All neurohospitalists should maintain accreditation in Advanced Cardiovascular Life Support. Relevant courses are available from local hospitals and from the American Heart Association (AHA). We also recommend revising EKG skills before starting on the ward. What follows is a brief revision of some important points.
CASE 19-1
You are rounding on the neurology ward, when one of the nurse trainees calls out for help. You arrive in the room directed by the nurse standing in the corridor. You see Mr. AM admitted under the care of the neurology team for suspected seizure. The patient is in a nonmonitored bed.
Check for response; an unconscious patient regardless of cause warrants an emergency alert.
Stabilize neck: If there is trauma, make sure the neck is secured and immobilized.
Check for airway: At the bedside, as first responder, you may secure the airway by three methods:
Hyperextend the neck if there is no contraindication
Place your fingers behind the mandibular angle and push forward.
Place an airway—one of the more convenient artificial airways is the “nasal trumpet.” It is inserted in the nares with the end lubricated with KY gel and the curvature facing down. It is advanced perpendicular to the coronal plane, and once in place, it is secured with tape.
Check breathing: Look for chest rising or auscultate. The shiny mirrored surface of the queen square hammer can also be placed under the nose to look for exhalation in the form of condensation.
Check pulse: The best places to look for a pulse are the carotid arteries bilaterally. Extend the fingers and place your hand in the coronal plane with the palmar surface facing backwards. Place the edges of the finger on the anterior edge of the sternocleidomastoid and press back and gently medially.
Call code: Do make sure code is called as soon as you suspect that the patient is unresponsive.
Institute basic life support: If a bag-and-mask device is available, stand at the head of the bed. It is often easier if the wheel locks are released and the bed is pushed forward. The newer beds often do not have a headboard, which may impede access. The older ones are designed so that the headboard may be removed by pulling upward. The bag-and-mask is connected to the wall oxygen. The mask is then secured with the three lateral digits, while the little finger is placed behind the angle of the jaw. The other hand is used to compress the bag. A good seal and chest movement confirms correct technique. The nurse may start chest compression. If the bed is high, it needs to be lowered so that her extended arms are roughly perpendicular to the sternum. The palmar surface of one hand is placed on the dorsum of the other and the fingers are interlocked as to keep the fingers off the ribs. The compressions are then applied as fast as physically possible. Rescue breaths are delivered every 5 seconds and the pulse rechecked every 2 minutes.
Gain access: If no intravenous (IV) access exist then access should be instituted. As a rule, use the largest cannula that you think you can insert in a given vein. Comfort is not a consideration here, a short large-bore cannula should be inserted in each cubital fossa when possible. If veins cannot be found in the cubital fossa then the cephalic vein in the lateral aspect of the wrist and the external jugular vein may be alternatives. If no other access is possible, a femoral catheter may be inserted by someone with experience in placing them.
CASE 19-1 (continued)
You find that the patient is not breathing and does not have a pulse. You place a nasal trumpet and start BLS with the help of the nurse. Another nurse brings in the crash cart and establishes access. What do you do now?
Attach electrodes and paddles: Most modern defibrillators come with self-adhesive contacts. The optimal placement of the contacts is anterior-posterior: one is placed in the lower left precordium and the other between the scapulae at the back. Sometimes this configuration is not possible, especially with old-fashioned paddles, then the second paddle is placed on the right upper part of the precordium.
Decide whether or not the rhythm is shockable: Pulseless VT and VF are “shockable rhythms” and all else, including asystole and pulseless electrical activity, are non-shockable.
CASE 19-1 (continued)
The code blue team from ICU arrives. The self-adhesive contacts are placed.
Treatment of shockable rhythm has three moving parts:
Electrical shock: There are three different kinds of shocks delivered by defibrillators. Old-fashioned defibrillators delivered the electrical energy in one monophasic pulse. For these defibrillators, an energy level of 360 J was used in defibrillation. Most modern defibrillators deliver biphasic waves, which are more efficient and used at 120 or 150 J depending on the waveform delivered. Make sure the shock is unsynchronized. If not sure which defibrillator you are using then one may try 200 J until more experienced operators arrive.
Cardiorespiratory resuscitation: The patient is intubated. Chest compressions are renewed. The rhythm is checked every 2 minutes.
Intravenous medications: Three types of medication may be given during resuscitation:
Vasopressors: Vasopressors appear to improve outcomes during cardiorespiratory resuscitation supposedly because they improve the delivery of blood to the peripheries. Epinephrine is given at a dose of 1 mg every 3–5 minutes. One of the epinephrine doses may be substituted with vasopressin 40 units, but there is no evidence that this does anything other than complicate the routine. One may also add 40 mg methylprednisolone for “brain protection.” But this is not a routine part of resuscitation.
Antiarrhythmic agents: A bolus of 300 mg of amiodarone may be given as an IV push, followed by another 150 mg IV push of amiodarone if no success. Other agents used include lidocaine, procainamide, and sotalol.
Bicarbonate: Bicarbonate may be used with prolonged resuscitation to mitigate the effects of metabolic acidosis.
CASE 19-1 (continued)
The code blue team decides that the patient is not in a shockable rhythms.
Nonshockable rhythms include:
Asystole: An absence of mechanical or electrical activity of the heart.
Pulseless electrical activity: As the name suggests, this is electrical activity in the heart without effective cardiac output.
The treatment is similar to above but does not include shocks. In other words:
Cardiorespiratory resuscitation: The patient is intubated. Chest compressions are renewed. The rhythm is checked every 2 minutes.
Intravenous medications: Three types of medication may be given during resuscitation:
Vasopressors: Vasopressors appear to improve outcomes during cardiorespiratory resuscitation supposedly because they improve the delivery of the blood to the peripheries. A dose of 1 mg of epinephrine is given every 3–5 minutes. One of the epinephrine doses may be substituted with vasopressin 40 units, but there is no evidence that this does anything other than complicate the routine. One may also add 40 mg methylprednisolone for “brain protection.” But this is not a routine part of resuscitation.
Other agents: Atropine (1 mg × max of 3 doses) used to substitute some adrenalin injections but this is not recommended routinely. Another possible agent is aminophylline, a methylxanthine that antagonizes adenosine.
Bicarbonate: Bicarbonate may be used with prolonged resuscitation to mitigate the effects of metabolic acidosis.
The importance of the reversible causes of PEA and asystole is that their reversal is often the only chance the patient may have of surviving. The mnemonic to remember is 6H and 5T:
Hypovolemia: This is the most common cause of asystole and PEA in the pediatric population. In adults, hypovolemia may be caused by occult bleeding or dehydration. The latter is more common in the elderly, sometimes in the presence of nonketotic hyperglycemia. Fluid resuscitation with saline through alarge-bore cannula is the treatment.
Hypoglycemia: Hypoglycemia is often in response to overtreatment with insulin. Insulinoma is another cause of inadvertent hypoglycemia. Otherwise hypoglycemia may occur in critically ill patients and patients with end-stage liver failure; 50 mL of 50% dextrose may be given as a bolus, and a dextrose infusion may be started subsequently.
Hypothermia: There is a saying in emergency medicine “someone is not dead until they are warm and dead.”
Hydrogen ions: Acidosis can cause cardiac arrest. When suspected, bicarbonate is given. Ampules of bicarbonate are available in the crash cart. When giving bicarbonate, potassium should be rechecked soon after the return of circulation if it occurs because changes in pH can change the extracellular concentration of the potassium ion.
Hyperkalemia: For details please see chapter 12.
Hypokalemia: For details please see chapter 12.
Thrombosis, cardiac: Ischemic heart disease causing a large infarct may be responsible for cardiac arrest.
Thrombosis, pulmonary: A saddle embolus causing an outflow obstruction of the heart will lead to cardiac arrest.
Toxins and tablets: Overdose of medications such as beta-blockers and calcium channel blockers may lead to arrest. Before the arrest the patient may be bradycardic and it is possible to give isoproterenol or glucagon (bypassing the actual adrenergic receptor) for the former and calcium for the latter. Both aminophylline and atropine may be useful. However, if severe enough these often end up needing pacing, initially transthoracic and then transvenous when the cardiologist is available.
Tension pneumothorax: Trapping of air in a hemithorax leads to lung collapse. On auscultation the breath signs are reduced, while the percussion of the chest is drum like and resonant. The trachea and the mediastinum deviate to the opposite side.
Tamponade: Cardiac tamponade is caused by acute or subacute pericardial effusion squeezing the heart and reducing stroke volume. The common causes include uremia, pericarditis, cancer, trauma, myocardial rupture, hemorrhage in the context of a bleeding diathesis, and rarely aortic dissection. The classical signs of cardiac tamponade are summarized in Becktriad:
Raised jugular venous pressure (JVP)
Shock
Muffled heart sounds
The diagnosis is often on transthoracic echocardiography (TTE), and treatment is aspiration of fluid from the pericardial space. The latter should not be attempted by the neurohospitalist.
CASE 19-1 (continued)
The notes indicate that the patient is diabetic and admitted for chronic inflammatory demyelinating polyneuropathy (CIDP). All spirometry readings until now have been reasonable. The patient is found to be severely hypoglycemic. He is on several renally excreted hypoglycemic agents, but his renal function has declined since his course of IVIG for the CIDP for which he was hospitalized in the first place. The patient is given a bolus of dextrose and started on an infusion of a dextrose solution. The patient develops a pulse and BP starts to return.
With the return of spontaneous circulation the patient is often transferred to the ICU for a period of time: oxygenation, intravascular volume, and blood pressure are addressed. If there is a high suspicion of an acute myocardial infarction (MI) especially an STEMI, then interventions may be indicated. If the patient is not responsive and qualifies, then the patient may be cooled according to the institution’s cooling protocol.
CASE 19-1 (continued)
The ICU team transfers him to their unit and institutes the hospital’s hypothermic protocol.
The purpose of the cooling protocol is to improve neurological outcomes after cardiac arrest with return to spontaneous circulation. The patient should satisfy a number of criteria including early institution of CPR, relative cardiac stability after the return of circulation, nontraumatic arrest, low Glasgow Coma Scale (GCS), and absence of severe preprotocol hypothermia. The technique involves maintenance of a mild hypothermia (around 33°C) for 24 hours. The mechanics of the cooling is variable depending on the hospital but may be as simple as applying ice packs to the axillae, groins, and the neck. But it often involves the administration of chilled saline, cooling blankets, and cooling machines. Detailed protocol for electrolyte, temperature, and invasive monitoring should have been instituted in the given hospital before cooling is offered as treatment in a given institution (Figure 19-1).
Before the patient is cooled it may be worthwhile to make sure the following three things have been performed or are available:
Noncontrast CT of the head—This is not for prognostication but rather to look for edema or bleed, which may require immediate surgical intervention. Note that while the patient is cooled, neurological examination cannot detect deterioration in function, and doing CT of the head of a cooled patient is logistically difficult.
Baseline examination—This is often useful if no imaging can happen before cooling begins. Asymmetrical motor responses and blown pupils, for example, should prompt the neurologist to emphasize a need for emergent imaging.
Continuous EEG—The presence of continuous epileptiform activity is a poor prognostic factor that, if addressed, might improve outcomes.
Rewarming occurs over a period of 8–12 hours, and once the patient is rewarmed, the neurologist is often involved in assessing the extent of neurological damage. For this, clinical examination, EEG, and MRI may be useful. There are three rules of thumb that one may keep in mind:
Do not prognosticate a cooled patient: The examination is entirely noncontributory when the patient is cooled and sedated. EEG patterns such as burst suppression and status myoclonic epilepsy are also of dubious prognostic value in this setting.
Time gradation: The recovery of brain functions occurs with time after warming and weaning of sedation. The longer the patient continues to have neurological deficits, the poorer the long-term prognosis. The only exception to this is in patients with traumatic brain injury and minimally conscious state who may recover their neurological function after a long period of delay.
Spatial gradation: As a general rule the more caudal functions are more important for prognosis. So, the absence of brainstem reflexes is often a poor prognostic factor as are abnormal motor responses such as decorticate or decerebrate rigidity. If the brainstem function is intact then EEG and SSEP may give some indication of functions and connectivity rostral to the brainstem. Certain EEG patterns are traditionally associated with poor outcomes such as alpha coma, burst suppression, nonconvulsive seizures, myoclonic seizures, and, of course, electro-silence. MRI can be used to rule out structural damage to the brain.
CASE 19-2
You are paged by the ward nurse to see one of your patients who had presented to hospital with recurrent headaches. The patient has palpitations and is anxious. His blood pressure and saturations are stable. You ask the nurse what the rate is and whether the pulse is regular or irregular.
Irregular pulse is often associated with atrial fibrillation (AF), which only rarely leads to acute hemodynamic instability. A rate less than 150 per minute is also more likely to remain stable. Rate-related symptoms such as chest pain for a rate of less than 150 should also prompt further investigation because the rate by itself cannot explain such symptoms.
CASE 19-2 (continued)
You ask the nurse to do a stat EKG while you are on your way to see the patient.
Wide complex tachycardias: The most important thing to note on the EKG is whether the rhythm is wide complex or narrow complex. Most wide complex tachycardias are relatively ominous and require urgent input from the cardiologist.
Regular wide complex tachycardias: The regular wide complex tachycardias are either ventricular tachycardias or supraventricular tachycardias with aberrant conduction. If there is a history of aberrancy such as bundle branch block and the waveform is similar (albeit faster) to the admission EKG then one can try 6 mg of adenosine followed by 12 mg of adenosine while waiting for the cardiologist to arrive. If there is no history of bundle branch block then 300 mg of amiodarone as a push followed by another 150 mg in 15 minutes may be attempted while waiting for the cardiologist or the arrest team. In the latter case it may be appropriate to have the crash cart ready. If there is any deterioration in hemodynamic stability then the patient should be shocked.
Irregular wide complex tachycardias: Again if there is clear bundle branch block and the irregular rhythm is the exact same waveform then it is likely to be atrial fibrillation. If not or if not sure then do not use AV nodal blockers such as adenosine, digoxin, or calcium channel blockers. You may try beta-blockers or magnesium if torsade de pointes is suspected but have the crash cart ready and have the cardiologist or a similarly qualified person review the EKG.
Narrow complex tachycardia: These are typically more benign.
Irregular narrow complex tachycardia: This is usually atrial fibrillation. For more detail see below.
Regular narrow complex tachycardia: If the patient is stable then you can try 6 mg of adenosine followed by 12 mg. If it converts then the likely etiology is a re-entrant supraventricular tachycardia. Recurrence may be treated in the same way. In case of atrial flutter the slowing of the heart might reveal the underlying “saw tooth” appearance of atrial electrical activity. Cardiology consult often follows. If it does not convert then atrial flutter is the most likely diagnosis. This is treated the same way as atrial fibrillation.
CASE 19-2 (continued)
You review the EKG and find that the patient is in an irregular narrow complex tachycardia with a rate of roughly 130 bpm. You diagnose the patient with AF.
AF is a tachyarrhythmia that originates above the ventricle and is thus one of the supraventricular tachycardias. The rhythm is irregular, and there is an absence of P waves on the EKG. AF is relatively common, and the risk is increased in hospitalized patients especially in the presence of infections, electrolyte abnormalities, and dehydration. AF is of special interest to the neurologist because it is a major risk factor for cardioembolic strokes. Additionally in elderly patients with stiff hearts (diastolic failure) the loss of atrial push in AF increases their risk of congestive heart failure. AF may be paroxysmal or persistent. Its clinical significance is based on two parameters: rhythm and rate. The abnormal rhythm in AF means that the atria are not pumping blood and merely quivering in place. This increases the risk of stasis of blood and formation of atrial thrombosis. The higher rates seen in atrial fibrillation can lead to cardiac decompensation.
Steps in treatment:
Assess stability—If the patient is unstable then emergency medical system should be activated. Evidence of instability includes a significant drop in blood pressure, loss of consciousness, flash pulmonary edema, or crushing retrosternal chest pain.
Review the EKG. Look for ischemia and evidence of electrolyte abnormalities on the EKG.
Check the chart for potential triggers including electrolytes, TSH, and Hb. Normalize potassium and magnesium. Look for secondary causes including IHD, hypertension, valvular heart disease, alcohol, cardiomyopathy, thyrotoxicosis, sick sinus, and Wolff-Parkinson-White (WPW) syndrome. Systemic conditions associated with AF include infection, bleeding, electrolyte abnormality, and surgery.
Rate control to mitigate symptoms. Common medications include diltiazem, beta-blockers and digoxin, ACE inhibitors, amiodarone, and sotalol. The two more useful agents are:
IV metoprolol in increments of 5 mg to a maximum of 15 mg, then start oral metoprolol depending on blood pressure (eg, 50 mg POBID for a normotensive patient). Can use oral metoprolol with IV loading if the patient is asymptomatic.
IV diltiazem 10 mg and then infusion (5 mg per hour).
Calculate CHA2DS2–VASc Score (see below). Start anticoagulation ASAP if indicated.
Get a cardiology consult.
The management of AF depends on the type and duration of the arrhythmia.
From the point of view of duration, AF is classified as:
Recent—less than 48 hours. The optimal strategy is electrical or chemical cardioversion under the direction of the cardiologist.
Persistent—persists for days until it is cardioverted. The treatment is the same as above.
Permanent—more than 7 days and refractory to cardioversion or more than 1 year regardless of attempts to treat. Strategies may include rate control and possible anticoagulation. Ablation and pacing in problematic and symptomatic cases may be entertained.
Paroxysmal—several strategies may be used including “pill-in-the-pocket” technique, prophylaxis, or implantable defibrillator.
CHA2DS2–VASc Score—This is a simple heuristic tool used to decide whether to anticoagulate a patient with nonvalvular AF (NVAF). The scale itself is used to predict the annual risk of stroke, which increases as the score increases. However, the decision to anticoagulate is often taken when any of the risk factors are present. These include:
Congestive heart failure
Hypertension, even treated hypertension
Age >75 years (2 points)
Diabetes
Previous stroke (2 points)
Vascular disease
Age 65–74
Sex category: female=1, male=0
Warfarin or the novel oral anticoagulants (NOACs) are the choice of treatment. For details please refer to the pharmacology chapters in the same volume.
CASE 19-2 (continued)
You put the patient on telemetry, Q2h vitals, and activity as tolerated. You call a cardiology consult. The nurse asks whether she should add atrial flutter to the problem list. You inform her that the patient has AF and not flutter.
Atrial flutter is characterized by a regular atrial rhythm of roughly 300 bpm. When visible, the atrial baseline may adopt a saw-tooth appearance. Not all atrial pulses get through to the ventricle. Usually one in every n atrial pulses get to the ventricle in which case the nomenclature is atrial flutter with n:1 block. So, for example, if the patient has atrial flutter with 2:1 block, then half of the pulses are going to be getting to the ventricle so that the pulse rate is 300/2=150. Occasionally the block is variable and atrial flutter is irregular. In such cases it is difficult to differentiate atrial flutter from AF. The treatment and approach to atrial flutter are similar to AF except that atrial flutter is more resistant to treatment.
The most common supraventricular tachycardia is sinus tachycardia. As a general rule the cause of this is systemic disease such as infection, low blood pressure, anxiety, bleeding, and other disorders that cause reflex tachycardia. Another common pattern is atrial premature complex where a P wave is created at a location other than the sinus node. This changes the morphology of the P wave, the PR interval, and may lead to “missed beats.” This is relatively benign, and if symptomatic, a small dose of beta-blocker may be tried. Another important group of conditions are paroxysmal supraventricular tachyarrhythmias due to junctional rhythms or accessory pathways. These are narrow complex tachycardias with a heart rate often more than 200. During an attack, the patient has a feeling of impending doom and is very anxious. An emergency medical system activation should be done, and while waiting for the code team, boluses of adenosine 6–12 mg may be tried. Note that the EKG may flatline briefly after adenosine and before resuming, and that the sensation caused by this is extremely unpleasant for the patient.
As a rule, the cardiologist should be involved in the management of ventricular tachycardias from the start. It is sometimes difficult to figure out the border between multiple premature ventricular beats and VT. If the number of PVCs is less than 5 and the RR interval is less than 600 ms then one can watch these patients on telemetry. Anything more sustained, faster, or polymorphic should be brought to the attention of the cardiologist. Polymorphic VT, that is one where the ventricular waveform is variable, is inherently unstable and should prompt the activation of medical emergency team. Any tachycardia with hemodynamic compromise should similarly be coded.
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