Hs and Ts of ACLS

Knowing the Hs and Ts of ACLS will help prepare you for any ACLS scenario. Dont forget your Hs and Ts when using the ACLS Megacode Simulator. The Hs and Ts of ACLS is a mnemonic used to help recall the major contributing factors to pusleless arrest including PEA, Asystole, Ventricular Fibrillation, and Ventricular Tachycardia. These Hs and Ts will most commonly be associated with PEA, but they will help direct your search for underlying causes to any of arrhythmias associated with ACLS. Each is discussed more thoroughly below. The Hs include:

Hypovolemia, Hypoxia, Hydrogen /hypokalemia, Hypoglycemia, Hypothermia.

The Ts include:

ion

(acidosis), Hyper-

Toxins, Tamponade(cardiac),Tension pulmonary), andTrauma. Hypovolemia

pneumothorax,

Thrombosis

(coronary

and

Hypovolemia or the loss of fluid volume in the circulatory system can be a major contributing cause to cardiac arrest. Looking for obvious blood loss in the patient with pusleless arrest is the first step in determining if the arrest is related to hypovolemia. 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
Hypoxia or deprivation of adequate oxygen supply can be a significant contributing cause to cardiac arrest. You must ensure that the patients airway is open, and that the patient has chest rise and fall and bilateral breath sounds with ventilation. Also ensure that your oxygen source is connected properly.

Hydrogen ion (acidosis)

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.

Hyper-/hypokalemia

Both a high potassium level and a low potassium level can contribute to cardiac arrest. The major sign of hyperkalemia or high serum potassium is taller and peaked T-waves. Also, a widening of the QRS-wave may be seen. This can be treated in a number of ways which include sodium bicarbonate (IV), glucose+insulin, calcium chloride (IV), Kayexalate, dialysis, and possibly albuterol. All of these will help reduce serum potassium levels. The major signs of hypokalemia or low serum potassium are flattened T-waves, prominent U-waves, and possibly a widened QRS complex. Treatment of hypokalemia involves rapid but controlled infusion of potassium. Giving IV potassium has risks. Always follow the appropriate infusion standards. Never give undiluted intravenous potassium.

Hypoglycemia
Hypoglycemia or low serum blood glucose can have many negative effects on the body, and it can be associated with cardiac arrest. Treat hypoglycemia with IV dextrose to reverse a low blood glucose.

Hypothermia
If a patient has been exposed to the cold, warming measures should be taken. The hypothermic patient may be unresponsive to drug therapy and electrical therapy (defibrillation or pacing). Core temperature should be raised above 86 F (30 C) as soon as possible. The Ts include:

Toxins
Accidental overdose of a number of different kinds of medications can cause pulseless arrest. Some of the most common include: tricyclics, digoxin, betablockers, calcium channel blockers, and erythromycin). Street drugs and other chemicals can precipitate pulseless arrest. Cocaine is the most common street drug that increases incidence of pulseless arrest. ECG signs of toxicity include prolongation of the QT interval. Physical signs include bradycardia, pupil symptoms, and other neurological changes. Support of circulation while an antidote or reversing drug is obtained is of primary importance. Poison control can be utilized to obtain information about toxins and reversing agents.

Tamponade

Cardiac tamponade is an emergency condition in which 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. 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. The recommended treatment for cardiac tamponade is pericardiocentesis.

Tension Pneumothorax
Tension pneumothorax occurs when air is allowed to enter the plural space and is prevented from escaping naturally. This leads to a build up of tension that causes shifts in the intrathroacic structure that can rapidly lead to cardiovascular collapse and death. 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. Treatment of tension pneumothorax is needle decompression.

Thrombosis (heart: acute, massive MI)

Coronary thrombosis is an occlusion or blockage of blood flow within a coronary artery caused by blood that has clotted within the vessel. The clotted blood causes an Acute Myocardial Infarction which destroys heart muscle and can lead to sudden death depending on the location of the blockage. ECG signs indicating coronary thrombosis are 12 lead ECG with ST-segment changes, Twave inversions, and/or Q waves. Physical signs include: elevated cardiac markers on lab tests, and chest pain/pressure. Treatments for coronary thrombosis include use of fibrinolytic therapy, PCI (percutaneous coronary intervention). The most common PCI procedure is coronary angioplasty with or without stent placement.

Thrombosis (lungs: massive pulmonary embolism)

Pulmonary thrombus or pulmonary embolism (PE) is a blockage of the main artery of the lung which can rapidly lead to respiratory collapse and sudden death. 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. Treatment includes surgical intervention (pulmonary thrombectomy) and fibrinolytic therapy.

Trauma

The final differential diagnosis of the Hs and Ts is trauma. Trauma can be a cause of pulseless arrest, and a proper evaluation of the patients physical condition and history should reveal any traumatic injuries. Treat each traumatic injury as needed to correct any reversible cause or contributing factor to the pulseless arrest.

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

ACLS Drugs
Each of the ACLS Algorithms utilizes a number of drugs which we will classify as primary drugs. The primary drugs are the medications that are used directly in an ACLS Algorithm. Here are the Primary ACLS drugs broken down by ACLS Algorithm. Each is a link to its respective page which covers, in detail, all aspects of the medication and it use in each ACLS algorithm and in post resuscitation efforts.

ACLS Algorithms and Their Primary Drugs Vent. Fib./Tach.

Epinephrine Vasopressin Amiodarone Lidocaine Magnesium

Asystole/PEA
Epinephrine Vasopressin Atropine (removed from algorithm per 2010 ACLS Guidelines)

Bradycardia
Atropine Epinephrine Dopamine

Tachycardia
adenosine diltiazem beta-blockers amiodarone digoxin verapamil magnesium

Acute Coronary Syndromes

Oxygen Aspirin Nitroglycerin Morphine Fibrinolytic Heparin Beta-Blockers

therapy

Acute Stroke
tPA-tissue Glucose Labetalol Nitroprusside Nicardipine Aspirin plasminogen activator (D50)

Review of Respiratory Arrest

Respiratory Arrest simply means cessation of breathing. In ACLS, respiratory arrest typically means that a patients respirations are completely absent or inadequate to maintain oxygenation, but a pulse is present. Management Give Open Provide of respiratory arrest includes the following interventions: oxygen airway ventilation

the basic

Provide respiratory support with the use of artificial airways (OPA and NPA) Suction to maintain a clear airway Maintain airway with advanced airways During respiratory arrest, the ACLS provider should avoid hyperventilation of the patient. Hyperventilation is providing too many breaths per minute or too large of a volume per breath during ventilation. Hyperventilation may lead to increased intrathoracic pressure, decreased venous return to the heart, diminished cardiac output, and increased gastric inflation, all of which can decrease the likelihood of positive outcomes.

For patients with a perfusing rhythm deliver 1 breath every 5 to 6 seconds

Opening Airway
The most common cause of airway obstruction in a patient that is unresponsive is the loss of tone in the throat muscles. When loss of throat muscle tone occurs the tongue can fall back and obstruct the airway. This type of obstruction is easily prevented with a basic airway opening technique called the head tilt-chin lift. In the case that spinal injury is suspected, the jaw thrust maneuver can be utilized. This jaw thrust maneuver allows the BLS/ACLS provider to maintain a stable cervical spine.

ACLS Ventilation
There are 5 basic airway skills used to ventilate a patient. Basic ventilation skills are discussed in the BLS course and will not be discussed in detail here. The following is a list of the 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-toBarrier device (using a pocket mask); and 5.) Bag-mask ventilation.

Bag-Mask ventilation
Bag-Mask ventilation is the most common method of providing positive-pressure ventilation. Both the oropharyngeal airway and the nasopharyngeal airway may be used as adjuncts to improve effectiveness of patient ventilation. The oropharyngeal airway may only be used on the unconscious patient because it can stimulate gagging and vomiting in a conscious patient. The nasopharyngeal airway may be used on the unconscious patient or on the semiconscious patient and is also indicated if a patient has massive trauma around the mouth or wiring of the jaws.

Suctioning
If the airway is being maintained with the basic airway skills listed above, 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.

Limit 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
Advanced Airways used during ACLS include 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 (10-12 breaths per minute). You should be given adequate time to practice with these devices during your ACLS training before ACLS megacode testing.

Tachycardia and its ACLS Algorithm

Tachycardia/tachyarrhythmia is defined as a rhythm with a heart rate greater than 100 bpm. An unstable tachycardia exists when cardiac output is reduced to the point of causing

serious signs and symptoms. Serious signs and symptoms commonly seen with unstable tachycardia are: chest pain, signs of shock, SOA, altered mental status, weakness, fatigue, and syncope One important question you may want to ask is: Are the symptoms being caused by the tachycardia? If the symptoms are being caused by the tachycardia treat the tachycardia.

There are many causes of both stable and unstable tachycardia and appropriate treatment within the ACLS framework requires identification of causative factors. Before initiating invasive interventions, reversible causes should be identified and treated.

Causes
The most common causes of tachycardia that should be treated outside of the ACLS tachycardia algorithm are dehydration, hypoxia, fever, and sepsis. There may be other contributing causes and review of the Hs and Ts of ACLS should take place as needed. 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.

Once these causative factors have been ruled out or treated, invasive treatment using the ACLS tachycardia algorithm should be implemented.

A few helpful mnemonics: ABC=Airway, Breathing, Circulation OMI=Oxygenation, Monitor(EKG), IV ICEM=IV, CPR, ET intubation, Monitor(EKG)

Respiratory Arrest with a Pulse

ABC's...call for code cart/equipment, call 911 if outside hospital

OMI...begin oxygenation, Determine cardiac rythm with Monitor, establish IV Look for cause.

Acute Myocardial Infarction

ABC's...call for code cart/equipment, call 911 if outside hospital OMI...begin oxygenization, Determine cardiac rhythm with Monitor, establish IV Use appropriate algorithm Administer aspirin Anyalgesia (consider location if infarct) Consider anti-coagulants Twelve Lead EKG, labs Consider thrombolytics (ST changes, History, Signs/symptoms) Consider adjunctive therapy prn.

Refractory VF/ Pulseless

VT

ABC's OMI ICEM...IV access, CPR, ET intubation, Monitors Electrical Intervention... "clear" before each shock) Parmacologic intervention Consider possible causes such as Acute MI, Hypoxia, Hypoglycemia, Acidosis, etc.

o o o o o o o o o o o o o o o

o o o o o o

Electrical defibrillation (X 1) 360 joules( monophasic) 150-200 joules (biphasic with truncated exponential waveform) 120 joules (biphasic with rectiliniar waveform) 200 joules (biphasic unknown waveform) CPR for 2 minutes, then rhythm check Drugs may be administered in conjunction with CPR ! ! ! Epinephrine 1 mg IV, may repeat every 3-5 minutes OR Vasopressin 40 units VI single dose only Repeat defibrillation if still unsuccessful CPR for 2 minutes, then rhythm check Amiodarone 300 mg IV bolus OR Lidocaine about 1- 1.5 mg mg/kg (as 75-100 mg) IV, may repeat 0.5 0.75 mg/kg in 5-10 min (Max: 3 mg/kg); If needed tracheal administration 2-4 mg/kg Repeat defibrillation if still unsuccessful CPR for 2 minutes, then rhythm check May consider Magnesium sulfate 1-2 gm in 10 mL D5W if suspect hypomagnesemia Procainamide 30 mg.min IV infusion (Max: 17 mg/kg) Repeat defibrillation if still unsuccessful May consider Na bicarbonate 1 ampule IV ? if suspect acidotic (best check ABG first)

Bradycardia

ABC's OMI Consider possible causes such as Acute MI, Hypoxia, Hypoglycemia, Acidosis, etc. Parmacologic/Electrical Intervention If hemodynamically unstable, CPR for 2 minutes Atropine (.5 mg q 5 min...up to 3.0 mg total) Transcutaneous Pacing Initiate Dopamine drip (2-20 micrograms/kg/min) Initiate Epinephrine drip (2-20 micrograms/kg/min)

If all above fails, Tranvenous Pacing

Second and Third Degree

Blocks

ABC's OMI Parmacologic/Electrical Intervention Consider possible causes such as Acute MI, Hypoxia, Hypoglycemia, Acidosis, etc. Transcutaneous Pacing Initiate Dopamine drip (2-20 micrograms/kg/min) Initiate Epinephrine drip (2-20 micrograms/kg/min) If all above fails, Tranvenous Pacing

Unstable Tachycardia

ABC's OMI Sedate and Cardiovert Valium 2mg. IV increments (to 10 mg. max) OR Versed 2mg. IV increments (to 10 mg. max) VT & A-Fib- start at 100J A-Flutter & SVT- start at 50J

Stable Tachycardia

ABC's OMI

Supraventricular Tachycardia (stable)

ABC's OMI Vagal Maneuvers- Have patient "Bear-Down", or Carotid Massage) Adenosine- 6mg then 12mg (Max 18mg) Cardizem- .25 mg/kg/2min, 35mg/kg/2min after 15 min. Beta Blockers Verapamil- 2.5-5 mg/2 min...5-10 mg after 15 min. Digiatlis-(limited use in emergency situations)

Supraventricular Tachycardia (unstable)

ABC's OMI Consider meds. If meds ineffective sedate and then cardiovert (50-100-200-300-360J) Sedate with Valium 2mg. IV increments (to 10 mg. max) OR Versed 2mg. IV increments (to 10 mg. max)

Atrial Fibrillation/ Flutter- Stable

ABC's OMI Pharmacologic Intervention Cardizem- .25 mg/kg/2 min, .35 mg/kg/2 min after 15 min. Beta Blockers Verapamil- 2.5-5 mg/2 min...5-10 mg after 15 min. Procainamide- 20 mg/min up to 17mg/kg total. Digiatlis-(limited use in emergency situations)

Ventricular Tachycardia- Stable

ABC's OMI Pharmacologic Intervention o In unstable hemodynamically, stat unsynchronized cardioversion with 50 -100 joules, then o 200, or to 360 joules. o In stable patients, may use synchronized cardioversion. with 100 J, then 200, 300, 360 J prn o *** Premedicate with sedatives whenever possible !!! **** o Amiodarone 150 mg IV bolus over 10 minutes or

o o o

Lidocaine 0.5 - 0.75 mg/kg IV , then 1- 4 mg/min infusion or Procainamide 200 1000 mg IV at rate <25 50 mg/min. Wide complex tachycardia VT vs SVT of uncertain etiology treat it as VT, & IV Procainamide is the drug of choice, & ** IV Verapamil is contraindicated !

Pulseless Electrical Activity

ABC's ICEM Consider possible causes such as Acute MI, Hypoxia, Hypoglycemia, Acidosis, etc. Pharmacologic Intervention CPR for 2 minutes Epinephrine- 1 mg q 3-5 min or Vasopressin- 40 U IV push (single dose) CPR for 2 minutes Consider termination of efforts after 10 minutes

Asystole

ABC's ICEM confirm rythm in two leads. Pharmacologic Intervention Consider possible causes such as Acute MI, Hypoxia, Hypoglycemia, Acidosis, etc. CPR for 2 minutes Epinephrine 1.0 mg IV push, repeat every 3-5 minutes or Vasopressin- 40 U IV push (single dose) CPR for 2 minutes Atropine 1.0 mg IV push

 Consider termination of efforts after 10 minutes.