ACLS Flashcards
What is ACLS?
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.
An oropharyngeal airway (OPA) should only be insert on a patient who is ___________
Unconscious and has no gag reflex
An nasopharyngeal airway (NPA) can be inserted on a patient who is ___________
Unconscious or conscious
With or without a gag reflex
How many compressions per minute should be provided to an adult undergoing CPR? Recommended depth? Breathes per minute?
100-120 compressions per minute at depth of 2.0-2.5 inch
1 breath per 6 seconds (avoid excessive ventilation)
When using the bag-valve-mask resuscitator, depress the bag about halfway to deliver a volume of
___ to ___ mL.
When using the bag-valve-mask resuscitator, depress the bag about halfway to deliver a volume of
400 to 700 mL.
Define respiration, ventilation, and gas exchange.
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.
What are the primary muscles used for ventillation? Accessory muscles?
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.
What muscles are used for expiration? Forced expiration?
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.
What controls the impulse to breath? What factors affect the rate and depth of breathing?
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.
What factor factors affect hemoglobin’s affinity for binding with oxygen
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.
Respiratory compromise manifests along a continuum:
Respiratory distress
Respiratory failure
Respiratory arrest
Cardiac arrest
Signs and symptoms of respiratory distress may include:
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.
What can be used as an objective assessment of the severity of a patient’s respiratory distress?
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.
What is respiratory failure? What are the two types of respiratory failure?
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.
What range of ETCO2 is normal?
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.
What SaO2 and ETCO2 values are indicative of respiratory failure?
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.
Signs of respiratory failure could include:
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.
Define respiratory arrest.
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.
The gold standard for measurement of carbon dioxide levels is:
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.
Review some of the more common pulmonary and cardiac conditions that should be considered when assessing a patient with acute-onset respiratory distress.
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
Diagnostic tests that may be ordered during the initial evaluation of a patient with respiratory compromise include:
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.
What steps should you take on a patient coughing/choking with a suspected obstructed airway?
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.
Only perform a finger sweep if ___________
An object is seen.
Define Sinus Bradycardia. Causes? Signs/Symptoms?
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.
Define first-degree AV block. Causes? Signs/symptoms?
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.
Define second-degree AV block type 1. Causes? Signs/symptoms?
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.
Define second-degree AV block type 2. Causes? Signs/symptoms?
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.
Define third-degree AV block. Causes? Signs/symptoms?
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.
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.
Second-Degree AV Block Type I
Identify the rhythm:
Constant but long PR interval. Missing QRS complexes. More P waves than QRS complexes.
Second-Degree AV Block Type II
Tachyarrhythmias can be categorized as either:
Narrow complex or wide complex
Narrow-complex tachyarrhythmias include:
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.
