Triage/Legal & FINAL

Legal - Section 2: Review Quiz

1 1 out of 1 points Failure to obtain patient consent for an intervention such as an injection is considered which legal infraction? Selected Answer:a. Battery Answers:a. Battery b. Negligence c. Malfeasance d. Tort Question 2 1 out of 1 points Failure to recognize signs and symptoms (e.g., of bleeding) that a reasonable and competent nurse should know, resulting in severe bodily harm or death to a patient, can constitute criminal negligence in the eyes of the law. Selected Answer: True Answers: True False Question 3 1 out of 1 points What unique aspects of the ED make confidentiality especially difficult to maintain, and require even more vigilance from nurses to ensure confidentiality is protected? Selected Answer:e. All of the above Answers:a. Overcrowding b. High traffic areas c. Visible patient identifiers d. Social media e. All of the above Question 4 1 out of 1 points The use of social media when not at work to express personal opinions or frustrations about other health-care professionals or institutions is acceptable. Selected Answer: False Answers: True False Question 5 1 out of 1 points Which of the following are nurses legally mandated to report? Selected Answer:e. All of the above Answers:a. Abuse or neglect of a child b. Sexual abuse of a patient c. A gunshot or stab wound d. A communicable illness on the Public Health list e. All of the above Question 6 1 out of 1 points The legal age of consent in Canada is 16 years or older. Selected Answer: False Answers: True False Question 7 1 out of 1 points Professional liability insurance is optional in most provinces except for Quebec. Selected Answer: False Answers: True False Question 8 1 out of 1 points The precedent-setting case Kolesar v. Jeffries, 1976, dealt with which of the following elements of nursing practice? Selected Answer:b. Documenting contemporaneously Answers:a. Maintaining confidentiality when dealing with police b. Documenting contemporaneously c. Mandatory reporting of sexual assault d. The process for chain of custody with regard to forensic evidence Sunday, December 5, 2021 12:49:35 PM MST

BBBs

A bundle branch block (BBB) refers to a rhythm abnormality with impaired conduction through either the right (i.e., RBBB) or left bundle branch (i.e., LBBB), causing delayed depolarization of the ventricle on the affected side. BBBs may be either permanent or transient.BBBs complicate the novice ECG interpreter's efforts!In earlier sections, we referred to supraventricular rhythms (i.e., sinus, atrial, and junctional) as having normally-shaped QRS complexes less than 0.12 seconds in duration. Rhythms that have wide, bizarre-shaped QRS complexes were referred to as ventricular in nature; however, a BBB also contributes to a QRS complex that is greater than or equal to 0.12 seconds with an abnormal shape (aberrancy). QRS complexes due to a BBB may mimic those of VT; however, the other parameters do not change. Therefore, it may still be possible to identify the origin of the rhythm by assessing P waves and PRIs. Differentiating VT from aberrancy, as well as a RBBB from a LBBB, may require a 12-lead ECG as Lead II analysis alone is insufficient. If a wide QRS complex is detected, following patient assessment and treatment as required, a 12-lead ECG should be performed. Systematic analysis of the ECG is your best tool.BBBs are covered in more detail in the next module (Essentials of 12-Lead Electrocardiography). Intraventricular Conduction DelaysAs mentioned earlier, during depolarization of the ventricle, the left side of the interventricular septum is stimulated first (red arrow). The impulse then crosses the interventricular septum, followed by simultaneous depolarization of the right and left bundle branches (blue/green arrows). However, since the left ventricle has a larger mass than the right, the net wave of depolarization is towards the left.If there is a delay or blockage of conduction down one of the bundle branches, the ventricles will not depolarize (and therefore contract) simultaneously. It is possible for a delay or block to affect one of the fascicles of the left bundle branch; however, this module discusses only blockages of the left or right bundle branch, not fascicular blockages.In order to determine the presence of a bundle branch block (BBB), one must first ensure that the impulse is supraventricular in origin. In other words, the impulse arises from above the ventricles and is not ventricular in origin. The other criterion for the presence of a BBB is that the QRS duration is more than 0.12 seconds; however, it is possible to have an incomplete BBB with a QRS duration of 0.10-0.12 seconds. Note that factors other than BBBs may contribute to a wider than normal QRS complex, including Wolff-Parkinson-White (WPW) syndrome and hyperkalemia.The right bundle branch is thinner and more susceptible to damage than the left; therefore, right bundle branch blocks (RBBBs) are more common than left bundle branch blocks (LBBBs).With a RBBB, the impulse still stimulates the left side of the interventricular septum first and crosses the interventricular septum (red arrow) causing a small upwards deflection in the QRS of Lead V1; however, the right bundle branch cannot conduct the impulse (more on this in a moment). The impulse also continues down the left bundle branch to stimulate the left ventricle (green arrow), causing a deep downward deflection in the QRS in Lead V1. In order for the right ventricle to be depolarized, the impulse must then travel cell-to-cell over to the right ventricle (blue arrow), causing a late upwards deflection in the QRS in Lead V1.Overall, the QRS ends up with an rSR' configuration. The symbol ' indicates a second wave of the same type and is verbally referred to as "prime." The second R wave is taller and is therefore capitalized, whereas the first r wave is smaller, and identified by lower case. Verbally, this shape is described as "rSR prime". The rSR pattern is sometimes referred to colloquially as "rabbit ears".With a LBBB, the septum is depolarized by the right bundle branch (small arrow), which also depolarizes the right ventricle. In order for the left ventricle to be depolarized, the impulse must then travel cell-to-cell from right to left (LARGE arrow).Overall, the QRS ends up with a QS configuration. Due to abnormal depolarization, ST segments and T waves are usually altered during repolarization; therefore, the presence of a LBBB masks signs of ST elevation and T wave inversion in the event of ischemia.Not every BBB results in these classic configurations, which often causes confusion. One way to resolve this is to look at the last part of the QRS complex, also called the terminal force, specifically the last 0.04 seconds of the QRS complex. If this deflection is upward, a RBBB exists, resulting in late depolarization of the right ventricle (and therefore the upward terminal force in Lead V1). If this deflection is inverted, a LBBB exists, resulting in late depolarization of the left ventricle (and the wave of depolarization moving away from Lead V1).One way to remember this is to relate it to how one moves the turn indicator of a vehicle. To signal a right turn, the indicator lever is moved upward (up = RBBB) and to signal a left turn, the indicator lever is moved downward (down = LBBB).Evaluate the following ECGs for the presence of a bundle branch block.A small r wave in V1 followed by S and R' (rSR') indicates a RBBB. The terminal portion of the QRS complex is going up (turning right = RBBB).The terminal portion of the QRS complex is going down (turning left = LBBB). Putting it All Together In summary, 12- and 15-lead ECGs can be used to aid in diagnosing acute coronary syndrome (ACS), axis deviation, and BBBs. Although beyond the scope of this Module, they can also be used to assess for disorders such as pericarditis, hemiblocks, and chamber hypertrophy.Evaluate the following ECGs for the presence of myocardial ischemia or infarction, axis deviation, and bundle branch blocks.Leads V1 to V3 show ST elevation, small R progression. ST depression and inverted T waves are shown in Leads I, aVL, V5, and V6.There is left axis deviation at -30°.There is no BBB (QRS is normal width).2. ST elevation is shown in leads V1 to V3.The axis is normal.The QRS complex is normal width; there is no BBB.3. ST elevation is shown in leads V1, V2 and possibly V3.There is T wave inversion in aVL and V6.There is left axis deviation at -30 degrees.There is no BBB (QRS width is normal).4. There is ST elevation in leads II, III and aVF.There is ST depression in leads I, aVL and possibly V6There is ST depression and inverted T waves in V1 to V3 (could be reciprocal changes posterior wall - need 15-lead ECG).The axis is normal.There is no BBB.

Managing the Waiting Room

Ideally , patients presenting to the ED would be seen by a physician or advanced practice nurse immediately; however, this is rarely possible in today's busy hospitals. As mentioned earlier, nurses must remember that what ever the patient's presenting complaint(s), it may be perceived as a crisis or stressful situation to them. Having to wait in the waiting room while other patients are being called ahead of them may evoke feelings of frustration, anxiety, and anger. It is imperative that triage nurses demonstrate compassion, empathy, and open communication with patients in the waiting room. For example, the patient may be the only one in the waiting room but within the department, all available resources have been diverted to multiple trauma patients who have just arrived via EMS. In a situation like this, the triage nurse should communicate openly and honestly with the patient to inform them that while he/she understands their frustration, several critically ill patients have just arrived so the wait may be longer than anticipated. Patients may have the misconception that arriving via ambulance will bump them to the front of the triage line or be seen by a physician more quickly. The triage process is the same for patients who arrive via EMS or 'walk-in' (Gilboy, 2010, p. 68). Triage nurses must continue to communicate with patients in the waiting room, such as by providing updates on wait times if possible and performing reassessments as per CTAS guidelines. These strategies go a long way in demonstrating that the triage nurses and ED staff have not forgotten about them and that they are doing the best they can with available resources. Having said that, after being triaged and waiting for several hours, patients may decide to leave without being seen by a physician. Triage nurses are responsible for documenting patients' disposition while in the waiting room, thus policies and procedures must be in place to provide guidance as to how to handle these situations (Gilboy, 2013). Patients may or may not inform the triage nurse of their intent to leave the ED. If the patient does tell the triage nurse he/she is leaving, the triage nurse should use this opportunity to discuss the situation with the patient (Gilboy, 2013, pp. 71-72), as well as inform the charge nurse and physician if the patient has a significant injury or illness (Gilboy, 2010). If the patient decides to leave, many EDs require the patient to sign a form indicating they have been advised of the risk(s) in doing so. The triage nurse must also consider whether the patient has the capacity to make this decision on their own. If they do not, they can legally be stopped from leaving. If the patient leaves the department without informing triage staff, the triage nurse must document the time he/she first noticed the patient was no longer in the waiting room, as well as the nurse's actions to find the patient (e.g., overhead page x 3) (Gilboy, 2013, pp. 71-72).

CV Disorders / 12-Lead ECGs

Although the classification and risk stratification of ACS have been updated, the pathophysiological principles of stable and unstable lesions remain unchanged. Ischemic cardiac episodes that occur as a consequence of stable and mature plaque formation are usually fairly predictable (stable angina). The person with this condition may be able to predict what will cause and relieve anginal symptoms. However, stable and mature plaques can change suddenly; ruptures of small lesions often remain clinically silent, while more extensive plaque rupture may place the patient at higher risk for MI and sudden death. When the fibrous cap over a plaque ruptures, lipid is released into the bloodstream and a luminal thrombosis (blood clot) forms, obstructing blood flow.Plaque instability results in periods of occlusion and revascularization (unstable angina); it is most often an indication of impending plaque rupture with thrombosis formation that may lead to MI. In comparison to more stable lesions, the plaque and thrombotic situation is dynamic, that is, it is constantly changing. Patients in the NSTE-ACS risk group may have a more unpredictable pattern of chest pain. It either culminates in a MI or stabilizes with repair to the plaque.The clinical bottom line: low- and high-risk patients may be indistinguishable based on clinical presentation alone.Chest discomfort or painSensation of aching, squeezing, pressing, burning, and/or heaviness Low - / Intermediate risk ACS Predictable onset, typically occurs with physical exertion or following heavy meal Typically relieved with rest, nitroglycerin, and/or oxygen (O2)NSTE - ACS: pressure-type chest pain occurring at rest or with minimal exertion lasting ≥ 10 minutes (most common) Chest pain at rest, new onset of severe pain, or increasing pain occurring more frequently and with more severity. There may be a 'stuttering' recurrence of ischemic episodes that persist from days to weeks. Pain may not be relieved with rest, O2, and/or nitroglycerin; if it is relieved, it may return.Not to be confused with variant angina (Prinzmetal's angina), which occurs due to a spasm of a coronary artery. It is not caused by atherosclerosis, but may occur with or without the presence of atherosclerotic lesions (CAD). Variant angina often occurs at rest and tends to be cyclic in nature. Nitrates, such as nitroglycerin, or Ca2+ channel blockers (CCBs) are administered to dilate the coronary artery(ies).Retrosternal (behind the sternum, most common) or substernal (below the sternum), with possible radiation to the throat, jaw, and arm(s) (see Figure 14.2 in Urden et al, 2022, p. 306)Women may present with atypical patterns of pain (see Box 14.4 in Urden et al., 2022, p. 306); however, there is some controversy as to whether women always present with atypical symptoms. Mehta et al. (2016) summarize the symptoms of acute MI in women, including ethnic disparities, as follows:Compared with men, women are more likely to have high-risk presentations and less likely to manifest central chest pain. Pain in the upper back, arm, neck, and jaw, as well as unusual fatigue, dyspnea, indigestion, nausea/vomiting, palpitations, weakness, and a sense of dread, occur more frequently in women compared with men. Ischemic symptoms in young black women include unusual fatigue, shortness of breath, chest discomfort, or frequent indigestion, with older white women displaying fewer symptoms. Shoulder pain and arm pain are twice as predictive of an ACS diagnosis in women compared with men (p. 922).Diabetic patients may have altered sensation due to diabetic neuropathySilent ischemia: 1/3 of patients experiencing a MI do not report chest pain or other related symptoms; the only evidence of myocardial ischemia is demonstrated via ECG, specifically ST-segment monitoring.Perception of dyspneaUnexplained new-onset dyspneaIncreased exertional dyspneaSigns of heart failure (i.e., S4, mitral regurgitation, pulmonary vascular congestion)Nausea, vomiting, abdominal pain Presyncope / Syncope Palpitations, arrhythmias Atypical: epigastric pain, indigestion, stabbing or pleuritic pain, increased dyspnea without chest pain Electrocardiogram (ECG) changes Low - / Intermediate - risk ACS May be either normal or nondiagnostic (inconclusive, such as ST-segment deviation of < 0.5 mm or T wave inversion of ≤ 2 mm)ST-segment depression is depicted below in Figure 1.2T wave inversion is depicted in Figure 14.5 (Urden et al., 2022, p. 312), as well as below in Figure 1.2NSTE - ACSST-segment depression ≥ 0.5 mm or dynamic T wave inversionNon-persistent or transient ST-segment elevation ≥ 0.5 mm for < 20 minutes also includedSTEMIST-segment elevation in 2 or more contiguous leads or new LBBB> 2 mm in leads V2 and V3 and ≥ 1 mm in all other leads*2.5 mm in men < 40 years...1.5 mm in all women*Note: A small percentage of patients with normal ECGs may be found to have MI (AHA, 2016, p. 69).

Confidentiality: Clinical Case

An 18-year-old male patient arrives to the ED suffering from what he says is a headache. After triage, he is brought to your section and you begin to assess his neurological status. During your assessment, the patient confides in you that he doesn't really have a headache, but that he is really here because he is extremely stressed and is having some thoughts about killing himself recently. He then says he regrets coming here and not to tell anyone what he told you, as he has significant trust issues. This person has told you about his suicidal thoughts in confidence. You want to value his trust, but you are also very worried for his safety. Questions: What should you do? Is it mandatory to report suicidal ideation? This is a complicated issue. Reporting of suicide ideation is not legally mandatory, unlike child abuse, gunshot wounds, and certain communicable diseases. However, there are still both ethical and legal implications. Nurses are ethically obligated to address suicidal ideation because a patient's safety could be at risk, and should harm come to the patient by not addressing this disclosure, the nurse could be held legally liable for damages (CNPS, 2017). Consider again the principle of non-maleficence. We must further explore a disclosure of suicidal thoughts by asking the patient questions such as whether they have a suicide plan, if they have ever attempted suicide, or if they have weapons at home. As well, in the interest of patient safety, we should involve others such as a physician or mental-health worker in the circle of care in order for the patient to be further assessed regarding suicide risk. We must also document accordingly. Confidentiality can be compromised when harm to the patient could come from maintaining that confidentiality (Keatings & Smith, 2010).

Conduction pathway of the heart

An electrical stimulus is generated in a special part of the heart muscle called the sinus node. It's also called the sinoatrial node (SA node). The sinus node is a small mass of special tissue in the right upper chamber of the heart (right atrium). In an adult, the sinus node sends out a regular electrical pulse 60 to 100 times per minute. This electrical pulse travels down through the conduction pathways and causes the heart's lower chambers (ventricles) to contract and pump out blood. The right and left atria are stimulated first and contract to push blood from the atria into the ventricles. The ventricles then contract to push blood out into the blood vessels of the body. The original electrical impulse travels from the sinus node across the cells of your heart's right and left atria. The signal travels to the AV node (atrioventricular node). This node is located between the atria and the ventricles. In the AV node, the impulses are slowed down for a very short period. This allows the atria to contract a fraction of a second before the ventricles. The blood from the atria empties into the ventricles before the ventricles contract. After passing through the AV node, the electrical current then continues down the conduction pathway, through a pathway called the bundle of His, and into the ventricles. The bundle of His divides into right and left pathways (bundle branches) to give electrical stimulation to the right and left ventricles. Normally at rest, the heart contracts about 60 to 100 times a minute depending on your age. In general, your heart rate slows as you age. junctional conduction Junctional rhythms arise from an area surrounding the AV node. This area has the ability to take over the pacemaker function of the heart to maintain cardiac output if the SA node malfunctions and its impulse formation drops. The intrinsic rate of the AV junction is 40-60 bpm. This protective rhythm is called junctional escape rhythm. Enhanced automaticity of this area, which may result from ischemia, stress, stimulants, electrolyte imbalances, and digitalis toxicity, can cause the rate to be higher than the intrinsic rate. This could result in premature junctional complexes, accelerated junctional rhythm, or junctional tachycardia, each of which is described in more detail below. The term supraventricular tachycardia may be applied to any rhythm faster than 100 beats per minute arising from above the ventricles. Impulses of junctional origin are conducted in a retrograde fashion through the atrial tissue, producing inverted P waves in lead II. If atrial depolarization occurs before ventricular depolarization, the P wave will precede the QRS, but the PRI will be less than 0.12 second. If depolarization of the atria and ventricles occurs simultaneously, the P wave will be hidden in the QRS complex. Finally, if atrial depolarization occurs after ventricular depolarization, the P wave will follow the QRS. In impulses of junctional origin, conduction through the ventricles is normal, producing a normal, upright QRS. Junctional (junctional escape) rhythm is normally seen following a failure of the SA node to generate impulses at a sufficient rate. The AV junction takes over pacemaker function at an intrinsic rate of 40-60 bpm, with a regular rhythm. As discussed previously, the P waves are inverted in Lead II, because of retrograde conduction to the atria, and may occur before, during, or following the QRS complex. Ventricular conduction is not affected and occurs in a normal fashion, producing the normal QRS complex. Ventricular rhythms arise from pacemaker sites within the ventricular muscle or Purkinje fibres. The Purkinje fibres have the ability to take over the pacemaker function of the heart if both the SA node and AV junctions malfunction. The intrinsic rate of the Purkinje fibres is 20-40 bpm. The resulting protective rhythm is called idioventricular rhythm (or ventricular escape rhythm). Altered cellular function in the ventricles, which may result from ischemia, stress, stimulants, drug effects, or electrolyte imbalances, may result in PVCs, accelerated idioventricular rhythm (AIVR), ventricular tachycardia (VT), ventricular fibrillation (VF), or asystole.

Aortic aneurysms

Aortic aneurysms and aortic dissections are disease states that result from progressive atherosclerotic disease and systemic arterial HTN. Aortic Aneurysm Localized dilation of the arterial wall > 1.5 times its normal diameter is referred to as an aneurysm, and results in an alteration in vessel shape and blood flow. 'True' aneurysms involve dilation of the entire vessel wall. Aneurysms may be described in terms of their shape: fusiform (more common, diffuse dilations along arterial circumference) or saccular (localized balloon-shaped outpouching). Abdominal aortic aneurysm (AAA): 4 times more common than thoracic aneurysms, occurring more often in men; smoking is the leading risk factor for AAA, followed closely by age, HTN, lipid disorders, and atherosclerosis. Signs/Symptoms: most patients with AAA are asymptomatic, with abdominal or back pain being the most common symptom worsening pain signifies aortic expansion or rupture may be detected as a palpable, pulsatile mass with bruit located in the umbilical region of the abdomen, to the left of midlineperipheral pulses must be vigilantly assessed (as the AAA dissects/ruptures, peripheral circulation will be compromised) Treatment: control of HTN, smoking cessation; pain control serial ultrasounds to monitor progression surgical repair if > 5.5 cm in men (women if > 4.5-5 cm, due to higher risk of rupture) endovascular graft (less invasive surgical repair): graft placement through femoral artery, insertion of balloon stents Thoracic aneurysm: classified by anatomical location (i.e. aortic root, ascending aorta, aortic arch, descending aorta); etiology and treatment differ for each classification Signs/Symptoms: similar to AAA in that most are asymptomatic; symptoms related to size/location of aneurysmmay include: aortic insufficiency, pericardial tamponadehigh mortality for acute dissection/rupture (< 50% survive prior to hospitalization, 80% mortality at 24 hours) Treatment: control of HTN; pain control serial ultrasounds to monitor progression surgical repair if > 5.5-6 cm (depends on clinical situation, comorbidities) Aortic Dissection Aortic dissection occurs when the intimal layer of the aorta tears longitudinally, creating a false lumen through which the flow of blood further separates the vascular layers and extends the tear; it is the most common, and most fatal, condition related to the aorta (mortality increases 1% per hour). Risk factors include: gender (men are > 2 x more likely than women), > 60 years of age, HTN, cystic medial degeneration (genetic disorder of large arteries), pregnancy, and trauma. Signs/Symptoms: sudden, intense chest/abdomen/back pain ("tearing", "ripping"); as the tear (dissection) extends, pain radiates to the back or distally toward the lower extremitiessyncopeaortic regurgitation (murmur)altered/loss of peripheral circulationwidened mediastinum (on CXR)cardiac ischemia (if coronary arteries involved)cardiac tamponade (if aortic root involved)neurological deficits (if aortic arch vessels involved)decreased renal function (if renal arteries involved)Treatment: management depends on location, severity, and how quickly the patient is diagnosed control of HTN pain control\ surgical repair

Reassessment

As aforementioned, the triage process is ongoing until patients' disposition is known (e.g., assigned a bed in the ED, transferred to the ward or another facility, discharged home). The well-being and safety of patients in the waiting room or triage bed remain the responsibility of the triage nurse and ED staff; therefore, patients must be reassessed accordingly. "The extent of the reassessment depends on the presenting complaint, the initial triage level and any changes identified by the patient" (Murray et al., 2004, p. 422). Gilboy (2013) describes this dynamic process as "routine rounding" (p. 72). Reassessment principles and guidelines are described below. Patients who are alert and oriented with less urgent complaints should be advised to return to triage if their condition changes while waiting. CTAS guidelines recommend the following reassessment timeframes: CTAS level 1: continuous nursing care; CTAS level 2: every 15 minutes; CTAS level 3: every 30 minutes; CTAS level 4: every 60 minutes; and CTAS level 5: every 120 minutes. All reassessments and acuity changes must be documented; however, the initial triage level should never be changed. If the patient's condition changes, it should be documented as the reassessment triage acuity level in the triage record(CTAS National Working Group, 2013c, p. 53; Murray et al., 2004, p. 422).

Using Codes of Ethics for Guidance

As mentioned above, the Code functions as both an ethics reference and a regulatory document. How can we as emergency nurses use the Code and other codes of ethics to help us address ethical dilemmas we are confronted with in the ED? The Code encourages self-reflection and discussion, and asks nurses to ensure that they consider the following when engaging in ethical action: Am I acting in accordance with the Code? Am I practicing the way a reasonable and prudent nurse would practice in this situation? Am I acting with care and compassion in my relationships with others in this situation? Am I meeting professionals and institutional expectations in this action? (CNA, 2017) According to CARNA (2010), the following principles are central to ethical decision making: Autonomy Beneficence Non-maleficence Fairness or distributive justice (p. 10). When faced with an ethical dilemma, one can consider the following framework proposed by Keatings and Smith (2010, p. 78, 79): Determine who is involved (patient? family member? co-worker?). Describe the ethical issue at hand. Assess the situation (e.g., are there other factors that may influence the situation?). Clarify the values of the people involved (e.g., do the patient's cultural or religious beliefs influence this situation? What are my beliefs?). Explore each perspective involved in the dilemma. Identify ethical principles involved in this situation (e.g., justice, autonomy). Clarify any legalities involved (Am I legally obligated to choose a certain course of action?). Explore the options for courses of action (What potential consequences are there to each course?). Decide on a course of action. Determine an action plan (How can I carry out this plan? Who should be involved?). Evaluate the plan (What could have been done differently?).

Cardioversion vs defibrilation and indications for use

Atrial flutter is seen in patients with digitalis toxicity, rheumatic heart disease, hypoxia, and pulmonary disease. The severity of symptoms observed is dependent on the ventricular rate. With rapid ventricular rates, symptoms associated with decreased cardiac output may be noted. Atrial flutter typically converts to either sinus rhythm or atrial fibrillation. This arrhythmia is treated pharmacologically or with cardioversion. Radiofrequency ablation may be utilized for treating chronic or recurrent atrial flutter. ECG Features of Atrial Flutter Rhythm Rate P waves PR Interval QRSRegular with fixed conduction ratio; irregular with variable conduction Atrial: 250-440; ventricular: depends on AV conduction. Sawtooth appearance There are two approaches to treating atrial fibrillation: rate control and rhythm control. Rate control involves administration of medications to slow ventricular rate, but with no intention of converting the rhythm to sinus rhythm. Anticoagulation is also provided to prevent thrombosis formation. Rhythm control is achieved either pharmacologically or via cardioversion. When attempting to convert atrial fibrillation to sinus rhythm, caution must be used because of potential thrombus formation. Conversion to sinus rhythm may dislodge the thrombi, thus producing emboli. ECG Features of Atrial Fibrillation Rhythm Rate P waves PR Interval QRSIrregular Atrial: 350-600; ventricular: variable. None apparent; irregular, disorganized baseline fibulatory waves The term supraventricular tachycardia (SVT) refers to a group of rapid, regular rhythms that originate above the ventricles (i.e., in the SA node, atrial tissue, or AV junction); therefore, SVT encompasses rhythms such as sinus tachycardia, atrial tachycardia, atrial flutter, and junctional tachycardia. If it is possible to differentiate the exact type of tachycardia, then it is preferable to utilize the appropriate name of the rhythm, such as junctional tachycardia. However, due to the rapid rate, the P wave is often hidden within the previous T wave, making it difficult to determine the exact origin of the tachycardia. Typically, this occurs with rates of 180 bpm and above. The term SVT is used when rhythms are rapid and regular, QRS width is normal, and the exact type of the tachycardia cannot be determined. Treatment of SVT includes vagal maneuvers (e.g., Valsalva maneuver, carotid sinus massage), pharmacologic therapy (e.g., Adenosine), and cardioversion. Urgent and emergent arrhythmias may require treatment with countershock, of which there are two types: defibrillation and cardioversion. Countershock causes simultaneous depolarization of all cardiac cells, allowing the dominant pacemaker (SA node) to resume control of the heart. With defibrillation, the delivery of energy is not related to the patient's underlying cardiac rhythm. With cardioversion, however, the delivery of energy is timed to coincide with the patient's QRS, thus avoiding administration of energy during the vulnerable part of the T wave. DEFIBRILATION Indications for defibrillation include the following:Pulseless VT VF Sustained torsades de pointes (polymorphic VT)Early defibrillation is key to recovery of a normal rhythm.There are two types of defibrillators: monophasic and biphasic. The energy they deliver varies, but generally a monophasic defibrillator delivers 360 joules (J), while a biphasic defibrillator delivers between 120J and 200J.Most commonly, hands-free defibrillation pads are placed in the anterolateral position, shown below. The anteroposterior placement may also be used; however, data indicate no difference in success rates (Link et al., 2010).Prior to defibrillation, it is imperative to ensure that the area is clear of personnel. Pads must be placed on dry skin and at least 2.5 cm away from internal pacemakers. If transdermal medication patches are in place, they should be removed and the area wiped clean. CARDIOVERSION Indications for cardioversion include unstable patients with the following rhythms:SVT Atrial fibrillation Atrial flutter VT with pulse As previously indicated, monophasic and biphasic defibrillators deliver different amounts of energy. Cardioversion is synchronized to the patient's underlying rhythm. The machine searches for the tallest R wave (or deepest S wave) and delivers the energy immediately following it, thus avoiding delivery of energy during the T wave.The patient is most often aware of the procedure, thus prior administration of sedation and analgesia is recommended, time permitting. Other safety considerations are similar to those related to defibrillation.Identify at least three differences between cardioversion and defibrillation. List three safety considerations when using cardioversion and defibrillation.Differences between cardioversion and defibrillation Cardioversion is synchronized to the patient's underlying rhythm, while defibrillation is the random delivery of electricity. Cardioversion typically uses a lower electrical dosage than defibrillation. Cardioversion is utilized for unstable rapid arrhythmias, while defibrillation is used for potentially lethal rhythms such as VF and VT. The patient may be awake during cardioversion and therefore may require analgesia and sedation.2. Safety considerations when using cardioversion and defibrillation. Prior to defibrillation, the area must be cleared of personnel. Pads must be placed on dry skin and at least 2.5 cm away from internal pacemakers.If transdermal medication patches are in place, they should be removed and the area wiped clean.

Main drugs used for rhythms, mechanisms of action, indications for use

Atropine - used for heart block Adenosine - used for SVT Epinephrine - used for VF or VT

Etiology of CAD

Both modifiable and non-modifiable factors contribute to the development of CAD. Non-modifiable risk factors include age, gender, family history, and race. Modifiable risk factors include hyperlipidemia, HTN, high-fat diet, obesity, physical inactivity, and smoking. Diabetics are more likely to develop CAD than members of the general population. Metabolic syndrome is a combination of factors that elevates the risk of developing CAD. It is a process that leads to thickening and hardening of the artery walls, characterized by:Accumulation of lipids within the vessel wallsProliferation of vascular smooth muscle cellsFormation of scar and connective tissueThe areas of thickening and infiltration are often referred to as lesions or plaque. As shown in the diagrams below, plaque formation is progressive and may eventually occlude the vessel; more commonly, however, the plaque ruptures and breaks free. Over a period of years, the changes that occur as a consequence of this process can lead to clinical conditions such as the following: How does LDL cause plaque? In the early stages of atherosclerosis, LDL that has entered the artery wall attracts and is engulfed by important immune system cells called macrophages that ingest, or "eat," LDL particles. LDL-laden macrophages become foam cells that promote inflammation and further the development of atherosclerotic plaques. What effect does low-density lipoprotein (LDL) cholesterol have on the atherosclerotic process?Selected Answer:LDL causes the pathological process that occurs with atherosclerosis, creating the build of plaques within the arteries. The high levels of LDL in the blood cause inflammation and affect the endothelial lining of the arteries. Correct Answer:LDL cholesterol is usually described as the "bad" cholesterol because high levels are associated with an increased risk of ACS, stroke, and peripheral arterial disease. LDL cholesterol infiltrates the vessel wall, binds to cells beneath the endothelium, and has an inflammatory effect on the arterial wall. Very-low-density lipoproteins (VLDLs) contain 10-15% of the total serum cholesterol, with most of the triglyceride (TG).

Types of cardiomyopathy

Cardiomyopathies affect the myocardial (middle) layer of the heart. They are classified according to the structural abnormality and genotype (if known). There are two main categories of cardiomyopathies: extrinsic (caused by external forces, such as HTN and valvular dysfunction) and intrinsic (myocardial disease without an external cause). The three types of cardiomyopathy are: dilated, hypertrophic, and restrictive (see Figure 14-20 in Urden et al., 2022, p. 336). Hypertrophic (Obstructive) Cardiomyopathy Hypertrophic cardiomyopathy (HCM) is the second most common cause of sudden cardiac death (SCD) in the adolescent population, and the leading cause of sudden death in competitive athletes; SCD is thought to be due to ventricular dysrhythmias. In approximately 50% of cases, it is a familial disease with autosomal dominant inheritance.HCM is characterized by LV hypertrophy that primarily involves the interventricular septum; the RV may also be involved, but this presentation is less common. LV septal hypertrophy obstructs outflow through the aortic valve, especially during exercise. It pulls the papillary muscle out of alignment, causing a functional mitral regurgitation. Diastolic dysfunction is the most characteristic feature of HCM; the stiff, noncompliant heart muscle cannot fill adequately during diastole .Patient Presentation Patients with HCM are often asymptomatic, or present with mild symptoms such as dyspnea (exacerbated on exertion); presyncope or syncopal episodes are also common. Symptoms may be similar to those of HF, as well as chest pain and palpitations. S1 and S2 heart sounds are usually normal, but a fourth sound (S4) is heard in most patients. Treatment Beta-blockers are the mainstay of therapy for patients with HCM, thus decreasing ventricular workload. Antiarrhythmics may also be used to control/prevent atrial/ventricular dysrhythmias, as well as anticoagulants if AFib or ventricular thrombi are present. Implantable cardioverter defibrillators (ICDs) may be used to prevent SCD, as well as ablation of the interventricular septum. Dilated Cardiomyopathy Dilated cardiomyopathy (DCM) causes 25% of all cases of HF and is the primary indication for cardiac transplantation. Approximately 80% of DCM is of unknown etiology and is considered idiopathic; however, genetics, viral infections, toxin exposure, and excessive alcohol consumption are also risk factors for the development of DCM.DCM is characterized by progressive ventricular dilation, without hypertrophy, resulting in impaired pumping ability of one or both ventricles. Although all four chambers of the heart are affected, the ventricles are more dilated than the atria. Hemodynamically, dilated cardiomyopathy is characterized by bilateral impairment of contractility and EF (< 40%), which results in increased preload and decreased stroke volume (due to dilated heart). As the ventricles continue to dilate, the mitral and tricuspid valve leaflets separate leading to valvular insufficiency. DCM can be further divided into two categories: ischemic (e.g., MI) and nonischemic (e.g., infection, heavy alcohol use) cardiomyopathy. Patient Presentation As a result of systolic pump failure, the patient presents with symptoms of biventricular HF (e.g., dyspnea, fatigue, pulmonary congestion), with anginal chest pain occurring in approximately ⅓ of patients. Murmurs are frequently heard because the ventricular dilation displaces the papillary muscles of the AV valves and inhibits the leaflets from completely closing, as discussed above. CXR shows an enlarged cardiac silhouette and increased cardiothoracic ratio. Other sequelae include rhythm disturbances (e.g., AFib, ventricular ectopic beats), intracoronary thrombi, and hepatomegaly if significant tricuspid insufficiency. Treatment Interventions include those initiated for HF:Diuretics and nitrates to decrease preloadACE inhibitors to decrease afterloadPositive inotropic agents (e.g., Digoxin) to increase the force of contraction and stroke volumeBeta blockers (e.g., Carvedilol), administered cautiously to decrease HR and cardiac workloadAmiodarone, if ventricular ectopy and high risk of SCD Cardiac resynchronization therapy/ICDs Restrictive Cardiomyopathy Restrictive cardiomyopathy (RCM) is the least common form of cardiomyopathy. It is a heart muscle disease that results in restricted ventricular filling due to increased myocardial stiffness and noncompliance. The overall effect is diastolic dysfunction, DHF, and low cardiac output. Patient Presentation In addition to DHF, clinical manifestations include dyspnea, orthopnea, and liver engorgement. Increased jugular venous pressure (JVP), extra heart sounds (S3 and S4), and pericardial effusion may also be present. TreatmentMedical management of RCM is primarily symptom-focused. Beta blockers, diuretics, ACE inhibitors/ARBs, and Na+/water restrictions may be prescribed.

Reportable Conditions

Communicable Disease The ED often acts as the gatekeeper to health conditions that surface in the community. As such, emergency staff members are commonly involved in notifying medical officers of health about suspected or confirmed cases of infectious disease. Every province and territory has public health policy around reportable diseases and conditions, which should be clearly posted in emergency departments. Question to Ponder:Do you know where to find the list of reportable conditions at your workplace? Gunshot and Stab Wounds Since 2010, Alberta has had in place a Gunshot and Stab Wound Mandatory Disclosure Act, which makes it mandatory for: Staff working in health-care facilities such as emergency departments to report when a gunshot or stab wound is treated/treatment is offered. Staff to report these occurrences as soon as reasonably possible without interfering with the patient's treatment. Health-care facilities must have a designated individual (such as a safety officer) who is responsible to make these disclosures on behalf of the facility to local police (AHS, 2010). Health-care institutions are mandated to release the patient's name and injury type to the police. All provinces and territories have mandatory reporting regulations; nurses are encouraged to become familiar with their respective documents and ensure their workplace has institution-specific guidelines for reporting communicable diseases, gunshot wounds, and stab wounds. Communicating with Police A unique aspect of emergency nursing is frequent interaction with law enforcement. It is a common daily occurrence to receive patients who are victims of motor vehicle collisions, patients who are brought in under police custody and require emergency treatment, patients who are under the influence of alcohol or drugs, and patients who were injured while engaging in illegal activities. In these and many other cases, emergency nurses may be approached by police who are looking for specific information about patients. According to the CNPS (2014b): The criminal justice system is complex and its intersection with health care can lead to challenging legal, professional and ethical issues. Nurses should therefore understand their ongoing obligation of patient confidentiality, when they may disclose personal health information (PHI) to police, how much information to disclose, when they need to refer to a police inquiry to higher authority and when it would be prudent to decline to respond to police inquiries (p. 1).Confidentiality and Personal Health Information

Witnessing Unethical or Incompetent Care

Competence as an emergency nurse is of utmost importance in order to quickly intervene with patients and do so safely under the duress of high patient volume and little time. If a colleague is demonstrating incompetent or unethical practice, patient safety is at risk. It is important for nurses to know their obligations regarding patient safety—even when it comes to the practice of others. Practice Question 4 Unethical or Incompetent Care Review pages 33 to 35 in the Code, (Appendix B), and answer the following questions: Questions: What should we do if we see a colleague providing unethical or incompetent care to patients? What are our ethical responsibilities? What are our legal responsibilities? (More on this in the next section). Nurses are ethically obligated to "question, intervene, report and address unsafe, non-compassionate, unethical or incompetent practice ..." (CNA, 2017, p. 33). Nurses must also be "attentive to signs that a colleague is unable, for whatever reason, to perform their duties," and patient safety should be at the forefront (CNA, 2017, p. 33). For example, supervisors or managers should be alerted of any medication errors made by a colleague (if the colleague does not report this), misuse of restraints, any verbal abuse or belittlement of patients, or any breach of a patient's confidentiality by a colleague. Nurses may be found legally negligent if they are aware of a colleague's unethical or incompetent care and they withhold that information from their employers and the regulatory college, and a patient suffers damages from the actions. More on this topic in the next section.

Confidentiality and Personal Health Information

Consent Consent is defined as the patient's acknowledgement and acceptance of treatment (Hammond & Zimmerman, 2013, p. 5). As a reminder, there is no age of consent in Canada, such that a child's consent to or refusal of treatment is based not on their age, but by their ability "to understand the information that is relevant to making a decision about the treatment...and be able to appreciate the reasonably foreseeable consequences of a decision or lack of decision" (Government of Ontario, 2020, section 4[1]). Anyone intervening with a patient needs to obtain either verbal consent (the usual mode) and/or written consent (in the case of procedures) prior to doing so (CNPS, 2018). Informed Consent It is considered negligent to fail to disclose to patients all the risks associated with a procedure or intervention we are about to perform. Failure to obtain consent at all would legally be considered battery (Keatings & Smith, 2010, p. 163).Essential components of informed consent: Description of intervention to be performed Alternatives available to the intervention if applicable Risks and benefits of the intervention Patient's understanding of the risks, benefits, and alternatives (i.e., have them repeat to you their understanding of these) (McConnell, 2018, p. 678). Implied Consent This type of consent is inferred from patient conduct, for example, after a nurse explains that a patient is overdue for a tetanus shot, the patient exposes a shoulder for the injection (Keatings & Smith, 2010, p. 162). Implied consent also applies to situations when an "individual is in a life- or limb-threatening situation and is unable to provide expressed consent" (McConnell, 2018, p. 678). Capacity Integral to obtaining consent, is determining whether a patient has the capacity to make that decision. Capacity is the ability to make an informed decision about one's own care, such that there is understanding of the nature, risks, benefits, and consequences of consenting or refusing the intervention in question (AHS, 2020, p. 6). Practice Question 7 Read the article below, and answer the following questions regarding consent and capacity: Canadian Nurses Protective Society (CNPS). (2018, June). Consent to treatment: The role of the nurse. https://cnps.ca/article/consent-to-treatment/ (Original work published 1994) Questions: How do you determine that your patient has the capacity to consent? What is considered valid consent by the Canadian court system? A patient can also be deemed legally incapacitated to make health-care related decisions by a formal, in-depth process (discussion of which is beyond the scope of this module), where either written advance directives are activated, or there is a substitute/alternate decision-maker appointed for decision making going forward. In the ED setting people may approach you looking for patient information, and may present themselves to you as a person legally able to make decisions for your patient. Let's address some important definitions related to capacity and decision making: Co-Decision Maker In most jurisdictions, if a person is impaired but can still participate in decision-making, another person may be appointed by court as a co-decision maker to assist in making medical decisions. This could be a family member or a friend selected by the patient (AHS, 2020, p. 6). Legal Guardian In most cases, the legal guardian of a minor is a parent with custody; however, we must not assume that is always so. A legal guardian could be either a relative or non-relative who has court-appointed guardianship for that child (Keatings & Smith, 2010, p. 178, 179). Substitute Decision-Maker (SDM) This is a legal concept used to describe someone who is by law entitled to make decisions for a patient who lacks capacity (Government of Ontario, 2020). Power of Attorney (POA) for Personal Care This is a type of substitute decision maker who is court-appointed to make health-related decisions for a patient once he or she loses capacity to do so (Keatings & Smith, 2010, p. 176). Living Will A specific legal document drawn up directing the care a patient wishes to have (usually at end-of-life), that takes effect once a patient is incapacitated (Government of Alberta, 2009; Keatings & Smith, 2010, p. 173). Advance Directives These directives are synonymous with living wills, which can be verbal (but are usually written) instructions that outline a person's specific wishes for care if rendered incapacitated (Keatings & Smith, 2010, p. 160). The most typical example of a written advance directive is a do-not-resuscitate order (DNR) (Keatings & Smith, 2010). Personal Directives In Alberta, personal directives are used instead of POAs for personal care or living wills; they are essentially the same, wherein a legal document allows a person to name an agent to make decisions on her or his behalf once incapacitated, and includes specific instructions regarding elements of healthcare such as resuscitation wishes (AHS, 2020). Specific Decision-Maker If a patient is incapacitated (either formally declared so, or is very ill and/or under the influence of a mind-altering substance), and there is no formal legal decision-maker such as a SDM, POA or agent listed in a personal directive, and the decisions that must be made are time-sensitive, consent can be obtained by choosing a specific decision-maker in the following ranked order: spouse or adult interdependent partner; adult son or daughter; father or mother; adult brother or sister; grandfather or grandmother; adult grandson or granddaughter; adult uncle or aunt; or adult nephew or niece (Province of Alberta, 2013, p. 8). AND . . . the relative selected: is 18 years of age or older; is willing and available to make the decision; is able to make the decision; has been in contact with the Patient in the previous 12 months; has knowledge of the Patient's wishes respecting the decision or of the beliefs and values of the Patient; and does not have a dispute with the Patient that might affect his/her ability to perform the duties of a Specific Decision-Maker (Province of Alberta, 2013, p. 71). Note that criteria for specific decision-makers may vary slightly between provinces and territories. Do-Not-Resuscitate (DNR) The issues around DNR orders will be further explored in the End of Life Issues module, but resuscitative decisions are so prominent in the ED that some review must be part of this module as well. As mentioned earlier, DNR is one of the most common advance directives, but often brings with it family dynamics and questions about decision making which can be challenging to address in the chaotic ED setting (ENA, 2018c). Unfortunately, a great many people do not have advance directives in place, and decisions about resuscitation are often left to a time when a person's health has deteriorated, making decisions around DNR challenging for everyone involved (ENA, 2018c). It is important that emergency nurses advocate for advanced care planning, and educate patients and their families about planning options (ENA, 2018c). The concept of DNR is not a clear one, and leaves open to interpretation whether it implies no resuscitation efforts at all (such as intubation, fluids, and transfusion), or just no CPR. It can also lead to confusion and worry by patients who may be afraid that DNR will mean "do not treat," and health-care providers may misinterpret it this way as well.It is very important that nurses and physicians ascertain a patient's DNR status as soon as possible in the emergency department, and that patients understand the implications of DNR. If the patient does not have the capacity to determine their status and there is no written DNR order, we must determine who has the legal authority to make decisions for that patient (as above in the section on capacity). Emergency nurses need to know their own provincial regulations when it comes to DNR, as some provinces (Ontario, for example), legally allow SDMs, POAs, and others with legal decision-making power to oppose a DNR order after a patient no longer has capacity to decide or is unconscious (Government of Ontario, 2020; Wright, 2015). That being said, most provincial and territorial laws make it illegal for legally binding DNR orders made when a patient was of sound mind to be disregarded by POAs or physicians.

Murmurs (systolic vs diastolic)

Disorders of the aortic valve Aortic stenosis is characterized by valvular inflammation, fibrosis, and calcification; the valvular pathogenesis results in a structural resistance to ejection and an increased afterload. The LV becomes hypertrophied and dilated in order to compensate, greatly increasing myocardial O2 consumption. Patients have difficulty increasing their cardiac output because of the obstruction, and therefore experience symptoms similar to those of HF (e.g., angina, exertional dyspnea, syncope), and SCD. Patients with aortic stenosis present with a systolic murmur best heard over the aortic area of the precordium.Aortic regurgitation (insufficiency) results in backward flow from the aorta to the LV. The aortic valve is normally closed during ventricular diastole (relaxing, filling); however, in aortic regurgitation, the thickened and retracted valve permits blood return from the aorta to the LV. This causes decreased forward cardiac output, but an increase in LV volume and pressure which eventually backs up into the LA and pulmonary vasculature. Patients present with a low diastolic pressure, widened pulse pressure, and a bounding pulse. Recall that the coronary arteries are perfused during diastole, thus aortic insufficiency may also result in angina symptoms. Fatigue, dyspnea (also on exertion), and palpitations, in addition to a diastolic murmur best heard over the aortic area of the precordium, are also likely manifestations. Aortic stenosis is characterized by valvular inflammation, fibrosis, and calcification; the valvular pathogenesis results in a structural resistance to ejection and an increased afterload. The LV becomes hypertrophied and dilated in order to compensate, greatly increasing myocardial O2 consumption. Patients have difficulty increasing their cardiac output because of the obstruction, and therefore experience symptoms similar to those of HF (e.g., angina, exertional dyspnea, syncope), and SCD. Patients with aortic stenosis present with a systolic murmur best heard over the aortic area of the precordium.Aortic regurgitation (insufficiency) results in backward flow from the aorta to the LV. The aortic valve is normally closed during ventricular diastole (relaxing, filling); however, in aortic regurgitation, the thickened and retracted valve permits blood return from the aorta to the LV. This causes decreased forward cardiac output, but an increase in LV volume and pressure which eventually backs up into the LA and pulmonary vasculature. Patients present with a low diastolic pressure, widened pulse pressure, and a bounding pulse. Recall that the coronary arteries are perfused during diastole, thus aortic insufficiency may also result in angina symptoms. Fatigue, dyspnea (also on exertion), and palpitations, in addition to a diastolic murmur best heard over the aortic area of the precordium, are also likely manifestations. disorders of the tricuspid valve In adults, valvular disorders of the right side of the heart are less common than those of the left side. They are most commonly associated with left-sided disorders resulting from rheumatic fever. Tricuspid stenosis is similar to mitral stenosis in that it limits blood flow from the RA into the RV. The RA becomes enlarged, and volume overload in the systemic venous system causes JVD, ascites, peripheral edema, and possible hepatomegaly and splenomegaly. Patients with tricuspid stenosis present with a diastolic murmur best heard over the tricuspid area of the precordium.Tricuspid regurgitation results in backward flow from the RV to the RA. During ventricular systole, the regurgitant tricuspid valve allows blood to flow retrogradely into the RA, thus causing atrial enlargement and increased systemic venous engorgement. The symptoms are similar to those of tricuspid stenosis, except that patients present with a systolic murmur best heard over the tricuspid area of the precordium.

Confidentiality

Each province and territory has its own privacy laws, but they all stem from the Federal Privacy Act, and the Personal Health Information and Electronic Documents Act (Office of the Privacy Commissioner of Canada, 2018). It is important that nurses become familiar with confidentiality standards as outlined by their regulatory college. Nurses have both an ethical and a legal responsibility to respect and maintain privacy and confidentiality of patients. Hammond & Zimmermann (2013) highlight the importance of confidentiality to the relationship emergency nurses have with their patients, and point out that patients have an expectation that their personal health information will be respected and confidentiality maintained. Recall from the Code (CNA, 2017, pp. 14-15): Nurses must take reasonable measures to make sure that confidential information is not overheard. Nurses collect, use, and disclose health information on a need-to-know basis, and in accordance with privacy laws. Nurses must disclose only what is necessary and within the circle of care. Avoid patient identifiers when discussing a clinical case with other nurses, unless absolutely necessary or within the circle of care. Nurses must refrain from accessing patient information when not within the circle of care, and from accessing information of a family member or friend. What makes maintaining confidentiality in the emergency department particularly challenging? Overcrowding: this unavoidable state within emergency departments makes confidentiality difficult to maintain and makes it difficult to obtain histories and accurately assess patients while at the same time trying to respect patient privacy and confidentiality (Rapaport, 2018). However, in a lawsuit, systemic issues such as overcrowding will not absolve individual practitioners of responsibility if their care falls below standard expectations (CNPS, 2010, para. 2). Visible patient identifiers: white boards, charts, et cetera can be scattered on desks. High stress environment: it is difficult to ensure that all charts are closed and patient identifiers secured when nurses are pulled away from charting to attend to an emergency. Often, priorities reflect responsive patient care, and privacy and confidentiality can be compromised unintentionally as a result. Emergency nurses must remain mindful of this. High traffic areas: family members often wander through the department looking for their loved ones, and can stumble upon an open patient chart or overhear a phone call at the desk. With a lack of beds, patients may receive care in the hallway or behind a simple curtain, allowing private information about patients to freely float around the department. Read Read the following articles, which highlight the realities of overcrowding and hallway health care as a unique challenge to the emergency department, and describe the impact of such challenges on patient care and confidentiality: Rapaport, L. (2018, February 28). Another reason to worry about overcrowded emergency rooms. Thomson Reuters, Reuters Health. https://www.reuters.com/article/us-health-emergency-overcrowding-hallway/another-reason-to-worry-about-overcrowded-emergency-rooms-idUSKCN1GC2WQ Stoklosa, H., Scannell, M., Ma, Z., Rosner, B., Hughes, A., & Bohan, J. S. (2018). Do EPs change their clinical behaviour in the hallway or when a companion is present? A cross-sectional survey. Emergency Medicine Journal, 35(7), 406-411. https://emj.bmj.com/content/emermed/35/7/406.full.pdf Note: While the article by Stoklosa et al. (2018) is about ED physicians, the message could easily translate to the challenges experienced by emergency nurses. Another major challenge to maintaining confidentiality in the ED is social media. There is no denying that "the ease with which information can be distributed presents challenges to both privacy and professionalism" (ENA, 2018d, p. 2). Read Read ENA's position statement on social media, which poses a good reminder to emergency nurses about the expectations for sensible use of this ubiquitous technology, and how detrimental it can be to use social media to post about patients or an institution. Emergency Nurses Association (ENA). (2018). Position statement: Social networking by emergency nurses. https://www.ena.org/docs/default-source/resource-library/practice-resources/position-statements/socialnetworkingbyernurses.pdf?sfvrsn=5e069b1a_8 As a real-life recent example of the legal and ethical implications of social networking, follow the link below outlining the case of a Saskatchewan RN who was found guilty of professional misconduct after she posted online her personal thoughts about the care provided to her grandfather at another health-care facility: CBC News. (2016, December 3). Nurse who 'vented' online found guilty of professional misconduct. CBC. https://www.cbc.ca/news/canada/saskatchewan/srna-discipline-social-media-nurse-saskatchewan-1.3880351 Consider these questions when you review this case: Why was the RN found guilty of professional misconduct when she wasn't working as a nurse at the facility at the time the comments were made? What impact did her public comments have on the staff working at the facility in question? How do you think these comments might change public perception of the workplace in question?

ECG complexes and what each component represents

Each small square of the ECG graph paper is 1 mm × 1 mm (Figures 1.4 and 1.5). In basic ECG interpretation, the horizontal markings are of greater significance than the vertical markings because they measure the elapsed time, or the time taken for individual events. Each small marking represents 0.04 seconds, and these are grouped in sets of five by heavier lines that represent 0.20 seconds (5 × 0.04 = 0.20). Thus, a complex that extends over 3 small squares represents 0.12 seconds (3 × 0.04 =0.12). Most single-lead monitoring is performed using Lead II. When using Lead II, the monitor will assign the role of negative electrode to the electrode located on the upper right chest. The electrode located on the lower left chest will be assigned the role of positive electrode. If using a three-cable system, the remaining electrode will be ground. If using a five-cable system, any of the other electrodes can theoretically be the ground, but traditionally it is the electrode located on the upper left chest. The advantage of Lead II is that it generally produces clear, upright waves and complexes that represent atrial and ventricular depolarization. These events are produced by vectors (electrical currents) traveling through the heart tissues toward the positive electrode. When current flows toward a positive electrode, the resulting waveform is upright. This is demonstrated in Figure 1.7a. Waveforms are created on an ECG by electrical currents as they travel through the cardiac tissue. If these currents, or vectors, are travelling toward a positive electrode, a positive (upright) deflection will result. Conversely, if the vector is traveling away from the positive electrode, a negative (inverted) deflection is seen. If the vector is moving perpendicularly toward a point between the negative and positive electrodes, the wave is biphasic (a combination of positive and negative deflections).The size of the muscle mass involved will determine the amplitude of the wave produced. Thus, the wave produced by the depolarization of the atria will be smaller than the wave (or complex) resulting from the depolarization of the ventricles, which represent a larger muscle mass.A period of no electrical activity will produce a flat line, or isoelectric line. P Wave The first wave seen on the ECG is the P wave produced by the depolarization of the atria. This is a small, upright, rounded deflection. The sinoatrial (SA) node generates the impulse, which then travels rapidly throughout atrial tissue toward the atrioventricular (AV) node. The mean, or average, direction of the current is toward the positive electrode of Lead II, and therefore causes an upright deflection (Figure 1.9.)If the P wave is inverted in Lead II, it indicates that the SA node was not the source of atrial depolarization. Similarly, if the P wave is absent, this also implies that the SA node is not firing. Normally, the P wave is followed by a QRS, but this is not always the case (Figure 1.10). PR Interval The PR interval (PRI) indicates the time taken from the start of atrial depolarization until the end of conduction through the AV node. The PRI is normally between 0.12 - 0.20 seconds (Figure 1.11). A PRI less than 0.12 seconds indicates that (a) the source of the impulse is not the SA node, or (b) the impulse bypasses the AV node completely, such as occurs with an accessory pathway. Longer values are produced by impaired conduction through the AV node (Figure 1.12). QRS Complex The QRS complex represents the time required for the depolarization of the ventricles. It is composed of a group of waves (Q, R, and S) that are produced by changing vectors as the ventricles are activated. Not all of these waves may be readily visible in the complex due to various factors; thus, in bedside monitoring, they are not examined individually, but as a whole.The QRS is measured from the point at which the first wave leaves the baseline until the point at which the last wave begins to flatten out into the ST segment (J point, J junction). This end point could be above, below, or on the baseline. Generally, the QRS complex is considered normal if it is less than or equal to 0.11 seconds in duration (< 0.12 seconds) (Aehlert, 2013; American Heart Association, 2011), meaning the complex originated from above the ventricles; however, a QRS of 0.11 seconds may be considered borderline (Morton et al., 2013). Wider QRS complexes (≥ 0.12 seconds) indicate slowed or abnormal conduction through the ventricles resulting from bundle branch blocks (BBBs), abnormal conduction pathways, or ectopic impulse generation (Figures 1.13 and 1.14) .Difficulties are often experienced by novice practitioners in the measurement of the QRS complex. Remember, this measurement should be done from the beginning of the complex to the end, that is, from the point it leaves the baseline to the J point. Because of altered shapes of the QRS complex and positioning of the ST segments, it is sometimes difficult to locate these points. ST Segment The ST segment starts at the end of the QRS complex (J point) and ends with the onset of the T wave. It depicts events from the end of ventricular depolarization to the beginning of ventricular repolarization. This segment is normally flat or isoelectric in comparison to the PR segment. Elevation or depression greater than one millimetre (one small square) in two or more contiguous leads may indicate pathology. This may be the result of many different factors, including myocardial ischemia and infarction, pericarditis, ventricular hypertrophy, and digitalis effect. If a change in ST segment is noted, it is recommended that a 12- or 15-lead ECG be obtained. The ST segment is shown in Figure 1.15. T Wave The T wave begins as the tracing moves from the ST segment and ends when the wave returns to the baseline. It represents ventricular repolarization. The normal T wave is rounded and slightly asymmetrical, with the initial slope steeper than the downward slope, and is normally in the same direction as the preceding QRS complex. As with changes in the ST segment, alterations in the T wave indicate abnormal ventricular repolarization, which may be a result of myocardial ischemia and infarction, abnormal serum potassium levels, and drug effects (e.g., procainamide, quinidine). Figures 1.16 and 1.17 demonstrate the T wave. QT Interval The QT interval is measured from the onset of the QRS complex to the end of the T wave. It indicates the time taken for ventricular depolarization and repolarization. The QT interval is dependent on the heart rate, age, and gender, with a shorter interval occurring with faster heart rates. Thus, the value for a normal QT interval is not a fixed time. Instead, a normal guideline would be one half the distance between two consecutive R waves (i.e., less than one half the RR interval). The QT interval is often corrected (QTc) for heart rate by using the formula QTc = QT divided by square root of RR interval. Normal QTc is less than 0.46 seconds in women and less than 0.45 seconds in men. A prolonged QT interval indicates that the time for depolarization and repolarization of the ventricles is increased. This may have serious consequences because it leaves the heart vulnerable to lethal dysrhythmias resulting from electrostimulation during the relative refractory period. Causes of prolonged QT intervals include electrolyte imbalances, drug toxicity, and slow heart rates (bradycardias) (Figures 1.18 and 1.19). U Waves U waves may or may not be present on an ECG. If present, a U wave is seen as a small, rounded deflection following the T wave and preceding the next P wave, and represents the latter phase of ventricular repolarization. A U wave may be the result of electrolyte imbalance, medications, hyperthyroidism, or long QT syndrome.

Nursing Qualifications and Competency

Emergency nursing is unique in that its body of knowledge encompasses all physiological processes from birth to death, requiring skilled application of the nursing process to patients of all ages and acuity within a stressful, chaotic and dynamic environment (NENA, 2018). NENA is the professional association for emergency nurses in Canada and, as such, sets the scope and standards of Canadian practice for emergency nursing. The triage process requires the knowledge and experience of a seasoned emergency nurse. The triage nurse must be able to rapidly assess patients' needs (physiological, psychosocial, spiritual) while taking into account patient flow through the ED and broader system (i.e., inpatient units, patient transfers, diagnostic imaging) (NENA, 2018). The specific qualifications of the staff emergency nurse are outlined below, followed by the additional qualifications of the triage nurse. Staff Emergency Nurse Minimum TWO years acute care, medicine/surgery experience in an active treatment setting is preferred Emergency nursing recognizes the need to develop and train new graduates in the skills and knowledge needed to become specialized as an emergency nurse Competence in: Basic Life Support (BCLS) protocols Advanced Cardiovascular Life Support (ACLS) protocols Pediatric Advanced Life Support (PALS) protocols Additional Courses and Qualifications recognized by NENA: Emergency Practice, Interventions and Care - Canada (EPICC) Trauma Nursing Core Course (TNCC) Emergency Nursing Pediatric Course (ENPC) Course on Advanced Trauma Nursing (CATN II) Emergency Nurse Certified (C)anada (ENC(C)) Current registration (RN) with Provincial/Territory Body Successfully completes a comprehensive orientation program to ensure competency in the care of the patient (NENA, 2018, p. 1) Triage Nurse The triage nurse shall meet specified qualifications for employment (in addition to those stipulated above). Minimum TWO years recent emergency nursing practice Demonstrated competence in emergency nursing practice Displayed acquisition of advanced assessment, interviewing and interpersonal skills Trained in current Canadian Triage and Acuity Scale (CTAS) (NENA, 2018, p. 1) Travers (2018) identifies the following more specific qualifications of the triage nurse: Strong interpersonal skills; Ability to conduct a brief, focused interview; Strong physical assessment skills; Ability to make rapid, accurate decisions; Ability to work collaboratively with other members of the health care team; Ability to adjust to workload fluctuations; Ability to effectively communicate understanding of patient and family expectations; Understand cultural and religious concerns that could arise at triage; and Possess knowledge of specific institutional policies affecting triage [e.g., patient diversion] (pp. 23-24). It is important for the emergency nurse to remember that triage does not end once an acuity level is assigned by the triage nurse. Triage is a "snapshot of the patient's status at the time of initial presentation to the ED" (Travers, 2018, p. 23). Patients' conditions and priorities of care may change after triage, thus all emergency nurses must possess the necessary competencies to safely care for patients with varying acuity levels.

Endocarditis vs pericarditis

Endocarditis Infectious endocarditis results in bacterial or fungal growths most commonly found on the leaflets of cardiac valves. Other cardiac structures may also be involved, including the chordae, chamber walls, and fistulas. The highest incidence of endocarditis is found among IV drug abusers and patients with a pre-existing structural (valve) abnormality. Complications include HF and systemic emboli, which markedly decrease circulation to vital organs. Patient Presentation The patient may present with fever, fatigue/malaise, as well as muscle and joint pain; cough and pleuritic chest pain are also common symptoms.Blood cultures and a CXR are utilized to diagnose endocarditis, in addition to an ECHO which provides better visualization of the cardiac valves. Treatment Management of endocarditis involves long-term IV antimicrobial therapy. When the patient has stabilized, valve surgery may be required to repair or replace the affected valve(s). Nursing interventions include timely antimicrobial administration, symptom relief (e.g., analgesia), vigilant physical assessment to identify new emboli, and patient education. Pericarditis Pericarditis is inflammation of the pericardial layer (pericardial sac). The damaged epicardium becomes rough and inflamed, and the capillaries that supply the pericardium become permeable to plasma proteins. This results in an exudate that varies in type and amount according to the causative agent; the exudate irritates the pericardium, and pericarditis occurs. The more extensive the inflammation, the more exudate effuses into the space between the parietal and visceral layers . If this pericardial effusion is significant, a pericardiocentesis may be required to remove excess fluid from the pericardial space. If the condition progresses, accumulated fluid may compress the adjacent cardiac structures and impair cardiac filling, resulting in cardiac tamponade. Cardiac Tamponade Cardiac tamponade can present as either a symptom or an injury; it may be associated with pericarditis, pericardial effusion, trauma, and a ruptured or dissecting aneurysm. It is due to the progressive accumulation of blood or fluid in the pericardial sac (space). If the fluid entering the pericardial space increases to the point that diastolic filling is compromised, a tamponade

Treatment of ACS

First 10 minutes Assess vital signs, including SpO2 (continuous cardiorespiratory monitoring) Obtain 12-lead ECG, and 15-lead/right-sided ECG if indicated Establish IV access Obtain blood for laboratory studies (i.e., complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine (Cr), glucose, magnesium (Mg2+), Ca2+, phosphorus (PO4-), [activated] partial thromboplastin time (aPTT), prothrombin time/international normalized ratio (PT/INR), creatine kinase-muscle/brain (CK-MB), and/or troponin (I or T) Obtain brief focused history, perform physical examination Complete fibrinolytic checklist, assess for contraindications Obtain and review portable chest x-ray (CXR) within 30 minutes of arrival (rule out aortic dissection)**Results of CXR, cardiac markers, and other laboratory investigations should not delay reperfusion therapy** Patient General Treatment The following initial steps should be taken for all patients who present with signs/ symptoms suggestive of ischemia or infarction:Oxygen, if hypoxemic (SpO2 ≤ 90%) or signs of heart failure Start at 4 L/min, titrate to maintain SpO2 ≥ 90% Aspirin inhibits platelet aggregation (thromboxane A2 production) and should be administered as soon as possible after patient presentation; platelets are the principal and earliest participants in thrombus formation, whose inhibition has also been shown to reduce coronary reocclusion and other recurrent events. Unless the patient has a true allergy to aspirin or a recent history of gastrointestinal (GI) bleeding, the initial dosage is 162-325 mg chewed. Other non-steroidal anti-inflammatory drugs (NSAIDs) cannot be substituted for aspirin due to increased risk of mortality. Nitroglycerin is administered sublingually (pill or spray), and is one of the first medications given to reduce myocardial workload. It is a potent venodilator, thus reducing venous return, preload, myocardial wall tension, and myocardial O2 consumption. It also dilates coronary arteries and therefore increases coronary artery blood flow. Nitroglycerin may cause hypotension, reflex tachycardia, and headache.Nitroglycerin should be given with caution in the following circumstances:Systolic blood pressure (SBP) < 90 mmHg or > 30 mmHg below baseline Severe bradycardia or severe tachycardia Suspected RV or inferior wall infarction Patient has taken medication for erectile dysfunction (e.g., sildenafil, vardenafil) within past 24 hours, or tadalafil within 48 hours Opiate (e.g., Morphine). Morphine may be given IV to help control chest pain that is unresponsive to nitrates. It is a venodilator that helps to redistribute volume away from the heart, thus decreasing preload and cardiac workload. Morphine also decreases systemic vascular resistance (SVR), which reduces LV afterload (AHA, 2016).In the case of NSTE-ACS, however, morphine must be used with caution due to its association with increased mortality .Monitor the patient to ensure appropriate response to treatment, and adjust treatment as indicated Observe for adverse side effects of treatmen tCarefully observe for progression to more severe ischemia or infarction Treatment of Low- / Intermediate-risk ACS Treatment for this group involves potential admission to an ED chest pain unit or appropriate bed for further monitoring and/or intervention. The interventions outlined above, as well as select adjunctive therapies (e.g., beta-blockers), treadmill stress test and/or serial ECGs and cardiac biomarkers are recommended (Amsterdam et al., 2014). Treatment of NSTEMI (NSTE - ACS) Abnormal biomarkers distinguish a NSTEMI from unstable lesions (angina). Early risk stratification of NSTEMI is the cornerstone of treatment in order to identify high or intermediate risk patients who require cardiac catheterization. Initial treatment of a NSTEMI includes the interventions described above.Without visual confirmation of ST-segment elevation on the 12-lead ECG, patients cannot receive immediate IV fibrinolytic agents, but they can be appropriately managed in the cardiac catheterization laboratory (i.e., percutaneous coronary intervention [PCI], see below) and receive glycoprotein (GP) IIb/IIIa inhibitor therapy. Treatment of STEMI Ultimately, the goal is to optimize O2 supply to the area of the heart that is affected, in other words, to improve O2 supply while reducing myocardial O2 demand. Most out-of-hospital deaths due to STEMIs are the result of the sudden development of VFib. The vast majority of deaths due to VFib occur within the first 24 hours of symptom onset, and of these, over ½ occur in the first 30 minutes. As outlined above, steps should be taken to ensure patients receive prompt assessment, diagnosis, and interventions from the moment they arrive in the emergency department (ED) or critical care area.A patient with ST-segment elevation of at least 1 mm in two contiguous leads (next to one another) should be considered a candidate for reperfusion therapy to restore blood flow to the infarcted area of the myocardium. There are three reperfusion approaches: pharmacological fibrinolytic therapy, PCI, and coronary artery bypass grafting (CABG). Short- and long-term outcomes are improved regardless of whether reperfusion is achieved via fibrinolytics or PCI, although PCI is the preferred reperfusion strategy. A discussion of CABG is beyond the scope of this module. As the reperfusion method is being selected, routine management of the STEMI patient includes the interventions outlined above where appropriate (i.e., oxygen, aspirin, nitroglycerin, morphine). Fibrinolytic Therapy The main goal of fibrinolytic therapy is prompt restoration of full coronary arterial patency, and should be administered within 30 minutes of first medical contact or hospital arrival (ED door-to-needle time). Fibrinolytic therapy should be considered in patients who present with ST-segment elevation > 2 mm in leads V2 and V3 and 1 mm or more in all other leads, or by new/presumed new LBBB (AHA, 2016). Fibrinolytic therapy is generally recommended if the onset of symptoms is within 12 hours of presentation, with qualifying ECG findings, and if PCI is not available within 90 minutes of first medical contact. It may be considered beyond this timeframe in the setting of persistent chest discomfort and ST-segment elevation (AHA, 2016).A risk assessment for bleeding must be performed before administering fibrinolytics. Absolute contraindications to receiving fibrinolytic therapy include the following:Any previous intracranial hemorrhage Known structural cerebral vascular lesion (e.g., arteriovenous malformation [AVM]) Known intracranial neoplasmIschemic stroke within the past 3 months (except acute ischemic stroke being treated with fibrinolytics) Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses)Significant closed head or facial trauma within the past 3 months The two broad categories of fibrinolytics are fibrin-selective and non-selective agents. Fibrin-selective agents are clot-specific and lyse clots quickly, while non-selective agents (e.g., Streptokinase) provide more systemic and prolonged lytic states (less commonly used today).Fibrin-selective agents include tenecteplase (TNK), alteplase (tissue plasminogen activator, tPA, rt-PA), and reteplase (recombinant plasminogen activator, rPa). Protocols exist regarding administration of fibrinolytics; it is imperative to monitor the patient for occult or overt bleeding after treatment with a fibrinolytic agent. Percutaneous Coronary Intervention (PCI) 'Primary' PCI is the recommended method of reperfusion therapy, and should be performed within 90 minutes of hospital arrival (ED door-to-balloon inflation). Procedures presently available include percutaneous transluminal coronary angioplasty (PTCA), coronary atherectomy, coronary stent placement, and brachytherapy. The most commonly performed procedures are PTCA and stent placement. With PTCA, a wire is placed across the lesion and a prepared balloon is placed over the wire and inflated several times to push back the plaque (see Figure 15.11 in Urden et al., 2022, p. 384). 'Rescue PCI', now referred to as pharmacoinvasive strategy, refers to PCI performed within 6-12 hours of ineffective fibrinolysis in patients who continue to experience myocardial ischemic symptoms 90 minutes post-fibrinolysis.Coronary stents are designed to be expanded and implanted into the lesion of the coronary artery to prevent restenosis after PTCA. Stents are coated with a drug or material to prevent or lessen the normal inflammatory response that could contribute to restenosis (see Figure 15.14 in Urden et al., 2022, p. 385).Coronary atherectomy is a procedure in which plaque is removed by a burr rotating at high speeds. Brachytherapy involves local radiation of the coronary artery wall. Adjunctive Therapies Nitroglycerin IV Routine use of nitroglycerin via IV is not recommended and has not been shown to reduce mortality in STEMI (AHA, 2016). Its indications for use include the following:Recurrent or persistent chest discomfort, unresponsive to sublingual doses STEMI complicated by pulmonary edemaSTEMI complicated by hypertension (p. 72)Clinical goals Ischemic chest discomfort Titrate to effect (e.g., start at 5-10 mcg/min, titrate upwards in 5 mcg increments until chest discomfort relieved) Maintain SBP > 90 mmHg Limit drop in SBP to 30 mmHg below baseline if hypertensive Pulmonary edema / Hypertension Titrate to effectLimit drop in SBP to 10% of baseline if normotensive Limit drop in SBP to 30 mmHg below baseline if hypertensive (p. 72) Glycoprotein IIb/IIIa (GP IIb/IIIa) Inhibitors These drugs essentially act as a Teflon coating to prevent platelets from binding to each other (prevent fibrinogen binding and platelet aggregation). Three commonly used GP IIb/IIIa inhibitors are abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat). Abciximab is less specific to GP IIb/IIIa receptors than eptifibatide and tirofiban.P2Y12 Inhibitors Clopidogrel (Plavix) is a thienopyridine that irreversibly binds to a specific platelet receptor (P2Y12 receptor antagonist), thus preventing platelet activation and aggregation. It is used in conjunction with aspirin, or as a replacement if the patient is allergic to aspirin, as well as prior to invasive procedures (e.g., PCI). Of note, the prolonged, irreversible binding increases the risk of undesired effects (e.g., bleeding); therefore, clopidogrel should be stopped one week prior to planned PCI. Lastly, clopidogrel requires hepatic activation thus patient responses may be variable. Ticagrelor (Brilinta) is also a P2Y12 receptor antagonist, but it reversibly binds to the specific platelet receptor and does not require hepatic activation. As a result, it produces greater platelet inhibition with a faster onset of action and less variability among patients.Heparin (Unfractionated, Low-molecular Weight Heparin [LMWH]) Heparin is commonly administered as an adjunct to PCI and fibrinolytic therapy (fibrin-specific agents only). Other high risk conditions (e.g., atrial fibrillation, venous thromboembolism, prolonged bed rest) may also warrant the use of heparin. LMWH has been shown to reduce recurrent ischemic events in unstable angina, NSTEMI, and during invasive diagnostic procedures (e.g., PCI) (Amsterdam et al., 2014).Anticoagulants (e.g., heparin) prevent clot formation and/or enlargement, but do not dissolve clots that have already formed. Fibrinolytics, however, cause clot lysis. Direct Thrombin Inhibitors Bivalirudin is a newer anticoagulant that acts as a direct thrombin inhibitor. It may be given alone or with GP IIb/IIIa inhibitors, and is used as a procedural anticoagulant for PCI. Its effects are dose-dependent and coagulation times return to normal within 1 hour of discontinuing the infusion due to its short half-life.Argatroban is reserved for use in ACS patients (prophylaxis, treatment, PCI) with heparin-induced thrombocytopenia (HIT). Beta-blockersBeta-blockers combat myocardial ischemia by reducing heart rate (HR) and contractility, and thus decrease myocardial O2 consumption (improve morbidity and mortality). They are given as soon as possible after MI, as well as for long-term therapy post-MI, and intermediate - low risk patients.Beta-blockers that are selective to cardiac tissue (beta-1) are preferred because they have minimal effect on beta receptors in bronchial airways (beta-2).Avoid if: heart failure, low cardiac output, hemodynamic instability; prolonged PR interval, second/third degree AV blocks; asthma, reactive airway disease Calcium Channel Blockers (CCBs)CCBs decrease HR and contractility and may be used in patients who do not tolerate beta-blocking agents or if beta-blockers are ineffective.Angiotensin-converting Enzyme (ACE) InhibitorsACE inhibitors prevent the formation of ACE, thus inhibit the formation of angiotensin and aldosterone, and reduce cardiac workload. ACE inhibitors prevent ventricular remodeling (dilation) and preserve ejection fraction (EF). They are given within 24 hours of STEMI unless contraindicated (coughing is a common side effect). If patients do not tolerate ACE inhibitors, angiotensin receptor blockers (ARBs) are the alternative

Treatment Heart Failure

HF Diganosis HF is not diagnosed according to left- or right-sided dysfunction per se, but rather according to the symptoms (e.g., dyspnea, congestion, decreased peripheral perfusion) and documented or suspected systolic and/or diastolic dysfunction (McKelvie et al., 2013). The diagnosis of HF will also reflect whether it is acute or chronic, which will ultimately guide the treatment process as well. The Canadian Cardiovascular Society (CCS) recommends the following criteria for the diagnosis of HF:thorough clinical evaluation of hemodynamic profile \use of diagnostic scoring system laboratory testing brain natriuretic peptide (BNP): endogenous substance secreted by the ventricles when they are overfilled; proportional to end-diastolic pressure useful in distinguishing between pulmonary-related and HF-related causes of dyspnea (pulmonary-related dyspnea should not result in elevated BNP levels) also useful for risk stratification and prognostic management troponin: slight/mild elevation may be seen in HF during acute decompensation, but does not necessarily indicate MI other initial blood tests: CBC, Cr, BUN, glucose, sodium (Na+), potassium (K+), thyroid functionECG and CXR within 2 hours of initial presentationechocardiogram (ECHO) within 72 hours of presentation (unless previous ECHO within 12 months or significant change in clinical status)coronary angiography (if angina, suitable for revascularization, to visualize cardiac anatomy) (McKelvie et al., 2013, pp. 169-173) heart failure treatment The HF itself should be treated according to the underlying cause, and whether it is deemed acute or chronic. As you can see in the table below, the goal of acute HF management is restoring hemodynamic stability; the treatment of chronic HF is dependent upon whether the patient has preserved or reduced EF. The CCS guidelines identify the following interventions for acute and chronic HF, depending on the clinical situation (e.g., renal function, comorbidities, ethnicity): ACUTE or CHRONIC Preserved EF (pEF)(> 40%) Reduced EF (rEF)(< 40%) O2 (with caution if no hypoxemia) Maintain SaO2 > 90%***main approach is to control factors that lead to HTN & MI*** Bilevel positive airway pressure (BIPAP) Continuous positive airway pressure (CPAP)***routine use of BIPAP/CPAPnot advisable*** Endotracheal intubation(if above methods fail, cardiogenic shock) ACE inhibitors ARBs(if other non-HF indications for their use)ACE inhibitorsARBsDiuretics (PO & IV)**mainstay of treatment** Diuretics(congestion, edema) Diuretics(reduce worsening HF) Vasodilators(e.g., nitroglycerin) Mineralocorticoid receptor antagonists (MRAs)(e.g., Spironalactone)***caution regarding↑ K+*** Beta-blockers(continue if chronic use, unless symptomatic [hypotension/ bradycardia]; not shown to improve outcomes) Beta-blockers(rate control) Beta-blockers(combined with ACE inhibitors)CCBs(only if preserved EF [> 40%] and atrial fibrillation [AFib]) CCBs(rate control) Digoxin(AFib, sinus rhythm with symptoms ) Tolvaptan (vasopressin antagonist)(symptomatic/severe hyponatremia, refractory to diuresis)(McKelvie et al., 2013)_________________ Figure 2.2. Treatment algorithm for acute heart failure. Reprinted from "2017 Comprehensive Update of the Canadian Cardiovascular Society Guidelines for the Management of Heart Failure", by J. A. Ezekowitz et al., 2017, Canadian Journal of Cardiology, 33, p. 1369. (https://doi.org/10.1016/j.cjca.2017.08.022)Further to the HF guidelines described above by McKelvie et al. (2013) and Ezekowitz et al. (2017), the overall goals of HF management are described below. Reduce preload Individuals with HF have excess preload, which leads to decreased stroke volume and cardiac output. Preload may be reduced by administering diuretics, such as Furosemide (Lasix), to lower circulating blood volume. Morphine or nitrates (e.g., Nitroglycerin) may achieve an acute reduction of preload by increasing venous dilation and redistributing blood away from the heart. Reduce afterload A reduction in afterload causes an inverse improvement in stroke volume and cardiac output. ACE inhibitors or ARBs may be prescribed to reduce afterload; however, they are not recommended in the acute stage of HF. In acute situations, Nitroglycerin may be used to induce arterial vasodilation and reduce afterload.Improve contractility Digoxin inhibits the Na+-K+-ATP-ase pump, which indirectly increases the amount of intracellular Ca2+ and improves contractility. Digoxin may be prescribed for patients who continue to experience moderate-severe HF symptoms, despite remaining in sinus rhythm; digoxin is also recommended in chronic AFib that is refractory to beta-blocker therapy or when beta-blockers cannot be used. It is of particular benefit to patients with rEF, and is more effective at controlling ventricular response when combined with beta blockers. The CCS advises against the routine use of inotropes if the patient is hemodynamically stable. In acute cases, agents such as Dopamine, Dobutamine, or Milrinone may be given IV. Dopamine and Dobutamine both act via stimulation of beta receptors. Milrinone is a phosphodiesterase-3 inhibitor that increases the amount of intracellular Ca2+; it also enhances uptake of Ca2+ during diastole and therefore improves cardiac muscle cell relaxation .Decrease cardiac workload Beta-blockers reduce HR and contractility; however, stroke volume, cardiac output, and EF must be monitored regularly. Resynchronize ventricular function Biventricular pacing may help to resynchronize ventricular function. Patient education Patients with HF are encouraged to be active participants in their care. Strategies to prevent exacerbations include providing information about fluid and Na+ intake, as well as exercise. Patients are instructed to limit fluid intake to 6-8 cups/day (including the fluid in foods). To monitor fluid retention, patients should be advised to obtain daily weights, ensuring the same scale is used every day; daily weights should be measured in the morning before breakfast, and a weight change of more than 2 kg (4 lb) in 2 days (or 2.5 kg [5 lb] in one week) should be reported. Guidelines may be provided to enable patients to adjust their diuretic therapy if a smaller change in daily weight is noted. Na+ intake should be limited to < 2 g/day from all sources. Exercise is best planned for short periods throughout the day, allowing for frequent rest periods (for more information, see Heart and Stroke Foundation of Canada, 2018).

Emergency Department Overcrowding

In Canada, emergency department overcrowding (EDOC) has been a key health care issue for decades. The most common cause of EDOC is the number of admitted patients in the ED who are waiting for an inpatient bed, as opposed to the misconception that inappropriate use of the ED is the culprit (Affleck et al., 2013). Other contributing factors are described below, and are largely due to capacity and efficiency limitations. These may include: inefficient use of acute care beds, including access to diagnostic services; shortage of acute care beds (inadequate number of beds, beds blocked); staff shortage in ED (e.g., physicians, nurses); other staff shortages that support patient flow and operational processes, such as administrative support and program staff (e.g., consultations); limited community care resources (e.g., home care, long-term care, rehabilitation services); fragmented integration of community and hospital-based resources; ineffective or lack of communication between hospital physicians and primary care providers upon patient discharge; and confusion regarding who is accountable for the patient at different times during their care (Affleck et al., 2013, p. 362). If the demand for emergency care exceeds an ED's capacity to provide appropriate and quality health care within a given timeframe, the following ill effects may result: patient suffering; prolonged wait times; deteriorating levels of service; adverse patient outcomes; and decreased ability to retain experienced emergency health care providers (Affleck et al., 2013, p. 359). In 2000, Canada had 3.8 hospital beds (acute and psychiatric care) per 1,000 Canadians. In 2015, Canada had 2.6 hospital beds per 1,000 Canadians, ranking 32nd out of 35 Organisation for Economic Co-operation and Development (OECD) countries (the average was 4.7) (OECD, 2017). As of 2017, the number of hospital beds per 1,000 Canadians had further decreased to 2.5 (OECD, 2019). This results in most hospitals functioning at or above 95% capacity, which does not allow for any flexibility within the system. It should also be noted that up to 20% of inpatients occupying acute care beds are those who require an "alternate level of care" (Affleck et al., 2013, p. 363), such as the elderly; however, they are not able to access community and post-acute care services due to inadequate services in these areas as well (Affleck et al., 2013). Various strategies have been implemented to address EDOC across Canada, as the performance among hospitals varies widely. Affleck et al. (2013) categorize these strategies as input, throughput, and output solutions, and are outlined as follows: Input solutions Improve primary care access (e.g., increase resource allocation to provide for more PCPs, thus limiting non-urgent use of EDs); and Improve emergency medical services (EMS) coordination (e.g., increase funding to allow for nurses to take over the care of patients who arrive via ambulance, thus facilitating EMS to get back on the road) (p. 365). Throughput solutions Engage in quality improvement processes (e.g., LEAN); Improve ED staffing, as well as matching staffing to patient demand (e.g., increase staff during peak patient arrival times); Use medical directives (e.g., sending patients for x-rays from triage if certain criteria are met); Use 'fast track' areas for patients presenting with non-urgent signs/symptoms or conditions that could likely be treated quickly (e.g., digit injury requiring splinting, minor laceration requiring suturing); Use 'rapid assessment zones' (e.g., patient is stable enough to wait in a chair, but requires a stretcher for an electrocardiogram); Establish ED observation units (e.g., patient requires a short stay in hospital for observation, thus freeing up a bed in the ED); and NENA suggests that a decision regarding a patient's disposition should be made within 24 hours and the ED should not be utilized as a holding unit for admitted patients (NENA, 2015). Improve teaching strategies (e.g., streamline process of junior resident assessing patient, which slows down decision-making and patient throughput) (pp. 365-367). Output solutions Implement overcapacity protocols (e.g., ED diversion protocols); and Implement formalized hospital-wide flow policies and processes (e.g., discharge planning, outpatient referrals and specialist follow-up) (p. 367).

Duty to Report

In a previous section of this module, we briefly touched on nurses' duty to report substance misuse by a colleague in the workplace. According to the CNA (2017), nurses have an ethical responsibility to report any circumstance when a patient's safety is at risk, but we also have a legal responsibility, which is outlined by our provincial and territorial Health Acts. Nurses are required to report to their managers and/or regulatory colleges, unsafe situations that could put patients at risk. "Nurses are attentive to signs that a colleague is unable, for whatever reason, to perform their duties. In such a case, nurses will take the necessary steps to protect the safety of persons receiving care" (CNA, 2017, p. 17). You will find within all provincial and territorial standards for practice that nurses have a duty to report unsafe conduct; for example, CARNA (2013) states in its standards, "the nurse reports unprofessional conduct to the appropriate person, agency, or professional body" (p. 8).In many cases, failure to report negligent or unethical conduct could in and of itself constitute professional misconduct, and those professionals who fail to report may end up sharing in legal ramifications (Keatings & Smith, 2010). In addition to the above, nurses are specifically legally mandated to: Report any sexual abuse of any client by a healthcare provider (CARNA, 2019, p. 8). Self-report any guilty criminal offenses or any findings of professional misconduct, and any pending investigations into their conduct (CNO, 2019a). Report to local child and family protective services any suspected physical, emotional, sexual abuse, or neglect of a child (Government of Ontario, 2017). This cannot be delegated, and the nurse who suspects the abuse must be the one to report it to the authorities (Foxman, 2015, p. 13).

Internal Factors Leading to Ethical Distress

Internal factors stem from the nurse's own personal values and can lead to ethical distress in the workplace. Remember that we as practitioners need to be attuned to our own personal belief system. There may come a time in our practice when we are asked to do things that strongly conflict with our own moral code. Conscious Objection For personal, religious, or other reasons, we may have strong moral opposition to certain practices or occurrences in health care, to a point that we feel that we cannot be a part of them. This is known as conscientious objection, and may exist regarding such things as suicide attempts, abortion, organ donation, or medical assistance in dying (MAID). Questions to Ponder: What do we, as emergency nurses, do if we know this about ourselves? Are these moral conflicts incompatible with emergency nursing? How do we reconcile a conscientious objection with our duty to care for patients? What are the legal implications of refusing to provide certain care? Keep in mind: nurses cannot legally abandon their patients. As with many ethical issues, the legalities involved are intertwined and difficult to separate. This is the case with conscientious objection, such that nurses have an ethical obligation to practice in a way that is consistent with their professional ethics and personal beliefs, but they also have a legal and contractual obligation to their employers to provide the care their patients require (Keatings & Smith, 2010, p. 349). There is a proper process to be followed in declaring conscientious objections: Prior to employment we must bring these moral issues to the attention of future employers. This is done in anticipation of events at work, not during an emergency situation. In an emergency, nurses have an ethical responsibility to protect patients from harm (beneficence and non-maleficence) If a situation arises while providing care, one must continue to provide care until alternative arrangements can be made (CNA, 2017, pp. 36-37). Important: Nurses must ensure that their conscientious objection is based on personal values and ethics and not prejudice or convenience (CNA, 2017, p. 37). Nurses must ensure not to try to influence the patient's opinions, values, and beliefs to align with theirs (Keatings & Smith, 2010, p. 204). In the case of medical assistance in dying (MAID), nurses have no legal or ethical obligation to participate (CNA, 2017, p. 35).

Legal Issues in Emergency Nursing

Introduction Ethics and legalities in nursing overlap significantly, but are distinct (CNA, 2017, p. 4). In arguably one of the most chaotic of environments for nursing practice, the emergency setting brings unique and heightened legal challenges. It is paramount that emergency nurses understand the legal implications of their practice and know where to locate resources that can help them with decision making. In this next section we review our legal structure in Canada, and discuss important legal obligations of nursing practice in an emergency-nursing context. Case studies and thought-provoking questions are utilized to help facilitate the application of legal decision making to emergency nursing practice situations. Module Objectives After completing this module, you will be able to: Describe the basic structure of the Canadian legal system. Understand the fundamental difference between civil and criminal law as it relates to emergency nursing. Relate other legal concepts such as negligence and tort, as they pertain to nursing. Understand the importance of confidentiality, duty to report, reportable conditions, and consent and capacity. Have an understanding of the legal issues around the provision of emergency treatment, advance directives, do-not-resuscitate orders, communicating with police, forensic evidence, and documentation in the emergency setting. Identify the professional liability insurance that is available to nurses, why such insurance is a requirement for nurses in Canada, and how it protects you. Identify legal resources to aid in decision making in practice. Relate legal issues to an emergency room setting with case studies and review questions.

Telephone Triage

It is not uncommon for EDs to receive calls from the public seeking medical advice, such as how they can treat reported signs and symptoms and whether they should be seen by a physician in the ED. Telephone triage is defined as, "the practice of performing a verbal interview and making an assessment of the health status of the caller" (ENA, as cited in Gilboy, 2013, p. 72). The Canadian Nurses Protective Society (CNPS, 2008) identifies the provision of telephone advice as a high-risk practice, specifically that "the absence of face-to-face contact increases the risk" (p. 1). Information obtained from the patient or third party (e.g., parent/caregiver) may be "inaccurate, incomplete or misleading" (CNPS, 2008, p. 1), thus the triage nurse must tread with extreme caution when eliciting and providing information to ensure adherence to professional and legal standards. The American College of Emergency Physicians' (ACEP's) position regarding telephone triage stipulates that medical assessment or management should not be provided by telephone (ACEP, 2019). Although currently under review, ENA's position statement on telephone advice supports that of the ACEP, specifying that triage nurses should inform the caller of the ED's hours of operation (e.g., 24 hours/day in urban areas) and that they are welcome to present to the ED to be assessed by a physician (Gilboy, 2013). All ED nurses should be familiar with the department's policies and procedures surrounding telephone triage and the provision of telephone advice. In many provinces across Canada, telehealth or telepractice has become a specialty in and of itself, requiring formalized training and education programs (Canadian Nurses Association [CNA], 2017).

Basic ECG Interpretation (various rhythms)

Junctional (Junctional Escape) Rhythm Junctional (junctional escape) rhythm is normally seen following a failure of the SA node to generate impulses at a sufficient rate. The AV junction takes over pacemaker function at an intrinsic rate of 40-60 bpm, with a regular rhythm. As discussed previously, the P waves are inverted in Lead II, because of retrograde conduction to the atria, and may occur before, during, or following the QRS complex. Ventricular conduction is not affected and occurs in a normal fashion, producing the normal QRS complex.Junctional escape rhythms are seen in situations of MI, hypoxia, electrolyte imbalances, and drug toxicity. The rate may be insufficient to provide adequate cardiac output, resulting in related signs and symptoms. Treatment is aimed at increasing the heart rate and treating the underlying cause.ECG Features of Junctional Escape RhythmRhythm Rate P waves PR Interval QRSRegular 40-60 bpm Inverted; before, during or after QRS. < 0.12 secs < 0.12 secs Accelerated Junctional Rhythm Accelerated junctional rhythm resembles junctional escape rhythm in all respects except that its rate is 60-100 bpm. Accelerated junctional rhythm is due to enhanced automaticity. All conduction and resulting ECG features are the same as previously discussed. Causes of accelerated junctional rhythm include digitalis toxicity, MI, and hypokalemia. Treatment focuses on management of the underlying cause.ECG Features of Accelerated Junctional RhythmRhythm Rate P waves PR Interval QRSRegular 60-100 bpm Inverted; before, during, or after QRS. < 0.12 secs < 0.12 secs Junctional Tachycardia Junctional tachycardia is a junctional rhythm that exceeds 100 bpm, also due to enhanced automaticity. The conduction and ECG features are the same as those seen in other junctional rhythms, differing only in the increased rate. Causes of junctional tachycardia are similar to those of accelerated junctional rhythm. With sustained tachycardia, the patient may present with symptoms of decreased cardiac output. Treatment of junctional tachycardia includes treating the underlying cause, vagal manoeuvres, drug therapy, and electroshock.ECG Features of Junctional Tachycardia Rhythm Rate P waves PR Interval QRSRegular > 100 bpm Inverted; before, during or after QRS < 0.12 secs < 0.12 sec Supraventricular Tachycardia (SVT) and Paroxysmal Supraventricular Tachycardia (PSVT) The term supraventricular tachycardia (SVT) refers to a group of rapid, regular rhythms that originate above the ventricles (i.e., in the SA node, atrial tissue, or AV junction); therefore, SVT encompasses rhythms such as sinus tachycardia, atrial tachycardia, atrial flutter, and junctional tachycardia. If it is possible to differentiate the exact type of tachycardia, then it is preferable to utilize the appropriate name of the rhythm, such as junctional tachycardia. However, due to the rapid rate, the P wave is often hidden within the previous T wave, making it difficult to determine the exact origin of the tachycardia. Typically, this occurs with rates of 180 bpm and above. The term SVT is used when rhythms are rapid and regular, QRS width is normal, and the exact type of the tachycardia cannot be determined. Treatment of SVT includes vagal maneuvers (e.g., Valsalva maneuver, carotid sinus massage), pharmacologic therapy (e.g., Adenosine), and cardioversion.The term paroxysmal refers to the sudden onset and/or cessation of a rhythm. When occurring with SVT, this is referred to as paroxysmal supraventricular tachycardia (PSVT). PSVT may be further differentiated into either atrioventricular nodal reentrant tachycardia or atrioventricular reentrant tachycardia, both of which are beyond the scope of this 9-section module/course.ECG Features of Supraventricular TachycardiaRhythm Rate P waves PR Interval QRSRegular 100-280 bpm With rapid rates, will be hidden within previous T wave. Not measurable if P waves hidden. < 0.12 secs Route of Conduction ventricular rhythms Up until this point, we have been looking at supraventricular rhythms (those originating from above the ventricles). In relation to Lead II, we have seen how these rhythms progressively alter their ECG characteristics as they change sites of origin along the cardiac conduction system. To review, sinus rhythms have upright P waves and upright QRS complexes; the PR and QRS intervals are normal. Atrial rhythms arise from an abnormal focus within the atria, thus giving them an abnormal P wave and variable PRI while maintaining the normal width of QRS. Junctional rhythms have inverted P waves in Lead II, shortened or non-existent PRIs, and normal QRS complexes.Ventricular rhythms arise from pacemaker sites within the ventricular muscle or Purkinje fibres. The Purkinje fibres have the ability to take over the pacemaker function of the heart if both the SA node and AV junctions malfunction. The intrinsic rate of the Purkinje fibres is 20-40 bpm. The resulting protective rhythm is called idioventricular rhythm (or ventricular escape rhythm). Altered cellular function in the ventricles, which may result from ischemia, stress, stimulants, drug effects, or electrolyte imbalances, may result in PVCs, accelerated idioventricular rhythm (AIVR), ventricular tachycardia (VT), ventricular fibrillation (VF), or asystole.The ventricular impulse does not travel through normal conduction pathways in the ventricles, but is conducted more slowly from cell to cell; therefore, ventricular rhythms result in a wide (≥ 0.12 seconds) and abnormally-shaped QRS complex. These complexes may be upright or inverted, depending on the origin within the ventricles. If there is a visible P wave, it is not associated with the ventricular complex; thus, PRIs are not measured. ST segment and T waves are usually opposite in direction from the QRS because both depolarization and repolarization are abnormal. Premature Ventricular Complex A premature ventricular complex (PVC), or premature ventricular contraction, is caused by early depolarization of tissue within the ventricles. PVCs are characterized by widened and abnormal complexes that occur early, disrupting the underlying rhythm. They are most often associated with a compensatory pause in which measurement between the R wave preceding the PVC and the R wave following the ectopic beat is equal to double the RR distance in the underlying rhythm. If the PVCs are all of the same configuration or shape, they arise from a single focus and are termed uniform (unifocal). Similarly, PVCs of varying configurations come from different sites and are termed multiform (multifocal). As we have learned, this change in shape is due to their differing relationships with the positive electrode.ECG Features of Premature Ventricular Complex Rhythm Rate P waves PR Interval QRSInterrupts regular underlying rhythm. That of underlying rhythm. Not associated None Bizarre shape;> 0.12 secs.Isolated uniform PVCs require monitoring, but generally do not require treatment. Increasing frequency, coupling (two together), and multiform PVCs may be warnings signs of a potential onset of lethal dysrhythmias. PVCs may occur in fixed, reoccurring patterns such as bigeminy (every second complex), trigeminy (every third complex), and so on. PVCs that do not interrupt the underlying rhythm are referred to as interpolated.Sample ECG 6.4. Sinus rhythm with bigeminy of PVCs .Of particular significance is the R-on-T phenomenon. In this case, the PVC falls on the T wave of the previous complex. If the PVC occurs during the last half of the T wave when the ventricles are only partially repolarized, repeated ventricular stimulation may occur, resulting in potentially lethal dysrhythmias (e.g., VF).Figure 6.2. Sinus rhythm with one R-on-T PVC.As discussed previously, it is important when reporting findings to identify the underlying rhythm as well as the frequency and characteristics of the PVCs (e.g., sinus bradycardia with frequent PVCs, bigeminy, etc.). Idioventricular Rhythm (Ventricular Escape Rhythm) Idioventricular rhythm (ventricular escape rhythm) results from the failure of pacemaker sites in the SA node and AV junction to produce impulses. Since the only remaining source of automaticity is within the ventricles, there will be no resulting P waves.This rhythm typically produces insufficient cardiac output because of its slow rate and lack of atrial kick. Treatment includes addressing the cause, drug administration (e.g., Atropine), and pacemaker use. The rhythm may be referred to as agonal if the rate is less than 20 bpm.ECG Features of Idioventricular Rhythm (Ventricular Escape Rhythm)Rhythm Rate P waves PR Interval QRSRegular 20-40 bpm Usually none visible. None > 0.12 secs; wide, bizarre shape. Accelerated Idioventricular Rhythm (AIVR) Accelerated idioventricular rhythm (AIVR) is a faster version of idioventricular rhythm with a rate of 40-100 bpm, and is generated by a ventricular focus with enhanced automaticity. AIVR is seen in the presence of an inferior MI and during reperfusion therapy with fibrinolytics. Treatment of AIVR depends on the cause and how well the patient tolerates the rhythm, as the ventricular rate is usually sufficient to provide adequate cardiac output. Usually, AIVR is transient and does not require treatment, but agents to increase the rate of the SA node (e.g., Atropine) may be administered, as well as consideration of pacemaker use.ECG Features of Accelerated Idioventricular RhythmRhythm Rate P waves PR Interval QRSRegular 40-100 bpm Usually none visible. None Abnormal shape;> 0.12 secs.ECG Sample 6.8. Accelerated idioventricular Ventricular Tachycardia (Monomorphic) Ventricular tachycardia (VT) is a regular, rapid, wide-complex arrhythmia usually originating from one focus within the ventricles. VT may develop without warning or may be preceded by PVCs, particularly those occurring in pairs, runs, or R-on-T situations. It may also be non-sustained, lasting for less than 30 seconds, in which case significant hemodynamic compromise is unlikely. Alternatively, sustained or incessant VT will seriously compromise cardiac output (become pulseless) and may degenerate into VF and cardiac arrest.ECG Features of Ventricular TachycardiaRhythm Rate P waves PR Interval QRSRegular 100-250 bpm Usually none visible. None Wide (≥ 0.12 secs) Polymorphic Ventricular Tachycardia Polymorphic ventricular tachycardia (VT) is a rapid ventricular rhythm in which the pattern of QRSs changes in shape, amplitude, and width from beat to beat, typically due to multiple irritable foci within the ventricles. One type of polymorphic VT is torsades de pointes (TdP), which, translated from French, means twisting of the points. In TdP, the QRSs appear to 'twist' around the isoelectric line, deflecting downward and then upward in a repeating pattern. TdP is associated with factors that cause a prolonged QT interval (refractory period). Treatment includes correcting causative factors, overdrive pacing, and antiarrhythmic drugs that do not further prolong the QT interval (e.g., Magnesium sulfate).ECG Features of Torsades de PointesRhythm Rate P waves PR Interval QRSRegular or irregular Typically 200-250 bpm; may be 150-300 bpm. Usually none visible. None Wide (≥ 0.12 secs); gradual change in polarity from positive to negative, and back. Upgrade to remove ads Only CA$44.99/year Ventricular Fibrillation In ventricular fibrillation (VF), which is analogous to atrial fibrillation, the ventricles are stimulated in a chaotic and rapid manner, causing them to quiver and 'fibrillate'. This rhythm results in no effective cardiac output (pulseless), which is reflected on the monitor by an irregular baseline and no identifiable QRS complexes. This may be described as either coarse ventricular fibrillation, or fine ventricular fibrillation. Coarse VF causes larger fibrillation waves, is generally of more recent onset, and is more successfully treated than fine VF.VF may occur without warning, but it is more often preceded by PVCs or VT.It is absolutely essential that you correlate the ECG findings with the patient's physical condition because VF can resemble ECG artifact. If the patient is alert and has a pulse, check the monitoring system.ECG Features of Ventricular FibrillationRhythm Rate P waves PR Interval QRSIrregular None None None None Ventricular Standstill ('P' Wave Asystole) Ventricular standstill is the absence of electrical activity in the ventricles, resulting in no cardiac output. The atria continue to depolarize, producing P waves, but there is no QRS following; this is often referred to as 'P' wave asystole.Once again, it is absolutely imperative that you correlate ECG observations with the patient's clinical condition. If the patient is conscious and has a pulse, this is not ventricular standstill. Check the monitoring system.ECG Features of Ventricular StandstillRhythm Rate P waves PR Interval QRSAtria: regular or irregularVentricles: none (no QRS) Atria: variableVentricles: none (no QRS) Present, but no associated QRS None None Asystole Asystole is the absence of any electrical activity in the heart. The difference between asystole and ventricular standstill is that ventricular standstill has P waves but no QRS, whereas asystole has no electrical activity at all. In both cases, there will be no cardiac output. In the absence of any electrical activity, the ECG shows a straight line.ECG Features of AsystoleRhythm Rate P waves PR Interval QRSNoneNoneNone None None Route of Conduction Av block Atrioventricular (AV) blocks indicate impaired conduction through the AV node and are characterized by prolonged PRIs or the absence of AV conduction.AV blocks are identified by the degree of conduction compromise. First-degree AV block is the most benign in that all impulses are conducted, but take longer than normal to travel through the AV node. First-degree AV block is characterized by a PRI consistently longer than 0.20 seconds. Second-degree AV block indicates that some impulses are not conducted to the ventricles. Type I second-degree block (Mobitz type I; Wenckebach) produces gradually increasing PRIs until there is a P wave without a QRS following. In type II second-degree block (Mobitz type II; Classical), there is a constant PRI until, without warning, there is a P wave without a QRS following. In second-degree 2:1 conduction, every other P wave is blocked resulting in inconsistent AV nodal conduction, thus determining the PRI is not possible. Third-degree AV block (complete heart block) indicates there is no conduction across the AV node, with ventricular activity relying on an escape pacemaker site, such as the AV junction or purkinje fibres.When reporting an AV block, indicate the underlying rhythm, type of AV Block, and any escape rhythm noted. AV Block Comparisons First-DegreePRI constantPRI prolongedOne P wave to each QRSRegular atrial rhythm; regular ventricular rhythmSecond-Degree, Mobitz Type IPRI variesPRI progressively gets longer until there is a P wave without a QRS followingRegular atrial rhythm; irregular ventricular rhythmSecond-Degree, Mobitz Type IIPRI constantPRI normal or prolongedRegular atrial rhythm; irregular ventricular rhythm (unless conduction ratio is consistent, such as 2:1 conduction)Second-Degree, 2:1 ConductionEvery other P wave is blocked so that it is not possible to determine if the PRI varies (therefore, it is not possible to determine if this is a Mobitz Type I or Mobitz Type II block).Regular atrial rhythm; regular ventricular rhythm (but at half the rate of the atria)Third-Degree, CompletePRI variesP waves have no relationship to QRS (P waves may be found hidden in QRS complexes and T waves)Regular atrial rhythm; regular ventricular rhythm (but at two different rates) First-Degree AV Block First-degree AV block is characterized as sinus rhythm with a prolonged PRI. Conduction follows the normal pathways so that no other alterations in the ECG occur. It is an asymptomatic rhythm and does not require treatment; however, the patient should be monitored to ensure that it does not progress to a more severe block. First-degree AV block may be congenital in nature, secondary to an inferior MI, or due to drugs that slow conduction through the AV node (e.g., beta-blockers, calcium channel blockers, Digoxin).ECG Features of First-Degree AV BlockRhythm Rate P waves PR Interval QRSRegular That of underlying rhythm; atrial rate = ventricular rate. Normal, upright; one P wave before each QRS complex. Constant; > 0.20 secs. < 0.12 secs. Second-Degree AV Block Type I (Mobitz Type I, Wenckebach) Second-degree AV block type I is characterized by a progressively increasing PRI until a point where conduction is blocked completely and there is a P wave without a QRS following ("Long, longer, lack...Wenckebach"). The atrial rhythm is regular, while the ventricular rhythm is generally regularly irregular in a pattern. Second-degree AV block type I may result from an inferior MI or drugs that slow conduction through the AV node.This is generally not a serious form of AV block and needs only to be monitored for progression to a more critical variety.ECG Features of Second-Degree AV Block Type IRhythm Rate P waves PR Interval QRSAtrial: regular;ventricular: irregular due to missing QRS complexes. Atrial: that of underlying rhythm; ventricular: less than atrial rate, depending on number of QRS complexes dropped. Normal, upright, more P waves than QRS complexes Progressively lengthens until there is a P wave without a QRS following. Normal (< 0.12 secs) where present.Sample ECG 7.2. Second-degree AV block type I. Second-Degree AV Block Type II (Mobitz Type II, Classical) Like second-degree AV block type I, second-degree AV block type II is characterized by P waves that do not have a QRS following. The atrial rhythm is regular, but the ventricular rhythm is irregular due to the block. Unlike in Type I block, however, the PRI remains constant until there is a P wave without a QRS afterwards. Given that this block may occur in the bundle of His, a widened QRS complex reflecting the slight slowing of ventricular conduction may be seen. In this block, we may see only an occasional missing QRS complex or several consecutively absent complexes. Second-degree AV block type II may result from an anterior MI or drugs that slow conduction.Second-degree AV block type II is the more serious of the second-degree blocks, with increased risk of progressing to third-degree AV block. The number of blocked complexes will directly affect the cardiac output; therefore, pharmacologic and pacemaker interventions must be considered.ECG Features of Second-Degree AV Block Type IIRhythm Rate P waves PR Interval QRSAtrial: regular;ventricular: irregular. Atrial: that of underlying rhythm; ventricular: depends on number of dropped complexes. Normal, upright; more P waves than QRS complexes. Constant; may be normal or prolonged. Normal or wide, depending on level of block in AV area. Second-Degree AV Block 2:1 Conduction Second-degree AV block 2:1 conduction is characterized by failure of every other atrial impulse to be conducted through the AV node. Because there are no consecutively conducted beats, one is unable to determine if the PRI progressively lengthens or is constant. Thus, it is not possible to clearly determine if second-degree AV block 2:1 conduction is due to a Mobitz type I or Mobitz type II block.Rhythm Rate P waves PR Interval QRSAtrial: regular;ventricular: irregular. Atrial: that of underlying rhythm; ventricular: half of the atrial rate. Normal, upright; more P waves than QRS complexes. Unable to determine if constant or prolonged as there are no consecutive beats. Normal or ≥ 0.12 secs. Third-Degree (Complete) AV Block Third-degree AV block occurs when there is no conduction between the atria and the ventricles. The SA node continues to generate impulses, producing normal, upright P waves, but there is no relationship between the P waves and ventricular activity. Ventricular depolarization may occur as a result of a junctional or ventricular escape pacemaker, resulting in a QRS whose characteristics reflect the origin of the pacemaker (junctional = narrow QRS, ventricular = wide QRS). The rate of ventricular activity will dictate the amount of compromise to cardiac output, which typically requires pharmacologic and/or pacemaker interventions.ECG Features of Third-Degree AV BlockRhythm Rate P waves PR Interval QRSAtrial: regular;ventricular: irregular. Atrial: that of underlying rhythm; ventricular: that of escape rhythm. Normal; not related to QRS. Not measured. Depends on escape pacemaker: < 0.12 secs if junctional focus; ≥ 0.12 secs if ventricular focus.

Documentation in the Emergency Department

Keatings & Smith (2010) discuss the importance of documentation as paramount to professional nursing practice. Documentation in accordance with the standards of our regulatory bodies allows us to establish a permanent record of the nurse's assessment and monitoring of patients, and is often the only written evidence of the care a patient has received (Keatings & Smith, 2010). Failure to keep accurate and complete documentation can have serious legal consequences for health-care professionals (Keatings & Smith, 2010). According to the CNPS (2007), documentation is necessary for: Communication between health care providers; Meeting legislative requirements; Quality improvement; Research; and Legal proof of health care provided (p. 1). When it comes to documentation in the emergency department, here are some important considerations: The emergency nurse shall accurately document pertinent patient data, nursing interventions, and patient outcomes. Emergency nurses must document thoroughly, chronologically and continuously, based on the nursing process, patient outcomes, and in accordance with agency specific documentation. Charting should indicate if past medical records were ordered, received, or were not available. When rapid interventions are occurring, it is best to have a designated charter. Documentation for critically injured or ill patients should be recorded in an ICU-type charting style, indicating regular vitals and assessments being performed. Unusual occurrences not part of routine care should also be documented, including a description of the event in objective factual terms. For example, patient refusal of care or a patient leaving AMA. If a problem is found (e.g., esophageal intubation) documentation of resolution of the problem must follow. All communication attempts with other personnel (MDs, managers) as it relates to patient care should be documented. Charting must reflect all provincially specific laws, such as the patient's right to refuse treatment. The provision of discharge instructions should be clearly documented, and a copy of the discharge instructions provided should be included in the medical record (McConnell, 2018, p. 683; NENA, 2018, p. 15). Keatings and Smith (2010) also add that documentation should be concise, factual, and as objective as possible, without any lengthy gaps between entries. As well, entries such as "Slept well, had a good day" are of limited use, as they are too vague in meaning, and do not add to the nursing assessment. Documenting Contemporaneously With respect to the chaotic nature of the emergency department, arguably one of the most difficult practice standards to uphold is documenting contemporaneously, which refers to documentation done as close to the time of the event or intervention as possible. Documentation after the fact can be problematic for a couple of main reasons: Memory naturally fades over time, thus leading to more potential for notes to be unintentionally inaccurate. The later that notes are created after the event (even if labelled "late entry"), the less weight they hold in legal proceedings (Keatings & Smith, 2010, p. 225). Read Follow this link to read CNPS's "Ask a Lawyer", regarding the weight held by late-entry documentation. Canadian Nurses Protective Society (CNPS). (2019, June). Ask a lawyer: Documentation of late entries. https://cnps.ca/article/ask-a-lawyer-documentation-of-late-entries/ Consider also the renowned Supreme Court of Canada case of Kolesar v. Jeffries, 1976, which established precedent regarding the importance of contemporaneous charting. Follow the link below to a CNPS article that, among other things, highlights this ground-breaking case in nursing documentation that sparked the well-known adage, "if it wasn't charted, it wasn't done." Canadian Nurses Protective Society (CNPS). (2020, October). Quality documentation: Your best defence. infoLAW, 1(1). https://cnps.ca/article/quality-documentation/ Questions to Ponder: Can you think of a time that were so busy in your shift that you ended up doing most of your charting after the fact? Did you have trouble remembering all that you did during that shift? Is it possible that you charted some inaccuracies and missed details? If you were called to court to defend your practice during that shift, do you feel that your charting would support the care you provided? Read Follow the link below for another case on documentation (Case 2 in the article), that discusses the trickle-down effect that can happen when something as seemingly benign as a blood pressure reading is not captured in our documentation. This case reminds us how important the emergency nurse's assessment and documentation is, and that it is considered equal to that of the MD in the eyes of the law. Canadian Nurses Protective Society (CNPS). (2017, October). Lessons from the courtroom: Collaborative care. https://cnps.ca/article/lessons-from-the-courtroom-collaborative-care/ [Currently under review] Charting by Exception Charting by exception is often seen in busy health-care settings like the ED. Although a time saver, it is a contentious legal issue in the court system. Regulatory colleges and our court systems have neither rejected nor supported this form of documentation (Bryden, 2016, slide 42). The nature of charting by exception is to chart only abnormal findings. The CNPS (2014a, p. 1) highlights some key messages when it comes to this form of charting: Nurses who are considering charting by exception will want to understand the additional risks associated with that style of documentation. When charting by exception, it is important that nurses have a shared understanding of what is "normal" and "abnormal" in that practice setting and for each particular patient. Charting by exception is best implemented when approved and supported by employer and/or workplace policy to ensure consistency in charting practices among the care team. Charting by exception may not be appropriate in some care settings, for example, where the patient is receiving complex or critical care. The fact that assessments or interventions occurred should generally be noted in the health record, along with the nurse's most relevant findings, even where the nurse is charting by exception. Nurses should consider their legal and professional responsibility to document patient care. Read Follow the link below to a very interesting presentation sponsored by the Registered Nurses Association of Ontario's Legal Assistance Program and given by a lawyer. There is a section in this presentation on charting by exception that describes this form of documentation as risky from a legal perspective, and reviews some of the cases that highlight this risk: Bryden, C. (2016). Documentation & nursing: A legal perspective [PowerPoint slides]. Registered Nurses' Association of Ontario. https://rnao.ca/sites/rnao-ca/files/Documentation_and_Nursing.pdf Question to Ponder: How do you reconcile the legal risks of charting by exception, and the busy, time-constrained nature of the ED?

Emergency Severity Index

Like the MTS, the ESI is also an algorithm-based triage tool that evaluates patient acuity. However, the ESI is unique in that the categorization of patients also takes into consideration patients' resource needs. "If a patient does not meet high acuity level criteria (ESI level 1 or 2), the triage nurse then evaluates expected resource needs to help determine a triage level (ESI level 3, 4, or 5)" (Gilboy et al., 2011, p. 7). To illustrate, [a]cuity is determined by the stability of vital functions and the potential threat to life, limb, or organ. The triage nurse estimates resource needs based on previous experience with patients presenting with similar injuries or complaints. Resource needs are defined as the number of resources a patient is expected to consume in order for a disposition decision (discharge, admission, or transfer) to be reached (Gilboy et al., 2011, p. 7). The triage nurse arrives at the appropriate triage level by answering four key questions (or decision points): Does this patient require immediate life-saving intervention? Is this a patient who shouldn't wait? How many resources will this patient need? What are the patient's vital signs? (Gilboy et al., 2011, p. 7) These four key decision points, along with the applicable acuity level and resource needs, are illustrated below in Figure 5. As with any triage acuity scale, the ESI is recommended for use by experienced triage nurses and/or those who have undergone ESI-specific triage training (Gilboy et al., 2011).

Lab findings in ACS

MI results from complete coronary artery occlusion and consequent death (necrosis) of myocardial muscle cells distal to the occlusion. Ruptured plaque with thrombosis is responsible for approximately 90% of all MIs; new coronary artery thrombosis and coronary artery spasm (due to ruptured plaque) account for other causes.The following substances are biomarkers for MI (cardiac enzymes):Cardiac Troponin I (cTnI) and Troponin T (cTnT) are released following necrosis and rupture of myocardial cells, and are more sensitive to myocardial injury and infarction than CK-MB. Troponins rise within 3-6 hours after MI and peak in 12-48 hours (cTnI usually within 24 hours); they may also remain elevated up to 10-14 days. Troponin I or T should be measured upon arrival and within 3-6 hours of symptom onset, or beyond (i.e., patients with normal Troponin levels but intermediate- to high-risk for ACS).Note: Troponin levels are directly proportional to the size of infarct or myocardial damage (reassess on day 3 or 4 post-MI); however, elevated levels may also be due to myocardial necrosis unrelated to ACS (e.g., pulmonary embolus [PE], renal failure) Creatine kinase muscle-brain (CK-MB) is specific to cardiac muscle, and is indicative of myocardial damage if > 5% of total CK (with chest pain/other symptoms). It typically starts to rise 4-8 hours after myocardial necrosis, peaks in 15-24 hours, and returns to baseline within 48-72 hours. However, given the newer Troponin biomarkers, CK-MB is no longer useful for the diagnosis of ACS but may be used to estimate MI size.Myoglobin and C-reactive protein (CRP) are also no longer necessary for the diagnosis of ACS.The time from onset of occlusion to irreversible damage is primarily dependent on the amount of collateral flow to the affected area. If the area has no collateral flow and high O2 demands, the interval from onset of occlusion to irreversible damage ranges from 20-60 minutes. If the area has some collateral flow and low O2 demand, the window from occlusion to irreversible damage is approximately 2-6 hours.

ECG characteristics of ACS (How is ischmia/injury/infarction indicated on the ECG and which coronary artery is involved)

Myocardial ischemia and infarction both cause alterations that are usually seen on an ECG. An ST elevation myocardial infarction (STEMI) may demonstrate hyperacute T waves, T wave inversion, ST-segment elevation, pathological Q waves, and loss of R wave progression. A non-ST elevation myocardial infarction (NSTEMI) may demonstrate ST-segment depression and T wave inversion.It is not possible to distinguish a NSTEMI from unstable angina simply by assessing a 12-lead ECG. Further information is obtained by assessing cardiac markers, such as troponin levels.Electrocardiographic changes to T waves, ST-segments, Q waves, and R waves are described below.Hyperacute T Wave One of the earliest changes in the evolution of a transmural MI is the increased height of T waves ("hyperacute" or "tombstone" T waves). These are seen within minutes to hours of the onset of an MI.image13T Wave Inversion The T wave is normally seen in the same direction as the QRS that precedes it. Therefore, T waves are normally upright in leads I, II, aVL, aVF and V2 to V6. T waves are normally inverted in aVR. They may be upright or inverted in Leads III and V1. T wave inversion is illustrated in the image below .ST-segment ElevationThe ST-segment represents early repolarization of the ventricles and is normally at the same height as the PR segment. To determine the degree of displacement of the ST-segment, measure 0.04 seconds to the right of the J point. The J point is the place where the QRS complex and ST segment meet. ST segment elevation is associated with STEMI, pre-infarction, and pericarditis.ST segment depression is associated with NSTEMI and myocardial ischemia. ST elevation or depression is significant if it is:greater than 1 mm in two or more contiguous limb leadsgreater than 2 mm in two or more contiguous precordial leads Global ST elevation (ST elevation in almost all leads) may be indicative of pericarditis, as illustrated in the image below.Pathological Q WavesA pathological Q wave is greater than 0.04 seconds wide and more than 25% of the height of the preceding R wave (except in Leads III and aVR). An abnormal Q wave indicates death of myocardial tissue and may occur within hours or days after the onset of an acute MI. This is clinically significant because the necrotic area represented by the Q wave is no longer able to depolarize, providing clinicians with valuable prognostic information; however, it is not possible to determine when the infarction occurred. In addition, post-mortem research has shown that Q wave MIs tend to be larger (Delewi et al., 2013).In the image below, pathological Q waves can be seen in Leads V1-V6 indicating a previous anterior (anterolateral) MI. Also note the evidence of an evolving acute inferior MI shown by ST segment elevation is Leads III and aVF (Lead II also shows inverted T waves).Loss of R Wave ProgressionAs mentioned earlier, when looking at the anterior leads, the R wave of the QRS complex gets progressively taller from V1 to V6. This is called "R wave progression."With an anteroseptal MI, the R wave may not get progressively taller.

Drug Classifications

Normally, a cardiac impulse is conducted throughout the heart sequentially. With a re-entry circuit, however, abnormal cells alter conduction and allow cells to be activated more than once by the same impulse. In order for re-entry to occur, an area of slowed conduction and a one-way, or uni-directional, block are necessary. As the impulse circles a cell, or small group of cells, it is blocked in one direction, but can circle around in the other direction. When it meets the area of abnormality, the impulse is conducted through (remember, it was a one-way block only), but it is conducted slowly so that by the time it has passed through the area of abnormality, the other side has recovered and can be depolarized again. This sets up a circuit in which the same impulse goes around and around, causing repeated depolarizations. This differs from automaticity abnormalities in that the tissue is not repeatedly generating its own impulse. Instead, the impulse gets "stuck"; every time it goes around the circuit, it causes the depolarization of surrounding tissue.Medications and countershock both act to reset the re-entry circuit; however, the circuit may recur, particularly if the original problems of oxygenation, electrolytes, and acid-base status have not been addressed. Abnormal Impulse Conduction: Blocks With a block or delay of conduction, the tissue is unable to conduct the impulse normally through the conduction system. The impulse may be only delayed, affected by varying patterns of blockage, or blocked completely. Blocks in conduction may be transient or permanent and may occur anywhere along the conduction pathway, such as the SA node, AV node, or bundle branch network. Section 2: Antiarrhythmic Medications Antiarrhythmic medications are classified according to the dominant action on the cell. They are categorized as Class I, II, III, IV, and V (Miscellaneous).Class I Drugs: Sodium Channel BlockersThe main effect of Na+ channel blockers is on the fast-response cells. (Think back to the APs - which type of cell primarily depends on Na+ for depolarization?) By primarily blocking Na+ channels, these drugs slow depolarization during phase 0 and therefore prolong depolarization, as indicated by the dotted line in the image below. As a hint to help remember this class of drugs, many of them have "caine" in their names.Class I drugs are further subdivided into three categories, according to their effect on repolarization and their potency as Na+ channel blockers. These subsets are identified as Class IA, Class IB, and Class IC. Class IA Agents In addition to blocking Na+ (as all of the Class I drugs do), Class IA drugs also block K+ during repolarization; therefore, these medications have the potential to prolong the entire AP. On the electrocardiogram (ECG), this may be evidenced by widening of the QRS and a prolonged QT interval. Class IA medications can be used to treat both supraventricular (e.g., atrial fibrillation/flutter) and ventricular arrhythmias.Class IB AgentsIn addition to blocking Na+ channels, these drugs actually accelerate phase 3 repolarization and therefore do not prolong the AP or QT interval (and may actually shorten them). Class IB agents are used only to treat ventricular arrhythmias, such as ventricular fibrillation (VFib, VF) and/or ventricular tachycardia (VTach, VT).Class IC AgentsThese drugs are the most potent Na+ channel blockers of this class and have minimal effect on phase 3 repolarization. Some of these drugs may be associated with a higher mortality; however, a recent study indicates that these drugs may be useful in the treatment of atrial fibrillation (Stiell et al, 2011). Class II Drugs: Beta Blockers Beta-blocking drugs compete with endogenous catecholamines for available beta receptor sites on the cell membrane. As a hint, many of these drugs have "lol" at the end of their generic names (e.g., Metoprolol).An awareness of normal beta stimulation effects will enable you to anticipate the effects of beta-blocking agents. Beta blockers slow the influx of Ca2+ during the depolarization of slow-response cells, causing a decreased heart rate .Class II antiarrhythmic medications are used only for supraventricular rhythms, such as atrial fibrillation and atrial flutter; they have no effect on ventricular arrhythmias, such as VT and VF.Noncardioselective (e.g., propranolol, sotalol)Block beta-1 (heart, kidneys) and beta-2 receptors (lungs, liver, skeletal muscle)Beta-1 effectsCardiac: decreased heart rate, force of ventricular contraction, and impulse conduction through AV node (end result = decreased cardiac output)Renal: renin suppressionBeta-2 effectsRespiratory: bronchoconstriction, vasoconstrictionHepatic and skeletal muscle: decreased glycogenolysisContraindicated in heart failure, AV heart blocks, sinus bradycardia, asthma, bronchospasm; used with caution in diabetes (may mask symptoms of hypoglycemia)Cardioselective (e.g., metoprolol, atenolol)Block beta-1 receptors (heart, kidneys)Cardiac effects: as aboveRenal effects: as aboveContraindicated in sinus bradycardia AV heart block greater than first degree; used with caution in heart failure, asthma, diabetes Minimal beta-2 blockade, thus safer than propranolol in asthma and diabetes; may mask symptoms of hypoglycemia (Burchum & Rosenthal, 2019, pp. 164-171)Vasodilating (e.g., labetalol, carvedilol)Block alpha-1 receptors (vascular smooth muscle), resulting in vasodilation, as well as beta-1 and beta-2 receptors Alpha-1 effects: dilation of arterioles, veins Decreased systemic and peripheral vascular resistance Beta-1 effects: as above Beta-2 effects: as above (may vary from drug to drug)May also exacerbate bradycardia, AV heart blocks, and asthma Venous alpha-1 blockade may produce postural hypotension (Burchum & Rosenthal, 2019, p. 519)As a review, identify three cardiac effects of beta stimulation. In addition, state one respiratory effect of beta stimulation.Identify two cardiac effects of beta blockade.State one potential respiratory effect of beta blockade. Cardiac effects of beta stimulation Increased heart rate Increased force of myocardial contractionIncreased speed of conduction through the AV nodeThe respiratory effect of beta stimulation is bronchodilation.Two cardiac effects of beta blockade Decreased force of myocardial contraction (negative inotropic effects)Decreased speed of conduction through the AV node (AV blocks) (negative chronotropic effects)One potential respiratory effect of beta blockade is bronchoconstriction. Class III Drugs: Potassium Channel Blockers There is no short-cut method for remembering this group of drugs, unlike the "caines" and the "lols." Class III agents slow down phase 3 repolarization, prolong the refractory period, and lengthen QT intervals.Although amiodarone actually has properties of all classes of drugs, its main effect is that of a K+ channel blocker.Class III agents can be used to treat both ventricular and supraventricular arrhythmias. Upgrade to remove ads Only CA$44.99/year Class IV Drugs: Calcium Channel Blockers Class IV drugs are similar to beta-blocking agents in their effects; however, the mechanism of action differs. Calcium channel blockers (CCBs) slow the entry of Ca2+ into the slow-response cells and thus, slow automaticity and heart rate.Remember that Ca2+ is required for contraction; therefore, anything that inhibits the entry of Ca2+ into the cell will decrease contraction.Class IV drugs are used to treat supraventricular arrhythmias, such as atrial flutter and atrial fibrillation. Hypotension is a common side effect, and should be used with caution in heart failure, AV blocks, or bundle branch blocks (BBBs). Class V Drugs: Miscellaneous, Unclassified AdenosineAdenosine inhibits impulse formation in the SA node and slows conduction through the AV node. It is used to convert stable supraventricular tachycardias (SVTs), including PSVT, as well as AV nodal and reentrant tachycardias (e.g., Wolff-Parkinson-White [WPW] syndrome). Side effects include flushing, dyspnea, chest pain or tightness, hypotension, sinus arrest, and AV blocks. Adenosine has a very short half-life and is usually cleared from the body within 10 seconds.AtropineAtropine is classified as an anticholinergic drug, thus it acts mainly on the vagus nerve by blocking the effects of acetylcholine thereby affecting vagal tone. It increases SA nodal impulse formation and decreases AV nodal conduction time and effective refractory period; the end result is increased heart rate and conduction velocity. Atropine is used in symptomatic sinus bradycardia and second-degree AV block type I; it is unlikely to be effective for second-degree type II and third-degree heart block unless the block is located in nodal tissue. Side effects include tachycardia and other anticholinergic effects (e.g., pupil dilation, dry mouth).MagnesiumMagnesium plays a role in suppressing the amplitude of early afterdepolarizations (EADs) by inducing resting depolarization and blocking the influx of Ca2+. Side effects include central nervous system (CNS) and respiratory depression, vasodilation, and hypotension; it should also be used with caution in renal failure. It is the treatment of choice for torsades de pointes (a type of polymorphic VT) and may be helpful in the treatment of both supraventricular and ventricular arrhythmias. Antiarrhythmic Drug Summary Class Classification Examples Indications ECG EffectsClass IA Sodium channel blockers Quinidine Procainamide Disopyramide Supraventricular and ventricular arrhythmias(e.g., AFib - Procainamide [pharmacologic cardioversion] Widened QRS Prolonged QT interval Class IB Sodium channel blockers Lidocaine Mexiletine Tocainide Ventricular arrhythmias(e.g., Refractory VFib - Lidocaine) Shortened QRS and QT interval Class IC Sodium channel blockers Flecainide Encainide Propafenone Supraventricular and ventricular arrhythmias Prolonged PR interval and QRS duration Class II Beta blockers Esmolol Metoprolol Propranalol Supraventricular arrhythmias only(e.g., AFib - Metoprolol [rate control]) Bradycardias AV blocksProlonged PR interval Class III Potassium channel blockers Amiodarone Ibutilide Sotalol Dofetilide Supraventricular and ventricular arrhythmias(e.g., VFib 2nd line - Amiodarone) Prolonged QT interval Class IV Calcium channel blockers Diltiazem* Verapamil** Nifedipine Supraventricular arrhythmias(e.g., AFib - Diltiazem [rate control])AV blocks Prolonged QT interval* Hypotension** Reflex tachycardia Adenosine Miscellaneous N/ASVT Wide QRS complex tachycardia (regular, monomorphic only) Bradycardia AV blocks Asystole Atropine Miscellaneous N/ASymptomatic sinus bradycardia 2nd-degree AV block Type I Tachycardia Bradycardia(if dose < 0.5 mg) Magnesium Miscellaneous N/A Torsades de pointes (treatment of choice)Supraventricular and ventricular arrhythmias Ventricular arrhythmias (due to digitalis toxicity; life-threatening)Bradycardia AV blocks Inotropic Medications Cardiac Glycosides Digoxin is classified as a cardiac glycoside. Its mechanism of action is mainly the inhibition of a component of the Na+/K+/ATP pump, which results in Na+/Ca2+ exchange and subsequent increased intracellular Ca2+. The net effect is increased force of myocardial contraction, lending to its use in heart failure. At therapeutic levels, digoxin also increases vagal tone resulting in decreased SA and AV nodal conduction. The main therapeutic effects of digoxin are decreased ventricular response (rate control, such as in atrial fibrillation) and symptom management in severe heart failure.Side effects of digoxin can either be therapeutic (digitalis 'effect', as noted above) or toxic. Therapeutic ECG effects include PR interval prolongation, ST-segment depression and T wave abnormalities (inverted, flattened, or biphasic; 'scooping' or 'sagging' ST-T complexes), QT interval shortening, and prominent U waves. Toxic effects (digitalis 'toxicity') include physical signs/symptoms, such as lethargy, visual disturbances (e.g., "halo"), hallucinations/delirium, severe headache, diarrhea, and abdominal pain. Toxic ECG effects include frequent ventricular ectopy (i.e., bigeminy, trigeminy) and almost any dysrhythmia (except for sinus tachycardia, SVT, and rapid atrial fibrillation) (Wetherell, 2015).In Figure 16 below, note the biphasic T wave (initial negative deflection, terminal positive deflection) and prominent U wave superimposed on the T wave. Sympathomimetic Agents Sympathomimetic agents stimulate adrenergic (i.e., alpha, beta) receptors, producing similar effects to those seen in stimulation of the sympathetic nervous system. These agents may be endogenous (i.e., epinephrine, dopamine, norepinephrine) and synthetic (i.e., dobutamine, isoproterenol). They are most commonly used in the management of hypotension, shock, and other hemodynamically unstable conditions. Receptor selectivity of sympathomimetic agents varies widely and their effects are dose-dependent (see Table 15.19 in Urden et al., 2022, p. 412). While these agents play a vital role in restoring and maintaining hemodynamic stability, they also have the potential to produce significant adverse effects at higher doses or with prolonged use. Dopamine Dopamine is one of the most commonly used drugs in emergency and critical care settings in the management of hemodynamically unstable patients. As a chemical precursor to norepinephrine, it stimulates both alpha- and beta-receptors, as well as dopaminergic receptors. It is used as a second-line agent in symptomatic bradycardia (after atropine) and for hypotension with signs and symptoms of shock. Intravascular volume must be corrected prior to initiating a dopamine infusion ("top up the tank first") (American Heart Association [AHA], 2016).Low dose (<3 mcg/kg/min), often controversially referred to as "renal dose": stimulates dopaminergic receptors which results in renal and mesenteric vasodilation, and subsequent increase in renal perfusion and urine output. Despite an increase in urine output, acute kidney injury remains a potential complication in the hypotensive or shock patient.Intermediate dose (3-10 mcg/kg/min): beta-1 receptors are stimulated, leading to increased cardiac contractility and cardiac output, as well as norepinephrine release.High dose (11-20 mcg/kg/min): alpha effects (vasoconstriction) predominate (Dirks & Waters, 2022, p. 412; Overgaard & Dzavik, 2008, p. 1047).The typical infusion rate of dopamine ranges from 2 to 20 mcg/kg/min and is titrated to patient response, slowly tapered accordingly (AHA, 2016, p. 174). Dobutamine Dobutamine mainly produces beta-1 adrenergic effects (enhanced cardiac contractility), in addition to slight beta-2 (mild vasodilation) and alpha (vasoconstriction) adrenergic effects. Due to its strong beta-1 inotropic effects, it has less of an influence on heart rate (weak chronotrope). Dobutamine is a primary drug used in the management of heart failure due to its mild vasodilatory effects. The net effect of beta-2 and alpha stimulation is mild vasodilation, making it suitable for patients with heart failure who cannot tolerate vasodilator therapy.Low dose (< 15 mcg/kg/min): increased cardiac contractility with little effect on peripheral vascular resistance (net effect of beta-2 and alpha receptor stimulation described above).High dose (≥ 15 mcg/kg/min): vasoconstriction predominatesThe typical infusion rate of dobutamine ranges from 2 to 20 mcg/kg/min and is titrated to patient response, slowly tapered accordingly (Dirks & Waters, 2022, p. 411; Overgaard & Dzavik, 2008, pp. 1047-1048). Epinephrine Epinephrine (Adrenalin) is an endogenous catecholamine produced by the adrenal glands. It has a strong affinity for both alpha- and beta-receptors, with its effects also being dose-dependent. Beta effects predominate at low doses, whereas high doses result in alpha effects. Epinephrine 1:10,000 concentration is administered intravenously in profound bradycardia or hypotension, as well as cardiac arrest; this must not be confused with the 1:1,000 concentration that is administered intramuscularly or subcutaneously in anaphylaxis. Low dose (< 2 mcg/kg/min): stimulates beta-receptors leading to increased heart rate, cardiac conduction, contractility, and vasodilation, with the net effect being increased cardiac output.Intermediate dose (2-8 mcg/kg/min): beta-1 effects predominate; however, alpha mediated vasoconstriction and increased peripheral vascular resistance occur.High dose (9-20 mcg/kg/min): alpha and beta-1 effects predominate (Dirks & Waters, 2022, p. 412; Overgaard & Dzavik, 2008, p. 1048). Norepinephrine Norepinephrine (Levophed), also an endogenous catecholamine, produces similar effects as epinephrine with the exception of beta-2 effects; it only stimulates alpha and beta-1 receptors, with minimal effect on heart rate. Norepinephrine's potent alpha effects are evident at lower doses, with massive vasoconstriction occurring as the dose is titrated upwards. This agent is mainly used as a vasopressor in shock states.Low dose (< 2 mcg/kg/min): stimulates alpha-receptors leading to increased peripheral vascular resistance, as well as modest beta-1 receptor mediated increase in cardiac contractility and cardiac output.High dose (2-16 mcg/kg/min): massive alpha effects (vasoconstriction) predominate (Dirks & Waters, 2022, p. 412; Overgaard & Dzavik, 2008, p. 1048). Vasopressor Medications Vasopressin The sympathomimetic agents described above are often used for their vasopressor effects; however, the increased afterload (systemic vascular resistance [SVR]) produced by these drugs forces the damaged heart to work even harder.Vasopressin is a synthetic form of antidiuretic hormone that exerts its effects by stimulating vascular smooth muscle receptors, thereby causing less stress to the heart; vascular receptors are also located in the renal tubules, which lead to water reabsorption when activated. Vasoconstriction of capillaries and small arterioles are the major effects of vasopressin. Vasopressin is said to increase the vascular sensitivity to norepinephrine, thus may be used as an adjunct to norepinephrine in refractory shock (Dirks & Waters, 2022, p. 415; Overgaard & Dzavik, 2008, p. 1051).Vasodilator MedicationsThe table below outlines some of the most commonly used vasodilator medications in emergency and critical care settings. Their respective drug classifications, indications for use, mechanisms of action, and related nursing considerations are described.described.Classification (with examples)Indications Mechanismof Action Nursing Considerations Direct smooth muscle relaxants(e.g., nitroprusside, nitroglycerin, hydralazine)Nitroprusside: hypertensive emergencies, severe heart failure (HF)Nitroglycerin:acute HF, acute coronary syndrome (ACS; unstable angina, myocardial infarction [MI])Hydralazine: hypertension (HTN), pre-eclampsia Activation of nitrous oxide causes direct vascular smooth muscle vasodilation; decreases peripheral vascular resistance Nitroprusside:potent, rapid venous/arterial vasodilation Nitroglycerin:venous/ arterial vasodilation (> venous; > arterial at higher doses), reduces cardiac filling pressures, pulmonary congestion, cardiac workload/O2 consumption; dilates coronary arteriesHydralazine:potent arterial dilation Hypotension(compensatory mechanisms: reflex tachycardia, sodium/water retention)Headache Nitroprusside:toxicity (confusion, nausea, tinnitus); renal dysfunction Nitroglycerin: hypotension, reflex tachycardia, headache; decreased efficacy with prolonged useHydralazine:reflex tachycardia Calcium channel blockers Dihydropyridines(e.g., nifedipine, nicardipine)Non-dihydropyridines Benzothiazines (e.g., diltiazem)Phenylalkylamines (e.g., verapamil)Dihydropyridines:HTN, including stroke; vasospastic angina Non-dihydropyridines:angina, HTN, dysrhythmias (rate control)Dihydropyridines:block calcium channels in coronary and cerebral vessels (arterial vasodilation); no direct effect on automaticity, conduction, contractility Non-dihydropyridines:block calcium channels in heart and blood vessels (coronary and peripheral vasodilation, SA and AV node blockade, decreased force of contraction) Dihydropyridines:hypotension, reflex tachycardia; flushing; headache Non-dihydropyridines:dizziness, headache; flushing, peripheral edema, HF; constipationAngiotensin-converting enzyme inhibitors(ACEIs)(e.g., captopril, enalapril, ramipril)HTNHFPost-MIDiabetic/Non-diabetic nephropathy Prevents conversion of angiotensin I to angiotensin II (renin-angiotensin-aldosterone [RAAS] system); decreases afterload (causes vasodilation)Limits ventricular modeling post-myocardial infarction, HF Hypotension Non-productive cough (may not tolerate)Hyperkalemia Renal failure (if renal stenosis)AngioedemaLiver dysfunctionAngiotensin II receptor blockers(ARBs)(e.g., candesartan, losartan, valsartan) HTN HF Post-MI Diabetic nephropathy(mainly when ACEIs not tolerated) Direct blockade at angiotensin II receptor site; decreases afterload (causes vasodilation)Limits ventricular modeling post-myocardial infarction, HF Renal failure (if renal stenosis)Angioedema Alpha-adrenergic blockers Labetalol:acute stroke, hypertensive emergencies, acute aortic dissection Phentolamine:catecholamine-induced HTN (e.g., pheochromocytoma) cocaine toxicity, extravasation of vasopressors (prevents necrosis), reversal of soft tissue anesthesia (reverses local anesthetic-mediated vasoconstriction)Labetalol:peripheral arterial/venous alpha receptor blocker (vasodilation); cardioselective beta-1 receptor blocker (decreased force of contraction, rate of conduction) Phentolamine:Nonselective peripheral arterial alpha blocker (arterial vasodilation) Labetalol: orthostatic hypotension, syncope, AV blocks; bronchospasm; fluid/water retention (long-term therapy) Phentolamine:orthostatic hypotension, reflex tachycardia; nasal congestion FIND ANSWERS BELOW !! Which of the following cardiovascular drugs is most appropriate in the treatment of symptomatic bradycardia?Dobutamine Digoxin Dopamine Norepinephrine The nurse is caring for a patient receiving a nitroprusside infusion. Which of the following signs and symptoms is indicative of toxicity? Hypotension Reflex tachycardia Headache Tinnitus With regards to sympathomimetic drugs, what is meant by the term "dose-dependent"? Include specific examples in your answer. Click here to view the suggested answers. Dopamine is most appropriate in the treatment of symptomatic bradycardia due to its beta effects.d. Tinnitus is indicative of thiocyanate toxicity due to prolonged infusion of nitroprusside. With regards to sympathomimetic drugs, the term "dose-dependent" refers to the range of drug effects that are produced at varying drug dosages. In other words, when the dose of the drug is changed, the effects also change. This is largely due to the drug's specificity and/or affinity for alpha- and beta-receptors.With epinephrine, for example, beta-adrenergic (beta-1 and beta-2) effects are more pronounced at lower doses, whereas alpha-adrenergic (alpha-1) effects predominate at higher doses. This principle also applies to dopamine; at low doses, dopamine mainly binds to dopaminergic receptors, producing vasodilation. As the dose increases, beta-1 and alpha-1 receptors are stimulated causing increased heart rate, cardiac output, and vasoconstriction, respectively.

Ethical and Legal Obligations: Clinical Case

Nurse A. is working the evening shift at the rural ED where she is employed. Nurse A. is a devoutly religious person, and has strong moral opposition to abortion. As an emergency nurse, she was fairly confident that abortion would rarely be encountered in this setting, and it was one of the main reasons she has never worked in a gynecological nursing setting. During this shift, Nurse A. receives a 25-year-old female patient, who had a pregnancy termination two days ago. She is having heavy vaginal bleeding, decreased level of awareness, and has a fever. Right away, Nurse A. can tell that this presenting history is influencing her feelings toward the patient. She goes through the motions of getting the patient attached to the monitor, doing baseline vitals, and starting an IV and fluids—but she feels inside that she will not in good conscience be able to take care of this person given her conscientious objection to abortion. Questions: What are Nurse A.'s ethical obligations to this patient? What are Nurse A.'s legal responsibilities to this patient? Answer - Ethical and Legal Obligations: Clinical Case In the interest of the principals of beneficence, non-maleficence, and promoting justice, Nurse A. is ethically obligated to provide care for this individual as this patient presents with an emergent condition. In order not to abandon her patient, she is legally and contractually obligated to provide the necessary care to this patient until other arrangements or handover to a colleague can occur.

Negligence and Duty: Clinical Case

Nurse S. is an emergency room nurse with 15 years' experience. Newly divorced, she has recently started going to more social events in an effort to meet new people. Nurse S. ended up going to a party the night before her scheduled shift, and was drinking until about three hours before the start of her 7:00 a.m. shift in emergency. This was highly out of character for her. Instead of calling in sick (which she hates to do), she decided to go to work as she was only working a short day. She was still quite intoxicated. As is the case for most shifts at the busy urban ED where Nurse S. is employed, she hit the ground running, taking over care for a patient who was suffering from an acute MI and awaiting transfer to the cath lab for cardiac stenting. She receives report from her co-worker, who comments on her looking hung-over or even still drunk. Nurse S. shrugs off the comment and the night shift nurse goes home. The patient was having persistent chest pain, was on a nitroglycerin drip, and a heparin drip. He was also receiving intermittent injectable morphine for pain. Nurse S. does not remember at shift change to ensure that all monitor alarms are set and parameters are appropriate. Nurse S. was feeling a bit fuzzy-headed as she was still under the effects of the alcohol. Her patient begins complaining of worsening chest pain, so Nurse S. decides to increase his nitroglycerin drip by the standard 10 mcg increment from his current dose of 40 mcg/minute. Nurse S. does not check the patient's blood pressure prior to increasing the dose, and in error actually increases the dose to a dangerous 500 mcg/minute instead of the intended 50 mcg. She is distracted by her colleague calling for help with a new trauma patient that had arrived in the next room, cancels the alarm on her patient's IV pump without looking at the alarm message (which was to alert her of this maximal dose) and goes over to see if she can help her colleague. While Nurse S. is in the next room, her patient's blood pressure undergoes a precipitous drop and he loses consciousness. Because the alarms are not set properly, this goes unnoticed, and the patient goes into cardiac arrest from prolonged hypotension. Nurse S. returns to her patient to check his pain level, finds that he is without vital signs and calls a Code Blue, but he cannot be revived. Questions: Describe how Nurse S.'s actions can be seen as criminal negligence. Is Nurse S.'s intoxication a defense for her actions? What was the duty of the night-shift nurse if she suspected that Nurse S. had been drinking? reach of duty to care, where her actions were a substantial departure from what is expected, and severe damages to patient resulting in death (Keatings & Smith, 2010). No, in fact this may add to the recklessness of her behaviour, and actually support her actions as criminal in nature (Keatings & Smith, 2010). Duty to report (discussed further in upcoming section), and ethical obligation to ensure safe patient care.

Providing Care in a Communicable Disease Outbreak or Pandemic

Nurses have historically put themselves in harm's way in order to care for people living in war-torn areas, poverty, and poor sanitation. They have also been at the forefront in dealing with outbreaks of communicable disease, or even more widespread pandemics. Emergency nurses are the gatekeepers for communicable disease right from triage, and should screen for febrile respiratory illness and travel history to help contain suspected communicable disease right away. These efforts by nurses at times risk their own personal health for their professional, ethical, and legal duty to care for others. Questions to Ponder: When does our profession ask too much? Can a nurse choose to withdraw or refuse care? What ethical principle comes to mind when considering care during outbreaks? According to the CNA (2017, p. 38), the concept of unreasonable burden comes into play when there are disproportionate threats to our personal or our family's wellbeing, or when resources are not adequate to allow safe care in accordance with our professional standards. Read

Location of Care

Once the triage nurse has assigned an acuity score, he/she utilizes this information to select the most appropriate location of care for the patient. Urban EDs typically have designated trauma and resuscitation areas (CTAS level 1 and 2), monitored beds with continuous cardiorespiratory monitoring capabilities (CTAS level 2 and 3), unmonitored beds for stable urgent and non-urgent conditions (CTAS level 3 to 5), fast-track or ambulatory care areas for minor 'walking wounded' (CTAS level 4 and 5), and an area allocated for patients with acute mental health conditions (wide range of acuity levels). Some also have rooms designated for specific types of complaints, such as ocular ('eye room') and gynecological ('gyne room') problems. In regional, community, or rural settings, however, EDs may not be designed to accommodate certain conditions as easily. The triage nurse must use his/her advanced critical thinking and decision-making skills to ensure that patients will be able to receive the care they need in the area to which they are assigned. For example, in a rural setting, the patient who presents with suspected cardiac-type chest pain should be assigned to a bed with portable continuous cardiorespiratory monitoring and within view of the nurses' station, as opposed to the procedure room down the hall. The patient with an apparent communicable disease who presents to a community urgent care center should be assigned to a private room that can accommodate infection control protocols (e.g., negative pressure, airborne/droplet/contact precautions), rather than the ambulatory care area where beds are separated by curtains. Staffing requirements should also be considered when assigning location of care. Inappropriate nursing staff mix (i.e., skill mix, levels of experience) can lead to feeling extremely distressed and overwhelmed, particularly in a chaotic and unpredictable environment such as the ED (Wolf et al., 2017). By communicating regularly and openly with the charge nurse or supervisor, the triage nurse can keep abreast of the staffing situation in the department which will facilitate assigning the patient to the right area at the right time (and to the right nurse). To illustrate, here is an example: A patient with an acute myocardial infarction arrives requiring immediate fibrinolytic therapy, but all the monitored beds or those allocated to emergent patients are occupied. The only available bed in the ED is in the nonurgent, unmonitored area and the nurse assigned to this patient care area is a new graduate. Where should the patient be assigned? Should the patient be assigned to the empty bed with a portable cardiac monitor at the bedside so fibrinolysis can get underway? Time is muscle, right? Right, but also wrong. Assigning a patient to an area that is ill-equipped to facilitate fibrinolytic therapy and to a nurse with limited emergency nursing experience places the patient and nurse at significant risk. In this case, the triage nurse should inform the charge nurse that a bed for a CTAS level 2 patient is required; the charge nurse could then consult with the nursing staff in that area to determine if any of their patients are stable enough to be moved to a less acute area or perhaps arrange to have an admitted patient transferred to the ward as soon as possible. One of the most important roles of the triage nurse is problem-solving; he/she must be intimately familiar with departmental and institutional policies and processes. Note: The purpose of this module is to provide an introduction to triage, thus students are only expected to become familiar with general triage principles and processes and have a basic understanding of CTAS acuity levels. ***If a patient looks sick and you are not sure, triage them as Level I or II*** (Beveridge et al., 2018, para. 4)

Modifiers (First Order, Second Order)

Once the triage nurse has chosen the appropriate CEDIS complaint, and considered information gathered from the critical 'first look' and triage interview, the next step is the selection of relevant modifiers. In most cases, more information is needed to aid in triage decision-making. "Modifiers provide additional acuity information to the presenting complaint and help assign the appropriate CTAS level" (CTAS National Working Group, 2013c, p. 21). First Order Modifiers: broadly applicable to a majority (but not all) of CEDIS complaints, prioritized according to ABCDE as follows: Vital signs (supported by 'critical look', if applicable) Respiratory distress (Airway, Breathing) E.g., Moderate respiratory distress with oxygen saturation (SpO2) < 92% = CTAS level 2 Hemodynamic status (Circulation/Control of hemorrhage) E.g., Blood pressure (BP) and heart rate (HR) at lower limit of normal, no other evidence of hemodynamic compromise = CTAS level 3 Level of consciousness (Disability) E.g., Unconscious, unable to protect airway = CTAS level 1 Temperature (Environmental) E.g., Immunocompromised, fever > 38ºC (> 17 years of age) = CTAS level 2 E.g., Temperature > 38ºC or < 36ºC (0-3 months of age) = CTAS level 2 Other first order modifiers are then considered and applied, as relevant: Pain severity (central, peripheral; acute, chronic) E.g., Moderate pain (score 4-7), central location, acute = CTAS level 3 Bleeding disorder (e.g., hemophilia, liver disease, anticoagulant use) E.g., Femur fracture, patient taking anticoagulants = CTAS level 2 Mechanism of injury (MOI) Refers to the transfer of energy from the environment to the patient; provides insight regarding "how much energy or force was applied to the patient's body structures and organs" (CTAS National Working Group, 2013c, p. 28) E.g., General trauma, Fall from > 18 feet = CTAS level 2 (CTAS National Working Group, 2013c, pp. 22-29, 48) It should be noted that not all presenting complaints require modifiers. For example, the patient who arrives in cardiac arrest is assigned a CTAS level 1 because no other information is needed to determine acuity rating. The patient who arrives with a complaint of chest pain of apparent cardiac origin is assigned an acuity rating of level 2, unless they are in shock or experiencing severe respiratory distress (level 1) (CTAS National Working Group, 2013c). Second Order Modifiers: specific to a limited number of complaints, most often applied after selection of presenting complaint and first order modifiers have not assigned a higher acuity level (more information still needed, additional features that influence acuity rating) (CTAS National Working Group, 2013c, p. 21). Blood glucose and degree (severity) of dehydration are examples of second order modifiers that may lead to the assignment of a higher acuity level (CTAS National Working Group, 2013c, p. 29). In some cases, first order modifiers may not be applicable to the presenting complaint in which case second order modifiers are the main determinant of acuity level assigned. E.g., CEDIS presenting complaint = Pregnancy issues > 20 weeks; second order modifier = vaginal bleeding 3rd trimester (CTAS level 1) (CTAS National Working Group, 2013c, p. 57)

Professional Liability Insurance

Our world is becoming increasingly litigious, and health-care professionals are being held to higher and more rigorous standards for care (Keatings & Smith, 2010). It has become a requirement in Canada for nurses to have professional liability insurance over and above the liability protection their employers provide. With the exception of Ontario and Quebec, CNPS liability coverage is automatically available to nurses through their respective Colleges or their Registered Nurses Associations (CNPS, 2019). Ontario and Quebec nurses can obtain extra professional liability insurance through their associations, or they can purchase CNPS coverage independently or through membership with the Canadian Nurses Association (CNPS, 2019). Read Follow the links below to read more about professional liability protection, what is covered, and what is not. Canadian Nurses Protective Society (CNPS). (2020). Services. Retrieved September 7, 2020, from https://cnps.ca/services/ Registered Nurses' Association of Ontario (RNAO). (2013). CNO's professional liability protection requirement. https://rnao.ca/sites/rnao-ca/files/3_Ways_to_Meet_CNOs_PLP_Requirement_-_RNAO_Membership_Factsheet_revised_11_29_2013.pdf Practice Question 9 Professional Liability Insurance Questions: What are the three main components of liability protection? If someone complains about you to your College, are you covered for that investigation? Professional Liability Insurance Legal advice, assistance with legal proceedings, and risk management and education. No, you would need to purchase supplementary liability insurance (see the CNPS website).

The Nature of Emergency Nursing

Practice environments greatly affect a nurse's ability to maintain standards of ethical practice (CNA, 2017). During this next section, consider the following question: Question to Ponder: What are the unique ethical challenges that emergency nurses face? History of Emergency Nursing The provision of emergency nursing care to patients can be traced back to Florence Nightingale. In 1854, she led fellow nurses onto the battlefield during the Crimean War to provide care to ill and injured soldiers. They rapidly sorted the ill and injured to identify those most in need of nursing care and urgent intervention (known today as triage). Nightingale and her colleagues were also instrumental in decreasing morbidity and mortality rates by instituting hygiene standards and patient safety measures (Gebbie & Qureshi, 2006). In addition to tending to patients' physical needs, Nightingale was credited for recognizing that patients also required social care, and that these two dimensions were not mutually exclusive (MacMillan, 2012). These early characteristics of emergency nursing care continue to be fundamental competencies of today's emergency nurse. Emergency care continued to evolve throughout the 20th century as the environment within which it was provided transitioned from first aid rooms, to emergency rooms, to much larger specialized emergency departments (EDs) (Solheim, 2016). In Canada, emergency medicine became recognized as a specialty in 1981 (Canadian Association of Emergency Physicians, 2016). In 1982, emergency nursing followed suit and embarked on a path toward specialization with the establishment of the National Emergency Nurses Association (NENA); designation as a specialty was granted in 1991 (NENA, 2018), followed by the development of the first certification exam in emergency nursing by the CNA in 1994 (West et al., 2011). As the national voice for emergency nurses, NENA continues to promote emergency nursing by facilitating professional development, advocating for emergency nursing issues, and developing practice guidelines and standards to ensure the highest quality emergency nursing care (NENA, 2018). Nature of Work To understand and effectively manage the ethical dilemmas that may be encountered during emergency nursing practice, health-care providers must be familiar with the nature and scope of emergency nursing practice. NENA (2018) describes the nature of emergency nursing as follows: Unlike many nursing specialties, emergency nursing transcends any narrow confines, and includes the provision of care that ranges across all demographics and physiologic processes: from birth to death; health promotion to end of life care; behavioral health to infectious illness; chronic disease to sudden health collapse; intermittent crises to progressive decline in health. The application of the nursing process to patients of all ages requiring stabilization and/or resuscitation for a variety of illnesses and injuries defines the nature of emergency nursing practice. Addressing the need or perceived need, for unplanned emergent care in an unscheduled manner, with an expanded potential for a stressful, chaotic environment defines the character of emergency nursing (p. I). The scope of emergency nursing includes: Triage and prioritization Stabilization and resuscitation Assessment, nursing diagnosis, planning, and implementation of interventions where limited data may be available, followed by evaluation of patient response Provisions of care in uncontrolled and/or unpredictable situations Crisis interventions to meet the needs of unique patient situations Emergency operations preparedness Education of the patient and community to facilitate attainment of an optimal level of wellness Wellness initiatives directed to patient and community, particularly related to disease and injury prevention Research Management Education and mentorship Advanced practice Forensic nursing (NENA, 2018, p. II). When looking at the unique environment of the emergency department (ED), we begin to see that ethical practice is influenced by both external and internal factors.

Ethical - Section 1: Review Quiz

Question 1 0 out of 1 points What does research show to be among the most ethically distressing situations emergency nurses face? Selected Answer:a. Trying to balance life with family responsibilities Answers:a. Trying to balance life with family responsibilities b. Working with colleagues whom the nurse feels are incompetent c. Providing aggressive care that is considered futile d. Watching patients suffer in spite of pain management efforts e. b, c, and d Question 2 1 out of 1 points Ethical distress can manifest in nurses as: patient avoidance, lateral violence toward co-workers, and practice errors. Selected Answer: True Answers: True False Question 3 1 out of 1 points If a nurse has a conscientious objection to a specific aspect of care that may be required in the ED, he or she must do which of the following: Selected Answer:d. Both b and c Answers:a. Avoid that aspect of care whenever possible, as there is no ethical obligation to provide care that the nurse objects to b. Provide care despite the objection, until alternate arrangements can be made c. Notify the employer of this objection prior to starting employment if possible d. Both b and c Question 4 1 out of 1 points According to CARNA (2010), the ethical principles central to decision making include: autonomy, beneficence, non-maleficence, and distributive justice. Selected Answer: True Answers: True False Question 5 1 out of 1 points Which ethical principle comes into question when considering offering health-related advice to someone over the telephone? Selected Answer:c. Non-maleficence Answers:a. Beneficence b. Ethical dilemma c. Non-maleficence d. Distributive justice Question 6 1 out of 1 points When can patient confidentiality ethically and legally be breached? Selected Answer:b. When harm may come to a patient if confidentiality is maintained Answers:a. When a police officer requests it b. When harm may come to a patient if confidentiality is maintained c. When discussing an interesting case in a debriefing session d. For research purposes Question 7 1 out of 1 points What resources can emergency nurses access for assistance with ethical dilemmas? Selected Answer:e. All of the above Answers:a. The CNA's Code of Ethics b. Provincial and territorial regulatory colleges c. Local union representatives d. Hospital ethics committees e. All of the above

Confidentiality and Personal Health Information

Questions: Who are the custodians of personal health information (PHI)? What are the five exceptions to maintaining patient confidentiality? What should you do if you aren't sure whether PHI can be disclosed to the police? Confidentiality and Personal Health Information Health-care practitioners who are independent are custodians of PHI, as is anyone who is an employee of a custodian of PHI, which is the case for hospitals or clinics (CNPS, 2014b). As such, a nurse in an emergency department would have to check with her or his supervisor, manager, or privacy officer to get permission to disclose PHI that is legally requested. Five exceptions:Court orders such as search warrants or subpoenas.Public safety, such as in a case where a clear and imminent threat of bodily harm or death exists.Legislative duties: This applies when there is a reportable injury or illness such as a gunshot wound or an infection that is reportable to Public Health, such as HIV. Another example would be suspected abuse of a child.Police investigation involving the patient.Police investigation involving a nurse, such that interviews of fellow nurse co-workers may involve divulgence of some patient information in order to discuss conduct of the nurse in question (CNPS, 2014b, para. 6-13). We must not look to police to decide whether PHI should be released. Just because police ask for information doesn't mean we are legally obligated to breach patient confidentiality and provide it. If not clear and outlined in a warrant, nurses must ensure they know which persons at their institution have the authority to make disclosure decisions, so that they can consult with such an authority (CNPS, 2014b, para. 15).

Rural Triage

Rural health care settings are unique in many ways, such as limited medical and nursing staff. Lack of 24-hour physician coverage in the ED is not uncommon practice in rural EDs across Canada. As a result, rural ED physicians may not be able to assess non-urgent patients within the CTAS timeframe guidelines, leading to the implementation of a medical directive permitting specially-trained emergency nurses to refer CTAS level 5 patients to an alternate, more appropriate, health care provider or to return to the ED at a later time. The following criteria must be met for the medial directive to be implemented: ED physicians may not be on site. There is a protocol for ambulances to call ahead when patients are level 1 or level 2. Nursing staff can initiate resuscitation. Physician-directed care may be provided in person, by telephone or by medical directives (CTAS National Working Group, 2013c, p. 61). CTAS level 5 patients may be deferred to another health care provider or time if: The patient is 6 months of age or older. Vital signs are deemed satisfactory by the nurse and temperature is 35ºC-38.5ºC (38.3ºC for age > 60 years). After the nursing assessment, there is no clinical indication that the patient may require urgent physician attention. Where the nurse is unsure, telephone consultation with the physician has determined that the problem is non-urgent. Appropriate hospital policies and medical directives are in place. There is agreement between medical and nursing staff to accept the process (CTAS National Working Group, 2013c, p. 61

ACS (stable vs unstable angina, STEMI vs NSTEMI)

ST-segment deviation:Low - / Intermediate risk ACS (stable angina)Normal or nondiagnostic changes in ST-segment or T waveHigh-risk non-ST-elevation ACS (NSTE-ACS)Unstable angina and non-ST-segment elevation MI (NSTEMI)ST-segment depression or dynamic T wave inversion; strongly suspicious for ischemiaST-segment elevation MI (STEMI, or new/presumably new left bundle branch block (LBBB) An acute MI may be described in relation to ST-segment elevation on the 12-lead ECG. If there is ST-segment elevation in specific cardiac leads, it is known as an ST-segment-elevation MI (STEMI). A STEMI involves all three cardiac layers - endocardium, myocardium, and epicardium; it may also be referred to as a transmural, full thickness, or Q-wave MI. Significant ECG changes include the presence of Q waves, elevated ST-segments, and T wave abnormalities, such as T wave inversion. Pathological Q waves are a late finding in MI, signifying myocardial necrosis.If there is no ST-segment elevation on the ECG, but symptoms persist and biomarkers are elevated, then it is called a non-ST-segment elevation MI [NSTEMI]. Not all MIs cause damage to all three layers of the heart; therefore, the ST-segment is not always elevated. If the infarction and subsequent cell and muscle necrosis are not full thickness, or transmural, ST-segment elevation may not occur because some of the muscle in the area can still be repolarized normally. However, ST-segment depression and/or T wave inversion may be noted. In this case, the definitive diagnosis may be made by elevation of specific cardiac biomarkers (i.e., Troponin) or in the cardiac catheterization laboratory. NSTEMI may also be referred to as a subendocardial, partial thickness, or non-Q-wave MI.Specific zones of myocardial tissue affected by a MI are depicted in Figure 14.4 (Urden et al., 2022, p. 311).Zone of ischemia (penumbra). The outermost region of the infarcted myocardial area is composed of viable cells, thus priority is given to saving this viable muscle by reperfusion. Repolarization in this zone is temporarily impaired, as indicated on the ECG by ST-segment depression or T-wave inversion. If reperfused, repolarization of this tissue will eventually be restored. Zone of injury. Between the ischemic and infarcted zones lies the zone of injury, which is composed of injured, but still potentially viable, tissue; cells in this area do not fully repolarize due to deficient blood supply. The ECG shows ST-segment elevation. Fibrinolytics or PCI (angioplasty) are used to restore blood supply.Zone of infarction. This is the innermost area of dead muscle (necrosis) in the myocardium, which is replaced by scar tissue as healing occurs. On the ECG, new pathologic Q waves reflect a lack of depolarization from the cardiac surface involved in the MI. These Q waves may be permanent, or disappear several months or years later. Complications that may occur subsequent to any type of MI include premature contractions, ventricular tachycardia (VTach/VT), and ventricular fibrillation (VFib/VF).Locations of STEMIs and NSTEMIs are identified in Figure 14.6 (Urden et al., 2022, p. 312).

Safety and Security

Safety and Security Workplace violence in health care is on the rise, with nurses (male and female) reported to be most at risk (Shields & Wilkins, 2009; International Council of Nurses [ICN], 2009). In the ED, the triage nurse is typically the first point of contact with the health care system for patients, families, and other individuals (e.g., visitors). Many factors contribute to violence and safety issues in the ED: Environment - fast-paced, stressful, overcrowding, long wait times; patients presenting under the influence of drugs and alcohol, mental health issues; gang violence (Gilboy, 2013, p. 70); Staffing - inadequate staffing levels and supervision; demanding workloads occurring in emotionally charged environment; Shift work - EDs are typically open 24 hours/day, thus nurses work at night; Security - public's movement is unrestricted in many EDs (may come and go anytime), emphasizing the importance of wearing employee identification badges in full view at all times; Close contact - triage nurse's station is often unprotected from the public (e.g., no glass separating patient from nurse); nurses perform interventions that require close physical contact with the public; and Privacy - patients may feel lack of personal space in the ED (violation of privacy) (ICN, 2006, p. 3). Many EDs are equipped with panic buttons at triage, doors with restricted access, or security guards; however, triage staff need to keep a close eye on the waiting room to observe for situations that may escalate to violence. Triage nurses should also observe for signs of increasing agitation during the triage interview (e.g., clenched fist, foul language) and, if observed, attempt to deescalate the situation with a calm, caring, and nonconfrontational demeanor. When triaging psychiatric patients, the triage nurse must determine if it would be safe for the patient to wait in the waiting room, or rather be taken to a secure treatment room within the department (Gilboy, 2013). Nurses should not be expected to tolerate abuse or violence in the workplace, either directed at themselves or others. It is imperative that nurses are aware of available resources within their workplace.

Heart Failure

Section 2: Altered Mechanical Function Circulation of blood through the vascular system depends on the cardiac pump. Alterations in the heart's mechanical function are usually a consequence of structural changes that increase or decrease cardiac compliance. Heart failure (HF) is a type of cardiac dysfunction in which the pumping action of the heart no longer meets the needs of the body, thus tissues cannot be adequately perfused; it is most often caused by CAD and myocardial damage to the LV. Other etiologies include valvular dysfunction, cardiac infection (e.g., myocarditis, endocarditis), cardiomyopathy, and uncontrolled HTN. Left-sided HF, with subsequent lung congestion, may be referred to as congestive heart failure (CHF), although this term is becoming less common. As you learned in NURS 460, four main mechanisms are involved in maintaining cardiac reserve in both normal and failing hearts.The sympathetic nervous system (SNS) activates alpha- and beta-adrenergic receptors. Alpha receptors cause vasoconstriction, while beta receptors increase heart rate, circulation, conduction, and contraction.The renin-angiotensin-aldosterone system (RAAS) releases aldosterone to retain sodium and water from the kidneys, thus increasing circulating plasma volume. Angiotensin II is released to increase systemic vascular resistance (SVR) and, therefore, BP .The Starling mechanism refers to the relationship between preload and resultant myocardial stretch of the ventricle, and how these two concepts affect the force of ventricular ejection. With initial increases in ventricular volume and stretch, contractility improves; however, as heart failure progresses, excess preload causes impaired contractility and overdistention of the ventricle (see Urden et al., 2022, p. 184) Myocardial hypertrophy is an enlargement of the ventricles to compensate for the lack of cardiac output.Whatever the cause of HF, the result is always decreased stroke volume and cardiac output. If the heart is unable to pump the blood out of the ventricles efficiently, the ejection fraction (EF) is diminished. An EF < 30% is strongly associated with ventricular dysrhythmias and an increased risk of death.A failing heart is unable to eject enough blood to meet the body's O2 needs. Blood accumulates in the ventricles, eventually causing backup and congestion downstream. HF may be classified as left- or right-sided, and as systolic or diastolic.

Acuity Rating Systems

Several different triage acuity (or severity) rating systems are used around the world, with severity scales ranging from three-level to five-level. Triage acuity scales are evaluated for validity and reliability. Validity refers to whether the triage acuity scale measures what it is supposed to measure. Does each triage level reflect a difference in severity (e.g., admission rates for acutely ill patients should be higher than for those who are not deemed acutely ill) (Gilboy, 2013, p. 63)? Reliability refers to the "degree of consistency (or agreement) among those using the method" (Gilboy, 2013, p. 63). In other words, does each triage nurse assign the same acuity rating to the same patient? Does each triage nurse assign the same acuity rating to a similar group of patients (e.g., chest pain)? Neither a busy ED with minimal patient throughput nor a particular triage nurse, for example, should influence the acuity rating assigned (Gilboy, 2013). Unlike three-level or four-level scales, five-level acuity rating systems allow for more comprehensive discrimination and definition of presenting signs/symptoms that are classified under each level. Five-level scales have demonstrated higher reliability, validity, as well as increased stability across nurses. Furthermore, five-level scales have shown to be safer with regards to the under-triaging and over-triaging of patients (Travers et al., 2002, p. 399). If patients are under-triaged, their safety may be compromised, whereas over-triage may lead to premature exhaustion of ED resources (Fernandes et al., 2005). Five-level acuity rating systems used around the world include the Australasian Triage Scale (ATS), Manchester Triage System (MTS), Emergency Severity Index (ESI), and CTAS. These scales assign severity scores in descending order of acuity. For example, level 1 refers to immediate threat to life while level 5 refers to nonurgent signs and symptoms. Each of the first three scales will be briefly discussed, followed by an in-depth review of CTAS.

Canadian Triage and Acuity Scale

Since the 1990's, CTAS has been the standard of emergency care in Canada for 'sorting' and 'prioritizing' patients based on their acuity level and needs. In addition to prioritization of care, the tool facilitates monitoring of patient flow and care processes (CTAS National Working Group, n.d., para. 1). The utilization of CTAS allows nurses and physicians to: triage patients according to the type and severity of presenting signs/symptoms; ensure that the sickest patients are seen first when ED capacity has been reached or exceeded due to visit rates or reduced access to other services; and ensure that a patient's condition and need for care is reassessed while in the ED (CTAS National Working Group, n.d., para. 2). The Canadian Emergency Department Information System (CEDIS) has been instrumental in the gathering and analyzing of national ED data. Since its inception in 2001, CEDIS has facilitated the national standardization of presenting complaint lists that form various patient case-mix groups (e.g., chest pain, cardiac features). The development of these standardized data sets allows for "quality improvement, research, and benchmarking at a local, regional and national level" (Grafstein et al, 2003, p. 27). In 2003, the CTAS National Working Group utilized the aforementioned CEDIS complaint lists as the foundation for further development of CTAS. Today, adult and pediatric case-mix groups included in CTAS are based on presenting complaint(s) and CTAS triage level (Grafstein et al., 2003). The triage level assigned using CTAS criteria is a mandatory data element to be used in all Canadian hospital EDs for reporting to the Canadian Institute for Health Information. Note: It is important for you to know the policies and procedures of your agency. An overview of CTAS documents and publications is available at the following URL address: http://ctas-phctas.ca/

Characteriscis of various rhythms

Sinus Tachycardia Sinus tachycardia also follows the normal route of conduction, thus all aspects are normal with the exception of rate, which is greater than 100 bpm (usually 100-160 bpm). Sinus tachycardia is a normal physiological response to the body's requirement for increased blood flow (oxygen). Some experts believe that, "A heart rate > 150/min is an inappropriate response to physiologic stress...or other underlying conditions" (AHA, 2011, p. 115). Conditions that produce sinus tachycardia include stress, fever, hypovolemia, pain, caffeine, nicotine, and certain drugs that increase sympathetic or decrease parasympathetic tone. In terms of cardiac pathology, it may be seen secondary to MI of the anterior wall. It is managed by treating the underlying cause.ECG Features of Sinus TachycardiaRhythm Rate P waves PR Interval QRSRegular 100-160 bpm Normal in configuration and duration; one P wave precedes each QRS complex. Normal(0.12-0.20 secs) Normal(<0.12 secs) Sinus Arrhythmia Sinus arrhythmia differs from NSR only in its irregular rhythm. It is commonly seen in children and young adults (Huff, 2006). The rate may be between 60-100 bpm, but is more commonly associated with sinus bradycardia. Characteristically, the rate increases slightly with inspiration and decreases with expiration in response to respiratory influence on the vagus nerve. Assuming respiration is regular, it is a recurring pattern and may be considered as regularly irregular. This arrhythmia has no clinical significance.ECG Features of Sinus ArrhythmiaRhythm Rate P waves PR Interval QRSRegularly irregular Normal 60-100 bpm or slow < 60 bpm Normal in configuration and duration; one P wave precedes each QRS complex. Normal(0.12-0.20 secs) Normal(< 0.12 secs) Sinus Arrest and Sinoatrial (Sinus Exit) Block Now things become a little more challenging. In both sinus arrest and sinoatrial block, we see an interruption in the underlying sinus rhythm, as a result of which one or more cardiac cycles are missing (dropped beats). It is important to remember that there is no ECG representation of the SA node impulse, which initiates the depolarization of the atria and the rest of the heart. Imagine for a moment that this impulse is seen as a spike preceding each and every P wave under normal circumstances. In sinus arrest, there would be no spike apparent because the SA node would not fire. Consequently, the rest of the cycle would also not occur. Sinoatrial block, also referred to as Sinus exit block, is similar, yet different. In that case, the SA node would fire (producing our imaginary spike), but it would not be conducted to the atria and the rest of the heart. Again, what we see on the ECG would be a period of one or more missing cycles. These arrhythmias may result from increased vagal tone, SA node damage, specific drugs, hyperkalemia, and coronary ischemia.Differentiating between these two arrhythmias on an ECG may be difficult; however, in sinus arrest, you will note that the RR interval is irregular. That is, the R wave following the pause does not occur on schedule.ECG Features of Sinus Arrest and Sinoatrial BlockRhythm Rate P waves PR Interval QRSUnderlying rhythm is regular; irregular during pause. Underlying rate is usually 60-100 bpm, but may be faster or slower, depending on SA node activity. Present and normal in underlying rhythm; absent during pause. Normal in underlying rhythm; absent during pause. Normal in underlying rhythm; absent during pause.Sample ECG 4.5. Sinus arrest._____________Sinoatrial block, on the other hand, will be observed to have regular RR intervals (with the exception of the period of pause). The R wave following the pause occurs on schedule.Sample ECG 4.6. Sinoatrial block. Route of Conduction atrial arrhythmia Atrial arrhythmias arise from atrial tissue, not from the SA node. As a result, the vectors of depolarization are abnormal, resulting in an abnormally shaped P wave. Because of the multitude of potential originating sites, the resulting P wave may be upright, inverted, or biphasic. The atria are capable of generating impulses at rapid rates. At faster rates, the AV node selectively blocks some of the impulses in an attempt to produce a near-normal ventricular rate and cardiac output. The PRI varies slightly, depending on the pacemaker location, but it will still be within normal limits. The QRS is normal. Multifocal Atrial Rhythm In multifocal atrial rhythm, as the name suggests, the rhythm arises from different foci within the atria. Because of the shifting of atrial vectors in relation to the positive lead, the identifying features of this rhythm are a changing P wave shape and a slight variation in the PRI. The strip needs to be long enough to confirm at least three different P wave shapes. The rhythm may be regular or slightly irregular, the rate is 60-100 bpm (or slower), and the QRS is unaffected. The causes of this rhythm include digitalis toxicity and underlying cardiac disease.This rhythm may also be called wandering atrial pacemaker. If the rate is greater than 100 bpm, it is referred to as multiform (or multifocal) atrial tachycardia.ECG Features of Multifocal Atrial RhythmRhythm Rate P waves PR Interval QRSRegular or slightly irregular 60-100 bpm; may be slower. Differing shapes and directions Premature Atrial Complex (PAC) The premature atrial complex (PAC) is an early occurring beat initiated by an ectopic pacemaker in the atria. Because of its prematurity, it overrides the ability of the SA node to initiate depolarization. The PAC is followed by a pause, usually called non-compensatory. This occurs because the SA node has been depolarized by the ectopic impulse and must 'reset' itself. The PAC may be conducted or non-conducted. The conducted PAC is characterized by an early, abnormal P wave, perhaps an altered PRI, and a QRS that may resemble the QRS complexes of the underlying rhythm. If, however, the PAC is sufficiently premature, the impulses are conducted to the ventricles before they have completely repolarized. This produces a widened QRS with an aberrant shape resembling a right bundle branch block (RBBB). The non-conducted PAC occurs so early that the ventricles are completely refractory to stimulation. This situation is demonstrated on the ECG by an early and abnormal P wave that is not associated with a QRS following.ECG Features of Premature Atrial ComplexRhythm Rate P waves PR Interval QRSUnderlying regular rhythm is interrupted by PACs. That of underlying rhythm. Normal in underlying rhythm; abnormal in PAC and may be hidden in preceding T wave. Normal in underlying rhythm; normal, slightly altered, or absent in PAC. Normal in underlying rhythm; may be normal, wide, abnormally shaped, or absent in PAC. Atrial Flutter Atrial flutter is depicted by an atrial rate of 250-440 per minute, which produces characteristic sawtooth 'flutter' waves seen on the ECG. Because atrial rates are so rapid, the AV node usually blocks at least half of the atrial impulses in order to protect the ventricles from rapid rates. If the AV node accepts atrial impulses in a consistent pattern, the ventricular rhythm will be regular. Further detail can then be added in terms of the ratio of atrial impulses to ventricular impulses (A/V conduction ratio). In a typical case of atrial flutter, the atrial rate might be 300 per minute; since the AV node usually blocks at least half of those impulses, the ventricular rate might be 150. The simplest method of determining the conduction ratio is to divide the atrial rate (e.g., 300) by the ventricular rate (e.g., 150). This example would then be described as atrial flutter with 2:1 conduction. Other conduction ratios (i.e., 3:1, 4:1) may also be seen; however, even conduction ratios (2:1, 4:1) are more common.In contrast, if the AV node accepts atrial impulses inconsistently, the ventricular rhythm will be irregular. Since it is not possible to further differentiate the conduction ratio, the rhythm is simply described as atrial flutter with variable conduction.Atrial flutter is seen in patients with digitalis toxicity, rheumatic heart disease, hypoxia, and pulmonary disease. The severity of symptoms observed is dependent on the ventricular rate. With rapid ventricular rates, symptoms associated with decreased cardiac output may be noted. Atrial flutter typically converts to either sinus rhythm or atrial fibrillation. This arrhythmia is treated pharmacologically or with cardioversion. Radiofrequency ablation may be utilized for treating chronic or recurrent atrial flutter.ECG Features of Atrial FlutterRhythm Rate P waves PR Interval QRSRegular with fixed conduction ratio; irregular with variable conduction Atrial: 250-440; ventricular: depends on AV conduction. Sawtooth appearance Atrial Fibrillation Atrial fibrillation is an arrhythmia of the heart involving an atrial rate of 350-600 per minute. This produces characteristic 'fibrillatory' waves that generate an irregular baseline on the ECG. The extremely rapid and disorganized atrial activity causes the atria to quiver rather than contract in a regular fashion. As seen with atrial flutter, the AV node blocks most of the atrial stimuli and selectively transmits impulses to the ventricles. There is no fixed pattern of conduction through the AV node, producing an irregular ventricular response.Acute causes of atrial fibrillation include drug toxicity and stress. Chronic causes include valvular disease, hyperthyroidism, and pulmonary disease. With atrial fibrillation, the patient may exhibit signs of decreased cardiac output due to lack of atrial contraction (atrial kick) and rapid ventricular rate. Because the atria quiver rather than contract as a unit, thrombi may form due to stasis of blood. Treatment of atrial fibrillation focuses on eliminating the cause, converting to sinus rhythm if possible, controlling ventricular rates, and preventing thrombosis.There are two approaches to treating atrial fibrillation: rate control and rhythm control. Rate control involves administration of medications to slow ventricular rate, but with no intention of converting the rhythm to sinus rhythm. Anticoagulation is also provided to prevent thrombosis formation. Rhythm control is achieved either pharmacologically or via cardioversion. When attempting to convert atrial fibrillation to sinus rhythm, caution must be used because of potential thrombus formation. Conversion to sinus rhythm may dislodge the thrombi, thus producing emboli.ECG Features of Atrial FibrillationRhythm Rate P waves PR Interval QRSIrregular Atrial: 350-600; ventricular: variable. None apparent; irregular, disorganized baseline fibulatory waves Route of Conduction junctional Junctional rhythms arise from an area surrounding the AV node. This area has the ability to take over the pacemaker function of the heart to maintain cardiac output if the SA node malfunctions and its impulse formation drops. The intrinsic rate of the AV junction is 40-60 bpm. This protective rhythm is called junctional escape rhythm. Enhanced automaticity of this area, which may result from ischemia, stress, stimulants, electrolyte imbalances, and digitalis toxicity, can cause the rate to be higher than the intrinsic rate. This could result in premature junctional complexes, accelerated junctional rhythm, or junctional tachycardia, each of which is described in more detail below. The term supraventricular tachycardia may be applied to any rhythm faster than 100 beats per minute arising from above the ventricles. Impulses of junctional origin are conducted in a retrograde fashion through the atrial tissue, producing inverted P waves in lead II. If atrial depolarization occurs before ventricular depolarization, the P wave will precede the QRS, but the PRI will be less than 0.12 second. If depolarization of the atria and ventricles occurs simultaneously, the P wave will be hidden in the QRS complex. Finally, if atrial depolarization occurs after ventricular depolarization, the P wave will follow the QRS. In impulses of junctional origin, conduction through the ventricles is normal, producing a normal, upright QRS. Premature Junctional Complex (PJC) A premature junctional complex (PJC), or premature junctional contraction, is a junctional beat that occurs prematurely in an underlying rhythm. It is caused by enhanced automaticity in the AV junction. Because of its narrow QRS complex, it can be mistaken for a PAC. In order to justify classifying a premature beat as being junctional in origin, one must clearly identify a PRI less than 0.12 seconds, a P wave that may be hidden within the QRS, or a P wave after the QRS.Isolated PJCs do not require treatment; however, the patient must be monitored for increasing frequency of these ectopic beats.One may also see a junctional beat occurring late rather than early in the underlying rhythm. These are termed junctional escape complexes and occur when there is a slowing of the underlying rhythm. Escape complexes are due to a normal safety mechanism and are not the same as premature ectopic beats.ECG Features of Premature Junctional ComplexRhythm Rate P waves PR Interval QRSUnderlying regular rhythm is interrupted by PJCs. That of underlying rhythm. Normal underlying rhythm; inverted and before, during, or after QRS in PJC. Normal in underlying rhythm;< 0.12 secs in PJC if measurable. < 0.12 secs

Australasian Triage Scale

The ATS is the standard for triage in EDs within Australia. Figure 1 below outlines the five levels, time to treatment, and performance thresholds of the ATS. The 'time to treatment' indicates the maximum timeframe within which a patient should receive assessment and medical intervention (Gilboy, 2013). Performance indicators reflect the "minimum percentage of presentations per ATS category that are expected to achieve the ideal time-to-treatment criteria" (Australian Government Department of Health and Ageing, 2009, p. 12). One must remember that these are ideal waiting times; if these performance indicators are not met, an organizational review and subsequent implementation of measures to meet patients' clinical needs are required (Australian Government Department of Health and Ageing, 2009). Figure 1. Australasian Triage Scale. Reprinted from Emergency Triage Education Kit: Triage Workbook (p. 12), by Australian Government Department of Health and Ageing, 2009, Commonwealth of Australia. Retrieved May 12, 2021, from https://www1.health.gov.au/internet/main/publishing.nsf/Content/387970CE723E2BD8CA257BF0001DC49F/$File/Triage%20Workbook.pdf The ATS uses "clinical descriptors or conditions that correspond to a specific severity level" (Gilboy, 2013, p. 64). The triage nurse assigns the patient a severity category based on his/her response to the following question: "This patient should wait for medical assessment and treatment no longer than..." (Gilboy, 2013, p. 64). Of note, the 'time' to treatment begins as soon as the patient enters the ED. With the ATS, vital signs are only obtained by the triage nurse if more information is required to assign a severity category (Gilboy, 2013). Using the primary assessment format, Figure 2 below provides a summary of adult physiological predictors of the ATS.

The Canadian Legal System: A Review

The Canadian legal system, with the exception of Quebec, abides by a system called English Common Law. The Quebec legal system is known as French Civil Law or Civil Code (Keatings & Smith, 2010, p. 88). The origins of these systems date back to the early settlers of our nation. Quebec was initially settled by the French and ruled by the kings of France under French civil law, while the rest of Canada is a confederation of former British colonies and territories, and adopted the legal structure of their English, Scottish, Welsh, and Irish colonists (Keatings & Smith, 2010, p. 88). The main difference between the two systems is that French civil law is "codified" into a single document known as the civil code, while the British common law is heavily centred around case law, which involves published judicial opinions where precedent has been set (Keatings & Smith, 2010, p. 88, 89). Below are some brief descriptions of key legal documents, concepts, and terms: The Canadian Charter of Rights and Freedoms This has been an integral part of the Canadian Constitution since 1982, and was devised to guarantee many basic human rights and fundamental freedoms (Government of Canada, 2018). The Charter can be used to challenge in a court of law certain injustices that surface in society (Government of Canada, 2018). This document states that "any person charged with an offense has the right ... to be presumed innocent until proven guilty according to the law in a fair and public hearing by an independent and impartial tribunal" (Keatings & Smith, 2010, p. 109). As such, two key legal concepts can be highlighted, namely presumption of innocence and burden of proof. Civil Law Civil law is a body of rules and legal principles that govern relations and respective rights and obligations among individuals, corporations, and other institutions (Keatings & Smith, 2010). For example, it would encompass legal proceedings concerning contracts, property, family, marriage and divorce, tort and negligence, health, wills and inheritance, copyright, and employment (Keatings & Smith, 2010, p. 98). Criminal Law Criminal law is federal legislation based on the Criminal Code of Canada; this realm of law prohibits harmful or undesirable conduct and sets out the processes followed by the Crown regarding such criminal acts as assault, impaired driving, robbery, et cetera. (Ontario Ministry of the Attorney General, 2020). Health-care related crimes that would constitute criminal conduct include such acts as drug diversion, patient abuse, criminal negligence causing death, and sexual assault or misconduct (McConnell, 2018, p. 676). Tort Tort is a civil (as opposed to criminal) wrongdoing committed by one person against another, such as assault or defamation (Keatings & Smith, 2010, p. 194). This is perhaps the most significant area of law for nurses, as their conduct must meet the standards of care outlined by their regulatory college—if a nurse does not meet professional standards and unintentionally causes harm to a patient, that is actually considered a tort in the eyes of the law. Battery Battery is intentional harmful or offensive non-consensual contact brought to another person, for example directly striking someone, or indirectly causing someone to fall and subsequently be harmed (Keatings & Smith, 2010, p. 194). However, the contact does not need to be violent to be construed as battery, for example, if a nurse administers an injection without patient consent this could be construed as battery (Keatings & Smith, 2010, p. 194). Assault This is a similar concept to battery, but must include actual or threatened intent to harm another through contact, and as such is a more violent concept (Keatings & Smith, 2010, p. 195). Negligence This involves a non-intentional tort that is essentially a wrongful "inaction." In a nursing context, negligence must include these three elements: Duty of care owed to the plaintiff (e.g., a patient or client). Breach of duty of care by the defendant (a nurse or physician) by failure to administer treatment or provide health care in accordance with a particular standard of care. Patient suffers damages as a direct result of the breach of the duty of care (Keatings & Smith, 2010, p. 197). Example: A nurse who fails to stay up to date with the standards of care as outlined by the regulatory college risks employing out-dated methods and would be found negligent should the nurse's conduct come into question and a patient was harmed in any way (Keatings & Smith, 2010, p. 197). There is a substantial difference between civil and criminal negligence, such that the latter would apply if a nurse acted in a way not expected by a reasonable nurse, that is, the nurse knew the conduct in question was poor but did it anyway, or was not acting in a way expected of him or her by the respective regulatory body and/or institution (Keatings & Smith, 2010, p. 201). Question to Ponder: Can professional negligence be considered a criminal act?The answer to this question is yes. Conduct that is a substantial departure from what one would expect from a reasonable and competent nurse can be considered criminal negligence when significant harm comes to the patient, such as bodily harm or death (Keatings & Smith, 2010, p. 201).Some examples of negligence that could be considered criminal: Failure to detect signs and symptoms of bleeding, resulting in hemorrhage and death. Failure to properly position a patient during a procedure, resulting in limb paralysis. Failure to check properly or administer correctly a medication resulting in patient death. Failure to properly monitor a restrained patient, resulting in asphyxia and brain damage, or even death. (McConnell, 2018, p. 677) Malfeasance This legal act constitutes a breach of criminal law with actions that are in accordance with one's duty to care, but done so poorly that damages result, such as extreme bodily harm or death (Keatings & Smith, 2010, p. 110). Nonfeasance A failure to act in accordance with one's duty to care would be considered nonfeasance, for example, if extreme negligence resulted in severe bodily harm or death (Keatings & Smith, 2010, p. 110).As you can see, there are many nuances to these legal concepts, and more than one concept may apply.Consider the following clinical case.

Ethical Principles

The Code identifies the ethical values and commitment required to practice as a registered nurse (RN) in Canada. Its purpose is two-fold: firstly, it serves as an aspirational tool outlining the ethical values and responsibilities expected of RNs, and secondly, it is a regulatory tool. As a self-regulating profession in Canada, nurses are bound by the ethical values and responsibilities outlined in the Code to ensure the provision of safe, competent, and ethical care to the public (CNA, 2017, p. 2). "The Code also serves as an ethical basis from which nurses can advocate for quality practice environments that support the delivery of safe, compassionate, competent, and ethical care" (CNA, 2017, p.2). Note that in June 2018, CNA members voted in favor of expanding its membership to also include licensed and registered practical nurses (LPNs, RPNs) (CNA, 2018). The membership amendment is expected to take effect in the coming months, thus a revised Code will be published to encompass practical nurses as well. In the meantime, practical nurses remain bound by their respective provincial regulatory body's Code of Ethics. With the broader societal goal of addressing social injustices in mind, the CNA (2017) lists the main concepts of ethical responsibilities in nursing as: Providing safe, compassionate, competent and ethical care Promoting health and wellbeing Promoting and respecting informed decision-making Honouring dignity Maintaining privacy and confidentiality Promoting justice Being accountable (p. 3)

Manchester Triage System

The MTS is the predominant triage acuity scale used in the United Kingdom. Unlike the ATS which consists of five severity levels based on clinical descriptors, the MTS is an algorithm-based risk management tool consisting of 52 flow charts describing patients' presenting signs and symptoms. Within each flow chart, there are six key discriminators: life-threatening, hemorrhage, pain, conscious level, temperature, and acuteness (time since onset of illness or injury) (Ganley & Gloster, 2011, p. 51). These discriminators are then utilized to select one of the five clinical priorities (levels of severity) and a color (red, orange, yellow, green blue - in descending order of severity) with maximum waiting time from the flow chart (Ganley & Gloster, 2011). Figures 3 and 4 below provide an example of a flowchart specific to presenting signs and symptoms related to abscesses and local infections, as well as the five categories with maximum times to be seen, respectively.

Ethics Resources

The following resources may be useful to you in completing this module, and in your practice as a nurse: CNA's Code of Ethics for Registered Nurses CARNA's Ethical Decision-Making for Registered Nurses in Alberta: Guidelines and Recommendations All provincial and territorial regulatory colleges have practice and decision-making support; for example, the College of Nurses of Ontario's (CNO's) Ask Practice feature has a whole section on ethics and practice. Ethics committees Clinical ethicists Safety and privacy officers Local unions

Presenting Complaint

The initial assessment interview with the triage nurse often sets the tone for a patient's overall experience in the ED. Triage nurses must engage in empathetic and nonjudgmental communication with patients, and recognize that a patient's presenting complaint or condition, no matter how minor, may be perceived as a crisis or stressful situation to them (Gilboy, 2013). As mentioned earlier, the purpose of CEDIS is the development and provision of a national data set for EDs across the country, thus enabling "regional, provincial, and national comparisons, for evaluation, quality improvement and research applications in both rural and urban settings" (CTAS National Working Group, 2013a, slide 25). The foundation of these data sets is the complaint list, consisting of 17 categories and 167 different complaints for adult and pediatric patients. While it is beyond the scope of this module to review all 167 complaints, the CEDIS categories for adult and patients are outlined below in Figure 10. Although currently under revision, the complete CEDIS complaint list, including those specific to pediatrics, can be found at the following link: https://caep.ca/wp-content/uploads/2016/03/nacrs_presenting_complaint_list_v2_0_en_fr_pdf_pdf.pdf The first step in the 'triage interview' is determining the patient's primary complaint, which may prove to be a challenging task particularly when it is difficult to identify the patient's most significant concern. Given developmental level, triaging pediatric patients can also be quite challenging; parents/caregivers are relied upon for subjective information (i.e., CIAMPEDS) when the patient is young, while adolescent patients are typically able to provide the necessary information. Patients may present with multiple complaints or conditions, thus triage nurses must possess strong interpersonal skills to ensure time is used wisely (Gilboy, 2013). The triage interview questioning should begin with the reason for the ED visit, ensuring the patient's (or caregiver's, if pediatric patient) own words are documented. If the patient arrives via ambulance, emergency services personnel provide most of the relevant information; however, the triage nurse should still verify information with the patient. Open-ended questions are generally most effective when determining the reason for ED visit. Here are a few examples: "What brings you to the emergency department today?" "What seems to be the problem today?" "How can we help you today?" If the patient presents with several complaints, "What is different now? What was it that made you come in today?" (Gilboy, 2013, p. 67). Once the triage nurse has determined the patient's chief complaint, a brief medical history should be obtained. A mnemonic, such as AMPLE (Allergies, Medications, Pertinent/Past medical history, Last meal/bowel movement/menses, Events/Environment related to complaint) may be used to focus the interview and obtain necessary subjective information. Objective data is also a key component of triage information. A rapid, focused physical assessment related to the chief complaint should be performed, if warranted. Inspection and palpation are the primary physical assessment techniques utilized by the triage nurse; however, there may be cases in which auscultation should also be performed (e.g., pleuritic signs/symptoms). If a patient presents with a wound dressing insitu, for example, the triage nurse should remove the dressing to examine the extent of injury (inspection) and administer limited first aid if warranted (e.g., pressure dressing, splinting) (Gilboy, 2013). When assessing peripheral perfusion, palpation should be performed to assess peripheral pulses, skin temperature, and capillary refill. However, "the role of obtaining vital signs at triage is controversial...the triage policy of each ED should address when and whether vitals signs need to be measured" (Gilboy, 2013, p. 67). The patient who arrives actively seizing does not need vital signs obtained at triage and should be taken immediately to the resuscitation area, while the patient who arrives complaining of dysuria should have vital signs assessed to support the acuity rating (level 3 or 4) and assignment to the waiting room. Ultimately, the decision to obtain vital signs at triage is patient and situation specific. The triage interview should take no more than 2 to 5 minutes (Gilboy, 2013), thus the triage nurse must possess excellent critical thinking, decision-making, and multi-tasking skills. When determining the patient's presenting complaint, the goal is to "select a complaint that will enable the assignment of the highest appropriate acuity level" (CTAS National Working Group, 2013a, slide 24). For example, if a patient presents with shortness of breath and a minor laceration to the hand with no bleeding or obvious neurovascular compromise, the selected complaint should be related to 'Respiratory (RESP)'.

Emergency Treatment

The law in all provinces and territories in Canada allows health-care professionals to administer emergency treatment even if patient consent cannot be obtained (Keatings & Smith, 2010). When treatment is considered essential and potentially life saving in a situation when seconds count and it must be administered right away, "healthcare providers will be absolved of any liability for administering treatment, provided there is no gross negligence on their part" (Keatings & Smith, 2010, p. 171). However, other challenging situations present themselves in the emergency department ...Right to Refuse Treatment. Practice Question 8 Treatment Decisions: Clinical Case A woman presents to the ED by EMS, profusely bleeding and barely conscious. The emergency physician decides that the woman requires a blood transfusion because her blood pressure is quickly dropping and the bleeding has been difficult to control. She orders transfusion of three units of packed red blood cells to be administered stat by the emergency nurse. However, the nurse finds a card on the patient's person that indicates that the patient is a Jehovah's Witness, and it clearly specifies: no blood transfusions. The card also outlines alternatives to blood that could be administered. The physician decides that the transfusion is a necessary life-saving intervention and does not change the order in spite of this new information. (Adapted from Keatings & Smith, 2010, p. 163) Questions: What is the nurse's legal obligation in this case? Is the physician legally entitled to supersede a patient's clearly written wishes when in an emergent life-saving situation? Is informed consent the same as informed refusal? Leaving Against Medical Advice Although discharging patients from the ED falls under the responsibility of the emergency physician, nurses play a key role in ensuring that a patient's capacity to make that decision is recognized and further assessed by the physician, and, that the patient is educated on the necessity of the care being declined, and in documenting these efforts along with an institution-specific form for leaving against medical advice (AMA) signed by both patient and physician. Clinical Case: Treatment Decisions The nurse must not follow the order of the physician to carry out a blood transfusion against the patient's written wishes. Both the physician and the nurse are considered equally liable in the eyes of the law regarding the provision of treatment (Keatings & Smith, 2010). No, the physician is not entitled to supersede a patient's clearly written wishes. Implied consent when a patient is either unconscious or deemed incompetent to decide on emergently necessary treatment does not apply when there are clearly written wishes (Keatings & Smith, 2010). Informed consent is not the same as informed refusal. As discussed previously, informed consent is a legal requirement for health-care providers; however, "there is no corresponding doctrine of 'informed refusal' requiring or authorizing a healthcare practitioner to proceed with emergency treatment when the practitioner has not been able to inform the patient of all the consequences and risks of refusing treatment" (Keatings & Smith, 2010, p. 165). In other words, health-care providers are required to explain why they recommend certain care, but patients are not required to explain why they do not consent, and they are not required to hear all the reasons why you feel they should consent ... confusing?

More Ethical Dilemmas in the Emergency Department Palliative and End-of-Life Care in the ED

The provision of palliative or end-of-life care in the chaotic emergency setting is a common source of ethical distress for nurses, and can lead to ethical dilemmas. Revels et al. (2016) aptly describe in their research the nature of the ED as having distinctly different goals from that of palliative care; in short, life-saving versus quality-of-life-enhancing (para 2). Question to Ponder: How do we reconcile these two very different goals within the same setting? The issues surrounding this broad topic will be explored in detail in a separate module in this course, but you are encouraged to review the following article: Read Revels, A., Goldberg, L., & Watson, J. (2016). Caring science: A theoretical framework for palliative care in the emergency department. International Journal for Human Caring, 20(4), 206-212. http://doi.org/10.20467/1091-5710.20.4.206 Do-Not-Resuscitate (DNR) As in the case of palliative care, ethical concerns around DNR will be further explored in the End of Life Issues module and later in this module, but some examples of ethical dilemmas with DNR include: Scenario: A patient clearly states to the emergency nurse and physician that they do not wish to be resuscitated, but doesn't yet have a formalized signed legal order. In some provinces such as Ontario, a family member with decision-making rights for the patient can dispute the patient's expressed wishes for DNR once the patient is unable to decide for themselves (unconscious, confused). This can cause ethical distress for nurses who are prevented from acting in accordance with patient wishes. Scenario: Consider a palliative patient who is nearing end-of-life, but who wants to be resuscitated even if those efforts would be futile. As mentioned above, administration of what is considered to be futile care has been found to be one of the most distressing things nurses experience in the emergency department. Read Read the following articles that discuss some of the ethical and legal considerations around resuscitation: Canadian Nurses Protective Society (CNPS). (2006). Consent for CPR. infoLAW, 15(2). https://cnps.ca/article/consent-for-cpr/ Blackwell, T. (2014, September 3). Toronto hospital illegally imposed 'do-not-resuscitate' order against wishes of dying man's family: Medical board. National Post. https://nationalpost.com/news/canada/toronto-hospital-illegally-imposed-do-not-resuscitate-against-wishes-of-dying-veterans-family-medical-board Telephone Advice People often call the emergency department looking for medical advice, however, even though the emergency nurse may altruistically want to give advice over the phone to ease a person's concern, this is a slippery legal slope, can actually be dangerous to the individual, and should be avoided (Heilicser, 2013, p. 47). Giving advice over the phone could unintentionally deter a patient from seeking the care they need, which is not only unethical, but could be considered legally negligent. As such, a nurse must consider the principle of non-maleficence or "do no harm" when confronted with this ethical challenge, as one never wants to engage in practice that could cause patient harm (CARNA, 2010, p.11). Confidentiality Legally, nurses are expected to maintain privacy and confidentiality within the confines of the professional standards of our regulatory bodies, and that of our contractual agreements with our employers. However, confidentiality may be questioned when confronted with certain disclosures that may lead to patient harm or imply certain safety risks. This sometimes results in ethical dilemma.

Critical Look (Rapid Visual Assessment)

The purpose of the critical 'first look' is to rapidly identify those patients in need of immediate resuscitative or emergent care (CTAS National Working Group, 2013a). This rapid assessment should take no longer than 3 to 5 seconds (CTAS National Working Group, 2013c) and requires the triage nurse to use his/her senses, particularly observation, listening, and smell (Gilboy, 2013). When triaging adult patients, the triage nurse performs a brief primary assessment to determine the presence of any critical findings related to Airway, Breathing, Circulation/Control of hemorrhage, Disability, and Exposure/Environmental controls (ABCDE) (Travers, 2018). The triage nurse assesses pediatric patients for related critical findings as well; however, the PAT is utilized because it provides a "rapid assessment of the pediatric patient's overall physiological stability and the development of an overall general impression (i.e., looks good versus looks bad) (Romig, as cited in Emergency Nurses Association [ENA]), 2012, p. 54). From across the room, the PAT allows the triage nurse to determine 'how sick' the child is and 'how quick' the child should receive care. Table 2 below describes findings the triage nurse should be observing for during the rapid across-the-room assessment. Table 2. Information obtained during the across-the-room assessment. Across-the-room Assessment Sense Findings Observe Airway patency Respiratory rate, obvious distress, use of O2 devices Signs of external bleeding Level of consciousness: interacting, unconscious; crying, moaning Signs of pain: grimacing, holding, guarding Skin color/condition Chronic illness: cancer, chronic obstructive respiratory disease (COPD), neuromuscular disorders Deformities Body habitus: cachectic, morbidly obese Activity: ability to ambulate, balance, bear weight General behavior: agitated, angry, flat affect Presence of splints, dressings, casts, medical equipment Clothing: clean, appropriate Listen Abnormal airway sounds Speech pattern, tone of voice, language Interactions with others Smell Stool, urine, vomit, ketones, alcohol Poor hygiene, cigarettes, infection, chemicals There may be occasions when the nurse must reprioritize the steps of the triage process. Resuscitative and emergent care and interventions must never be delayed due to triage assessment. Patients requiring resuscitation, for example, should be immediately assigned to the resuscitation area and triage documentation may be completed when time permits. In the case of patients requiring emergent care or those at risk of serious illness, triage may be performed at the bedside. Stable patients presenting with apparent urgent, less urgent, and non-urgent signs and symptoms can be triaged in the triage area, unless their condition becomes unstable (CTAS National Working Group, 2013a). Infection Control The importance of infection control during the triage process cannot be overstated. Every ED should have an infection control process in place for resuscitative or emergent patients who 'bypass triage' and are directly transported to patient care areas. "Patients stable enough to triage should be assessed for communicable disease risk" (CTAS National Working Group, 2013a, slide 23). For example, droplet precautions should be initiated for patients who are coughing or vomiting (older children may wear a mask if coughing), while contact precautions should be considered for those who present with diarrhea or wound drainage (CTAS National Working Group, 2013a). Patients, particularly children, presenting with a rash may also be at high risk of communicable disease (e.g., varicella, meningococcemia), thus immunization status is a critical piece of information. Most EDs in Canada require the triage nurse to ask specific questions regarding communicable disease risk (e.g., recent fever, cough, contact with anyone who is ill, travel out-of-country), the answers to which may influence the assigned acuity score and location of care (e.g., isolation room).

Triage Pitfalls

The triage environment is one of high stress, organized chaos, and dynamic change. Triage nurses may encounter unsuspected or hidden difficulties while engaging in the triage process. Although not exhaustive, the following list provides a summary of pitfalls of which triage nurses should be aware: 'Up triaging': Assigning a higher triage acuity level to ensure patient safety is acceptable practice in some situations, thus triage nurses should not be afraid to do so if warranted. Not recognizing hemodynamic compromise in children: Pediatric patients are able to compensate hemodynamically for a longer period of time than adults, thus triage nurses must be able to recognize the clinical significance of hypotension or hypovolemia (sudden drop in blood pressure is indicative of shock). Not recognizing the significance of perineal or limb complaints: severe or disproportionate pain in the perineal region or a limb should be considered a 'red flag'. Necrotizing fasciitis is a significant concern in these patients; a 6-inch area of black skin may become 6 to 8 times as large within 1 hour of delay of treatment. This tends to be more dangerous in patients with perineal complaints as it is difficult to assess the area at triage. Not recognizing that mental health presentations may be as acute or dangerous as a medical or surgical one: Mistriaging mental health/behavioral changes poses a major risk for the triage nurse and patient. Intracranial lesions, central nervous system infection, and delirium (due to infection, drug interaction, metabolic disturbances) are the most common causes of acute mental health deterioration and must be considered prior to assigning an acuity score. In addition, new onset bizarre behavior may actually be due to an acute medical problem. Not assessing neurovascular status of distal limb: Patients presenting with limb complaint(s) must have neurovascular status of the affected limb assessed, including distal areas (e.g., digits). Allowing negative feelings about a patient to influence acuity score: Subjective and objective data obtained from the triage interview should be the only information considered when assigning acuity score. Mistaking patient fears as anxiety: In the absence of physiological findings, patient statements such as "I can't breathe" or "I'm going to die" may be misconstrued as simple anxiety (CTAS National Working Group, 2013c, p. 60).

Triage Process

The triage of any patient begins from across the room, with a critical or 'first look' of the patient's presenting condition. This is followed by determining the patient's risk for infectious disease and maintenance of infection control (e.g., need for droplet or airborne precautions). The triage nurse then performs a rapid assessment of the patient's presenting complaint(s), assigns an appropriate acuity level, and directs the patient to an appropriate location of care and resources (CTAS National Working Group, 2013a; NENA, 2014). It is important to note that triage is an ongoing process. Patients' acuity and condition may change while in the waiting room, for example; therefore, the triage nurse must reassess patients on a regular basis, as per patient need and ED guidelines. Triage is typically performed at a designated location (e.g., triage desk) and begins as soon as the patient enters the ED; however, it may occur anywhere in the ED, such as in the hallway during times of waiting room overcrowding or resuscitation room during a cardiac arrest (Travers, 2018). Figure 7 below illustrates the steps in the triage process for adult patients. The triage process for adult and pediatric patients is the same, but a few key differences in the principles of adult and pediatric triage should be noted. The 'first look' or across-the-room assessment is based on the Pediatric Assessment Triangle (PAT), which includes general appearance, work of breathing, and circulation to skin (see Figure 8 below) (Horeczko et al., 2013). Pediatric-specific modifiers are used when triaging children (e.g., no tone, unable to support head). Presenting complaint is identified AND the mnemonic CIAMPEDS1 is utilized. The significance of presenting complaints and symptoms differ (e.g., consolable vs. inconsolable). Anatomic and physiologic assessments for pediatrics differ (e.g., smaller airway, less circulating blood volume). Symptom reports may not accurately reflect the child's condition (e.g., change in behaviour is often a 'red flag'). The impact of age/development and psychosocial considerations is significant (e.g., emotional response, interaction with caregiver). Developmentally-appropriate assessment and interview techniques are required when triaging pediatric patients (age-specific). Other circumstances may also need to be considered: prematurity, congenital anomalies, metabolic disease, technologically-dependent, developmentally challenged, and/or child maltreatment. Age guidelines for pediatrics may differ from institution to institution; however, children from birth up to and including 16 years of age are generally considered to be pediatric. Note: Patients older than 16 years of age who are challenged and technologically-dependent may also be considered to be pediatric (CTAS National Working Group, 2013b, slides 3-8). 1CIAMPEDS: Chief complaint,

External Factors Leading to Ethical Distress

These factors are mainly systemic issues, which are seen as "undermining the integrity of ED clinicians to uphold their ethical obligations to provide safe, respectful, and equitable care..." (McLelland et al., 2016, p. 1). This can lead to ethical or moral distress in health-care providers (McLelland et al., 2016). What are some examples of external factors? High volume of patients, many of whom don't have a primary care provider. Understaffing of departments. Time pressures exerted by institutional requirements, such as new initiatives implemented to help curb wait times, or data collection requirements. Lack of resources to properly address social issues, mental health, addictions. Lack of inpatient beds available, leading to "hallway nursing" and ED flooded with inpatients. Lack of alternate levels of care available, such as long-term care, palliative care, complex continuing care for chronic conditions (McLelland et al., 2016). Can you think of any other external factors that lead to ethical distress? What common patient characteristics contribute to ethical distress in the ED? High acuity level. Multiple comorbidities and/or poorly managed chronic conditions. Complex mental-health issues. Palliative status with no advance care planning in place, which can lead to aggressive medical management or "futile care." Because of these complexities, emergency nurses often feel that there is only time to address the very highest priority of patient care needs, and many other social issues— complex medical issues, timely transfer and discharge—all get pushed aside in the interest of time, rendering nurses feeling like they have provided substandard care. This is ethically distressing! Falcó-Pegueroles et al. (2015) and Fernandez-Parsons et al. (2013) highlight some specific scenarios in the ED that nurses find particularly ethically distressing: Patient suffering in spite of pain management strategies such as analgesia and/or sedation. Working with other health-care professionals they feel are incompetent. And performing enhanced testing and/or administering treatments seen as futile for a patient with an irreversible terminal illness.

Triage Overview

Triage is defined as "a sorting process that utilizes critical thinking and a standardized set of guidelines, in which an experienced Registered Nurse [RN] assesses patients upon arrival to the Emergency Department [ED]" (National Emergency Nurses Association [NENA], 2019, p. 1). The purpose of triage is to collect information that will inform decision-making regarding the urgency of ill or injured patients' medical and/or psychological needs (Travers, 2018). Put more simply, Gilboy (2013) states the purpose of triage is to "put the right person in the right place at the right time for the right reason" (p. 61). Triage serves as more than a tool to score the severity of a patient's condition; it also serves as a common language within the ED as a whole (Gilboy, 2013). Not only is the "process of triage...essential for safe and appropriate care of the emergency department patient" (NENA, 2019, p. 2), triage data is utilized to monitor departmental acuities (e.g., to ensure adequate staff-patient ratios), as well as inform decision-making regarding institutional and strategic operational plans (e.g., role of the ED within the institution or health care region) (NENA, 2019). The goals of triage are described as follows: to rapidly identify patients with urgent, life threatening conditions; to determine the most appropriate treatment area for patients presenting to the ED; to provide ongoing assessment of patients; to provide information to patients and families regarding care and services expected, as well as waiting times; to decrease congestion in emergency treatment areas; and to contribute information that helps to define departmental acuity (Beveridge et al., 2018, para. 2). The triage nurse is generally the first point of clinical contact for patients presenting to the emergency department (ED). This nurse is responsible for evaluating the urgency of the situation, conducting the initial rapid assessment, and determining the level of care and resources required. ***The purpose of this module is to provide an introduction to triage, in particular the Canadian Triage and Acuity Scale (CTAS). Completion of this module does not infer qualification to triage patients in the ED.***

Forensics: Evidence Collection

Unique to the ED is the increased likelihood that a nurse will be responsible for collecting and preserving medical evidence, and thereby required to follow the chain of custody for evidence transfer (Hammond & Zimmermann, 2013). The chain of custody is the act of collecting, protecting and labelling evidence, until safely transferred to law enforcement as applicable (Hammond & Zimmermann, 2013).Examples of situations that may require evidence collection: Legal requests for blood/urine specimens related to alcohol illicit drug use. Abuse (child abuse, domestic violence, sexual assault, elder abuse). Death by trauma or work-related accident. Unexplained and/or sudden deaths that will require coroner's inquest (Hammond & Zimmermann, 2013). As highlighted in the previous section, documentation in accordance with standards is paramount to ensuring accurate records. When collecting and transferring evidence, it is essential that nurses document contemporaneously̶—note what evidence was collected, that the evidence was labelled, and who the evidence went to and at what point in the chain of custody.

Preload vs afterload

What does preload mean? Preload is defined as the stretch of myocardium or end-diastolic volume of the ventricles and most frequently refers to the volume in a ventricle just before the start of systole. Afterload is the pressure that the heart must work against to eject blood during systole (ventricular contraction). Afterload is proportional to the average arterial pressure.[1] As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles respectively. Afterload changes to adapt to the continually changing demands on an animal's cardiovascular system.[1] Afterload is proportional to mean systolic blood pressure and is measured in millimeters of mercury (mm Hg).

Locations of MI and related complications

complications during hospitalization for acute myocardial infarction may include cardiogenic shock acute heart failure right ventricular infarction mechanical complications, such as left ventricular (LV) septal rupture, LV free wall rupture, mitral regurgitation, and LV aneurysm electrical complications, such as ventricular arrhythmias, atrial fibrillation, and atrioventricular block ischemic complications, such as reinfarction, infarct extension, and postinfarction Specific leads of the standard ECG correlate with areas of the left ventricle (LV). The LV is divided into four walls: anterior (front), lateral (left side), inferior (bottom), and posterior (back). The RV may also experience infarction, but assessment of this requires more than the standard ECG, as explained below. The module on 12- and 15-lead ECGs discusses RV infarction more extensively. Anterior Wall Infarction or Injury The left coronary artery (LCA) splits into the left anterior descending (LAD) and left circumflex (LCx) arteries. The LAD artery supplies blood to the anterior wall of the interventricular septum, left atria, and anterior wall of the LV. The anterior LV is reflected in leads V1 to V4 on the ECG; therefore, with a STEMI of the anterior wall, ST-segment elevation is expected in leads V1 through V4 of the 12-lead ECG (see Figure 14-7 in Urden et al., 2022, p. 312).V1 and V2 represent the interventricular septum.V3 and V4 represent the anterior wall of the left ventricle.Anteroseptal wall MIs are the most common type of infarction, and have the potential to cause many complications: Cardiogenic shock may occur due to damage to the LV (unable to generate adequate cardiac output).Heart blocks: the LCA supplies a large portion of the bundle branch network, thus bundle branch blocks (BBBs), second degree atrioventricular (AV) blocks, or third degree AV blocks may occur.Sinus tachycardia is common as a result of compensatory mechanisms in response to decreased blood pressure (BP).Ventricular septal defect (VSD): the LAD artery supplies a large portion of the interventricular septum which, if damaged, may result in a VSD post-infarction.Other potential complications: ventricular aneurysm and papillary muscle rupture, with subsequent valvular regurgitation. Lateral Wall Infarction or Injury The LCx artery supplies the left lateral wall of the LV and the left atria (LA), as well as the posterior wall of the LV in some patients. Lateral wall infarctions are usually extensions of anterior or inferior infarctions. On the ECG, the left lateral wall of the LV is reflected in leads V5, V6, I, and aVL. With a STEMI of the lateral wall of the LV, ST-segment elevation is expected in leads V5, V6, I, and aVL (see Figure 14-8 in Urden et al., 2022, p. 314).In approximately 45-50% of patients, the sinoatrial (SA) node is supplied by a branch of the LCx artery; in 10% of patients, the AV node is also supplied by a branch of the LCx artery. Therefore, complications of lateral wall infarction or injury may include SA node dysfunction and AV blocks; LV dysfunction also may occur. Inferior Wall Infarction or Injury The right coronary artery (RCA) supplies the right atrium (RA) and RV. In most patients, the inferior (bottom) wall of the LV is supplied by the acute marginal branch of the RCA. On the ECG, the inferior surface of the LV is depicted in leads II, III, and aVF (see Figure 14-9 in Urden et al., 2022, p. 315). Approximately 40% of inferior wall MIs involve the RV; therefore, a RV infarction should be suspected when changes are seen in the inferior leads, and a right-sided ECG or 15-lead ECG should be obtained.In approximately 50-55% of the population, the RCA supplies the SA node; in approximately 90% of the population, the RCA supplies the AV node. Therefore, bradyarrhythmias and AV blocks may occur following an inferior wall MI. Posterior Wall Infarction or Injury A posterior wall MI occurs as a result of blockage of the posterior descending artery which, in most people, branches from the RCA; however, it may also arise from the LCx artery. No leads in the standard 12-lead ECG directly view the posterior wall of the heart; a posterior wall infarction or injury is diagnosed by reciprocal changes in the anterior leads V1 to V4. ST-segment elevation and the presence of Q waves in the posterior wall will manifest as the opposite: ST-segment depression and tall R waves in the anterior leads. Alternatively, the 12-lead ECG can be flipped over and turned around: looking from the reverse side of the ECG, one can note ST-segment elevation and the presence of Q waves. Additional leads also may be used to view the heart's posterior surface. Right Ventricular Infarction or Injury A RV infarction occurs when there is a blockage in the proximal section of the RCA, which places all of the RV and inferior wall at risk. To detect RV injury or infarction, electrodes can be placed over the right precordium (15-lead ECG). In a 15-lead ECG, lead V4 electrode is moved to the right side of the precordium and becomes V4R; leads V5 and V6 are moved to the patient's back and become V8 and V9, respectively. If leads are moved away from the standard 12-lead ECG sites (such as with a right-sided or 15-lead ECG), the ECG must be labelled accordingly. Reciprocal change is a very important ECG finding, not only supporting the diagnosis of STEMI but also indicating a high-risk patient. Reciprocal change is defined as ST-segment depression occurring on an ECG which also has ST-segment elevation in at least 2 leads in a single anatomic segment.

legal documentation

kkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkjkkkkkjjjjkkkkkkkkkkkkjjjj

S/s of left vs right sided heart failure

left sided If the LV is affected, systemic cardiac output decreases resulting in increased pulmonary pressures and pulmonary congestion. Compensatory mechanisms are initiated, causing tachycardia, tachypnea, and systemic vasoconstriction. The following symptoms are related to decreased forward flow and downstream congestion in the lungs: Confusion, agitation Cool, pale peripheries Hypotension Tachypnea Tachycardia Sluggish capillary refill Decreased urine output Bi-basilar crackles Productive cough Hemoptysis Cyanosis Pulmonary edema Pulmonary HTN S3 and S4 heart sounds Pink frothy sputum (late sign of extreme pulmonary congestion) Patients with left-sided heart failure may have abnormalities of the heart muscle (i.e., LV), predisposing them to systolic or diastolic failure. Systolic Heart Failure Systolic heart failure (SHF), also called heart failure with reduced ejection fraction (HFrEF), occurs when contractility during systole is impaired, thus decreasing stroke volume, cardiac output, and EF (< 40-50%); the most common presentation is LV systolic dysfunction. Symptoms include fatigue, limited exercise tolerance, dyspnea, and fluid overload. The goal of therapy is to improve contractility. Diastolic Heart Failure Diastolic heart failure (DHF), or heart failure with preserved ejection fraction (HFpEF), occurs when stiff and fibrotic cardiac muscle impairs the heart's ability to relax and fill, which is most often due to LV dysfunction. Patients with DHF have limited exercise tolerance because the noncompliant ventricle cannot increase stroke volume. The goal of therapy is to improve diastolic relaxation. Right Sided HF RV HF may occur secondary to RV infarction or tricuspid valve dysfunction. In addition, because myofibrils are continuous throughout the heart, RV failure may occur as a result of LV failure (most common). In other words, single-sided failure will eventually cause failure of the other side. The following symptoms of right-sided HF are related to decreased forward flow and downstream congestion of vessels and organs that drain into the venous system:Peripheral edema Hepatomegaly Splenomegaly Ascites Jugular venous distension (JVD) Increased central venous pressure (CVP) Indigestion Anorexia