Cardiac Arrest

Cardiac Arrest
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Terms in this set (101)
-plays role in rate of impulse formation, speed of conduction, and strength of contraction
-PNS and SNS
-Vagus nerve stimulation-> slows firing of SA node; slows impulse conduction of AV node= decrease in HR
-Sympathetic nerve stimulation-> increases SA node firing;AV node impulse conduction and cardiac contractility= increase in HR
Ventricular dysrhythmiasstart above AV nodeEctopic dysrhythmiasoutside conduction systemConduction blocks dysrhythmiasproblem w/impulse conductionAntidysrhythmic Drugs-classified according to how/where they affect the cardiac cells - 4 classes: 1 (1a, 1b, 1c), II, III, IVAntidysrhythmic Drugs MOACorrecting abnormal cardiac electrophysiologic functionAntidysrhythmic drugs contraindications-heart blocks -allergies -cardiogenic shock -may worsen current dysrhythmiasAntidysrhythmic drugs adverse effects-hypersensitivity reactions: N/V, headache, dizziness -pro-dysrhythmic -QT prolongation -unpredictableBrady dysrhythmias categories-Sinus bradycardia -Heart block -AtrialSinus Bradycardia-SA node fires ar <60 bpm -Athletes and SleepSinus bradycardia occurs b/c-Valsalva maneuver( bearing down when having a bowel movement) -hypothermia -medications -vagal stimulationSinus brady cardia treatment/meds-treatments depends on symptoms -Meds: Atropine -Transcutaneous pacing or permanent pacemakerAtropine: Med class, MOA-Anticholinergic -Blocks action of neurotransmitter acetylcholine -Allows SNS to dominate -Blocks inhibitory vagal effects on pacemaker cells-> Increased HR -Works on conduction system of heartAtropine Indicationssinus bradycardiaAtropine Contraindications-Allergies -Glaucoma -poor intestinal motilityTachy-dysrhythmias Categories-Atrial-> Afib -Ventricular-> Ventricular fibrillation, ventricular tachycardia -Supraventricular -JunctionalAtrial Fibrillation (Afib)-disorganization of atrial electrical activity-> multiple ectopic foci -Rapid atrial contractions-> loss of effective atrial contractions -Underlying heart disease; can develop acutely -Decreased CO d/t atrial kickControlled afib60-100 bpmUncontrolled afib>100 bpmAfibv treatment Goals-Decrease rate -prevent stroke -convert to NSRAfib treatment: Drugs for rate control-Calcium channel blockers -Beta blockers -Amiodarone or Digoxin -Electrical cardioversion -continue anticoagulantsAmiodarone adverse effects-75% -Corneal microdeposits-> visual halos, photophobias, dry eyes -Pulmonary toxicity-> fibrosis -Proarhythmic -Long 1/2 life (will take 2-3 months to get out of system)Amiodarone drug interactionsdigoxin and warfarinAmiodarone MOA and use-Very effective -Prolongs action potential duration and effective refractory period is cardiac tissues -Blocks alpha and beta adrenergic receptors of SNS -Use: Afib, VTACH, VfibAmiodarone AdministrationPO, IVAfib increases risk of...stroke -blood can pool in the heart's upper chambers and form clots -break free and travel= strokeSupraventricular Tachycardia (SVT)-Atrial tachycardia, paroxysmal supraventricular tachycardia -ectopic focus; above bundle of His -re-excitement of the atria -PAC may triggerSVT: Healthy heart d/t....-over exertion -emotional stress -deep inspiration -stimulantsSVT also d/t-digoxin toxicity -coronary heart disease (CAD)SVT HR150-220 bpmSVT manifestations-Decreased CO -hypotension '-palpitations -dyspnea -anginaAdenosine Class and moa-unclassified Antidysrhythmic -Slows conduction time through AV nodeAdenosine: indicationsSVTAdenosine (Half life, IV)-half life-> 10 seconds; only IV and FAST -IV-> close to the heart as possible (Antecubital) -IV dose RAPIDLY-> 1-2 seconds; 20 ml flushAdenosine pt education-may feel chest tightness -minimal adverse effectsSVT treatment: Vagal maneuversValsalva, Carotid massage, Coughing, ice water, gaggingSvt Treatment: drug therapy-adenosine -convert SVT to NSRSVT treatment: Synchronized cardioversion-for SVT or ventricvular tachydysrhythmias (with a pulse) -Shock on R wave of QRS complex -increases joules as neededCardioversion: nonemergencysedate the ptcardioversion: emergencycardioversion ASAPCardioversion: if pulseless or ventrivular fibrillation->defibrillatorVentricular tachycardia (VTACH)•Run of 3 or more PVCs; 150-250 bpm •Ectopic foci fire repeatedly •Sustained or nonsustained •Ominous sign •Electrolyte imbalances, drug toxicity, MI, CAD, etc. •Stable or unstable •Unstable = pulseless VTACH (pVT) •Treated immediately!VTACH treatment-Does the pt have a pulse? -pulseless= EMERGENCY -pulse= medications -epinephrine and shock -amiodaroneVentricular fibrillation (V-fib)-firing of multiple ectopic foci in ventricles -cause ventricules to twitch or 'quiver' -unable to pump blood-> no CO -HR is not measurableVfib causes-acute MI -HF -Acidosis -HyperkalemiaVfib treatment-ACLS -defib -epinephrine -amiodaronevfib goals-CPR -defib -vfib defibvfib/pVT treatment (SCREAM)-Shock -CPR -Rhythm -Epi -Amiodarone -Medications (Lidocaine)code blue-pt stopped breathing/no pulsse -resuscitation efforts -begin ACLS -Specialized team -different if on floors compared to icu or edRapid response-pt declining -change in vs -change in mental status, stroke-like symptoms, difficulty breathing -'doesnt look right' -intervene -may turn into code -specialized team -not in ed, icurapid response goalprevent code blue from happeningCardiopulmonary arrest key points-early cpr!!! -minimal interruptions -quality compressions -100-120 per/min -2-2.4 in depth -EARLY defib -'edison is the medicine'Cardiopulmonary arrest-cardiac arrest -heart stops -cessations of breathing -medical emergency -'code blue' -code team -BLS -ACLS (advanced cardiac support)initiation of code blue-CPR immediately -series of events, PMHx, lab results -provide oxygemn-> ambu bag -attatched monitor pads -defib-> shockable rhythm -pulseless VTACH pr ventricular fib (pVT/VF) -medsWhat;s happening during a code•Roles are being assigned •IV access •Advanced airway •Placing pads •Labs drawn (full rainbow) •Blood glucose monitoring •Calling family •Consoling family •Documentation, runner, crash cartCode blue participants•Physician/Intensivist/Resident/NP/PA •Critical care RN (unless in ICU or ED) •RN à code cart •RNà documentation •RN/PCA/Nurse's aid/student à runner •RN/IV team à IV access •RN à Family support •Respiratory therapist •Supervisor/Nurse managerDefibrillationthe use of electrical shock to restore the heart's normal rhythm -monophasic (360 joules) or biphasic (120-200 joules) -manual or automatic deviceManual defibrillationinterpret heart rhythms, determine need for shock, and deliver shockautomatic external defibrillator (AED)detects rhythm and tells user to deliver shockshockable rhythmsVentricular Fibrillation & Ventricular Tachycardianon-shockable rhythmsPEA (pulseless electrical activity) and asystoledefibrillation only indicated for.. and goalv-fib and pulseless VTACH -most effective when myocardial muscle cells are no anoxic or acidotic -Goal: rapid defib (within 2 minutes)Epinephrine class and moa-Adrenergic drug -vasoconstructive drug, vasopressive drug, pressor, inotrope -MOA: binds to receptor and causes physiologic response -Avcts on both alpha and beat receptorsAdrenergic receptors: alpha vs beta (Alpha 1)-vascular smooth muscle; heart -stimulation by NE= constriction -CONSTRICTS ARTERIESAdrenergic receptors: alpha vs beta (Beta 1)-vascular smooth muscle; heart -Stimulated by NE and epi= increased HR, force of contraction and speed of conduction -CONSTRICTS HEART VESSELSAdrenergic receptors: alpha vs beta (Beta 2)-smooth muscle coronary blood vessels and lungs -activated by epi= vasodilation -DILATE LUNGSEpinephrine Contraindications-allergy -sever hypotensioEpinephrine adverse effects-increased HR -palpitations -dysrhythmias -fluctuations in BP Toxicity/overdose: seizures and HTNEpinephrine continued (life, used for, administriation during...)-short 1/2 life -pulseless VT, Vfib, Asystole, PEA -administration during cardiac arrest: q 3-5return of spontaneous circulation (ROSC)-return of a pulse for at least 20 min -not necessarily favorable -20-25% survival ratePost-Resuscitation Goals***-optimize hemodynamis -reperfusion -targeted temp. management -therapeuitc hypothermia -reduce mortality; improve neurologic outcomes -decrease in core temp -slow rewarming of the bodycerebrovascular accident (CVA)-aka stroke -results in infarction-> cell death -ischemia of hemorrhage -functions of the brain that were controlled by the effective are are impaired or lost -immediate medical attention is requiredStroke Pathophysiology-brain reuires continous supply of blood -provide o2 and glucose to neurons -blood flow(BF)-> 750-1000 ml/min -If BF is interrupted: neurologic metabolism is altered-> 30 seconds; metabolism stops-> 2 min; cell death-> 5 minTypes of stoke: Ischemic- 87% -Inadeqaute blood flow to the brain -blockage of a cerebral artery by a blood clot -thrombotic -embolicIschemic Stroke: thrombotic-most common (60%) -injury to blood vessel wall and formation of clot -narrowed vessel becomes occluded= infarction - extent depends ononset, area damaged, and collateral circulation -unlikely to see decrease LOC 24 hrsIschemic stroke: thrombotic risk factorsHTN and DMIschemic stroke: Embolic-2nd most common cause of stroke -embolus lodges and occludes cerebral artery -starts in endocardium-> plaque breaks off-> enters circulation -travels upward to cerebral circulation and lodges in narrow vessel -afib, MI, ineffective endocarditisIschemic stroke: embolic less commonAir and fat emboliHemorrhagic stroke-weakened blood vessels rupture -bleed into the brain -Aneurysms and AVMs -Cells begin to die -Bleeding into the brain tissue (Intracerebral) -Bleeding into the subarachnoid space or ventricles (subarachnoid hemorrhage SAH)Ischemic stroke drug therapy-fibrinolytic therapy •Reestablish blood flow à prevent cell death •Recombinant tissue plasminogen activator (tPA) •Produces localized fibrinolysis à binds to fibrin in thrombi •Plasminogen à plasmin (enzyme) à digests fibrin & fibrinogen •Clot breakdown •MUST be given within 3-4.5 hours of onset of s/s •Must control BP (SBP <185)Stroke Alert•Different terms depending on the facility •Signs and symptoms of stroke •Slurred speech, weakness, asymmetry, incontinence •Ischemic vs Hemorrhagic •Neurological change •Need to ACT FAST •Stroke AlertGolden Hour (Time is Tissue)-CT scan -Glucose and NIHSS -Fibrinolytic therapy -Thromboectomy -Further workup -'Door to needle time'Pulseless Electrical Activity (PEA)=organized electrical activity seen on EKG -Pt has NO pulse; NO mechanical acitivity -common after defibrillation -poor prognosisPEA CausesH's and T'sPEA treatmentTreat underlying cause-> CPR, EpinephrineAsystole-absence of ventricular electrical activity -May see P wave -NO ventricular contraction; no depolarization -Pt is unresponsive, pulseless, and apneic -IMMEDIATE ATTENTION-> lethalAsystole causes-heart disease -conduction issuesAsystole treatment-CPR -EpinephrinePEA and Asystole treatment-P: Pump; start compressions -E: Epinephrine -A: Assess cause-> 5 H's and T'sPEA H's and T'sH's: 1. Hypoxia 2. Hydrogen ion (acidosis) 3. Hyper or hypokalemia 4. Hypothermia 5. Hyper or hypoglycemia T's: 1. Toxins 2. Tamponade (cardiac) 3. Tension pneumothorax 4. Thrombosis (pulmonary) 5. Thrombosis (cardiac) 6. TraumaPremature Atrial Contraction (PAC)-contraction starting from ectopic focus in the atrium -sooner than expected -often benign -d/t emotional stress, fatigue, heart dx -healthy person-> palpitations -Frequent PACs= Prewarn of dysrhythmiaspremature ventricular contraction (PVC)-Ectopic focus in ventricles -QRS complex wide and distorted -3 or more= Vtach -R on T phenomenon -Stimulants, electrolyte imbalances, hypoxia, fever -treat the cause -NO meds to treat