ACLS

Question 1

What is ACLS?

Answer 1

ACLS stands for Advanced Cardiovascular Life Support. In ACLS, healthcare professionals use a set of algorithms to treat conditions ranging from cardiac arrest and myocardial infarctions (heart attacks) to stroke and other life-threatening emergencies.

Part of ACLS involves healthcare professionals interpreting a patient’s heart rhythm using an electrocardiogram. Based on this heart rhythm, decisions are made regarding treatment options.

ACLS providers must have the skills and knowledge to place advanced airways and insert an IV (Intravenous) or IO (Intraosseous) line for the administration of fluids and medications. And they must have a thorough understanding of all the medications available to them that are used to treat for the variety of heart rhythms and conditions they will encounter.

Question 2

An oropharyngeal airway (OPA) should only be insert on a patient who is ___________

Answer 2

Unconscious and has no gag reflex

Question 3

An nasopharyngeal airway (NPA) can be inserted on a patient who is ___________

Answer 3

Unconscious or conscious

With or without a gag reflex

Question 4

How many compressions per minute should be provided to an adult undergoing CPR? Recommended depth? Breathes per minute?

Answer 4

100-120 compressions per minute at depth of 2.0-2.5 inch

1 breath per 6 seconds (avoid excessive ventilation)

Question 5

When using the bag-valve-mask resuscitator, depress the bag about halfway to deliver a volume of
___ to ___ mL.

Answer 5

When using the bag-valve-mask resuscitator, depress the bag about halfway to deliver a volume of
400 to 700 mL.

Question 6

Define respiration, ventilation, and gas exchange.

Answer 6

Respiration (the process of moving oxygen and carbon dioxide between the atmosphere and the body’s cells) includes ventilation (the mechanical process of moving air into and out of the body) and gas exchange (the molecular process of adding oxygen to, and removing carbon dioxide from, the blood).

Effective respiration relies on effective functioning of the respiratory system, the cardiovascular system and the nervous system.

Question 7

What are the primary muscles used for ventillation? Accessory muscles?

Answer 7

The diaphragm is the primary muscle responsible for ventilation. The external intercostal muscles, located between the ribs, synergistically act with the diaphragm during inspiration to expand the rib cage. When ventilation demands increase, the body recruits accessory muscles for assistance. The sternocleidomastoid, scalene and upper trapezius muscles are the body’s accessory muscles of inspiration.

Question 8

What muscles are used for expiration? Forced expiration?

Answer 8

Expiration is a passive action that occurs when the diaphragm and external intercostal muscles relax. During active (forced) expiration, the internal intercostal muscles, the rectus abdominis and the external and internal oblique muscles are recruited as accessory muscles of ventilation.

Question 9

What controls the impulse to breath? What factors affect the rate and depth of breathing?

Answer 9

The impulse to breathe is controlled by respiratory centers in the brain stem that regulate nerve impulses to the diaphragm and intercostal muscles.

The respiratory centers receive input from chemoreceptors located throughout the body. These chemoreceptors detect changes in arterial oxygen and carbon dioxide content and in arterial pH, all of which affect the rate and depth of breathing.

Question 10

What factor factors affect hemoglobin’s affinity for binding with oxygen

Answer 10

Many factors can affect hemoglobin’s affinity for binding with oxygen and the strength of the bond, including blood pH, carbon dioxide levels, body temperature and 2,3-bisphosphoglyceric acid (a substance in red blood cells that is affected by increased oxygen needs or with impaired oxygen delivery). These factors can cause the curve to shift to the right or to the left.

Question 11

Respiratory compromise manifests along a continuum:

Answer 11

Respiratory distress
Respiratory failure
Respiratory arrest
Cardiac arrest

Question 12

Signs and symptoms of respiratory distress may include:

Answer 12

Dyspnea.
Speech dyspnea (i.e., the need to pause between words to take a breath) or an inability to speak.
Changes in breathing rate or depth.
Tachycardia or bradycardia.
Decreasing SaO2 levels (however, SaO2 levels may be unaffected in some patients).
End-tidal carbon dioxide (ETCO2) levels that are initially low (less than 35 mmHg) but with increasing distress move into the normal range (35 to 45 mmHg) and then become elevated (greater than 45 mmHg).
Decreased, absent or abnormal breath sounds (e.g., wheezes, crackles, rhonchi).
Use of accessory muscles to assist in breathing, evidenced by supraclavicular, suprasternal, intercostal or substernal retractions.
Tripod positioning (leaning forward with the hands supported on the thighs or other surface).
Diaphoresis (the skin is often cool and clammy).
Irritability, restlessness or anxiety.
Changes in level of consciousness.
Cyanosis.

Question 13

What can be used as an objective assessment of the severity of a patient’s respiratory distress?

Answer 13

Capnography can provide an objective assessment of the severity of a patient’s respiratory distress. Arterial carbon dioxide (PaCO2) values can also be used and are more accurate than capnography, but require arterial sampling and do not provide a continuous output. Some respiratory conditions can make the absolute values or even capnography unreliable. For this reason, it is good clinical practice to correlate capnography with PaCO2 values. In conditions where the absolute value may not match the PaCO2 value, the trend in capnography values is usually accurate.

Early on in respiratory distress, the patient will tend to hyperventilate, which leads to hypocapnia and is reflected by a low ETCO2 value (i.e., less than 35 mmHg). As the patient’s respiratory distress increases and the patient begins to tire, the ETCO2 value may return to the normal range (35 to 45 mmHg). But with the onset of respiratory failure, the ETCO2 level will increase to greater than 45 mmHg, indicating hypoventilation.

Question 14

What is respiratory failure? What are the two types of respiratory failure?

Answer 14

Respiratory failure occurs when the respiratory system can no longer meet metabolic demands. There are two types, hypoxic respiratory failure (characterized by a PaO2 < 60 mmHg) and hypercapnic respiratory failure (characterized by a PaCO2 > 50 mmHg), but patients can also have a combined form. Hypoxic failure is most often associated with ventilation–perfusion mismatch, whereas hypercapnic failure is most often associated with decreased tidal volume or increased dead space. Most patients with respiratory failure need ventilatory assistance in addition to supplemental oxygen. Respiratory failure must be addressed quickly to prevent respiratory arrest. In clinical care, initial recognition of respiratory failure is based on clinical signs.

Question 15

What range of ETCO2 is normal?

Answer 15

35-45mmHg

A normal capnogram is square with a flat baseline, a flat plateau and an ETCO2 value between 35 and 45 mmHg. The square waveform indicates that carbon dioxide flow is not obstructed; the flat plateau means that the patient is exhaling carbon dioxide to the peak level, and the flat baseline means that the patient is not rebreathing carbon dioxide.

Question 16

What SaO2 and ETCO2 values are indicative of respiratory failure?

Answer 16

An SaO2 less than 90% (PaO2 less than 50 mmHg) or a low PaO2 despite compensation and/or an ETCO2 value greater than 50 mmHg or a PaCO2 that is elevated and not reflective of ventilatory effort is indicative of respiratory failure.

Question 17

Signs of respiratory failure could include:

Answer 17

Signs of respiratory failure could include:

Changes in level of consciousness.
Cyanosis.
SaO2 less than 90%.
ETCO2 greater than 50 mmHg.
Tachycardia.
A decreased or irregular respiratory rate.

Question 18

Define respiratory arrest.

Answer 18

Respiratory arrest is complete cessation of the breathing effort. The body can tolerate respiratory arrest for only a very short time before the heart stops functioning, leading to cardiac arrest.

Question 19

The gold standard for measurement of carbon dioxide levels is:

Answer 19

The gold standard for measurement of carbon dioxide levels is arterial carbon dioxide (PaCO2)

However, this requires arterial sampling and is not continuous, making capnography beneficial. In several respiratory conditions and emergencies, the ETCO2 value may not correlate with the PaCO2 value. In most conditions, while the absolute value does not correlate, the trends do correlate, allowing the use of capnography to monitor a patient’s improvement or decline. It is good clinical practice to correlate ETCO2 values with PaCO2 values. When and how often to obtain an arterial sample to correlate depends on clinical judgement, resources and the patient’s condition.

Question 20

Review some of the more common pulmonary and cardiac conditions that should be considered when assessing a patient with acute-onset respiratory distress.

Answer 20

PULMONARY:
Pulmonary embolism
COPD exacerbation
Asthma exacerbation
Pneumonia
Pneumothorax
Noncardiogenic pulmonary edema/acute respiratory distress syndrome (ARDS)

CARDIAC:
Cardiogenic pulmonary edema/congestive heart failure (CHF)
Acute coronary syndromes (ACS)
Cardiac tamponade
Acute valvular insufficiency

Question 21

Diagnostic tests that may be ordered during the initial evaluation of a patient with respiratory compromise include:

Answer 21

Blood gases (arterial or venous).
Serum cardiac markers.
A basic metabolic panel.
A toxicology screen.
Chest radiography, chest computed tomography (CT) or both.
A 12-lead ECG.
Bedside echocardiography or ultrasonography.

Question 22

What steps should you take on a patient coughing/choking with a suspected obstructed airway?

Answer 22

Then provide up to 5 back blows until the obstruction is relieved. If the obstruction is not relieved, transition to up to 5 abdominal or chest thrusts. If necessary, continue with cycles of 5 back blows followed by 5 abdominal or chest thrusts until the obstruction is relieved or the patient becomes unresponsive.

Question 23

Only perform a finger sweep if ___________

Answer 23

An object is seen.

Question 24

Define Sinus Bradycardia. Causes? Signs/Symptoms?

Answer 24

Sinus bradycardia is identical to normal sinus rhythm, except the rate is less than 60 bpm. Cardiac activation starts at the SA node but is slower than normal. Sinus bradycardia may be a normal finding in some patients, but in others it is a pathologic finding.

Causes of sinus bradycardia include:
Vagal stimulation.
Myocardial infarction.
Hypoxia.
Medications (e.g., β-blockers, calcium channel blockers, digoxin).
Coronary artery disease.
Hypothyroidism.
Iatrogenic illness.
Inflammatory conditions.

Sinus bradycardia may not cause signs or symptoms. However, when sinus bradycardia significantly affects cardiac output, signs and symptoms may include:
Dizziness or light-headedness.
Syncope.
Fatigue.
Shortness of breath.
Confusion or memory problems.

Question 25

Define first-degree AV block. Causes? Signs/symptoms?

Answer 25

First-degree AV block is characterized by a prolonged delay in conduction at the AV node or bundle of His. The impulse is conducted normally from the sinus node through the atria, but upon reaching the AV node, it is delayed for longer than the usual 0.2 second. In first-degree AV block, although the impulses are delayed, each atrial impulse is eventually conducted through the AV node to cause ventricular depolarization. Causes First-degree AV block may be a normal finding in athletes and young patients with high vagal tone. It can also be an early sign of degenerative disease of the conduction system or a transient manifestation of myocarditis or drug toxicity. Signs and Symptoms First-degree AV block rarely produces symptoms.

Question 26

Define second-degree AV block type 1. Causes? Signs/symptoms?

Answer 26

In second-degree AV block type I (also called Mobitz type I or Wenckebach block), impulses are delayed and some are not conducted through to the ventricles. After three or four successive impulse delays, the next impulse is blocked. After the blocked impulse, the AV node resets, and the pattern repeats. Second-degree AV block type I usually occurs at the AV node but may be infranodal. Causes Because the block usually occurs above the bundle of His, conditions or medications that affect the AV node (such as myocarditis, electrolyte abnormalities, inferior wall myocardial infarction or digoxin) can cause second-degree AV block type I. This type of arrhythmia can also be physiologic. Signs and Symptoms Second-degree AV block type I rarely produces symptoms. Some patients may have signs and symptoms similar to sinus bradycardia.

Question 27

Define second-degree AV block type 2. Causes? Signs/symptoms?

Answer 27

In second-degree AV block type II (Mobitz type II), the block occurs below the AV node, in the bundle of His. As with second-degree AV block type I, some atrial impulses are conducted through to the ventricles, and others are not. However, there are no progressive delays. The blocked impulses may be chaotic or occur in a pattern (e.g., 2:1, 3:1 or 4:1). In high-grade second-degree AV block type II, the ratio is greater than 2:1 (i.e., 3:1, 4:1, or variable). Causes Second-degree AV block type II is always pathologic. It is usually caused by fibrotic disease of the conduction system or anterior myocardial infarction. Signs and Symptoms Patients may present with light-headedness or syncope, or they may be asymptomatic. The clinical presentation varies, depending on the ratio of conducted to blocked impulses.

Question 28

Define third-degree AV block. Causes? Signs/symptoms?

Answer 28

In third-degree (complete) AV block, no impulses are conducted through to the ventricles. The block can occur at the level of the AV node but is usually infranodal. Pacemaker cells in the AV junction, bundle of His or the ventricles stimulate the ventricles to contract, usually at a rate of 30 to 45 bpm. This means that the atria and ventricles are being driven by independent pacemakers and are contracting at their own intrinsic rates (i.e., 60 to 100 bpm for the atria and 30 to 45 bpm for the ventricles), a situation known as AV dissociation. Causes Degenerative disease of the conduction system is the leading cause of third-degree AV block. This arrhythmia may also result from damage caused by myocardial infarction, Lyme disease or antiarrhythmic drugs. Signs and Symptoms If ventricular contraction is stimulated by pacemaker cells above the bifurcation of the bundle of His, the ventricular rate is relatively fast (40 to 60 bpm) and reliable, and symptoms may be mild (such as fatigue, orthostatic hypotension and effort intolerance). However, if ventricular contraction is stimulated by pacemaker cells in the ventricles, the ventricular rate will be slower (20 to 40 bpm) and less reliable, and symptoms of decreased cardiac output may be more severe.

Question 29

Identify the rhythm: Each impulse is delayed a little more than the last until eventually one impulse is completely blocked, the ECG shows progressive lengthening of the PR interval with each beat, then a P wave that is not followed by a QRS complex (a “dropped beat”). After the dropped beat, impulse conduction through the AV node resumes and the sequence repeats.

Answer 29

Second-Degree AV Block Type I

Question 30

Identify the rhythm: Constant but long PR interval. Missing QRS complexes. More P waves than QRS complexes.

Answer 30

Second-Degree AV Block Type II

Question 31

Tachyarrhythmias can be categorized as either:

Answer 31

Narrow complex or wide complex

Question 32

Narrow-complex tachyarrhythmias include:

Answer 32

Narrow-complex tachyarrhythmias include... sinus tachycardia, atrial flutter, atrial fibrillation and supraventricular tachycardia. These tachyarrhythmias usually originate in the atria or AV node and run normally through the bundle branches, producing a normal QRS complex.

Question 33

Wide-complex tachyarrhythmias include:

Answer 33

Wide-complex tachyarrhythmias originate in the ventricles and include... ventricular tachycardia (monomorphic and polymorphic) and ventricular fibrillation. The cardiac arrest rhythms—pulseless ventricular tachycardia and ventricular fibrillation. Supraventricular tachycardia with aberrant conduction can also produce a wide-complex tachyarrhythmia.

Question 34

Is ventricular tachycardia is a wide-complex tachyarrhythmia or narrow-complex tachyarrhythmia? What are the subtypes of ventricular tachycardia?

Answer 34

Wide-complex tachyarrhythmia Subtypes: monomorphic and polymorphic Monomorphic ventricular tachycardia occurs when there is only one ectopic focus in the ventricles. The QRS complexes are abnormal but all look the same. Polymorphic ventricular tachycardia occurs when there are two or more ectopic focus. The QRS complexes are abnormal and differ in shape/size.

Question 35

Define sinus tachycardia.

Answer 35

Sinus tachycardia is the most common tachyarrhythmia. It is identical to normal sinus rhythm, except the rate is between 100 and 150 bpm. Sinus tachycardia is a normal physiologic response when the body is under stress (such as that caused by exercise, illness or pain). When it is a pathophysiologic response, it may be associated with heart failure, lung disease, shock or hyperthyroidism.

Question 36

Define atrial flutter. Causes? Signs/symptoms?

Answer 36

Atrial flutter is caused by an ectopic focus in the atria that causes the atria to contract at a rate of 250 to 350 bpm. The underlying mechanism of atrial flutter is most often a re-entrant circuit that encircles the tricuspid valve annulus. Causes This rhythm is often seen in patients with heart disease (such as heart failure, rheumatic heart disease or coronary artery disease) or as a postoperative complication. Signs and Symptoms Patients may be asymptomatic or present with shortness of breath, palpitations, effort intolerance, chest constriction, weakness or syncope.

Question 37

Define supraventricular tachycardia (SVT). Causes? Signs/symptoms?

Answer 37

Supraventricular tachycardia (SVT) is an arrhythmia originating above the ventricles. In general, the rate is greater than 150 bpm, which helps to differentiate SVT from sinus tachycardia. SVT can be classified as AV nodal re-entrant tachycardia (AVNRT), AV-reciprocating tachycardia (AVRT) and atrial tachycardia. Causes This rhythm is seen in patients with: Low potassium and magnesium levels. Family history of tachycardia. Structural abnormalities of the heart. Adverse reactions from certain pharmacologic agents (e.g., antihistamines, theophylline, cough and cold preparations, appetite suppressants). Certain medical conditions (e.g., cardiovascular disease, long-term respiratory disease, diabetes, anemia, cancer). Illicit drug use. Signs and Symptoms Patients may present without symptoms or with dizziness or light-headedness, dyspnea, palpitations (including pulsations in the neck area), diaphoresis, ischemic chest pain, hypotension, fatigue, vision changes and syncope.

Question 38

How can you distinguish sinus tachycardia from supraventricular tachycardia (SVT)?

Answer 38

The rate is greater than 150 bpm.

Question 39

Define atrial fibrillation. Causes? Signs/symptoms?

Answer 39

Atrial fibrillation is caused by multiple ectopic foci in the atria that cause the atria to contract at a rate of 350 to 600 bpm. Rarely, the atrial rate may be as high as 700 bpm. The AV node only allows some of the impulses to pass through to the ventricles, generating an irregularly irregular rhythm that is completely chaotic and unpredictable. Causes Atrial fibrillation can occur in young patients with no history of cardiac disease. Acute alcohol toxicity can precipitate an episode of atrial fibrillation in otherwise healthy patients. However, atrial fibrillation commonly occurs in the presence of underlying heart disease, lung disease, hyperthyroidism or myocardial infarction. Signs and Symptoms Patients with atrial fibrillation may be asymptomatic. However, ventricular rates greater than 100 bpm are usually not tolerated well because the filling time for the ventricles is significantly reduced. Symptoms may include shortness of breath, palpitations, chest pain, light-headedness, dizziness and fatigue. Hypotension, syncope and heart failure can occur.

Question 40

Define ventricular tachycardia. Causes? Signs/symptoms?

Answer 40

Ventricular tachycardia occurs when a ventricular focus below the bundle of His becomes the new pacemaker. The ventricles contract rapidly (usually at a rate faster than 100 bpm) and usually with a regular rhythm. The rapid ventricular rate significantly diminishes cardiac output and can only be sustained for a short period before the patient becomes hemodynamically compromised. Ventricular tachycardia can quickly turn into ventricular fibrillation, leading to cardiac arrest. Causes Ventricular tachycardia usually occurs in the presence of heart disease or damage, such as that caused by acute or remote myocardial infarction or cardiomyopathy. There is a significant risk for ventricular tachycardia after myocardial infarction, and this risk can last for weeks, months or years. Ventricular tachycardia may also be precipitated by medications that prolong the QT interval, including amiodarone or other antiarrhythmics and certain antibiotics and antidepressants. Electrolyte derangements (including hypocalcemia, hypomagnesemia and hypokalemia) can also be involved. Signs and Symptoms With sustained ventricular tachycardia, signs and symptoms of reduced cardiac output and hemodynamic compromise develop, including chest pain, hypotension and loss of consciousness.

Question 41

V-Tach and V-Fib are examples of ____-complex tachyarrhythmias.

Answer 41

V-Tach and V-Fib are examples of WIDE-complex tachyarrhythmias.

Question 42

Atrial flutter and atrial fibrillation are examples of ____-complex tachyarrhythmias.

Answer 42

Atrial flutter and atrial fibrillation are examples of NARROW-complex tachyarrhythmias.

Question 43

SVT is an example of wide or narrow complex tachyarrhythmias.

Answer 43

SVT most commonly produces narrow complexes but with aberrant conduction can also produce a wide-complex tachyarrhythmia.

Question 44

Identify the rhythm: P waves absent or abnormal. There is minimal to no beat-to-beat variability and the heart rate is greater than 150 bpm.

Answer 44

SVT

Question 45

Differentiate monomorphic ventricular tachycardia vs. polymorphic ventricular tachycardia.

Answer 45

Monomorphic ventricular tachycardia occurs when there is only one ectopic focus in the ventricles. The QRS complexes are abnormal but all look the same. Polymorphic ventricular tachycardia occurs when there are two or more ectopic focus. The QRS complexes are abnormal and differ in shape/size.

Question 46

What are the two types of bradyarrhythmias?

Answer 46

Bradyarrhythmias WITHOUT hemodynamic compromise Bradyarrhythmias WITH hemodynamic compromise

Question 47

What are the 1st and 2nd line therapies for Bradyarrhythmias WITH hemodynamic compromise?

Answer 47

First-line therapy is with atropine. Second-line therapies include transcutaneous pacing and β-adrenergic agonists. Consider implementing one of the second-line therapies immediately if the patient has second-degree AV block type II or third-degree AV block. Consider expert consult and transvenous pacing if first- and second-line therapies are not effective.

Question 48

What is atropine? Indication? Dosage? Max dose? Precautions?

Answer 48

Atropine is an anticholinergic drug that increases sinoatrial (SA) node firing to increase the heart rate. Give a 1-mg bolus intravenously every 3 to 5 minutes, up to a maximum dose of 3 mg. If the atropine is having no effect, do not wait to reach the maximum dose of atropine before initiating second-line therapies. Use atropine with caution in patients with acute coronary ischemia or myocardial infarction because in these patients, atropine can cause adverse effects, including ventricular tachycardia or ventricular fibrillation.

Question 49

What measure can be initially taken to slow the heart rate in a patient who is in SVT?

Answer 49

Vagal maneuver

Question 50

What medication is used to treat SVT?

Answer 50

Adenosine The initial dose of adenosine is 6 mg by rapid IV push, followed by a 10- to 20-mL normal saline flush. If rhythm not converted, then second dose of 12 mg adenosine followed by a 10- to 20-mL normal saline flush.

Question 51

Dose of atropine for treatment of hemodynamic unstable bradyarrhythmia?

Answer 51

1-mg atropine bolus intravenously every 3 to 5 minutes, up to a maximum dose of 3 mg.

Question 52

Initial dose of adenosine for treatment of SVT? Second dose if rhythm not converted?

Answer 52

6 mg by rapid IV push, followed by a 10- to 20-mL normal saline flush.

Question 53

If vagal manuever and two doses of adenosine (6mg IV bolus and by 12mg IV bolus) do not resolve SVT what do you do next?

Answer 53

Synchronized electrical cardioversion

Question 54

SVT treatment?

Answer 54

Vagal manuever --> 6mg adenosine --> 12mg adenosine --> synchronized electrical cardioversion

Question 55

Precipitating causes of ventricular fibrillation include:

Answer 55

``` Myocardial ischemia or infarction. Shock. Electrocution. Stimulant overdose. Ventricular tachycardia (including torsades de pointes). ```

Question 56

What is Torsades de pointes? Causes?

Answer 56

Torsades de pointes is a highly unstable form of ventricular tachycardia that may revert to sinus rhythm or degenerate into pulseless ventricular tachycardia or ventricular fibrillation. T ``` Causes: A congenital condition. Acute myocardial infarction. Medications (amiodarone or other antiarrhythmics, antibiotics, antidepressants, zofran) Drug–drug interactions. Electrolyte imbalances (low K, Mg, Ca) ```

Question 57

What is pulseless electrical activity (PEA)? Causes?

Answer 57

Pulseless electrical activity (PEA) is a term used to describe several rhythms that are organized on ECG (i.e., the QRS complexes are similar in appearance) but the patient has no appreciable pulse. The heart’s conduction system is functioning, but the myocardium is not contracting (or contracting too weakly) to produce cardiac output, or volume is not sufficient to maintain cardiac output. PEA may be seen immediately after successful defibrillation of a patient with ventricular fibrillation or pulseless ventricular tachycardia. But when PEA is the presenting rhythm (“primary PEA”), the underlying cause is usually a condition that either affects contractility or ejection (e.g., hypoxia, acidosis, anterior myocardial infarction) or leads to inadequate preload (e.g., severe hypovolemia, pulmonary embolism, tension pneumothorax, cardiac tamponade, right ventricular infarction).

Question 58

What is asystole? Causes?

Answer 58

In asystole, there is no electrical activity (flatline) and therefore no contraction. Asystole is often the terminal rhythm in untreated pulseless ventricular tachycardia or ventricular fibrillation, or when resuscitation efforts are unsuccessful. ``` Other causes include: Indirect lightning strike. Drowning. Narcotic drug overdose. Hypothermia. Pulmonary embolism. Hyperkalemia. Stroke. ```

Question 59

Untreated untreated pulseless ventricular tachycardia or ventricular fibrillation, or unsuccessful resuscitation efforts can lead to ______

Answer 59

Untreated untreated pulseless ventricular tachycardia or ventricular fibrillation, or unsuccessful resuscitation efforts can lead to asystole.

Question 60

_____ may be seen immediately after successful defibrillation of a patient with ventricular fibrillation or pulseless ventricular tachycardia.

Answer 60

Pulseless electrical activity (PEA) NOTE: PEA can also be a presenting rhythm (“Primary PEA”)

Question 61

What are the reversible underlying causes of cardiac arrest? What rhythm would be on the monitor to prompt you to think of these causes?

Answer 61

Whenever you have a patient in cardiac arrest with PEA or asystole think: "H's and T's" ``` Hypovolemia Hypoxia Hydrogen excess (acidosis) Hyper/Hypokalemia Hypothermia ``` ``` Toxins (cocaine, meth, heroin; overdoses of BB, CCB, digoxin, tricyclic antidepressant, opioids) Trauma Thrombosis (aka massive PE or MI) Tension PTX Tamponade ```

Question 62

Differential for PEA/asystole:

Answer 62

"H's and T's" ``` Hypovolemia Hypoxia Hydrogen excess (acidosis) Hyper/Hypokalemia Hypothermia ``` ``` Toxins (cocaine, meth, heroin; overdoses of BB, CCB, digoxin, tricyclic antidepressant, opioids) Trauma Thrombosis (aka massive PE or MI) Tension PTX Tamponade ```

Question 63

What are the shockable rhythms?

Answer 63

Ventricular fibrillation and PULSELESS ventricular tachycardia require defibrillation as soon as possible. Because shocks may not be successful or, in the case of successful defibrillation, the resultant rhythm may not be adequate to sustain perfusion or a pulse, resume CPR immediately after each shock. After every 2 minutes of CPR, reassess the rhythm (while minimizing interruptions to chest compressions) to determine next actions: If the rhythm is shockable, resume CPR immediately and administer 1 shock. If the rhythm is nonshockable, attempt to palpate a pulse. (It is only necessary to check for a pulse if an organized rhythm is present on the monitor.) If a definitive pulse is palpated, provide post–cardiac arrest care. If a definitive pulse cannot be palpated, resume CPR immediately and follow the code card pathway for a nonshockable rhythm.

Question 64

How long should you perform CPR after a shock before pausing compressions to conduct a rhythm check?

Answer 64

Immediately after the shock is delivered, resume CPR for 2 minutes before pausing compressions to conduct a rhythm check.

Question 65

When is epinephrine administered in a patient in pulseless V-Tach or V-Fib? Dose? How long before next administration?

Answer 65

After 2 shocks have been delivered. Epinephrine (1 mg IV/IO every 3 to 5 minutes) may be administered. The vasoconstrictive and positive ionotropic effects of epinephrine help to increase cerebral and coronary perfusion.

Question 66

How many shocks are given to a patient in pulseless V-Tach/V-Fib before epinephrine is administered?

Answer 66

2 shocks

Question 67

After the third shocks in a patient with pulseless V-Tach/V-Fib what should you administer next?

Answer 67

Amiodarone (antiarrhythmics) The initial dose of amiodarone is 300 mg administered as an IV/IO bolus. If the arrest rhythm persists, consider giving a second dose of 150 mg as an IV/IO bolus 3 to 5 minutes later. Alternatively, lidocaine may be used if amiodarone is not available. The initial dose is 1 to 1.5 mg/kg IV/IO, followed by 0.5 to 0.75 mg/kg IV/IO every 5 to 10 minutes, up to a maximum dose of 3 mg/kg.

Question 68

The initial dose of amiodarone? Second dose if the arrest rhythm persists?

Answer 68

The initial dose of amiodarone is 300 mg administered as an IV/IO bolus. If the arrest rhythm persists, consider giving a second dose of 150 mg as an IV/IO bolus 3 to 5 minutes later.

Question 69

If amiodarone is not available what other antiarrhythmic can be used? Dosage? Second dose if the arrest rhythm persists?

Answer 69

Lidocaine may be used if amiodarone is not available. The initial dose is 1 to 1.5 mg/kg IV/IO, followed by 0.5 to 0.75 mg/kg IV/IO every 5 to 10 minutes, up to a maximum dose of 3 mg/kg.

Question 70

What are the nonshockable rhythms?

Answer 70

PEA and Asystole Management of PEA or asystole involves providing continuous high-quality CPR, administering epinephrine (1 mg IV/IO repeated every 3 to 5 minutes) as early as possible and performing rhythm checks after every 2 minutes of CPR. Defibrillation is not indicated when the rhythm is PEA or asystole. It is extremely important to look for and address potential underlying causes of the cardiac arrest. PEA and asystole often have an underlying cause, and unless that cause is addressed, the resuscitative effort will not be successful.

Question 71

What is post–cardiac arrest syndrome?

Answer 71

Post–cardiac arrest syndrome, the pathophysiologic consequences of cardiac arrest comprise four key areas. The duration of the cardiac arrest (i.e., from collapse through ROSC) directly affects the severity of the post–cardiac arrest syndrome. Brain injury, caused by ischemia and cerebral edema, is a significant cause of morbidity and mortality in patients who achieve ROSC. Among patients who achieve ROSC, the short-term mortality rate is high. Myocardial stunning secondary to the ischemia/reperfusion response causes systolic and diastolic dysfunction, leading to hemodynamic instability in the immediate post-arrest period. The ischemia/reperfusion response can trigger a systemic inflammatory response, which can lead to multisystem organ dysfunction syndrome (MODS). The underlying cause of the cardiac arrest may continue to have pathophysiologic consequences during the post-arrest period.

Question 72

The ischemic conditions that comprise ACS can be subdivided into two categories:

Answer 72

The ischemic conditions that comprise ACS can be subdivided into two categories: STEMI and NSTE-ACS.

Question 73

Reperfusion therapy in the form of PCI or fibrinolytic therapy is recommended for all patients with STEMI and should be performed within _____ hours of the onset of symptoms.

Answer 73

12 hours

Question 74

Ideally, PCI is performed within ____ minutes of the patient’s first medical contact; this time frame is extended to ____ minutes if the patient must be transferred to a facility capable of performing the procedure. As the time from first medical contact to PCI increases, so does the mortality rate.

Answer 74

Ideally, PCI is performed within 90 minutes of the patient’s first medical contact; this time frame is extended to 120 minutes if the patient must be transferred to a facility capable of performing the procedure. As the time from first medical contact to PCI increases, so does the mortality rate.

Question 75

What is a stroke? Types?

Answer 75

A stroke is a sudden neurologic deficit that occurs because of impaired blood flow to part of the brain ISCHEMIC (87%) Ischemic stroke occurs when a blood vessel carrying blood to the brain becomes obstructed. Ischemic strokes account for about 87% of all strokes. Ischemic stroke is classified as thrombotic or embolic. HEMORRHAGIC (13%) Hemorrhagic stroke occurs when a blood vessel in the brain ruptures and pressure from the bleeding damages the brain tissue. This type of stroke is frequently caused by hypertension or aneurysms. Hemorrhagic strokes can be classified as intracerebral or subarachnoid.

Question 76

Ischemic strokes can be classified as either _____ or _____

Answer 76

THROMOBTIC STROKE A thrombotic stroke is most often caused by rupture of an atherosclerotic plaque in a cerebral artery, resulting in the formation of thrombus that occludes the artery. Patients frequently have a history of hypercholesterolemia and atherosclerosis. EMBOLIC STROKE An embolic stroke occurs when a plaque fragment or blood clot forms elsewhere within the circulatory system and travels to the cerebral circulation. Often the source of the embolus is a blood clot that forms in the heart or the large arteries in the upper chest or neck. Between 15% and 20% of embolic strokes are associated with atrial fibrillation.

Question 77

Hemorrhagic strokes can be classified as either _____ or _____

Answer 77

INTRACEREBRAL HEMORRHAGE Intracerebral hemorrhage, the most common form of hemorrhagic stroke, occurs when an artery located within the brain bursts, causing bleeding into the surrounding brain tissue. Intracerebral hemorrhage may be caused by an arteriovenous malformation, anticoagulant therapy or chronic hypertension, among other causes. SUBARACHNOID HEMORRHAGE Subarachnoid hemorrhage occurs when a blood vessel located on the surface of the brain ruptures, causing bleeding into the subarachnoid space. This type of hemorrhage is most often caused by a ruptured aneurysm but can also be caused by an arteriovenous malformation, bleeding disorder, head injury or anticoagulant therapy.

Question 78

For an acute ischemic stroke, when is fibrinolytic therapy ideally administered?

Answer 78

Within 60 minutes of the patient's arrival and within 3 hours of the onset of symptoms

Question 79

What stroke severity tool is used in the neurologic assessment of a patient having a stroke?

Answer 79

National Institutes of Health Stroke Scale (NIHSS)

Question 80

What imaging should be ordered on a patient having a stroke? Timeline?

Answer 80

Non-contrast CT or MRI scan of the brain within 10 minutes of the patient’s arrival, completed CT or MRI scan within 20 minutes and interpreted within 45 minutes.

Question 81

Treatment for hemorrhagic stroke?

Answer 81

Treatment depends on the cause and severity of the bleeding. Measures are taken to support the airway, oxygenation, ventilation and perfusion. In addition, care entails measures to control the internal bleeding, including consideration of reversal of anticoagulants, consideration of treatment of hypertensive crisis, management of increased intracranial pressure and treatment of seizures. A neurology or neurosurgical consult is necessary and the patient may need to be transferred to a comprehensive stroke center or a neurosurgical center for definitive care.

Question 82

Treatment for ischemic stroke?

Answer 82

Treatment for ischemic stroke is fibrinolytic therapy, endovascular therapy or both based on inclusion and exclusion criteria.