ACLS

Signs of Possible Stroke

-Sudden weakness or numbness of face, arm or leg, esp on one side of body -Sudden confusion -Trouble speaking or understanding -Sudden trouble seeing in one or both eyes -Sudden trouble walking -Dizziness or loss of balance -Sudden severe headache with no known cause

BLS Systemic Approach

1) Check responsiveness: tap and shout 2) Shout for nearby help/activate emergency response system and get the AED 3) Check breathing and pulse: check for absent or abnormal breathing by scanning chest movement for 5-10 secs. Check pulse for 5-10 secs (ideally check both pulse and breathing at the same time) Pulse--> start rescue breathing at 1 breath every 5-6 secs, check pulse every 2 min No pulse--> start chest compressions 4) Defib: if no pulse, check for shockable rhythm with AED as soon as it arrives. Follow each shock immediately with compressions *Minimize interruptions in chest compressions (no longer than 10 seconds)* *Compress the chest at least 2 inches at a rate of 100-120/min*

Post Cardiac Arrest Care Algorithm

1) Ensure adequate airway 2) Elevate head of be 30deg, reduces incidence of cerebral edema, aspiration, ventilatory assc pneumonia 3) Avoid hyperventilation (titrate O2 to lowest level req to achieve arterial sat of 94-99%): hyperventilation increases thoracic pressure, lowers CO, decreases cerebral blood flow *Brain injury and cardiovascular instability major factors that determine survival after cardiac arrest*

Stroke Care

1) Immediate general assesment within *10 min of arrival*, order urgent noncontrast CT 2) Immediate neuro assessment and CT scan within *25 min of arrival* 3) Interpretation of CT within *45 min of arrival* 4) Administration of fibrnolytic therapy within *1 hr of arrival* or *3 hrs from sx onset* Door-to admission time = 3 hours

VT Care

1) Shock 2) CPR for 2 min, establish IV or IO access 3) Shock 4) CPR for 2 min, administer 1 mg epi every 3-5 min 5) Shock 6) CPR for 2 min, administer amiodarone 300 mg, 150 mg bolus

Closed Loop Communication

1) Team leader gives a message/order to a team member 2) Team leader confirms that team member heard and understood message by receiving a clear response and eye contact 3) Team leader listens for confirmation of task performance from team member before assigning another task

Post Cardiac Arrest Care

After ROSC PCI: if coronary artery occlusion is suspected, rescuers should transport patient to facility capable of PCI. Decision to perform PCI can be made irrespective of presence of coma or decision to induce hyperthermia Glycemic control: Should not attempt to alter glucose concentration within a lower range because of increased risk of hypoglycemia Neurologic care: Pts treated w TTM--> prognostication of neuro fxn should be dealyed untial at least 72 hrs after return to normothermia Not treated w TTM--> earliest time is 72 hrs after arrest and potentially longer is sedation or paralysis confound exam

Anti-Arrhytmics

Amiodarone: treatment of VF or pulseless VT unresponsive to shock, CPR and vasopressor 300 mg IV/IO push followed by 150 mg IV/IO in 3-5 min if VF/pulseless VT persists Lidocaine: Given when amiodarone not available. Intial dose = 1-1.5 mg/kg IV/IO, repeat at 0.5-0.75 over 5-10 min intervals to a max dose of 3 mg/kg. Dose for ET is 2-4 mg/kg Magnesium: Given for pts with torsades 1-2 g IV/IO diluted in 10 mL over 5-20 min

ROSC

Coronary perfusion pressure (CPP) = aortic relaxation - right atrial relaxation pressure CPP correlates with myocardial blood flow and ROSC ROSC does not occur unless CPP>15 mmHg acheived during CPR

Acute Stroke Care

Critical decision point is performance and interperatation of noncontrast CT to differentiate bw ischemic and hemorrhagic stroke If CT is not available, stabilize pt and transfer to facility with capability Do not give aspirin, heparin, or rtPA until CT has ruled out hemorrhage *CT should be completed within 25 min of arrival and should be read within 45 min* Hemorrhage present: not a candidate for fibronlytics, consult a neurologist No hemorrage: candidate for fibronlytic therapy. If C/I, consider giving aspirin

Shock and Vasopressors

For persistent VF/pulseless VT, give 1 shock and resume CPR immediately for 2 min after shock When IV/IO access is available, give 1 mg epinephrine every 3-5 min during CPR after second shock--> vasoconstrictor, increases cerebral and coronary blood flow

Acute Coronary Syndrome

Half of the pts who die of ACS do so before reaching the hospital. VF or pulseless VT is precipitating rhythm in most of these deaths. VF most likely to develop in first 4 hrs after onset of Sx Primary goals: -identify pts with STEMI and triage for early reperfusion -relief of ischemic chest discomfort -prevention of MACE such as death, nonfatal MI, need for urgent postinfarct revascularization -Tx of acute, life threatening arrhythmias of ACS

IHCA Cardipulmonary Arrest

IHCA is commonly preceded by physiologic changes In recent studies, nearly 80% of hospitalized patients with cardioresp arrest had abnormal vital signs documented for up to 8 hours before actual arrest Many of these changes can be recognized by monitoring routine vital signs Intervention before clinical deterioration or cardiac arrest may be possible

Ventilations

If patient is in resp arrest with a pulse, deliver ventilations every 5-6 seconds with a bag mask or advanced airway device Recheck pulse every 2 min (no longer than 10 seconds) ET tube: continuous waveform capnography in addition to clinical assessment used to confirm and monitor placement of ET tube

Early defibrillation

Interval from collapse to defib is one of the most important determinants of survival from cardiac arrest Early defib is critical for pts with sudden cardiac arrest: -VT is common initial rhythm, pulesless VT rapidly deteroriates to VF (heart quivers, no blood pumped) -Electrical defib is the most effective way to treat VF -probability of succesful defib decreases quickly over time -VF deteriorates to asystole if not treated

Management of Resp Arrest

Interventions include: -Giving supplemental O2 -Opening airway -Providing basic ventilation -Using basic airway adjuncts -Suctioning *Avoid excessive ventilation*--> increases intrathoracic pressure, decreasing venous return and CO. Can cause gastric inflation and predisposing to vomitting or aspiration. Can also cause *cerebral vasoconsctriction*

Agonal gasps

Not normal breathing, may be present in first minutes after sudden cardiac arrest Usually looks like he is drawing air in very quickly Mouth may be open and jaw head or neck move with gasps Happen at a slow rate *sign of cardiac arrest*

Basic Airway Adjuncts

Oropharyngeal Airway (OPA): J-shaped device used in *unconscious* pts (check for intact cough and gag reflex) at risk for developing airway obstruction from tongue or relaxed upper airway muscles May also be used to keep airway open during bag mask ventilation and during suctioning of the mouth and throat in intubated pts to prevent them from biting ET tube

Oxygen and Drugs

Oxygen: EMS should administer oxygen if pt is dyspneic, hypoxemic, has obvious signs of HF, has arterial O2 sat less than 90%, or O2 sat is unknown Should titrate O2 to a sat of 90% or greater Aspirin: if pt has not taken aspirin and has no hx of allergy or recent GI bleed, give 160-325 mg to *chew*. Rectal suppositories can be given for pts with disorders of GI tract Nitroglycerin: give pt 1 sublingual tablet every 3-5 min for ongoing symptoms. Max dose = 3 tablets. Administer only if hemodynamically stable C/I w/ inferior wall MI and RV infarct, hypotension, bradycardia, tachycardia, or recent PDE-I use

Pulseless Electrical Activity

Patient is in cardiac arrest, has an organized rhythm on monitor but no pulse

12 Lead ECG

Patients with potential ACS arriving at the ED should receive a 12 lead ECG within first 10 minutes *Only means of identifying STEMI* If STEMI is identified, give fibronolytics within 30 min of arrival or perform PCI within 90 min

Capnography

ROSC recognized by abrupt increase in PETCO2 to >50 mmHg, consistent with substantial improvement in blood flow

Minimizing Interruptions in Cardiac Arrest

Shortening interval between last compression and shock by even a few seconds can improve shock success Minimize hands off interval between compressions and administering shock Ater verifying shockable rhythm and initiating charging, provider should resume chest compressions until defibrillator is fully charged

Targeted Temperature Management

Should be started in patients who remain comatose with ROSC after cardiac arrest Maintain a constant target temp between 32-36deg C for at least 24 hrs Optimal method is unknown, combination of rapid infusion of ice cold, isotonic, non glucose containing fluid, surface cooling devices, or ice bags are safe and effective Concurrent TTM an PCI is feasible and safe

Unstable Tachycardia

Signs and symptoms: hypotension, acutely altered mental status, signs of shock, ischemic chest discomfort, AHF *Rapid recognition that pt is significantly symptomatic and that symptoms caused by tachycardia*

Cardioversion

Synchronized shocks: recommend for pts with unstable SVT, unstable atrial fib, unstable atrial flutter, unstable regular monomorphic tachy with pulse Unsynchonized shock: pulseless pt, pt demonstrating clinical deteriorations (ie severe shock or polymorphic VT), unsure whether monomorphic or polymorphic VT present in unstable pt

Narrow QRS with Regular Rhythm

Terminating narrow complex SVT that are symptomatic but stable 1) Attempt vagal maneuvers 2) If does not respond, give adenosine: 6 mg IVP over 1 sec (follow with 20 mL saline), repeat with 12 mg if does not convert after 1-2 min Adenosine increases AV block, will terminate 90% of reentry arrhythmias within 2 min. Will not terminate A-flutter or A-fib but will slow AV conduction, allowing for ID of flutter or fib waves C/I: safe in pregnancy, may cause bronchospasm, DI w theophylline, caffeine or theobromine If rhythm converts w adenosine--> probably reentry SVT. Observe for recurrence. Treat recurrence w adenosine or longer acting AV nodal blocking agents (non DHP CCB or B blocker) If rhythm does not convert--> possibly atrial flutter, ectopic atrial tachy, or junctional tachy *AV nodal blocking drugs should not be used for pre-excited atrial fib or flutter. Tx unlikely to slow ventricular rate and may accelerate ventricular response. Avoid combining AV nodal blocking agents*

Assessing CPR Quality

Use quantitative waveform capnography in intubated pts to monitor CPR quality, optimize chest compressions, and detect ROSC during chest compressions Placement of invasive monitors usually not warranted but when available intra arterial relaxation and central venous oxygen sat helpful for optimizing CPR End tidal CO2: main determinant of PETCO2 is blood delivery to lungs. <10 mmHg during CPR suggests ROSC unlikely CPP: Increased CPP correlates with myocardial blood flow and ROSC. Surrogate for CPP during CPR is arterial relaxation. If <20 suggests ROSC unlikely Central venous oxygen sat: changes in SCVO2 reflect changes in O2 delivery due to changes in CO. Can be measured continuously by using oximetric tipped central venous catheters placed in SVC or pulmonary artery. If <30% suggests ROSC unlikely