CV II Exam 2 ACLS, Stroke, and Arrhythmias PDF

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CV II Exam 2: ACLS, Stroke, and Arrhythmias Hypertensive Crisis ● ● ● ● Pathophysiology: ○ Abrupt rise in systemic vascular resistance (SVR) from a known or unknown stimulus followed by compensatory mech arising from the vascular endothelium ○ HTN begets HTN ○ Urgency vs Emergency ○ Hypertensive urg...

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CV II Exam 2: ACLS, Stroke, and Arrhythmias Hypertensive Crisis ●

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Pathophysiology: ○ Abrupt rise in systemic vascular resistance (SVR) from a known or unknown stimulus followed by compensatory mech arising from the vascular endothelium ○ HTN begets HTN

○ Urgency vs Emergency ○ Hypertensive urgency: ■ Presentation: ● Abrupt rise in BP: SBP ≥ 180 mmHg, DBP ≥ 110 mmHg ● No signs of end organ damage ■ Result of noncompliance or inadequate tx ■ Reduce BP over a period of 24-48 H with oral meds ■ Prefer short acting: ACEi/ARB ○ Hypertensive emergency: ■ Presentation: ● Abrupt rise in BP: SBP ≥ 180 mmHg, DBP ≥ 110 mmHg ● Signs of end organ damage ■ D/t chronically elevated BP or de novo presentation ■ Immediate action should be taken to reduce BP but in a controlled fashion ■ NOT aimed at normalizing BP ■ Parenteral drug therapy and intensive care monitoring Clinical Presentation: ○ Majority of pts will have hx of BP elevation for years before HTN emergency ○ Clinical manifestations are directly related to type of end organ dysfxn ○ Most frequent presentation: ■ Chest pain, Dyspnea, Neurologic deficits ○ Absolute level of BP may not be as important as rate of increase ■ Organ dysfxn is uncommon w/ DBP < 130 mmHg0■ Except in children and pregnancy Initial management- HTN emergency: ○ No consensus on first line agent ○ Dictated by affected target organ ○ General goal: reduce BP by 10-15% over 30-60 min or MAP by 20-25% in first 60 min ■ Exceptions: ● Aortic dissection ● Acute intracranial bleed 1

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Pharmacologic agents: ○ Direct vasodilators: ■ Hydralazine: ● Greater effect on DBP than SBP ● Increases renal blood flow ● Onset of action 5-25 min; Effect of BP lasts up to 12 H ● Avoid in tachycardia, HF pts ● Good in renal trouble ● SE: rebound tachycardia ■ Fenoldopam: ● MOA: Peripheral dopamine-1 agonist ● Renal vasodilation ● Fast on and small t ½ ● Effect lasts 30-60 min ■ Want something fast on and fast off, that can be titrated and controlled well ○ Nitrates: ■ Sodium Nitroprusside ● Arterial and vasodilation; decrease preload and afterload ● Rapid onset ● Disadvantages: ○ Coronary steal (shunts blood from coronary arteries): can trigger acute MI ○ Increased intracranial pressures ○ Decreased cerebral blood flow ○ Cyanide toxicity, especially in renal failure ● Use the smallest amt for shortest time possible ● SE: tachyphylaxis: effects of drug stop after a certain amt of time ■ Nitroglycerin: ● Vasodilator, decreases preload, increased coronary blood flow, inhibits coronary vasospasm, and decrease myocardial O2 demand ○ Arterial dilation at high doses ● Fast on, fast off ● Tachyphylaxis is very common after 4 H of IV infusion ● SE: HA, tachycardia ○ Calcium Channel Blocker: ■ Nicardipine: ● 2nd gen DHP ● High selectivity for coronary and cerebral vasodilator activity ● Onset: 5-15 min, Duration: 3 H ● Recommended for acute ischemic stroke when SBP>220 or DBP >120 mmHg ● Need ICU monitoring of drips ■ Clevidipine ● Direct coronary vasodilator, increase coronary blood flow,increase SV & CO ● Lipid emulsion formulation: ○ Avoid in pts with egg or soy allergies ○ Change infusion line frequently ○ Hyperlipidemia, on TPN, pancreatitis ● Fast on, fast off 2

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Beta blockers ■ Pt needs to be euvolemic ■ Labetalol ● Alpha 1 and Beta 1 non selective receptor blocker (greater effect on Beta) ● Onset 2-5 min, Duration 2-4 H ● Commonly used in preg: can’t cross placenta easily ■ Esmolol: ● Cardioselective Beta blocking ● Reduces HR and myocardial contractility, no vasodilatory effect ● Rapid onset: 60 sec, Duration: 10-20 min ● ‘Ideal’ B blocker for critically ill pts ● Metabolised by RBC esterases (anemia may prolong half life) ■ CI: ● Heart block ● Severe bradycardia ● ADHF: esp in fluid overloaded pts ○ ACE I: Enalaprilat: ■ Onset: 15 min, Peak in 1 H ○ Alpha blocker: ■ Phentolamine ● Was agent of choice for catecholamine induced HTN emergency (cocaine) ● Immediate onset of action Major presenting symptoms: ○ Neurologic: ■ Failure of autoreg in sudden elevation in MAP → cerebral edema & microhemorrhages ■ Sx: HA, stupor, seizures, delirium, agitation, N/V, visual disturbances (spots) ■ Lower BP within 2-6 H by 25% ■ Preferred antihypertensive agents: ● Nicardipine ● Labetalol ● Fenoldopam ○ Myocardial Ischemia ■ Elevated SVR increases LV myocardial wall tension and oxygen demand ● Can lead to myocardial ischemia or even infarction ■ Preferred agents: ● Nitrates: lower LV preload and improve coronary blood flow ● B blockers (labetalol, esmolol): ↓ HR, ↓ afterload, & improves coronary perfusion ■ Avoid: Hydralazine d/t reflex tachycardia ■ Target BP goal: MAP between 60-100 mmHg ○ Acute HF: ■ Presents as acute pulmonary edema ■ 2nd most common sign of end organ damage ■ D/t reduction in both preload and afterload ■ Preferred agent: sodium nitroprusside ● ACEi will help reduce afterload and improve CO ● Clevidipine ● Loop diuretics will often need to be added for pulmonary edema 3

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Aortic dissection: ■ Differential dx for pts presenting with acute chest pain and elevated BP ■ High mortality during 1st H ■ Type A dissection: surgical emergency ■ Type B dissection: can be medically managed ● Want to get BP low to remove pressure from dissection and body can self repair ● Goals: SBP 90 ■ Complications occur with SBP >160, DBP >110 ○ Preeclampsia is distinguished from chronic HTN by proteinuria ■ Lab: >300 mg protein/24 H ○ Initial therapy: volume expansion, Magnesium sulfate for seizure prophylaxis and BP control ○ Agents: ■ No antihypertensive for preg specifically ■ Hydralazine ● Associated with more c sections, maternal oliguria, placental abruption ● Unpredictable hypotensive effect ■ Labetalol: both oral and parenteral ● Safe in breastfeeding 4

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Nicardipine Methyldopa: oral drug of choice, outpt treatment Avoid: ● Nitroprusside d/t cyanide ● ACEi/ARB: teratogenic Postoperative hypertension: ○ Significantly elevated BP w/in 1st 2 H after surgery ■ Sympathetic activation and adrenergic surge ○ May lead to neurologic, CV, or surgical site complications ○ Reversible contributors (treat first) ■ Pain, hypoxemia, hypercarbia, hypothermia, volume overload, anxiety ■ Withdrawal from withholding antihypertensive ■ Did they get B blocker before surg? ○ Pts with poorly controlled HTN: high risk ○ Tx should be focused on cause and ability to take oral meds ■ Restart home meds if there are no CI Hyperadrenergic States: ○ Most commonly related to drug overdoses (Cocaine, amphetamines, PCP) ○ Less common: pheochromocytoma, clonidine withdrawal, MAOI tyramine rxn ○ Caused by surge in catecholamine levels ○ Recommend goal is lower MAP by 20-25% ○ Agents depend on cause: ■ Nicardipine and fenoldopam in most cases ■ Pheochromocytoma an MAOI tyramine rxn: phentolamine, phenoxybenzamine, nitroprusside ■ Cocaine/amphetamine: add a benzodiazepine ■ Clonidine withdrawal: give clonidine Drugs used in Advanced Cardiac Life Support Chains of survival: ○ In hospital cardiac arrest:

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■ Out of hospital cardiac arrest:

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V Fib is the most frequent initial rhythm out of hospital cardiac arrest 5

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Value of chest compressions ○ Compression - ventilation ratio ■ No advanced airway: 30:2 ■ Advanced airway: no ratio, follow rates ○ 100-120 per minute ○ Ventilations q 6-8 sec ○ Better outcomes with fewer breaks in compressions Early Defibrillation ○ 1st line for V fib ○ Use of electrical current to produce myocardial depolarization to allow coordinated ctx to resume ○ Doesn't jump start heart: need shockable rhythm ○ With high quality compressions: proven to increase survival to hospital discharge BLS: ○ Chest compressions ○ Airway ○ Breathing ○ Highlights: ■ Immediate recognition of unresponsiveness, activation of emergency response system, and initiate CPR ■ Admin naloxone if opioid emerg suspected ■ Trained rescuers are encouraged to simultaneously perform some steps to reduce time to first chest compressions ■ Continued emphasis on high quality CPR for both lay rescuer and healthcare provider ACLS:

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Airway Breathing Circulation Algorithms: ■ Cardiac arrest: ● V fib ● V tach (pulseless VT) ● Pulseless electrical activity ● Asystole ■ Immediate post cardiac arrest care ■ Tachycardia with pulse ● Narrow QRS complex ● Wide QRS complex ■ Bradycardia with pulse Treatable causes: ○ Hypoxia ○ Hypovolemia ○ Hydrogen ions (acidosis) ○ Hypo/hyperkalemia ○ Hypothermia ○ ○ ○

Toxins Tamponade (cardiac) Tension pneumothorax 7

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○ Thrombosis (pulmonary) ○ Thrombosis (cardiac) Drug admin: ○ IV access ■ Central: ● Preferred ● Drug reaches central circ quickly ● May not be avail in most pts ■ Peripheral ● Can be used in most cases ● 1-2 min to reach central circ ● Should be followed by 20 mL bolus of IV fluid ● Consider elevating the extremity for 10-20 sec after admin ○ Intraosseous (IO) ■ Consider if IV access is unavailable ■ Safe and effective for fluid resuscitation, drug deliver, and blood sampling ● Dosing same as IV ■ Can be used in all ages ■ Most common site: proximal tibia ○ Endotracheal: ■ IV and IO preferred ■ Results in lower blood concentrations at comparable doses ● Recommend to use 2-2.5 times the IV dose diluted in 5-10 mL of SW or NS ■ Select drugs only ● Naloxone ● Atropine ● Vasopressin ● Epinephrine ● Lidocaine Drugs in Cardiac arrest: ○ Vasopressors: ■ Goal: increase myocardial and cerebral blood flow during CPR and achieve ROSC ● Shown to increase rate of return of spontaneous circulation (ROSC) ● Not shown to increase survival to hospital discharge ■ Don’t interrupt chest compressions or delay defibrillation ■ Agent: Epinephrine ● Vasopressin and Atropine were removed from past AHA updates ■ MOA: ● Alpha-adrenergic receptor stimulation ○ Vasoconstriction: prevents arterial collapse, increased coronary and cerebral perfusion, and increases coronary perfusion pressure (CPP) ○ May make Vfib more susceptible to defib ● Beta receptor stimulation ○ Increase myocardial O2 requirements ○ Impair O2 delivery and consumption ○ Increase lactate production in the post-resuscitation period ■ Dose: 1 mg IV/IO every 3-5 min 8

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● High dose (0.1-0.2 mg/kg) not recommended for routine use ● Use 1 mg/10 mL in codes ■ Admin as soon as feasible after onset of arrest d/t an initial non-shockable rhythm ○ Antiarrhythmics: ■ Amiodarone or lidocaine may be considered for VF/pVT that is unresponsive to defib ■ Useful for pts with witnessed arrest for whom time to drug admin may be shorter ■ Amiodarone: Dose: 300 mg IV/IO bolus, may repeat 150 mg IV/IO bolus ■ Lidocaine: Dose: 1-1.5 mg/kg IV/IO, may give addn’l 0.5-0.75 mg/kg IV/IO push ■ Magnesium ● Considered only in TdP with prolonged QT ● Not routinely used ● Dose: 1-2 g IV diluted in 10 mL of D5W or NS (50%, 500 mg/mL) ○ Steroids: ■ IHCA: ● Combo of methylprednisolone, vasopressin, & epi during arrest; hydrocortisone after ROSC ● Combo may be considered, not routinely used ■ OHCA: Not well studied, not part of routine use Not routinely recommended medications: ○ Vasopressin and Atropine: ■ No benefit for survival to hospital discharge when combined with epi ■ Dose: 40 units IV/IO ■ Doesn’t hurt pt but doesn’t help ○ Sodium Bicarb: ■ No benefit or poorer outcomes ■ May provide benefit in special situations ● Pre existing metabolic acidosis ● Hyperkalemia ● TCA overdose ■ Dose: 1 mEq/kg ● Flush line after use d/t incompatibilities ○ Calcium: ■ Variable results on ROSC, no studies show improved survival to hospital discharge ■ Possible benefit in special situations: ● Hyperkalemia, hypocalcemia ■ 1 gm CaCl = 3 gm Ca Gluconate ○ Beta blockers (Esmolol) ■ Limited evidence ■ Consider in pts who remain in persistent ventricular dysrhythmias despite multiple rounds of ACLS ● Might be causing adrenergic storm that could benefit from beta blockade ■ Dose: 500 mcg/kg + infusion up to 100 mcg/kg/min??? Meds in special circumstances: ○ Cardiac arrest associated with PE ■ Confirmed PE: Consider thrombolysis, even with chest compressions ■ Suspected PE: ● Consider thrombolysis, no consensus on inclusion criteria, timing, drug, or dose 9

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Alteplase: 50-100 mg IV/IO Admin: variable. Bolus +/- infusion ● Ex: 50 mg IV bolus + 50 mg IV bolus 15 min later ● Ex: 15 mg IV bolus + 85 mg IV over 90 mins ○ Assoc with Opioid Overdose: ■ Naloxone: ● Dose: 0.4-2 mg IM/IN (or IV) ■ Standard resuscitative measures should take priority over naloxone (CPR first) ■ Provide education to anyone in the room or close to pt for future knowledge ○ Assoc with poisoning: ■ IV Lipid Emulsion (ILE) ■ Failing other options. ■ MOA?: Lipids collect lipid soluble drugs ■ Dose: Using 20% soln ● 1.5 mL/kg (LBW) IV bolus over 1 min ● Infusion: 0.25 mL/kg/min for 30-60 ● Immediate Post-Cardiac Arrest Care: ○ Optimize ventilation and oxygenation ○ Treat hypotension ■ Avoid SBP 150 bpm) ○ Can be classified by QRS complex, HR, or regularity ○ Goal: prevent cardiac arrest ○ Similar to bradycardia algorithm ○ 1) Identify and treat underlying cause ○ 2) Stable vs unstable ■ Unstable: Hypotension, altered mental status, signs of shock, ischemic chest discomfort, acute HF ● If pt has severe sx: Synchronized cardioversion ASAP ■ Stable: Evaluate QRS interval ● Get expert opinion or utilize drug therapy ○ Examples: ■ Regular Narrow-Complex tachycardia ● Sinus tachycardia, sVT ● Non pharm Therapy: ○ Vagal maneuvers ■ Ex. carotid sinus massage 10

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■ Ex. Bearing down ○ Will slow ventricular rate and may assist in rhythm dx ○ Try while preparing drug ● Pharm therapy: ○ Adenosine: ■ Slows conduction through AV node to get normal rhythm back ■ Rapidly absorbed and metabolised ■ Dose: 6 mg initially, may repeat w/ 12 mg if rhythm doesn’t convert in 1-2 min (total 3 doses) ● Push fluid behind to get med to heart ■ SE: flushing, dyspnea, chest discomfort, brief bradycardia/asystole ● Educate pt on how they will feel (terrible) ○ Calcium channel blockers (Use IV for fast action) ■ Verapamil ● Don’t use in pts with impaired ventricular fxn or HF ● Dose: 2.5-5 mg IV bolus over 2 min, may repeat w/ 5-10 mg Q 15-30 min (total of 20 mg) ■ Diltiazem ● Dose: 15 mg IV bolus, mayi repeat w addn’l 20 mg in 15 min PRN, followed by infusion 5-15 mg/hr titrated to HR ● Used more than verapamil ○ Beta blockers (Ex. metoprolol) (Use IV for fast action) ■ Slow conduction by antagonizing sympathetic tone in nodal tissue Wide complex tachycardia ● VT or VF ● SVT with aberrancy ● Preexcited tachycardia (Wolff-parkinson-White syndrome) ● Presume unstable pts have VT and perform synchronized cardioversion immediately ● Therapy: ○ Adenosine: ■ May use adenosine for tx or dx if unable to determine the etiology of rhythm ■ Do not use adenosine for unstable, irregular, or polymorphic wide-complex ■ Dosing similar to narrow complex tachycardia ○ IV antiarrhythmic: amiodarone, procainamide, sotalol ■ In stable pt with monomorphic VT ■ Avoid procainamide or sotalol in pts with prolonged QT ■ Lidocaine is less effective: 2nd line ● Contraindication: verapamil unless tachycardia is known to be supraventricular with profound hypotension Irregular tachycardia ● A fib and flutter ● Rate vs Rhythm control ● Pts in AF >48 H: increased risk of cardioembolic events 11

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Don’t attempt cardioversion unless pt is unstable or adequately anticoagulated ● Therapy: IV ○ Beta blockers, Non-DHP CCBs, amiodarone, and digoxin ■ Torsades de Pointes: irregular tachycardia ● Subtype of polymorphic VT (abnormally long QT interval) ● Deteriorates to VT/VF easily ● Can result from meds, electrolyte/metabolic alterations, or congenital cause ● Therapy: ○ IV mag: 2 mg IV push (diluted) ○ May consider IV beta block or isoproterenol depending on QT ● Bradycardia with pulse: ○ HR < 60 bpm (generally African Americans > Caucasians ■ Sex: Men > Women ■ Family Hx: inherited coagulopathies ■ Low birth weight: Odds of stroke double for those with birth weights < 2.5 kg ○ Potentially modifiable: ■ Migraine with aura ■ Metabolic syndrome ■ Drug/EtOH abuse (esp cocaine, amphetamines, heroin) ■ Hemostatic and inflammatory factors ■ Homocysteinemia ■ Sleep disordered breathing (Sleep apnea, snoring) ■ Periodontal DZ ■ Infection DZ ○ Modifiable: ■ HTN ■ Smoking: Environmental exposure to smoke increases risk as well ■ DM ■ Oral Contraceptives 13

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● Obesity + HTN + OCP increase risk ● Increased risk with age ■ Postmenopausal hormone therapy (HRT) ■ Afib ■ Dyslipidemia ■ Obesity; Physical inactivity ■ Carotid stenosis; CHD/PAD ■ Pregnancy ■ Depression Goals of therapy for pts with acute ischemic strokes ○ Reduce ongoing neurologic injury and decrease mortality and long term disability ○ Prevent complications secondary to immobility and neurologic dysfxn ○ Prevent stroke recurrence Treatment and monitoring for primary prevention ○ Target modifiable, well documented risk factors ■ HTN, Cig smoking, Afib, DM, Dyslipidemia, Obesity ■ Use appropriate guideline therapy for each ○ ASA: Benefit remains unclear, currently not recommended Treatment of acute ischemic stroke ○ TIA: DAPT for 21 days post TIA to prevent stroke ○ AIS: ■ Airway support/ventilatory assistance ■ Supplemental O2 >94% ■ Fluids for hypotension and hypovolemia ■ Lower temperature in hyperthermia: temp >38 celsius ■ Glucose control (neuro sx, can’t tell if AIS tx is working unless these sx are cleared) ● Treat hypoglycemia 110 at time of tx ■ Maintain BP 0.5 sec ○ ECG: QRS amplitude is continually changing ○ Delayed ventricular repolarization d/t blockade of K conductance ○ Risk factors: ■ Non modifiable: ● Congenital long QT syndrome ● Females ● Increasing age ● Structural heart DZ (LV dysfxn) ● Impaired renal or hepatic fxn 21

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● Previous drug induced QT prolongation ■ Modifiable: ● Electrolyte abnormalities (low K, Mg, Ca) ● Bradycardia ● Starvation or obesity ● Medications ● Drug interxn ○ MOA of drug induced QT prolongation: ■ Risk factors must be present ■ + Meds: ● Use of >1 QT prolonging drug ● Cause electrolyte abnormalities ● Higher drug concentrations ● Impaired kidney or liver fxn ● Drug interactions → inhibit metabolism of another QT prolonging drug ■ QT prolonging drugs: ● Type 1a and III antiarrhythmics ● TCAs, SSRIs, Antipsych ● Trazodone ● Fluoroquinolones ● Azoles ● Macrolides ● Ondansetron ● Quinine ● Tacrolimus ○ Clinical presentation: ■ S/Sx dependent on heart rate (avg: 150-300 bpm) ■ Palpitations ■ Dizziness, lightheadedness ■ Dyspnea ■ Chest pain ■ Syncope ■ Hemodynamically unstable ■ Pulseless ■ May evolve into VF and result in sudden cardiac death ■ May terminate on it’s own Ventricular fibrillation ○ Char by irregular, disorganized, chaotic activity w/ rapid beats and no identifiable P waves or QRS complexes → absence of ventricular depolarization ○ No effective CO, pulse, or BP → sudden cardiac death ○ Etiology: ■ Ischemic heart DZ ■ MI ■ LV dysfxn ■ Medications ○ Clinical presentation: ■ Pulseless 22

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■ Loss of BP ■ Unresponsive ■ Collapse Sinus bradycardia: ○ HR < 60 BPM ○ May occur in young healthy individuals ○ Asymptomatic: don’t treat ○ Some pts (older) have sinus node dysfxn (sick sinus syndrome) ○ Increased Sx if poor LV fxn d/t decreased CO ○ Etiology: ■ Sick sinus syndrome (conduction DZ) ■ MI ■ Hypothyroidism ■ Hypothermia ■ High or low K ■ Systemic lupus erythematosus ■ Sleep apnea ■ Increasing age ■ Drugs: ● Beta blockers, diltiazem, verapamil, sotalol ● Antiarrhythmics ● Cisplatin ● Clonidine; Cocaine ● Digoxin ● Fluoxetine, citalopram ○ Clinical presentation: ■ Asymptomatic ■ Dizziness, lightheadedness ■ Fatigue ■ Syncope ■ Chest pain ■ Dyspnea, S/Sx CHF esp in pt with LV dysfxn Therapeutics of Arrhythmias Atrial fibrillation: ○ Complications: ■ Hemodynamic consequences: ● Loss of atrial mechanical fxn (decreased CO) ● Irregularity of ventricular response ● High HR ● Card...