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ACLS
| Question | Answer |
|---|---|
| VFib - VTach Meds (5) | Epinephrine, Vasopressin, Amiodarone, Lidocaine, Magnesium |
| Asystole - PEA Meds (2) | Epinephrine, Vasopressin |
| Bradycardia Meds (3) | Atropine, Epinephrine, Dopamine |
| Tachycardia Meds (7) | Adenosine, Diltiazem, Beta Blockers, Amiodarone, Digoxin, Verapamil, Magnesium |
| Acute Coronary Syndromes Meds (7) | (MONA) Morphine, Oxygen, Nitro, Aspirin, Fibrinolytic therapy, Heparin, Beta blockers |
| Acute Stroke Meds (5) | tPA, Glucose D50, Labetalol, Nitroprusside, Nicardipine |
| 5 H's - Name - When to use | Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hyper-/hypokalemia, Hypothermia [Hypoglycemia]. major contributing factors to pulseless arrest including PEA, Asystole, Ventricular Fibrillation, and Ventricular Tachycardia |
| 5 T's - Name - When to use | Toxins, Tamponade(cardiac),Tension pneumothorax, Thrombosis (coronary and pulmonary), [Trauma]. major contributing factors to pulseless arrest including PEA, Asystole, Ventricular Fibrillation, and Ventricular Tachycardia |
| Hypovolemia - What to look for? Most important 3 interventions. | Look for obvious blood loss is the first step. After CPR, the most import intervention is obtaining intravenous access/IO access. A fluid challenge or fluid bolus may also help determine if the arrest is related to hypovolemia. |
| Hypoxia - What to look for (4) | Ensure that the patient’s 1. airway is open, 2. chest rise and fall and 3. bilateral breath sounds with ventilation. 4. oxygen source is connected properly. |
| Hydrogen ion (acidosis) - how to evaluate - how to prevent Resp/Metabolic | To determine if the patient is in respiratory acidosis, an arterial blood gas evaluation must be performed. Prevent respiratory acidosis by providing adequate ventilation. Prevent metabolic acidosis by giving the patient sodium bicarbonate. |
| Hypokalemia - Signs (3) - Tx | Signs: flattened T-waves, prominent U-waves, and possibly a widened QRS complex. Treatment of hypokalemia involves rapid but controlled infusion of potassium.Never give undiluted intravenous potassium. |
| Hyperkalemia - Signs (2) - Tx (6) | Signs: taller and peaked T-waves, widening of the QRS-wave. Treatment: sodium bicarbonate (IV), glucose+insulin, calcium chloride (IV), Kayexalate, dialysis, and possibly albuterol. All of these will help reduce serum potassium levels. |
| Hypoglycemia - Tx | Treat hypoglycemia with IV dextrose to reverse a low blood glucose. Hypoglycemia was removed from the H’s but is still to be considered important during the assessment of any person in cardiac arrest. |
| Hypothermia | Tx: warming measures - Core temperature should be raised above 86 F (30 C) as soon as possible. The hypothermic patient may be unresponsive to drug therapy and electrical therapy (defibrillation or pacing). |
| Toxins - Most common types (5) | Accidental OD can cause pulseless arrest. Some of the most common include: tricyclics, digoxin, betablockers, and calcium channel blockers), and street drugs. Cocaine is the most common street drug. Use poison control. |
| Toxins - Signs (4) | ECG signs of toxicity include prolongation of the QT interval. Physical signs include bradycardia, pupil symptoms, and other neurological changes. |
| Tension Pneumothorax - Treatment | Air enters the plural space and is prevented from escaping leading build up of tension that causes shifts in the intrathroacic structure leads to cardiovascular collapse and death. Treatment of tension pneumothorax is needle decompression. |
| Tension Pneumothorax - Signs (7) | ECG signs include narrow QRS complexes and slow heart rate. Physical signs include JVD, tracheal deviation, unequal breath sounds, difficulty with ventilation, and no pulse felt with CPR. |
| Tamponade - Treatment | Fluid accumulates in the pericardium (sac in which the heart is enclosed). The buildup of fluid results in ineffective pumping of the blood which can lead to pulseless arrest. The recommended treatment for cardiac tamponade is pericardiocentesis. |
| Tamponade Signs (5) | ECG symptoms include narrow QRS complex and rapid heart rate. Physical signs include jugular vein distention (JVD), no pulse or difficulty palpating a pulse, and muffled heart sounds due to fluid inside the pericardium. |
| Thrombosis (heart: acute, massive MI) - Signs (4) | ECG signs during PEA indicating coronary thrombosis include ST-segment changes, T-wave inversions, and/or Q waves. Physical signs include: elevated cardiac markers on lab test. |
| Thrombosis (heart: acute, massive MI) - Tx (2) | Tx thrombosis BEFORE cardiac arrest - fibrinolytic therapy, or PCI (percutaneous coronary intervention) i.e. angioplasty with/without stentsment. Tx WITH cardiac arrest and without known PE, routine fibrinolytic tx given during CPR is not recommended |
| Thrombosis (lungs: massive pulmonary embolism) - Signs (6) | ECG signs of PE include narrow QRS Complex and rapid heart rate. Physical signs include no pulse felt with CPR. distended neck veins, positive d-dimer test, prior positive test for DVT or PE. |
| Thrombosis (lungs: massive pulmonary embolism) - Treatment (2) | Tx includes surgical intervention (pulmonary thrombectomy) and fibrinolytic therapy. |
| Trauma - Treatment | Treat each traumatic injury as needed to correct any reversible cause or contributing factor to the pulseless arrest. Trauma was removed from the T’s but is still to be considered important during the assessment of any person in cardiac arrest. |
| VF treated with CPR/AED - Equipment - First Intervention | VFib should be treated with CPR and an AED. Equipment: AED and a pocket mask. Rapid assessment and treatment using the CAB sequence of BLS should be performed as the first intervention. AED. Effective CPR and early defibrillation are the key to VFib. |
| CPR - When to use | Do CPR if no palpable pulse or undetermined pulse. Don't delay. When in doubt - CPR. CPR may be needed after successful defibrillation since spontaneous rhythms after defibrillation may not always produce adequate perfusion for several minutes. |
| AED - When to use (3) | Patient is not responsive, not breathing, no pulse. |
| Emergencies - Order | Emergencies are treated in the following order: Check patient responsiveness, activate EMS, and get the AED, then perform CABD’s of the BLS Primary Survey. |
| Airway Skills | Head-tilt chin lift and mouth-to-barrier device resuscitation. |
| Airway Management | 1. Give oxygen, 2. Open the airway 3.Provide basic ventilation 4. Provide respiratory support with the use of artificial airways (OPA and NPA) 5.Suction to maintain a clear airway 6.Maintain airway with advanced airways |
| Hyperventilation Causes (4) | Avoid hyperventilation-too many breaths/min or too large of a volume/breath. Leads to increased. intrathoracic pressure, decreased. venous return to the heart, decreased.cardiac output, and increased. gastric inflation |
| Ventilation - how often | For patients with a perfusing rhythm deliver 1 breath every 5 to 6 seconds. |
| Opening Airway - most common airway obstruction - how to fix | The most common cause of airway obstruction is the loss of tone in the throat muscles - tongue can fall back & obstruct the airway. This can be prevented with head tilt-chin lift. For suspected spinal injury, use jaw thrust maneuver to maintain c-spine |
| Opening Airway - maintain C-Spine | jaw thrust maneuver |
| 5 basic airway skills | 1.) Head tilt-chin lift; 2.) Jaw thrust without head extension for possible cervical spine injury; 3.) Mouth-to-Mouth ventilation; 4.) Mouth-to-Barrier device (using a pocket mask); and 5.) Bag-mask ventilation. |
| When to use the oropharyngeal airway | Only use on the unconscious patient because it can stimulate gagging and vomiting in a conscious patient. |
| When to use nasopharyngeal airway | On the unconscious, semiconscious patient or if a patient has massive trauma around the mouth or wiring of the jaws. |
| Most Common cause of unconscious patient (3) Treatment? | If the airway is being maintained, blood, secretions, and vomit become the primary causes of an obstructed airway in the unconscious patient. Suctioning should be used to clear the airway if it becomes occluded with these body fluids. |
| Suctioning - how long | Limit oral and endotracheal suctioning to 10 seconds or less to reduce the risks of hypoxemia. Monitor for changes in heart rate as oropharyngeal suctioning can cause vagal stimulation resulting in bradycardia. |
| Advanced airways | Combitube, LMA (Laryngeal mask airway), and ET tube (endotracheal tube). Once an advanced airway is in place, chest compressions are no longer interrupted for ventilations. 1 breath should be given every 6-8 seconds (8-10 breaths per minute). |
| Stroke Symptoms - Top 3 | 1. Facial Droop; 2. Arm drift; 3. Abnormal speech. |
| Step 2: ACLS Stroke Protocol - Prehospital | 1. Support the patients airway (and give O2 to 94%. 2..Perform Prehospital Stroke Assessment (CPSS) 3.Blood Glucose Check 4.Establish Time Zero - If possible bring a witness that can confirm the time of onset 5.Triage and Alert Stroke Center |
| Stroke - what should be done within 10 minutes (8) | •Neuro Screening: within 10 minutes of arrival. •ORDER Head CT: •Assess and treat ABC’s: •12-lead ECG to rule out myocardial infarction and arrhythmias. •Apply oxygen PRN sat>94%. •IV access •Activate the stroke team •Blood Glucose |
| Stroke - what should be done within 25 minutes (3) | A full general physical and neuro exam. The physical and neuro exam should be performed by a qualified physician and the physician should also gather a complete history on the patient. Finally, the physician will establish the time of symptom onset. |
| Stroke - Head CT timeline | The head CT scan done within 25 minutes of arrival. Read by a qualified physician within 45 minutes of arrival. |
| Stroke - no bleed (inclusion factors for tPA) (2) | 1.The patient must be 18 years or older. 2.The onset of symptoms must be less than 3 hours before beginning treatment. 3.The stroke appears to be causing measurable neurologic deficit. |
| Stroke - no bleed (exclusion factors for tPA) (9) | 1.Active bleeding 2.Hx of intracranial hemorrhage 3.Sx of SAH 4.Head trauma/stroke <3 months 5.High BP (185/110) 6.Art. puncture 7.Inc risk of bleeding rel to dse 8.BS<50 9.CT shows multilobar infarction with hypodensity |
| Stroke - no bleed (exclusion factors for tPA) explained | 6.Art. puncture at a noncompressible site < 7 days ago 9.CT shows multilobar infarction with hypodensity > 1/3 of the cerebral hemisphere. |
| Stroke - no bleed (exclusion factors for tPA) disease explained | 7.Inc potential for bleeding rel to dse - PLT<100,000, use of anticoagulants with INR>1.7 or PT > 15, or Heparin received < 48 hrs resulting in aPTT > the upper normal limit. |
| Stroke- most common side effects (4) | Intracranial hemorrhage, other forms of bleeding, angioedema and transient hypotension. |
| Stroke - what should be done within 60 minutes | All treatments up to this point should have taken place within the 60 minute window of time allowed before rtPA is started. The rtPA should be started within 60 minutes of arrival at the treatment facility. |
| tPA is made of what? (3) | Recombinant tissue plasminogen activators (rtPAs) include alteplase, reteplase, and tenecteplase (TNKase). |
| tPA bolus? Infusion? | rtPA is given IV 0.9 mg/kg with a maximum of 90 mg and is infused over 60 minutes with 10% of the total dose administered as an initial intravenous bolus over 1 minute. |
| What to do within 24 hrs of tPA? (2) | Once fibrinolytic therapy has been started, the patient should not receive any other type of anticoagulant therapy for 24 hours. Ideally, the patient should receive a repeat head CT scan after 24 hours to ensure the patient has no intracranial bleeding. |
| Insulin for Strokes? | Evidence shows hyperglycemia worsens outcomes, Control of hyperglycemia with insulin improves survival rates. In light of this, AHA now recommends considering the use of intravenous or subcutaneous insulin to control blood glucose level in stroke victims. |
| Hypertension after tPA - BP goals | After fibrinolytic therapy has been initiated, maintain BP - SBP<185 and DBP<110. This lowers the risk of hemorrhage related to the use of rtPA. |
| S/S Tachycardia (7) | chest pain, signs of shock, SOB, altered mental status, weakness, fatigue, and syncope - One important question: “Are the symptoms being caused by the tachycardia?” If the symptoms are being caused by the tachycardia treat the tachycardia. |
| The most common causes of tachycardia that should be treated outside of the ACLS tachycardia algorithm (4) | dehydration, hypoxia, fever, and sepsis. |
| Tachycardia treatments prior to ACLS | Administration of OXYGEN and NORMAL SALINE are of primary importance for the treatment of causative factors of sinus tachycardia and should be considered prior to ACLS intervention. |
| tachyarrhythmia (def) | When atrial fibrillation occurs with a (RVR) rapid ventricular rate (rate > 100 beats/min) |
| tachyarrhythmia | •palpitations or chest discomfort •shortness of air and possibly respiratory distress •hypotension, light-headedness and possibly loss of consciousness •peripheral edema, jugular vein distention, and possibly pulmonary edema |
| Afib - EKG signs | 1.No p-waves before the QRS on the ECG. 2.The heart rate will be irregular. When the HRis extremely rapid, it may be difficult to determine if the rate is irregular, and the absence of p-waves will be the best indicator of afib |
| Unstable tachycardia treatment | For the patient with unstable tachycardia due to a tachyarrhythmia, immediate cardioversion is recommended. Drugs are not used to manage unstable tachycardia. The appropriate voltage for cardioverting unstable atrial fibrillation is 120-200 J. |
| Contraindication for cardioversion | Cardioversion of stable atrial fibrillation should be performed with caution if the arrhythmia is more than 48 hours old and no anticoagulant therapy has been initiated due to the risk of emboli that can cause MI and stroke. |
| Aflutter is a type of | This abnormal heart rhythm technically falls under the category of supra-ventricular tachycardias. |
| Aflutter rate | Atrial Flutter will usually present with atrial rates between 240-350 beats per minute. These rapid atrial rates are caused by electrical activity that moves in a self-perpetuating loop within the atria. |
| Aflutter symptoms | •palpitations, chest pain or discomfort •SOB •lightheadedness or dizziness •nausea •nervousness and feelings of impending doom •symptoms of heart failure such as activity intolerance and swelling of the legs occur with prolonged fast flutter) |
| Aflutter treatment | Early cardioversion.Drugs are not used to manage unstable tachy. Aflutter sensitive to cardiovert lower energy shock (than afib). 20-50J is usu. enough. AHA recommends an initial shock dose 0f 50-100 J for cardioverting unstable atrial flutter. |
| Aflutter - EKG - cause | Self perpetuating loop in atria. Saw tooth flutter waves. Flutter waves are consistent. Ventricular rate is consistent |
| SVT - definition | SVT is a broad term for a number of tachyarrhythmias that originate above the ventricular electrical conduction system (purkinje fibers). |
| SVT - EKG | Classic Paroxysmal SVT has a narrow QRS complex & has a very regular rhythm. Inverted P waves are sometimes seen after the QRS complex. These are called retrograde p waves -The end result is a drop in cardiac output & hypotension. |
| SVT Signs - Stable (5), Unstable (2) | These symptoms occur more frequently with a heart rate >150 beats per minute: •Shortness of air (S) •Palpitation feeling in chest (S) •Ongoing chest pain (U) •Dizziness (S) •Rapid breathing (S) •Loss of consciousness (U) •Numbness of body parts (S) |
| Unstable SVT Treatment | Unstable patients with SVT and a pulse are always treated with cardioversion. The appropriate voltage for cardioverting SVT is 50-100 J. This is what AHA recommends and also SVT converts quite readily with 50-100 J. |
| Stable SVT Treatment | Vagal Maneuvers |
| Wide-complex tachycardias - name - how wide - deteriorates to what | monomorphic ventricular tachycardia and polymorphic ventricular tachycardia; Wide complex tachycardias are defined as a QRS of ≥ 0.12 second. These are the most common forms of tachycardia that will deteriorate to ventricular fibrillation. |
| monomorphic ventricular tachycardia - attributes - treatment | All of the QRS waves will be symmetrical. Each ventricular impulse is being generated from the same place in the ventricles. Treatment depends on whether the patient is stable or unstable. If unstable, the ACLS tachycardia algorithm should be followed. |
| polymorphic ventricular tachycardia - attributes - name a type - | The QRS waves will not be symmetrical. This is because each ventricular impulse can be generated from a different location. QRS is taller or wider. Torsades de Points. These tachycardias originate in the ventricles. |
| polymorphic ventricular tachycardia - stable vs unstable treatment | If polymorphic VT is stable the ACLS tachycardia algorithm should be used. Unstable polymorphic ventricular tachycardia is treated with unsynchronized shocks (defibrillation). Defibrillation is used because synchronization is not possible. |
| The initial recommended synchronized cardioversion voltage doses are as follows: SVT/aflutter/afib/vtach | Narrow regular (SVT and atrial flutter): 50-100 J; ---- Narrow irregular (atrial fibrillation): 120-200 J biphasic or 200 J monophasic; ---- Wide regular (monomorphic VT) : 100 J; ---- Wide irregular: defibrillation dose (not synchronized) |
| The fist question that should be asked when initiating the ACLS tachycardia algorithm is: | “Is the patient stable or unstable?” The answer to this question will determine which path of the tachycardia algorithm is executed. |
| Unstable tachycardia - treatment | Patients with unstable tachycardia should be treated immediately with synchronized cardioversion. If a pulseless tachycardia is present patients should be treated using the cardiac arrest algorithm. Adenosine for regular narrow complex Tachy. |
| Patients with stable tachycardia - next question for treatment | Treated based upon whether they have a narrow or wide QRS complex. |
| Tachycardia questions | Stable? Yes (treat). No -> Wide QRS? Yes (treat). No (treat). |
| Stable tachycardia (wide QRS) - treatment | Wide QRS (>0.12 sec) ->Stable (wide/regular/monomorphic) → adenosine → consider antiarrhythmic infusion (amiodarone, procainamide, sotalol) → get an expert |
| Stable tachycardia (narrow QRS) - treatment | Not Wide QRS (<0.12 sec) ->Stable (narrow QRS complex) → vagal maneuvers → adenosine (if regular) → beta-blocker/calcium channel blocker → get an expert |
| Unstable tachycardia s/s (5) | hypotension, altered mental status, signs of shock, ischemic chest pain, acute heart failure |
| The major ECG rhythms classified as bradycardia include: | Sinus Bradycardia, First-degree AV block, Second-degree AV block, Type I —Wenckenbach/Mobitz I, Type II —Mobitz II, Third-degree AV block complete block |
| The most common cause of PEA | hypovolemia |
| Question: What can sometimes be mistaken for asystole during a code? | fine ventricular fibrillation. Another way you can help determine the difference between asystole and fine VF is to increase the signal gain on the monitor. Increasing the signal gain will help you visualize any electrical impulses that indicate fine VF. |
| 2nd block type I Can be recognized by | observing and increasing PR interval with an eventual drop in a QRS complex. The PR interval will go longer, longer, longer, drop. |
| 2nd degree block type II can be recognized by | observing a missing QRS complex. Unlike 2nd block type I, the PR interval’s will all be the same. |
| The treatment for unstable third-degree AV block in ACLS is | transcutaneous pacing. |
| Symptomatic bradycardia exists when the following 3 criteria are present: | 1.) The heart rate is slow (less than 60 but usu less than 50; 2.) The patient has symptoms; and 3.) The symptoms are due to the slow heart rate. |
| Functional or relative bradycardia occurs when (2) ex. | a patient may have a heart rate within normal sinus range, but the heart rate is insufficient for the patients condition. An example would be a patient with an heart rate of 80 bpm when they are experiencing septic shock. |
| 3 medications that are used in the Bradycardia ACLS Algorithm. | atropine, dopamine (infusion), and epinephrine (infusion). |
| First drug used to treat bradycardia in the bradycardia algorithm, classification, what does it do | Atropine - classified as an anticholinergic drug and increases firing of the SA Node by blocking the action of the vagus nerve on the heart resulting in an increased heart rate. |
| Atropine, When to use caution | In the presence of myocardial ischemia and hypoxia since it increases oxygen demand of heart and can worsen ischemia. |
| Atropine dosing | The dosing for Atropine is 0.5 mg IV every 3-5 minutes as needed, and the maximum total dosage that can be give is 3 mg. |
| Atropine avoided when? | Atropine should be avoided in hypothermic bradycardia and it will not be effective for Mobitz type II/Second Degree Block Type 2 and Complete Heart Block (3rd degree block) |
| Dopamine infusion rate for brady | Dopamine: Second-line drug for symptomatic bradycardia when atropine is not effective. Dosage is 2-10 micrograms/kg/min infusion and titrate |
| Epinephrine infusion rate for brady | Can be used as an equal alternative to dopamine when atropine is not effective. Dosage is 2-10 micrograms/min and titrate to patient’s response. The goal of therapy is to improve the patient’s clinical status rather than target an exact heart rate. |
| The decision point for ACLS intervention in the bradycardia algorithm is determination of what? treatment? | Adequate perfusion. adequate perfusion -> observe and monitor. poor perfusion -> preparation for transcutaneous pacing should be initiated, and an assessment of contributing causes (H’s and T’s) should be carried out. |
| Preparation for TCP should be taking place when | as atropine is being given.f atropine fails to alleviate symptomatic bradycardia, TCP should be initiated. Ideally the patient should receive sedation prior to pacing.,If the pt is deteriorating rapidly, it may be necessary to start TCP prior to sedation. |
| TCP treatment of choice when? | For the patient with symptomatic bradycardia with signs of poor perfusion, transcutaneous pacing is the treatment of choice. |
| TCP rate, when to expedite? | Do not delay TCP for the pt with symptomatic brady with signs of poor perfusion. TCP rate should start at 60/min and adjust based on the pt’s clinical response. The dose is 2mA (milliamperes) above the dose that produces observed capture. |
| TCP is contraindicated for | hypothermia and asystole. |
| TCP - pulse check where | Assess with the femoral pulse. A carotid pulse should not be used as TCP can create muscular movements that may feel like a carotid pulse. |
| the most common rhythm present after defibrillation. | PEA - Patients with PEA usually have poor outcomes. |
| Positive outcome of an attempted resuscitation depends primarily on two actions | 1. Providing effective CPR; and 2. Identification and correction of the cause of PEA. |
| There are 2 medications used in the PEA algorithm, | epinephrine and vasopressin. These medications should be given while maintaining high-quality CPR. |
| PEA - when to give epi/vasopressin (doses) | Epinephrine (1 mg) every 3-5 minutes. Vasopressin (40 Units) can be given IV or IO to replace the first or second dose of epinephrine. |
| What have not been shown to increase survival from PEA | Vasopressors |
| What should be a high priority as a cardiac emergency progresses? | The identification and correction of the causes of PEA H's and T's |
| What is an important step in the ACLS protocol if the rhythm is asystole | Confirmation that a “flat line” is truly asystole. Fine VF can appear to be asystole, and a “flat line” on a monitor can be operator or equipment failure. 1. loose/disconnected leads 2. loss of monitor power 3. low signal gain on the ECG monitor. |
| Some of the most common reasons to stop or withhold resuscitative efforts are: | DNR status, Threat to the safety of rescuers, Family or personal information such as a living will or advanced directive Rigor mortis |
| Why is training emphasis is placed on the cardiac arrest algorithm. | Many of the patients that experience sudden cardiac arrest demonstrate VF at some point in their arrest, |
| What is the best scientific approach to restoring spontaneous circulation. | Rapid treatment of VF using the cardiac arrest algorithm |
| What are several important points that should be considered when initiating the cardiac arrest algorithm: | 1. High-quality CPR should be performed until the defibrillator is attached 2.Interruptions in compressions should be kept to a minimum. 2. rapid use of the defibrillator should be emphasized. 3.Use a manual defibrillator over an AED |
| Why should you use a manual defibrillator over an AED | The use of the AED can result in prolonged interruptions in chest compressions for rhythm analysis and shock administration. |
| Are stacked shocks used? | No. CPR is resumed for 5 cycles between each shock. |
| Biphasic means | The electrical current travels from one paddle to the other paddle and then back. The biphasic shock requires less energy to restore normal heart rhythm and reducea burns and cellular damage to the heart. Most defibrillators are biphasic. |
| VF and pulseless VT defib dose? | When using a biphasic defibrillator in VF and/or pulseless VT, you will use a dose of 120-200 Joules to shock. Start with 120J and increase the dosing in a stepwise fashion as needed. (Example: 120 J » 200 J » 300 J » 360 J.) |
| Announce shock: | To ensure safety during the shock, providers should always announce the following statement, “I am going to shock on three. One, I’m clear…Two, you’re clear…Three, everybody is clear.” |
| What is Synchronized Cardioversion, when is the shock? | It is a LOW ENERGY SHOCK that uses a sensor to deliver electricity that is synchronized with the peak of the QRS complex (the highest point of the R-wave). Syncs with the pts rhythm so that the shock is with or just after the peak of the R-wave. |
| The most common indications for synchronized cardioversion are | unstable atrial fibrillation, atrial flutter, atrial tachycardia, and supraventricular tachycardias. If medications fail in the stable patient with the before mentioned arrhythmias, synchronized cardioversion will most likely be indicated. |
| Synchronization avoids the delivery of a LOW ENERGY shock during | Cardiac repolarization (t-wave). If the shock occurs on the t-wave (during repolarization), there is a high likelihood that the shock can precipitate VF (Ventricular Fibrillation). |
| What is Defibrillation? | Unsynchronized cardioversion is a HIGH ENERGY shock which is delivered as soon as the shock button is pushed on a defibrillator. The shock falls anywhere within the cardiac cycle (QRS complex). |
| When is defib used? | Unsynchronized cardioversion (defibrillation) is used when there is no coordinated intrinsic electrical activity in the heart (pulseless VT/VF) or the defibrillator fails to synchronize in an unstable patient. |
| he vasopressors that can be used in the treatment of VF/Pulseless VT are | Epinephrine and/or Vasopressin. Epinephrine is primarily used for is vasoconstrictive effects. Vasopressin is also used for its vasoconstrictive effects and has been shown to have effects similar to those of epinephrine. |
| Why is vasoconstriction important during CPR | Vasoconstriction is important during CPR because it will help increase blood flow to the brain and heart. |
| When are rhythm checks performed? How long should they last? | After 5 cycles of CPR. Limit rhythm checks to less than 10 seconds to minimize interruptions in CPR |
| What antiarrhythmic medications are used in the pulseless arrest algorithm | Amiodarone, lidocaine, and magnesium |
| There are 4 rhythms that are seen with pulseless cardiac arrest. These four rhythms are | pulseless ventricular tachycardia (VT), ventricular fibrillation (VF), asystole, and pulseless electrical activity (PEA). |
| This is an outline of the 4 steps in the BLS Survey : | (1) Check responsiveness. Scan for breathing (scan 5-10 seconds). (2) Activate EMS. Get an AED. If 2 rescuers, 2nd person activates EMS and get AED (3) Circulation: Pulse Check (carotid) < 5-10 secs. No pulse ->CPR. (4) Defib. No pulse -> AED asap. |
| The ACLS Survey uses the ABCD model (A&B) | (A) Airway: Maintain airway and use advanced airway if needed. Confirmation placement of airway and secure. (B) Breathing: Give bag-mask ventilation, provide O2, avoid excessive ventilation. Monitor adequacy of ventilation. |
| The ACLS Survey uses the ABCD model (C&D) | (C) Circulation: Obtain IV access, attach ECG leads, identify and monitor arrhythmias, giving fluids if needed, and use defibrillation if appropriate. (D) Differential diagnosis: Look for reversible causes and contributing factors for the emergency. |
| ROSC | Return of Spontaneous Circulation |
| Topics of focus for post-cardiac arrest care include (5) | therapeutic hypothermia, hemodynamic and ventilation optimization, immediate coronary reperfusion with PCI (percutaneous coronary intervention), glycemic control, neurologic care and other technical interventions. |
| post-cardiac arrest care Therapeutic Hypothermia - Criteria | The decision point for the use of therapeutic hypothermia is whether or not the patient can follow commands. |
| post-cardiac arrest care Therapeutic Hypothermia - Methods and Temp goal | One of the most common methods used for inducing therapeutic hypothermia is rapid infusion of ice-cold (4° C), isotonic, non-glucose-containing fluid to a volume of 30 ml/kg. The optimum temp is 32-34 ° C (89.6 to 93.2 ° F). Maintain Temp 12 - 24 hrs |
| post-cardiac arrest care Therapeutic Hypothermia - How to measure temp | During induced therapeutic hypothermia, the patients core temperature should be monitored with any one of the following: esophageal thermometer, a bladder catheter in the nonanuric patients, or a pulmonary artery catheter if one is already in place. |
| post-cardiac arrest care Ventilation Optimization | Oxygen should be titrated to maintain an arterial oxygen saturation of ≥ 94%. Quantitative waveform capnography can be used to regulate and titrate ventilation rates during the post-arrest phase. |
| post-cardiac arrest care Excessive ventilation should also be avoided | because of the potential for reduced cerebral blood flow related to a decrease in PaCO2 levels. and of the risk of high intrathoracic pressures which can lead to adverse hemodynamic effects during the post arrest phase. |
| post-cardiac arrest care Hemodynamic Optimization BP | Hypotension, SBP < 90 mmHg ->fluids and vasoactive meds Objective is adequate systemic perfusion, and a mean arterial pressure of ≥ 65 mmHg should accomplish this. |
| post-cardiac arrest care Glycemic Control | Maintain glucose levels from 144-180 mg/dL, and since there is an increased risk for hypoglycemia in the post-arrest phase these more moderate levels should be maintained rather than normal levels of 80-110 mg/dL |
| Waveform Capnography what does it measure | It is a direct measurement of ventilation in the lungs, and it also indirectly measures metabolism and circulation. |
| Normal ETCO2 | in the adult patient should be 35-45 mmHg. |
| Two very practical uses of waveform capnography in CPR are: | 1.) evaluating the effectiveness of chest compressions; and 2.) identification of ROSC. Low ETCO2 value (< 10 mmHg) during CPR in an intubated patient would indicate that the quality of chest compressions needs improvement. |
| ETCO2 Goal in CPR | High quality chest compressions are achieved when the ETCO2 value is at least 10-20 mmHg. |
| ETCO2 in ROSC | When ROSC occurs, There will be a significant increase in the ETCO2. (35-45 mmHg) This increase represents drastic improvement in blood flow (more CO2 being dumped in the lungs by the circulation) which indicates circulation. |
| For the intubated patient in cardiac arrest, what is now considered the desired method for monitoring quality of chest compressions and determining when the patient has a ROSC. | quantitative waveform capnography, |
| Pulseless Ventricular Tachycardia is primarily identified by several criteria. | 1. rate is usually greater than 180 beats per minute and the rhythm generally has a very wide QRS complex. 2. the pt will be pulseless. (3)the rhythm originates in the ventricles. |
| Are all VTach pulseless? | Notherefore, pulselessness must be established prior to beginning an algorithm. This is accomplished simply by checking a carotid or femoral pulse.Many tachyarrhythmias of a rate >150 will deteriorate into pulselessness if timely treatment is not given. |
| The primary cause of VFib is | hypoxia (lack of oxygen) to the heart muscle which causes hyperirritability in the cardiac muscle tissue. As a result, multiple muscles cells within the ventricles simultaneously fire as pacemakers causing a quivering- ineffective for cardiac output. |
| Concern for Vfib | VF can rapidly lead to heart muscle ischemia and there is a high likelihood that it will deteriorate into asystole. |
| VFib treatment of choice | Ventricular fibrillation is always pulseless and must be confirmed by EKG or defibrillator monitor. Defibrillation is the treatment of choice and should occur as soon as possible. |
| What can all be seen with PEA. (3) | Sinus Rhythm, tachycardia, and bradycardia Performing a pulse check after a rhythm/monitor check will ensure that you identify PEA in every situation. |
| The most common cause in emergency situations is | Hypovolemia. others to consider are H’s and T’s. |
| How to treat PEA | PEA is treated by assessing and correcting the underlying cause. 6 H’s and 6 T’s of ACLS.When an underlying cause for pulseless electrical activity cannot be determined, PEA should be treated in the same fashion as asystole |
| The main treatment of choice for asystole is | the use of epinephrine and CPR. During asystole, there is no blood flow to the brain and other vital organs. This results in very poor outcomes if resuscitation is successful. |
| What to do if Asystole is on the monitor? | Ensure that all leads are connected properly. If all leads are properly connected, you should rapidly assess for any underlying causes for the asystole- H’s and T’s mnemonic. |
| First-degree Heart block or first degree AV block is | a disease of the electrical conduction system of the heart in which the PR interval is lengthened beyond 0.20 seconds. This lengthening of the PR interval is caused by a delay in the electrical impulse from the atria to the ventricles through the AV node |
| First-degree Heart block or first degree AV block treatment | Normally and in the case of ACLS, first-degree heart block is of no consequence unless it involves myocardial infarction or an electrolyte imbalance. |
| Second Degree Heart Block (Type 1) Also called Mobitz 1 or Wenckebach is | a disease of the electrical conduction system of the heart in which the PR interval has progressive prolongation until the atrial impulse is completely blocked. Once the p-wave is blocked, no QRS is generated, and the cycle begins again. |
| Second Degree Heart Block (Type 1) Also called Mobitz 1 or Wenckebach - One of the main identifying characteristics | is that the atrial rhythm will be regular. |
| Second Degree Heart Block (Type 1) Also called Mobitz 1 or Wenckebach treatment | Although second degree heart block type-1 is not clinically significant for ACLS, recognition of the major AV blocks is important because treatment decisions are based on the type of block present. |
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empyrean