as a result of impaired cardiac function or due to drug administration (nitrates, M.S.) Data (continued) Respiratory rate: Initially elevated. Should return to normal after pain relief • Patients with CHF, respiratory rate correlates with severity of condition Data (continued) Peripheral: How bad is the patient’s condition? • Pallor, cyanosis, diaphoreses, mottled, cool, peripheral pulses variable Temperature: Often increases 4-8 hours post MI Heart Sounds: muffled. murmurs may be transient or permanent Diagnosis Continuous cardiac monitoring 12 lead ECG Determine Location of infarct (next slide) Anterior Septal ST Leads 1, AVR, V1 through V4 Lateral Apical ST Leads 1, AVL V5 and V6 Posterior Recipical Changes V1,V2 No Q waves, Tall R’s St II,III,AVF Upright t wave ST Leads II, III, AVF Inferior Serum Markers Myoglobin • Elevated 1-4 hours after onset of MI, peaks 6-7 hours, normal in about 1 day • Lacks specificity, found in skeletal muscle Serum Markers (continued) Troponins: • Most recent marker, most sensitive and specific for cardiac damage • Elevated 3-12 hours after MI, Peaks in 24 hours, with TnI , returns to normal in 5-12 days • TnT may be elevated in patients with renal failure, which is not the case with TnI; therefore TnI is utilized. Interventions ABCs Oxygen IV or topical NTG, as B/P tolerated (B/P 100 or greater IV with normal saline, KVO Analgesia: M/S ASA 12 Lead ECG Blood samples for analysis Interventions (continued) If appropriate consider PTCA Follow ACLS Guidelines Prepare for Thrombolytic Therapy as appropriate Administer aspirin, nitrates, heparin, plavix, Integrillin, Lopressor, Morphine, antiarrhythmics Interventions (continued) Observe patient: • Bleeding, reperfusions dysrhythmias • Vital signs, ventricular ectopy, and other dysrhythmias • Heart and lung sounds • LOC Interventions (continued) Portable chest film ACLS measures Prepare for cath lab Educate and explain Allow visit from significant other Heart Failure & Cardiogenic Pulmonary Edema Clinical syndrome, can occur from any heart disease Pediatric..usually due to congenital heart defects Inability to discharge contents Inability to pump enough blood to meet metabolic needs Diagnostics Lab: • • • • • H& H Lytes BUN, Creatinine Liver function studies Cardiac enzymes (if AMI) • BNP B-type natriuretic peptide Radiologic: • often normal • pulmonary vasculature, edema, fluid • Cardiac silhouette may show cardiac enlargement, hypertrophy, dilation • Enlarged RA and RV • Pleural effusion • Valve calcifications Diagnostics cont’d ECG: nonspecific changes, electrolyte or drug induced dysrhythmias Echo: chamber size,wall thickness, thrombus formation, valvular function, pericardial disease Interventions ABCD Provide supplemental O2 IV Normal Saline ABGs and other labs Provide rest ECG continuous Monitor hemodynamics Administer Morphine Administer vasodilator • Decreases afterload, arterial dilations. Also preload Vasodilators (continued) NTG, Isosorbide • Increases venous pooling • NTG preferred in pulmonary edema, CAD since improves coronary artery perfusion • Venous dilation Vasodilators (continued) Diuretics: • Decrease preload • Foley catheter, possible • I&O • Monitor serum K+ Vasodilators (continued) ACE Inhibitors: • Captopril, Enalapril • Block formation of Angiotensin II, yields vasodilation • Reduce mortality, by improving cardiac function • Avoid overdiuresis • Cleared by kidney Hypertensive Emergencies Life-threatening elevation of B/P necessitating reduction to prevent end-organ damage and potential death Essential hypertension • unknown cause Secondary hypertension • elevated pressure whose cause is known (renal vascular disease) Produces changes in arterioles (necrosis and inflammation over time) causing decrease in bloodflow to end organs Accelerated and/or malignant • hypertension:Diastolic pressure higher than 140 mmHg Precipitating Factors Untreated/uncontrolled essential or secondary hypertension Poor patient compliance with antihypertensive medications Renal dysfunction Eclampsia of pregnancy (not tolerated well) Adrenergic crises AMI, Cerebral dysfunction Pituitary tumors Assessment History Severe H/A Epistaxis Family hx hypertension MAO inhibitors CAD, Renal Disease Diabetes, obesity, smoker, hyperlidemia, stress Exam Diastolic pressure exceeding diastolic or 120mmHG Retinopathy with exudates, Retinal hemorrhages Papilloedema (diastolic pressure > 140) H/A, confusion, restless stupor, somnolence Epistaxis Tachycardia Chest discomfort N&V Rales Oliguria, azotemia Diagnostics Lab: • ABG: metabolic acidosis • CBC HCT in renal failure, polycythemia in renal • Electrolytes: Hypocalcemia Hyponatremia aldosteronism causes hypokalemia ( half of patients) • Glucose: elevated in Cushing’s Syndrome, diabetes • BUN and creatinine elevated in renal disease • Uric acid: hyperuricemia in renal failure • U/A: proteinuria, possible renal dysfunction Radiologic Findings Chest film: cardiomegaly may be seen ECG: LV hypertrophy may be seen CT scan: Diffuse brain edema with hypertensive crises ECHO: diastolic function impaired. Interventions ABCD, O2, IV @ KVO rate ACLS protocols Administer medications NTP: • Most common and most effective • 0.5-10mcg/kg/min • Titrate with B/P • Watch for cyanide toxicity • Drug is light sensitive Interventions (continued) NTG: • Drug of choice for unstable angina and ischemia, LV failure, adrenergic crises • Provides immediate response Sympathetic Blocking Agent (Labetalol) • Alpha and beta blocker • Onset and cessation of action slower than NTP and NTG • Contraindicated in patients with heart failure, greater than 1st degree block, bradycardia, and reactive airway disease Interventions (continued) ACE Inhibitors • Used in presence of LV failure • Captopril: 6.25-50 mg orally every 30-45 minutes • Enalapril: 1.25-5 mg IV every 6 hours • Onset of action for both 10-15 minutes Interventions (continued) Calcium Channel Blockers • Nifidipine: 10 mg PO or sublingual (10-20 mg orally every 30-45 minutes of sublingually every 15 minutes) Beta Blocker: Metoprolol, Esmolol • Blocks effects of increased adrenergic tone • Metoprolol 5 mg IV every 5 minutes up to 15 mg total Interventions (continued) Administer diuretics Closely monitor patient’s response Continuous arterial monitoring Watch medication side effects Observe for signs of ischemia I&O Monitor for dysrhythmias Monitor for ↑ ICP Possible ICP monitoring Sudden chest pain may suggest aortic dissection Reassure patient/family Calm environment Questions????????