MedSurg III: Exam 3 Unit 5 PDF

MedSurg III: Exam 3 Unit 5: Complex Perfusion Problems I CH: 21, 22, 23, 25 Book & PPT, KEY POINTS, Lecture, Hemodynamic Monitoring  Continuous assessment of the CV system to dx & manage complex conditions using direct pressure monitoring systems  Centr...

MedSurg III: Exam 3 Unit 5: Complex Perfusion Problems I CH: 21, 22, 23, 25 Book & PPT, KEY POINTS, Lecture, Hemodynamic Monitoring  Continuous assessment of the CV system to dx & manage complex conditions using direct pressure monitoring systems  Central Venous Pressure o Measurement of the vena cava or right atrium and reflects the filling pressure of the right ventricle (preload). o Normal CVP is 2-6 mm Hg. o CVP > 6 mm Hg = elevated right ventricular preload  = HYPERVOLEMIA or right sided HF o CVP < 2 mm Hg = reduced right ventricular preload  = HYPOVOLEMIA  Dehydration/excessive blood loss/vomiting/diarrhea/ over diuresis o Used for infusing IVF, administering IV medications, and drawing blood specimens. o Preferred site if the subclavian vein Femoral vein avoided  Pulmonary Artery Pressure o To assess left ventricular function, etiology of shock, and evaluate the pt’s response to medical intervention o Assess  left ventricular function, Right atrial pressure  Pulmonary artery pressure, Pulmonary artery wedge pressure o NURSING ALERT  Pulmonary wedge pressure Evaluate the return of the pulmonary artery systolic and diastolic waveform displayed on the bedside monitor. o Normal PAP 8-20 mmHg  Intra-arterial blood pressure o Used to obtain direct and continuous BP measurements who have severe HTN or HYPOotension o Used for Frequent ABG measurements and blood samples. o Site: radial artery  Obtaining pressure o Sterile procedure o A disposable flush system  Never put dextrose normal saline ONLY  Heparin only by orders o A pressure bag placed around the flush solution maintained at 300 mmHg of pressure o A transducer to convert the pressure set a 0 o Monitor  NI o Hand Hygiene o Dressing change  Gauze dressings Q2days; Transparent dressings Q7days  Or whenever dressings become damp, loosened, or visibly soiled. o Assess catheter site (tenderness, fever, s/s systemic infection If infected pull the line and send to lab o Replace transducers, tubing, continuous-flush device, and flush solution every 96 hours or per policy o Bathing  Do not submerge the catheter site in water- NO baths ONLY SHOWER  Showering is permitted if the catheter and related tubing are placed in an impermeable cover. o Patient education ask patient to report any new discomforts from the catheter site.  o Keep patent and free of air bubbles o Checking the stopcock of the transducer is positioned at the level of the atrium before system is used to obtain pressures  Landmark is: phlebostatic axis. o Establish the zero-reference point to ensure fx HOB elevated to 60 degrees; reposition axis for accurate reading o Do not introduce anything else into but saline into pressure line (transparent dressing, no antimicrobial ointment)  Complications o Pneumothorax can occur during the insertion of the catheter o Infection – CLABSI if catheter is left in after 72-96 hrs = higher risk for infections take out ASAP if it’s not needed o Air embolis Cardiac Dysrhythmias Sinus Tach/Brady Sinus Tachycardia Sinus Bradycardia  Occurs when the Sinus node creates an impulse at a faster- than-normal rate.  Occurs when the SA node creates an impulse at a  Abnormal fast HR > 100 beats per minute. slower- than-normal rate o Compensatory response to increased demand for cardiac output or reduced stroke volume.  Slowed impulse generation by the sinus node o Sympathetic activation o Decreased parasympathetic activity  Unstable and symptomatic bradycardia is  Etiology frequently due to hypoxemia. o Fever o Hyperthyroidism  Other possible causes: o Pain o Increased metabolism o Low BP o Acute AMS (e.g., delirium); Acute o Hypoxia decompensated HF o Stress  Etiology: o Increased parasympathetic activity o Meds that stimulate the sympathetic o Sleep, Drugs, Increased Stroke vol. response o HTN o Physically Trained Individuals  Characteristics (ATHLETES) o Rate: > 100 bpm but less than 120 bpm o Rhythm: Regular o Vagal stimulation (vomiting, suctioning, o QRS Shape: Normal severe pain) o P Wave: Normal and consistent shape, always in front of the QRS o PR Interval: 0.12-0.20 seconds o Low metabolic needs low HR may be  Dx normal for some ppl like athletes o EKG  NI  Sleep, athlete, hypothyroidism o Assess cause o Perform vagal maneuvers   Carotid sinus massage o Meds (Nifedipine, amiodarone, metoprolol)  Gagging  Characteristics o Rate: Less than 60 bpm  Bearing down against a closed glottis o Rhythm: Regular (as if having a bowel movement) o QRS Shape: Normal o P Wave: Normal and Consistent Shape,  Forceful and sustained coughing always in front of QRS o PR Interval: 0.12-0.20 seconds  Applying a cold stimulus to the face  NI (such as applying an ice- cold wet towel o Assess cause to the face) o Prevent vagal stimulation o Withhold Drugs that cause Bradycardia o Monitor for Hemodynamic Instability  Beta-blockers  Medical  Calcium-channel blockers o Determined by the severity of s/s and o Monitor for Hemodynamic Instability directed at identifying and abolishing its  Tx cause. o Depends on Cause o Synchronized Cardioversion  electrical o Emergency Transcutaneous Pacing current given to sync pts QRS complex to  Medications stop an arrhythmia o Epinephrine (Adrenergic Receptor) o Atropine (Anticholinergic)  If the tachycardia is persistent and causing hemodynamic instability (acute  If the bradycardia is unstable-- (acute AMS, chest discomfort, hypotension) AMS, chest discomfort, or hypotension)  MedIcations  Give 0.5 mg of atropine rapidly as an o Adenosine (Calcium Channel Blockers) i (IV) bolus and repeat Q3 to 5 min until a max dosage of 3 mg is given. o Sotalol, Propranolol (Beta- Adrenergic Blockers) o if the bradycardia is unresponsive to atropineemergency transcutaneous or meds [dopamine, isoproterenol, or epinephrine], are given A-FIB/Flutter Atrial Fibrillation Atrial Flutter “A-FIB” “A-FLUTTER”  Irregular  Regular o Saw tooth impulse coming from same  Atrial depolarizations are blocked at the AV place Node  a few are reaching the ventricles and initiating ventricular contractions.  Occurs because of a conduction defect in the o Causes atria to quiver instead of contract atrium and causes a rapid, regular atrial impulse. forcefully. o Completely disorganized/ irregular  The atrial rate is faster than the AV node can atrial rhythm accompanied by an irregular conduct not all atrial impulses are conducted into  ventricular rhythm of variable rate  @ RISK for THROMBI/STROKE/BCLOT the ventricle  Characteristics o Rate: Atrial:300 -600 bpm; Ventricular: o causing a therapeutic block at the AV 120-200 bpm node. o Rhythm: Irregular o QRS: usually normal but may be abnormal  RF & s/s are the same as atrial fibrillation o P wave: No discernible P waves, cannot be measured, Irregular, and shape are referred as fibrillatory waves  Characteristics o PRI: cannot be measured o Rate: Atrial: 250-400 bpm; Ventricular: 75- o P:QRS ratio: Many:1 150 bpm  Etiology/ RF o Rhythm: Atrial: regular; Ventricular: BOTH o Increasing age (60-70) o QRS shape: Normal o HTN, DM, Obesity o P Wave: Saw toothed shape, referred as F o HF, Valvular heart disease waves o Obstructive sleep apnea o PR Interval: Difficult to determine o Alcohol consumption—  s/s o Chest pain,  moderate (1–3 drinks/day)  high (>3 drinks/day) o SOB o Hyperthyroidism o Low BP o Postoperative cardiac surgery o Smoking, Exercise  NI o Vagal Maneuvers o Cardiac ischemia, MI  Medical o Cardiac inflammatory disease o Antithrombotic Therapy similar to Atrial o Myocardial hypertrophy, fibrosis, or dilation Fibrillation o Atrial remodeling o Electrical Cardioversion  CM  Meds o Some patients are asymptomatic o Adenosine (Calcium Channel Blockers)  o Palpitations causes sympathetic block and slowing of o HF conduction through AV node o SOB  Given IV by rapid adm. and o Hypotension (low BP) immed. followed by a 20-mL o Dyspnea on Exertion saline flush and elevation of the o Fatigue arm with the IV line to promote o Pulse deficit—different between apical rapid circulation of the me. and peripheral o Irregular pulse (low cardiac output) pulse deficit  NI o History H&P o Stroke Risk Assessment o Monitor Lab (Coags and H/H)  Keep INR 2.0 and 3.0 o Electrical Cardioversion- Anticipate TEE performed to evaluate for atrial thrombi before cardioversion  Need consent  Tx o Prevent Emboli events o Electro-cardioversion  Indicated for pt with AFib that is hemodynamically unstable  Transthoracic echocardiogram (TEE) o Catheter Ablation  MEDS o Heparin @ hospital/ Coumadin @ HOME  Asystole  Also known as Sinus Arrest.  Results in zero CO  The absence of impulse initiation in the heart results in electrical asystole.  Etiology  NI o MI o High Quality CPR o Electrical Shock o Identifying underlying and contributing o Electrolyte Disturbances factors o Acidosis o IV initiation o Parasympathetic Activity o Prepare for intubation  S/S o Rapid cardiac rhythm analysis and o NO heartbeat, palpable pulse, Defibrillation as soon as it is available respirations  Medical o Intubation o DO NOT shock pt if there’s no electrical conduction no electricity for defibrillator to use  Meds o Epinephrine (Adrenergic agonist) o Push EPI then CPR to keep med pumping for p tbc their body can’t Premature Ventricular Contractions (PVC’s)  Impulse that starts in the ventricle and is conducted through the ventricles before the next normal sinus impulse  Ventricles do not activate the atria while the normal sinus rhythm is buried in the bizarre-looking QRS complex from the premature ventricular beat  The interval b/w the sinus beat preceding the premature beat and the sinus beat following the premature beat is twice the regular interval  Etiology  Characteristics  o CAD cardiac ischemia or infarction o Rate: depends on underlying rhythm o Drug Overdose o Rhythm: irregular due to early QRS o Electrolyte imbalance- o QRS: duration is 0.12 seconds or longer,  Hypokalemia shorten narrow shape is bizarre and abnormal resting period then ventricular starts o P wave: visibility of P wave depends on taking over timing of PVC, may be absent  Hyperkalemia elongates resting o PRI: if P wave is in front of QRS PRI is less period than 0.12 seconds  Hypomagnesemia o 2 PVC – couplet o Caffeine, Nicotine, Alcohol o 3 PVC – triplet o HF, Tachycardia o 4 PVC—Quadruple  Quadrigeminy (every o Digitalis Toxicity fourth complex is a PVC o Hypoxia o NS PVC NS PVS – bigeminy o Acidosis o PV looks different – multifocal  CM o PVS looks the same – unifocal o May be asymptomatic or may feel heart “skipped a beat”  Medication o Amiodarone (Potassium Channel Blocker)  NI o Monitoring patient for frequent PVCs V-Tach/FIB Ventricular Tachycardia Ventricular Fibrillation “V-TACH” “DEFIB V-FIB”  REGULAR  Irregular  3 or more PVCs in a row  Most common in pts with cardiac arrest  3 or more consecutive ventricular  Rapid, uncoordinated cardiac rhythm that results in complexes > 100 bpm ventricular quivering and lack effective contraction o The rhythm is regular, and complexes have o Decreased CO = decrease blood supply to the same configuration other tissue  Characteristics  Pt with larger MIs and lower EF at higher risk of  lethal VT. o Rate: ventricular >300 bpm  Emergency because the pt is unresponsive and o Rhythm: extremely irregular without a pulseless. pattern  Characteristics o QRS shape: irregular with changing o Rate: Ventricular: 100 to 200 bpm; Atrial: amplitudes depends o Rhythm: Regular  No recognizable QRS complexes o QRS Shape; 0.12 sec or more, bizarre,  Etiology abnormal shape o Premature heart beats, Accelerating V-Tach o P Wave: Difficult to detect (not in book o PR Interval: Difficult to detect o CAD  Etiology o Acute MI o Myocardial ischemia (MI) or infarction o Untreated VT o Damage to the myocardium alters o Cardiomyopathy conduction times and pathways o Acid-Base Imbalances/Electrolyte imbalances o High catecholamine levels o Electrical Shock o Abnormal Electrolytes  CM o Too much digoxin = toxic o Absence of audible HB, palpable pulse,  CM respirations o Decrease in CO = in loss of consciousness o Pulseless, Loss of Consciousness, Apnea o Unresponsive  NI o Pulseless or Pulse o Check pt FIRST CPR until defib is available  NI o Early defibrillation critical to survival o Monitor HR and rhythm o Assess hemodynamic stability o Education for ICD: Other people not going to get shocked  Medical o Amiodarone o EPI  Medical o Intubation w/ pulseless VT o Defibrillation o Cardioversion o Meds  Amiodarone (Potassium Channel Blocker)  Magnesium Sulfate o Unstable  compression and DEFIB VTach VFib   Stable with pulse cardioversion **KNOW  DEFIB Torsades – irregular defib (M- MEDS shaped) Give MAG  Unstable without pulse DEFIB know pt education care on internal defib Interventions (PT EDUCATION)  Pacemakers  ICD: External Defib (vest), Internal defib o Detects and determines life-threatening tachycardia or fibrillation through shock o May need temporary vest until implantation  Worn at all times except when showering  Change battery every day  Delivers shock within 1 minute after rhythm detected  Vest vibrates and alarm to warn shock imminent o Must continue with meds o NI  Same as pacemaker  If battery is weak in ICD you will see s/s prior to ICD Torsades de Pointe  M shaped  Patho o A polymorphic ventricular tachycardia preceded by a prolonged QT interval  Etiology o CNS disease o Med interactions  Ciprofloxacin  Erythromycin  Haloperidol  Lithium  Methadone o Electrolytes  Low potassium  Low calcium  Low magnesium o Congenital  CM  o Rhythm likely to cause the patient to deteriorate and become pulseless  EMERGENCY o Polymorphic VT  Medical o Defibrillate o CPR o Correcting electrolyte imbalance o Meds  MAG SULFATE Heart Blocks  A disturbance in conduction between the sinus impulse and its associated ventricular response called atrioventricular (AV) block  Etiology o Functional or Pathologic Defect in the AV Node, Bundle of His, or Bundle Branches o Myocardial Ischemia o Congenital Heart Defects  CM o Vary with the ventricular rate and severity of any underlying disease o Decreased heart rate o Decreased perfusion to organs  1st degree heart block o Prolonged PR interval > 0.20 seconds o No Treatment o When all atrial impulses are conducted through the AV node into the ventricle at a slower rate  2nd degree heart block (Type I) o PRI gets longer and longer until QRS “drops” o NO TX o Progressively lengthening intervals until one P wave is not conducted (QRS dropped) o Occurs when there is a repeating pattern in which all but one of a series of atrial impulses are conducted through the AV node into the ventricles o Each atrial impulse takes a longer time for conduction than the one before until one impulse is fully blocked  2nd degree heart block (Type II) o P-P reg, R-R reg – will progress to 3 degrees without Tx Pacer Tx o Occurs when only some of the atrial impulses are conducted through the AV node into the ventricles o Non conducted P waves with a consistent PR interval o Every PR interval is the same o Tx depends on how frequent QRS drop happens   Pacemaker (either for SA or AV node)  3rd degree heart block o NO P-QRS relationship at all emergency intervention needed Pacer TX o NO impulses are conducted from atria to ventricles (through AV node)  Atrium and ventricle contraction but not in synch o ECG shows regularly occurring P waves that are independent of the ventricular rhythm o Lethal arrhythmia o More P waves than QRS complexes o Tx  Pacemaker  External pacer right now then implantable pacemaker  NI o Physical Assessment o Cardiac Monitoring o If patient does not have symptoms; no treatment or decreasing the cause  MEDICAL: o Transcutaneous pacing (emergent- need right now)  Dislodgement of pacing electrodes  Pacemaker malfunction o Meds  ATROPINE (Anticholinergic)(works in SA node)  1st degree & 2nd degree T1 Pacemaker  Used when a patient has a permanent or temporary slower than normal impulse o Paces the atrium and then ventricle when activity is not sensed for a period of time.  Types o On-Demand pacing o Fixed pacing o Transcutaneous Pacing  Emergency  Temporary until insertion of actual pacer device  Temporary—emergent  In conscious pt to tx symptomatic or unstable bradycardia  Complications o Dislodgement of pacing electrode o Pacemaker malfunction o Inhibition of permanent pacemakers or reversion can occur with exposure to strong electromagnetic fields  Allows patient to safely use most household electronic appliances and devices  Medications o Atropine (Anticholinergic)  NI o Physical Assessment  Look at incisionObserved for bleeding, hematoma, infection  Look for spike on ECG  Spike in front of P wave – atrial pacer  Spike in front of QRS – ventricular pacer  Did device migrate o Cardiac Monitoring o If patient does not have symptoms; no treatment or decreasing the cause (i.e. withhold medication or treatment)  Education  o Will set off alarms at airport – take card from vendor o Avoid high magnetic system  Does not include TV, microwave o Avoid cellphone in shirt pocket o Pt with hiccups and a pacemaker is a priority pt o 2-4 wks takes tissues to heal o Electrodes can be dislodged o Do not raise arm above level of pacer o s/s of infx o no swimming until wound heals o chest pain  migration of the leads o when heart isn’t perfusion  can pass out o consistent wooziness CALL DR. Acute Coronary Syndromes  Coronary plaque rupture that develops into acute thrombus.  Prolonged or total disruption of blood flow to the myocardium o Clot formation begins with adherence of PLTs to the ruptured plaque, & attracts more PLTs and forms a plug. o Results in a thrombosis may partially or completely obstruct the artery and cause acute ischemia.  Ischemia of cardiac cells occurs when the oxygen supply is not sufficient to meet metabolic demands. o ACS occurs when sudden obstruction of coronary blood flood flow results in acute myocardial ischemia  ACS may present as unstable angina, MI, or sudden cardiac arrest  Unstable Angina o Occlusion is partial, or the clot is dissolved before the death of myocardial tissue.  REDUCED blood flow o Symptoms increase frequency and severity, not relived with rest or nitro o Reduced blood flow in a coronary artery due to rupture of an atherosclerotic plaque  MI—STEMI/NSTEMI o Complete blockage of vessel (tissue death)  Sudden cardiac death o A decrease in blood supple from CAD may cause the heart to abruptly stop beating  Etiology o Coronary Heart Disease (CHD) o Atherosclerosis  An abnormal accumulation of lipid, or fatty substances, and fibrous tissue in the lining of arterial blood vessel walls.  These substances block and narrow the coronary artery, resulting in decreasing blood flow to the myocardium. o Nearly all infarcts are located in the left ventricular wall. o May occur at any age, but frequency rises with advancing age. o Females younger than 45 years have a six-fold lower risk of MI than men of the same age. o After menopause, the rate of MI in women becomes equal by age 80. o Pt wrist will hurt  Dx o EKG  Myocardial Injury and Ischemia are indicated by ST-segment changes (elevation) o Labs  Elevated serum levels of myoglobin (protein), troponin, (protein) and creatine kinase (CK-MB/Enzyme) o Cardiac Catheterization o Echocardiogram- used to evaluate ventricular function o Troponin  Cardiac protein  Found in the cardiac muscle If found in bloodstream – heart damage   Not the Goldstar anymore bc other heart damage can mimic protein  Increase in the level of troponin in the serum  detected within a few hours during acute MI  Remains elevated for long period often as long as 2 weeks o CKMB  Heart muscle enzymes Cardiac specific isoenzyme  Found mainly in cardiac cells and therefore increases when there has been damage to these cells  Elevated CKMB is an indicator of acute MI  The level begins to increase within a few hours and peaks within 24 hours of an infarct  CM oAngina Pectoris  Chest pain by ischemia o SOB o Indigestion to Choking choking sensation is never normal o N/V, anxiety o Cool, pale, and moist skin.  may indicate cardiogenic shock o HR & RR faster than normal o Heavy sensation in the upper chest o Feeling of impending death o Crushing, chest pain that may radiate to the arm, shoulder, jaw, or back. o Numbness in arms, wrists, and hands o Pallor, Diaphoresis o Dizziness or Light-headed  Prevention o Controlling Cholesterol- Assess labs (KNOW NORMALS)  Low-Density Lipoprotein (LDL) < 100mg/dl  Total Cholesterol 40 mg/dl  Triglyceride < 150 mg/dl o Dietary Measures  small frequent meals o Low Saturated Fats and High Fiber o Weight Loss and Physical Activity o Smoking Cessation o Managing HTN o Controlling Diabetes  NI o Oxygen, 12 Lead EKG, Labs, Medications o Educate small frequent meals throughout the day o MONA  Morphine  Reduce pain and anxiety decrease HR  Reduce preload and afterload  Oxygen  Nitroglycerin  Vasodilate  Aspirin  Blood thinner o Bedrest- Flat and keep affected leg straight until sheath is removed o Repositioning logrolling o Assess site and monitor for bleeding, hematoma, numbness, tingling o Post-op  VS, Labs  Continuous Cardiac Monitoring  Meds Analgesics  Urine Output Monitoring  Smoking Cessation Counseling  Nicotine replacement   Removal of sheath at the end of procedure (vascular closure device, sutures, direct manual pressure, or compression device)  Removed after activated clotting time (ACT) labs indicate that the heparin is no longer active and clotting time is acceptable o Cath  Risk for bleeding  pressure on site for 15-20 min  s/s: pale, cold, numbness, delayed cap refill use doppler  Medical o Goal is to minimize myocardial damage, preserve myocardial function, and prevent complications. o Meds  Statins Antihyperlipidemic (Atorvastatin, Simvastatin)  cholesterol meds  Nitrate (Nitroglycerin)  Cardiac Selective Beta Blocker (Metoprolol)  Calcium Channel Blocker (Diltiazem)  Antiplatelet (Clopidogrel)  Opioid (Morphine)  Anti-platelet (Aspirin)  ACE Inhibitor (Lisinopril)  Anti-coagulant (Heparin) low molecular weight heparin  Glycoprotein (Eptifibatide)  Oxygen o Reperfusion Therapies- aimed at opening the blocked coronary artery o PCI: Percutaneous Coronary Interventions  Used to open the occluded coronary artery and promote reperfusion to the area deprived of oxygen.  Performed within 60 minutes from arrival to ED- Door to Balloon Time  Why is time so important  tissue/cardiac damage o Thrombolysis  Enzymatic digestion of thrombus to open lumen using streptokinase and tissue plasminogen activator (tPA)  Use when PCI is not available.  Should not be used in patients who are bleeding or bleeding disorders  Given within 30 minutes of presentation to the hospital- Door to Needle Time  KNOW CONTRAINDICATIONS***  Active bleeding  Bleeding disorder  Hx of hemorrhagic stroke  Hx of intracranial vessel malformation  Recent surgery/ trauma  Uncontrolled hypertension  Pregnancy o PTCA: Percutaneous Transluminal Coronary Angioplasty  Physical disruption of plaque to open lumen,  Catheter (sheath) inserted in the femoral or radial artery, up through the aorta, and into the coronary arteries.  Dye is injected (angiography) to identify location and extent of blockage.  assess allergies  Complications o Invasive Coronary Artery Procedures  Percutaneous Coronary Interventions (PCI)  Thrombolysis  Percutaneous Transluminal Coronary Angioplasty (PTCA)   CABG: Coronary Artery Bypass Graft (CABG) o The greater saphenous vein is removed from the leg and grafted to the ascending aorta to the coronary artery distal to the lesion. o Surgical placement of a new conduit to bypass the occluded area of the artery. o Indications  Angina uncontrolled with medication of PCI  Treat Left main coronary artery stenosis or multivessel CAD  Prevention and Treatment of MI, Dysrhythmias, or Heart Failure  Unsuccessful PCI  Bypassed arteries must have 70%+ occlusion  50% occlusion in the Left main coronary artery o Complications  Hypovolemia  MI  Hemorrhage  Stroke  Cardiac Tamponade  Acute Kidney Injury  Fluid Overload  Electrolyte Imbalances  Hypothermia  Hepatic Failure  Hypertension  Infection  Cardiac Failure o NI  o Geriatric Considerations  May not present with pain  Dyspnea  Weakness  Give Medications cautiously stay in body longer and don’t metabolize as fast Myocardial infarction  Complete occlusion  STEMI – o significant damage to myocardium (Necrosis) (complete blockage)  NSTEMI – o may be less damage to the myocardium (Ischemic process) (partial blockage)  less damage  If occlusion is complete, and if the thrombus persists long enoughirreversible damage to myocardial cells occurs= necrosis o  Tx o Use rapid transit to the hospital o Obtain 12-lead ECG to be read within 10 minutes o Obtain laboratory blood specimens of cardiac biomarkers troponin Begin routine medical Evaluate for indications for Continue therapy as interventions: reperfusion therapy: indicated:   Supplemental oxygen  Percutaneous coronary  IV heparin, low–molecular-  Nitroglycerin intervention weight heparin, bivalirudin,  Morphine  Thrombolytic (fibrinolytic) or  Aspirin therapy  Fondaparinux  Beta-blocker  Clopidogrel (Plavix)  Angiotensin-converting  Glycoprotein IIb/IIIa enzyme inhibitor within 36 inhibitor hours  Bed rest for a minimum of  Anticoagulation with 12–24 hours heparin and platelet  Statin prescribed at inhibitors discharge.  Statin. Sudden Cardiac Arrest  Unexpected death from cardiac causes within 1 hour of the onset of symptoms  In cardiac arrest the heart is unable to pump and circulate blood to the body’s organs and tissues  Etiology o CHD or Atherosclerosis o Hereditary o Structural or Electrical Abnormalities o Ventricular Fibrillation- most common o Bradycardia leading to Asystole  CM o Consciousness, pulse, and blood pressure are lost immediately o Ineffective breathing or gasping o Pupil dilation o Seizures may occur bc they’re not getting o2 o Pallor or Cyanosis o Brain damage irreversible  NI o CPR  check for responsiveness and breathing code blue/call 911  Chest compression if there’s no carotid pulse and no defibrillator is yet available DEFIB once available o AED o Maintaining Airway and Breathing o ACLS