objectives - amazon simple storage service online review cardiovascular emergencies cen online...

CEN Online ReviewCardiovascular Emergencies

CEN Online Review: Cardiovascular Emergencies — Chapter 1 1

Nicholas Nelson, MS, RN, CEN, CPEN, CCRN, CPN

Objectives1. Explain concepts related to the care of an ED patient experiencing a cardiovascular emergency.2. Describe various patient presentations related to cardiovascular emergencies.3. List interventions necessary for a patient presenting with a cardiovascular emergency.

CHAPTER 1Cardiovascular Emergencies

� Cardiac Output = Stroke Volume (SV) × Heart Rate (HR) � Heart rate

§ Normal heart rate: 60–100 beats/min (adult), varies by age (pediatrics) § Sympathetic nervous system (SNS)

· Heart rate is increased by stimulation of the SNS, which occurs from stress, anxiety, acute pain, release of catecholamines, hypotension, and drugs with positive chronotropic effects

§ Parasympathetic nervous system (PNS) · Heart rate is decreased by stimulation of the PNS, which can occur with vagus nerve stimulation, cardiac conduction abnormalities, and drugs with negative chronotropic effects

§ Heart rhythm · Certain dysrhythmias may impair adequate filling of heart chambers or result in loss of atrial kick (contributes 20–40% of ventricular filling in healthy adult)

� Stroke volume § Definition: Amount of blood ejected from each ventricle per contraction § Measured in milliliters per beat § Amount ejected from either ventricle is nearly equal in the healthy patient § Positively influenced by preload and contractility (strength of myocardial contraction)

Figure 1: Cardiac Output



§ Contractility · Definition: The strength of each myocardial contraction · Significantly contributes to cardiac output · Affected by preload (Frank-Starling law), afterload, electrolyte status, myocardial oxygenation, amount of functional myocardium, and drugs with inotropic effects

§ Preload · Definition: Volume of blood that results in pressure or stretch of the ventricles during diastole · Affected by amount of venous return to heart · Increased by peripheral venous constriction and alpha adrenergics (e.g., epinephrine, norepinephrine, and medium-to-high dose dopamine)

· Decreased as a result of decreased intravascular volume (e.g., hemorrhage, diuresis, vomiting or diarrhea, third spacing, or redistribution of blood flow), as well as vasodilators

§ Afterload · Definition: Resistance to ventricular emptying during systole · Negatively influences stroke volume · Increases with vasoconstriction or mechanical obstruction of ventricular outflow, such as aortic or pulmonic stenosis, hypertension, hypothermia, or in response to compensatory mechanisms associated with shock

· Decreases with hyperthermia, distributive shocks, or vasodilators � Adults increase cardiac output through heart rate and stroke volume � Young children lack the ability to increase stroke volume

§ Tachycardia is the primary mechanism for increased cardiac output

Table 1: Normal Hemodynamic Values

Parameter Adults/Adolescents Children Infants/Neonates

Cardiac Output 4–8 LPM 1.3–3 LPM 0.8–1.3 LPM

Stroke Volume 50–100 mL/beat 13–50 mL/beat 5–13 mL/beat

Heart Rate 60–90 beats/min Toddler: 80–130 beats/min School age: 75–100 beats/min

Infant: 80–160 beats/min Neonate: 70–170 beats/min

Blood Pressure Below 120/80 mm Hg Older than 1 year: (SBP) = (Age x 2) + 90

0–1 mo.: above 60 mm Hg 1–12 mo.: above 70 mm Hg

Central Venous Pressure/Right Arterial Pressure

4–10 mm Hg 2–6 mm Hg 0–8 mm Hg

� Mean arterial pressure § Definition: Average pressure over the entire cardiac cycle § [(2 × diastolic) + systolic]/3

� Pulse pressure § Definition: Difference between the systolic and diastolic blood pressures § Calculate via systemic pressure or pulmonary pressure § Low systemic pulse pressure (narrowing pulse pressure)

· Decreased left ventricular stroke volume, blood loss due to trauma, low stroke volume (e.g., related to shock or cardiac tamponade)



� High pulse pressure (widening pulse pressure) § May be transient and normal effect of activity (e.g., aerobic exercise) § Caused by chronic conditions (e.g., atherosclerosis, aortic regurgitation), or acute conditions (e.g., aortic aneurysm, aortic dissection, patent ductus arteriosus, endocarditis, anxiety, fever, pregnancy)

� Cushing triad § Indicative of increased intracranial pressure

· Widening pulse pressure (or hypertension) · Bradycardia · Irregular breathing patterns

Pharmacology � Chronotropes

§ Drugs that affect the heart rate (generation of electrical impulse) § At the SA node

� Inotropes § Drugs that affect contractility (force of contraction) of the heart

� Dromotropes § Drugs that affect automaticity (electrical impulse velocity) of the heart at the AV node

Alpha and Beta Receptors

Figure 2: Alpha Beta Receptors

VasodilatorsReview of commonly used vasodilators in the emergency setting or medications of patients who present to the ED.Monitor for hypotension and initiate appropriate intervention.

� Angiotensin-converting enzyme (ACE) inhibitors (-pril) § Affect the renin-angiotensin-aldosterone system (RAAS) by blocking conversion of angiotensin I to angiotensin II, which results in reduction of blood pressure in presence of hypertension, and reduction of afterload associated with heart failure

§ Decrease preload and afterload by vasodilation and diuresis § Adverse effects

· Monitor for dry cough, angioedema or rash (due to increased bradykinin, a potent vasodilator), and renal impairment (modest renal impairment is common during first few days of administration)

· Patients with adverse effects may need to be switched to angiotensin receptor blockers (ARBs) § Classified as category D for pregnant women; avoid during pregnancy


� Angiotensin receptor blockers (ARBs) (-sartan) § Inhibit angiotensin II receptors, which results in vasodilation and decreased aldosterone levels, increasing excretion of sodium and sparing of potassium

§ Indications include hypertension and heart failure § Only available in oral formulations § Adverse effects

· Hypotension, dizziness, headache, hyperkalemia, and (rarely) dry cough · Monitor blood pressure, heart rate, and electrolyte levels, and intervene appropriately

� Calcium channel blockers (-dipine) § Negative inotropic, chronotropic, and dromotropic effects

� Beta-blockers (-lol) § Negative inotropic, chronotropic, and dromotropic effects § Beta receptors § Classified as cardioselective (work on beta-1 receptors) and non-cardioselective (work on beta1 and beta2 receptors)

Figure 3: Beta Blockers



Table 2: Vasodilator Medications

Medication Therapeutic Effects Notes

Nicardipine Calcium channel blocker Coronary, peripheral vasodilator Monitor BP, HR continually (IV administration)

Labetalol Slows HR, decreases PVR, CO, BP Moderately decreases preload and afterload

Gradually lower BP to avoid cerebral ischemia/infarct, optic nerve infarction, angina, myocardial ischemia or infarct

Nesiritide B-type natriuretic peptide Venous, arterial vasodilator Monitor BP, HR continually (IV administration)

Nitroglycerin

Coronary artery dilator: improves collateral blood flow to ischemic myocardial tissue Peripheral vasodilator: strong preload reduction, mild afterload reduction

Must be mixed in glass bottle and may need special tubing Contraindicated within 24 hours of phosphodiesterase inhibitor use Potent venous and arterial vasodilator

Nitroprusside

Potentiates depolarizing neuromuscular blocking agents Decreases SVR Moderate preload reduction, strong afterload reduction

Caution with hyponatremia, hypothyroidism, severe hepatic or renal impairment May cause thiocyanate toxicity: hypotension, confusion, tinnitus, hyperreflexia, headache, vomiting, seizures Protect from light

Table 3: Vasopressor and Inotropic Medications

Medication Therapeutic Effects Notes

Epinephrine Increases CO, HR, SVR Relaxes bronchial smooth muscles

May cause hyperglycemia Titrate up to desired response

DOBUTamine

Decreases preload and afterload Increases contractility, SV, CO Does not increase oxygen demand (Beta1 stimulation)

Correct hypovolemia before administration Titrate based on patient condition, response

DOPamine Lower doses: increases contractility Higher doses: additionally increases vasoconstriction

Correct hypovolemia before or with administration Titrate based on patient condition, response

Milrinone Increases CO Decreases SVR Vasodilator

Monitor for ventricular dysrhythmias, SVT, hypotension, diuresis, hypokalemia Obtain liver enzymes, RFTs

Norepinephrine Increases CO, HR, SVR Increases BP, coronary blood flow Tissue necrosis with infiltration

Phenylephrine Decreases HR Increases SVR Increases systolic BP

Tissue necrosis with infiltration Administer IV fluids with persistent hypotension

VasopressinIncreases SVRCauses vasoconstriction, water retention, urine concentration

May be used to augment vasopressors



Table 4: Antidysrhythmic Medications

Medication Indications Therapeutic Effects Notes

Adenosine Paroxysmal SVT Wolff-Parkinson-White

Slows SA node and AV node conduction, heart rate

Rapid IV push with flush May cause transient heart block or asystole

Amiodarone Unstable VT/VF, SVTDecreases AV conduction Prolongs action potential, refractory period

Longer shelf-life when diluted in glass containers

Digoxin Atrial fibrillation/flutter, Paroxysmal SVT

Increased force of myocardial contraction Decreased SA, AV node conduction

Monitor serum drug levels

Diltiazem

Angina Hypertension Uncontrolled atrial fibrillation/flutter

Slows AV conduction Calcium channel blocker

Continuous ECG monitoring during IV infusion IV solution stable for 24 hours only

EsmololSinus tachycardia SVT Hypertension

Slows sinus heart rate Decreases cardiac output Reduces blood pressure

Administer via large bore IV infusion (not push)

IbutilideRapid conversion of atrial fibrillation/flutter of recent onset

Slows sinus node rate and AV conduction Dose-related prolongation of QT interval

Can cause torsades de pointes (polymorphic ventricular tachycardia) within 4–6 hours after administration

LidocainePVCs Ventricular tachycardia Ventricular fibrillation

Decreases depolarization, automaticity, excitability of ventricle during diastole

Monitor for central nervous system toxicity with repeated doses

Procainamide

Atrial fibrillation SVT PVCs Ventricular tachycardia

Increases threshold of ventricles, His-Purkinje fibers Decreases myocardial excitability, conduction velocity Depresses myocardial contractility

Monitor for paradoxical response with extremely rapid ventricular rate during treatment of atrial fibrillation Reduce infusion if QRS widens by 50% or rapid BP drop May lead to complete heart block with lower degree AV blocks

Propranolol SVT

Slows sinus HR Decreases cardiac output, blood pressure, myocardial ischemia severity

Maximum undiluted IV push rate is 1 mg/min Dilute in 10 mL D5W, administer 1 mg over 10–15 min

Verapamil Paroxysmal SVT Atrial fibrillation/flutter

Slows SA, AV conduction Causes vasodilation by decreasing peripheral vascular resistance

Avoid or use with caution with LV dysfunction Extreme caution with hypertrophic cardiomyopathy Caution with long-term beta-blocker therapy



CHAPTER 2Chest Pain

� Common complaint that may indicate a cardiac or non-cardiac problem � Goal is to identify ischemic chest pain as quickly as possible, with rapid and appropriate intervention � Risk factors

§ Previous diagnosis of coronary artery disease (CAD) § Angina pectoris § Myocardial infarction § Coronary artery stents § Pacemaker/automated internal cardiac defibrillator § Non-modifiable

· Age · Sex · Heredity

§ Modifiable · Weight/diet · Smoking cessation · Exercise · Stress management

� Clinical manifestations § Vary by vessel(s) involved § Pain or discomfort in chest, jaw, neck, left arm, epigastrium, or scapular region of back

· Some patients may deny pain and describe discomfort as ache, dullness, pressure, or tightness § Nausea or vomiting § Hemodynamic instability

· Hypotension or signs of decreased cardiac output or shock (cool, clammy, diaphoretic skin) · Shortness of breath · Dysrhythmias (tachycardia, bradycardia, bundle branch blocks, ventricular ectopy, ventricular fibrillation)

� Anxiety or impending sense of doom § May be in denial of signs or symptoms

� Assessment § OPQRST mnemonic

· Onset � When was the onset of this pain? What were you doing during the onset?

· Provoke, Precipitate, Palliate � What provokes or precipitates the pain? � What makes the pain better?

· Quality � What is the quality of the pain? � How do you describe the pain?

· Radiate, Region (location) � Does the pain radiate to other locations (such as referred pain)?

· Severity, associated Symptoms � What is the severity of your pain or rate the pain or discomfort on a scale of 0–10 � What other symptoms are associated with your pain? (e.g., nausea, vomiting, paresthesia, dizziness, syncope)



· Timing � What is the timing of the pain? � Does the pain come and go, wax and wane, or is it constant? � How long have you had the pain? (e.g., onset, duration, sudden or gradual)

Anginal Equivalents � Definition

§ Women, elderly, and diabetics often have atypical presentations § Often present with nonspecific symptoms or only one symptom instead of traditional cardiac chest pain

· Shortness of breath · Fatigue · Palpitations · Near syncope/syncope · Nausea, vomiting · Diaphoresis · Pain/discomfort rating for trending, treatment effectiveness

� Assessment § Laboratory studies

· Complete blood cell count (CBC), chemistry, electrolyte levels, coagulation studies, and cardiac enzymes · Troponin is the cardiac enzyme that is the best indicator of tissue damage due to myocardial ischemia or infarction

§ Radiology · May be indicated based on suspected cause · Chest X-ray · Echocardiogram · Doppler studies · Stress testing · Percutaneous catheterization intervention (PCI) with angiography

� Interventions § 12-lead ECG should be obtained within 10 minutes of arrival at ED, preferably before the administration of nitroglycerin if possible

§ History · Current medications

� Phosphodiesterase inhibitors § Sildenafil, tadalafil, vardenafil, avanafil § Recent use may lead to profoundly decreased cardiac output in the presence of inferior wall infarct or with concurrent nitroglycerin administration

� Ticagrelor § May have decreased effectiveness when combined with full dose of aspirin

· Cocaine � Stimulates alpha- and beta-adrenergic receptors � Use of beta blockers in the patient who has recently used cocaine leaves alpha activity unopposed � Results in additional coronary vasoconstriction and systemic hypertension



CHAPTER 3Pacemaker Therapy

� Indications § Profound, refractory bradycardia, heart block, or idioventricular dysrhythmias

� Transvenous pacing § Catheter electrode threaded into the right atrium or ventricle via the subclavian, internal jugular, brachial, or femoral vein

� Transcutaneous pacing § Procedure

· Place pad on the back at the mid-thoracic level of the spine and other pacing pad on the front of the chest at level of lead V3

· Emergency settings typically include fixed or demand (preferred) mode, a rate of 60–80 beats/min at 60–80 mA, gradually increasing mA until capture is obtained, then increasing by approximately 5–10 mA

Figure 4: Failure to Capture

By Michael Rosengarten BEng, MD.McGill [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons

� Electrical § Pacer spike precedes each QRS complex (ventricular pacing), P wave (atrial pacing), or P wave and QRS (atrioventricular pacing)

� Mechanical § Palpable pulse that correlates to each paced beat

� Lack of capture § Acidosis § Hypoxemia § Wires not appropriately connected § Wet/diaphoretic skin or electrodes



Cardioversion � Definition

§ Synchronized defibrillation § With spontaneous circulation, usually hemodynamically unstable

· Ventricular tachycardia with a pulse · Supraventricular tachycardia · Atrial fibrillation or flutter that is refractory to pharmacologic interventions

� Procedure § Activate synchronous (sync) mode § Marker will be present on cardiac monitor above each R wave § Hold defibrillation button until energy has been delivered § Sync mode must be reset with each energy delivery § Obtain 12-lead ECG prior to, during, and after cardioversion for cardiac/electrophysiology consultation, if possible

Defibrillation � Lack of spontaneous circulation � Nonsynchronous defibrillation � Most cardiac defibrillators are biphasic

§ Adjust joules based on manufacturer’s guidelines � Adults

§ Biphasic: 120–200 joules § Monophasic: 200–300 joules

� Pediatrics § 2 joules/kg, then 4 joules/kg § Maximum of 10 joules/kg

Note: The use of paddles requires the application of 25 pounds of pressure

Dysrhythmias � Definition

§ Abnormal cardiac electrical activity resulting in aberrant rhythms § May be asymptomatic or result in symptoms related to altered cardiac output

� Types § Bradycardia § Tachycardia § Supraventricular arrhythmias § Ventricular arrhythmias § Heart block

Bradycardia � Definition

§ Impaired or delayed electrical impulse · SA node or CNS activation of heart affected

§ Adults: below 60 beats/min § Pediatrics: age-specific

� Causes § Coronary artery disease § Aging § Respiratory (pediatrics) § Cardiac defects § Drugs (e.g., beta or calcium channel blockers, digoxin, clonidine)



� Clinical manifestations § Hypotension § Altered mental status § Shock § Chest pain § Acute heart failure

� Interventions § Reverse causative agent or correct underlying cause as appropriate § Stable

· Administration of atropine, IV crystalloid fluids · Asymptomatic bradycardia: observation

§ Unstable · Administration of dopamine/epinephrine infusion · Transcutaneous pacing

Tachycardia � Definition

§ Adults: HR above 100 beats/min (unstable above 150 beats/min) § Pediatrics: age-specific

� Causes § Acute pain, fever, activity § Coronary artery disease § Cardiac defects § Electrolyte imbalances § Excessive drug use/overdose

� Clinical manifestations § Anxiety, diaphoresis § Palpitations, chest discomfort § Shortness of breath § Dizziness, syncope § Hypotension, shock § Loss of vital signs § Mental status changes

� Interventions § Correct underlying problem

· Stable � Administer amiodarone (IVPB)

· Unstable � Cardioversion

§ Consider sedation prior to procedure as appropriate � Regular, narrow complex: 50–100 joules, biphasic � Irregular, narrow complex: 120–200 joules, biphasic

· Pulseless � Defibrillation and CPR � Administer epinephrine every 3–5 minutes � Administer amiodarone (IV)

§ Cardiac workup, electrophysiology consultation § Cardiac catheterization, lab, surgical intervention, placement of automatic implantable cardioverter defibrillator (AICD) and/or pacemaker



Supraventricular Dysrhythmias � Originate in atria � Premature atrial contractions (PACs) � Paroxysmal supraventricular tachycardia (PSVT) � Wolff-Parkinson-White

§ Fast heart rate because of extra (abnormal) pathway between the atria and ventricles § Impulse travels through normal route and extra pathway, causing impulse to travel through heart rapidly § Presence of delta-wave

Figure 5: Wolff-Parkinson-White Syndrome Figure 6: Delta Wave

Supraventricular dysrhythmias, https://commons.wikimedia.org/wiki/File%3AWPW.jpeg Image: Heilman, J., 2009 By Tom Lück (Own work) [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons

� AV node re-entry tachycardia § More than one pathway through the AV node

� Atrial fibrillation § Common irregular pattern § Many impulses that begin and spread through the atria with complete travel through AV node with lack of coordinated atrial activity

· Fibrillating (quivering) atria · Rapid ventricular response (RVR): ventricular rate above 100 beats/min

� Atrial flutter § One or more rapid circuits in the atrium which result in an organized and regular rhythm

· Sawtooth waves · Atrioventricular conduction

� Fixed (e.g., 2:1) � Variable

� Causes § Conduction abnormalities

· Coronary artery disease · Cardiac defects · Aging · Excessive drug use



� Clinical manifestations § 100–250 beats/min § Normotensive, hypotensive, or hypertensive § Shortness of breath, dyspnea § Palpitations, chest tightness § Mental status changes

� Interventions § Stable

· Vagal maneuvers · Pharmacologic cardioversion as appropriate

§ Unstable · Synchronized cardioversion

§ Heart rate greater than 150 beats/min · Cardioversion at 50–200 J (biphasic) · Administer amiodarone (IVPB)

Premature Ventricular Contraction � Electrical impulses originate in ventricles � Failure of the SA node or overriding of ventricle-generated impulses � Premature ventricular contractions (PVCs)

§ “Skipped” heartbeat sensation § Usually benign, but may be caused by specific condition and produce specific symptoms § May occur in bigeminy (every other complex), trigeminy (every third complex), etc. § Runs of three or more PVCs constitute ventricular tachycardia

� Ventricular tachycardia (VT) § With pulse or pulseless § Torsades de pointes

· Form of polymorphic VT · Rhythm seems to twist like streamers · QRS complexes have variable amplitude

� Ventricular fibrillation (VF) § Quivering of the ventricles § No coordination for filling or ejecting of blood in chambers

Figure 7: Premature Ventricular Contraction

By James Heilman, MD (Own work) [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons



� Causes § Blunt trauma § Underlying conditions (e.g., prolonged QT syndrome) § Diseased heart (e.g., heart failure, cardiomegaly, cardiac hypertrophy) § Severely hypoxic myocardium § Electrolyte disturbances (e.g., magnesium, potassium)

� Clinical manifestations § Heart rate: 150–300 beats/min § Palpitations, chest discomfort § Syncope § Dyspnea § Hypotension § Loss of vital signs

� Interventions § With a pulse

· Cardioversion (VT) · Administration of magnesium (torsades de pointes)

§ Pulseless · Defibrillation, CPR, epinephrine administration · Correct underlying causes

CHAPTER 4Heart Block: Atrioventricular Block (AVB)

� First degree § Usually benign § Characteristic

· Features prolonged PR-interval � Second degree, type I (Wenckebach)

§ Most common form of second degree AVB § Characteristics

· Gradual prolonging of the PR-interval and then eventually a blocked impulse that results in a P wave, but no QRS complex

· Following beat tends to feature a shortened PR-interval � Second degree, type II

§ Characteristics · Consistent PR-interval before QRS complexes, followed by a blocked P wave that lacks a QRS complex · Succeeding beats will have normal PR-interval

� Third degree (complete) § Disruption of electrical activity of atrium versus ventricles – no coordination between the two § Characteristics

· P-wave to P-wave intervals are consistent, as are QRS to QRS intervals, but some P waves may be hidden in QRS complexes

CEN Online Review: Cardiovascular Emergencies — Chapter 3 & 4 14


Figure 8: First Degree Figure 9: Second Degree Type I

By James Heilman, MD (Own work) [CC BY-SA 3.0 By Michael Rosengarten BEng, MD.McGill [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons

Figure 10: Second Degree Type II Figure 11: Third Degree

By <a href=”/wiki/User:Jmh649” title=”User:Jmh649”> By MoodyGroove at English Wikipedia (Own work) [Public domain], James Heilman, MD </a> [CC BY-SA 3.0 via Wikimedia Commons (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons

� Causes § Aging § Coronary artery disease § Drug overdose

� Interventions § Administration of atropine for low degree blocks

· Ineffective for high degree AVB, heart transplants § Transcutaneous pacing for high degree heart blocks, heart transplants § Identify and treat underlying cause (consider Hs and Ts)

· Hypovolemia · Hypoxia · Hydrogen ion (acidosis) · Hyper- or hypokalemia · Hyper- or hypoglycemia · Hypothermia · Toxins · Tamponade (cardiac) · Tension pneumothorax · Thrombosis (coronary and pulmonary) · Trauma



Sudden Cardiac Arrest � Definition

§ Failure of cardiac electrical system · Not a myocardial infarction

� Clinical manifestation § Asymptomatic (occurs too quickly)

� Risk factors § 80% have signs and symptoms consistent with:

· Coronary artery disease (CAD), myocardial infarction (MI) · Syncopal or near syncopal episodes · Exertional chest pain, dyspnea, or syncope · Heart failure or history of myocardial infarction · Ejection fraction less than 40% · Modifiable CAD risk factors:

� Hypertension � Diabetes � Obesity � Smoking � Hypercholesterolemia

� Interventions § Early intervention is essential for survival § Defibrillation, high quality CPR § Implanted cardiac defibrillator for future events

Cardiopulmonary Arrest � Causes

§ Trauma § Chronic or acute illness § Sudden cardiac arrest

� Basic life support interventions § Goals

· Recognition · Activation of emergency response · High quality chest compressions · Rescue breathing · Rapid defibrillation

� Interventions § Chest compressions

· Most important aspect of early resuscitation · Effective, continuous compressions allow for some cardiac perfusion and cardiac output · Push hard, fast

� Rate at least 100; 2015 AHA guidelines call for rate of 100–120 compressions per min � Adequate depth � Allow for chest recoil � Minimize interruptions

§ Airway · Advanced airway maneuvers (e.g., intubation) take time and can delay compression initiation

� Do not delay compressions or defibrillation for advanced airway insertion · Ensure airway patency using BLS maneuvers



§ Breathing · Assess the rise and fall of chest with depth and symmetry · Utilize bag-mask ventilation unless ineffective · Prevent hyperventilation — excessive administration of ventilations increases intrathoracic pressure, decreasing venous return to the heart

· Ratio of 30 compressions to 2 ventilations · Ventilate once every 5–6 seconds (8–10 per minute) if advanced airway is placed (2015 AHA guidelines)

§ Defibrillation · Early defibrillation has better outcomes · Perform CPR, including chest compressions, while defibrillator is charging · Immediately resume CPR after each shock for 2 minutes · No pulse checks unless organized rhythm is present

§ Medications · Follow medication administration with saline flush and circulate with chest compressions · Epinephrine (1:10,000)

� 1 mg IV/IO every 3–5 minutes · Amiodarone

� Lidocaine is an alternative

Family Presence � Potential benefits

§ Family is more likely to understand seriousness of patient’s illness or injury and see that all possible interventions were performed

§ Family is able to begin the grieving process § Family may be able to provide additional medical history and events surrounding arrest § Family’s fear and anxiety may be reduced and feelings of isolation may be minimized

� Perceived concerns § May interfere § Resuscitation activities may be misinterpreted, increasing potential for litigation § Events/procedures may be too traumatic § Response to grief may be anger or violence

� Procedure § Assign one staff member to family

· Physically remain with family · Explain treatment using simple, clear terms · Inform team if family is present · If possible, allow family to interact with patient during resuscitation efforts (such as holding hand or speaking to patient)

� Interventions § Pulseless ventricular tachycardia/ventricular fibrillation

· Rapid defibrillation · Administration of IV/IO epinephrine every 3–5 minutes · Administer IV/IO amiodarone for refractory ventricular fibrillation

§ Asystole/pulseless electrical activity · Identify and treat the underlying cause (consider Hs and Ts) · Administer high-quality CPR · Administer epinephrine IV/IO every 3–5 minutes



§ Symptomatic bradycardia · Obtain IV access and 12-lead electrocardiogram · Administer atropine 0.5 mg every 3–5 minutes as needed to a maximum of 3 mg total dose · Consider administration of isoproterenol for heart transplant patients · Consider initiation of transcutaneous pacing

Special Trauma Considerations � Very poor survival rates (0–3.7%) for traumatic causes of cardiopulmonary arrest, especially for those with massive hypovolemia

� Emergency thoracotomy § Has extremely high mortality rate § May be considered for penetrating injury with a short scene time and transport time and if objective signs of life are present upon arrival to the ED

§ Other indications for thoracotomy include massive intrathoracic hemorrhage, cardiac tamponade, and internal cardiac massage

� Ventricular fibrillation may be a cause of cardiopulmonary arrest in trauma patients, but not necessarily the cause of an initiating trauma

Special Pediatric Considerations � Causes of pediatric cardiopulmonary arrest are usually due to respiratory failure or shock

§ Apparent life-threatening event (ALTE) · A cause of cardiopulmonary arrest · Definition

� A color change, marked change in muscle tone, choking, or gagging § Sudden infant death syndrome (SIDS)

· A cause of cardiopulmonary arrest · Cause is unknown, associated with accidental suffocation · Occurs in infants less than 1 year of age, with peak incidence at 2–4 months of age

§ Interventions · High quality basic life support interventions are even more essential for correcting cardiopulmonary arrest in the pediatric patient

· Utilize current AHA Pediatric Advanced Life Support (PALS) guidelines · Facilitate family presence whenever possible

Special Pregnancy Considerations

Table 5: Causes of Maternal Cardiac Arrest

BEAU-CHOPS

Bleeding/Disseminated Intravascular CoagulationEmbolism (coronary, pulmonary, amniotic fluid)Anesthetic complicationsUterine atonyCardiac diseaseHypertension/Pre-eclampsia/EclampsiaOthers: Hs and TsPlacentae abruptio/previaSepsis



� Interventions § Follow standard AHA Advanced Cardiovascular Life Support (ACLS) guidelines § Provide chest compressions slightly higher anatomically § Manually displace the uterus to the left to prevent or correct vena cava syndrome § Initiate IV access above the level of diaphragm § Remove fetal monitoring devices prior to defibrillation § Identify and treat the contributing factors § Consider emergency Cesarean section if no maternal return of spontaneous circulation within 4 minutes of arrest

Successful Resuscitation � Early percutaneous coronary intervention (PCI) is the gold standard for myocardial infarction � Thrombolytic therapy is alternative where PCI is not available

§ Facilitate early transfer to a PCI-capable hospital after the administration of fibrinolytics or thrombolytics � Therapeutic hypothermia (targeted temperature management)

§ Only therapy shown to improve neurologic recovery after a return of spontaneous circulation (ROSC) with persisting neurologic deficits

§ Initiate immediately after ROSC when patient is comatose § Procedure

· Target temperatures of 32–34°C for 12–24 hours · Initiate continuous core temperature observation · Control shivering to prevent increased body temperature · Provide for sedation, analgesia, and neuromuscular blockade · Obtain baseline electrolyte levels and hourly glucose levels and correct as needed · Indwelling urinary catheter is often utilized and may also measure core body temperature




CHAPTER 512-Lead Electrocardiograms (ECG)

� Multiple vantage points of the heart � Useful for identifying various conditions, including acute myocardial infarction � Placement

§ Contiguous leads · Leads that look at a certain area of the heart · Consistent findings in at least two contiguous leads indicates ischemia, injury, or infarct

§ Reciprocal leads · Leads that oppose the contiguous leads, or those that look at the opposite area of the heart · Opposite changes from those found in contiguous leads may be present in reciprocal leads and help to confirm interpretation

Figure 12: Lead Placement


Table 6: 12-Lead ECG

Leads I, aVL — high-lateral leads Leads V1, V2 — septal leadsLeads II, III, aVF — inferior leads Leads V2, V3, V4 — anterior and septal leads Leads V1, V3, V4— anterior and septal leadsNote: aVR is not used for diagnostic purposes Leads V5, V6 — lateral chest leads

Table 7: ECG Alterations Related to Myocardial Infarction

Condition ECG Alteration

Ischemia Tall or inverted T-waves ST-segment depression (possible)

Injury Elevated ST-segment with reciprocal changes T-wave may invert in some leads

Infarction (acute) ST-segment elevation T-wave may be inverted

Infarction (old) Abnormal Q-wave Normalized baseline



Table 8: 12-lead ECG Changes in Myocardial Infarction

Arterial Involvement

Affected Area

Indicative Changes

Reciprocal Changes

AssessmentAssociated Arrhythmias

Potential Complications

Left Anterior Descending (LAD)

Anterior LV wall Anterior LV septum Apex LV Bundle of His Bundle branches

ST é :V1–4

Loss of R waves in precordial leads

ST ê :II, III, aVF

ê LV function ê CO, ê BP S3, S4 with HF Crackles with pulmonary edema

Right BBB, Left BBB AV blocks Atrial fibrillation Atrial flutter Ventricular tachycardia

Cardiogenic shock Left BBB Associated with high mortality

Right Circumflex Artery (RCA)

Lateral LV wall Posterior LV LA

ST é :I, aVL, V5–6

ST ê :II, III, aVF

Murmurs Mitral regurgitation

Bradycardia 2nd Degree Type I AVB

Cardiogenic shock

Right Circumflex Artery (RCA) (posterior descending)

Inferior/posterior LV AV node

ST é :II, III, aVF

Q waves:II, III, aVF

ST ê :I, aVL, V1–4

Symptomatic bradycardia ê BP, ê CO LOC changes Diaphoresis Murmurs

AV blocks Complete heart block 2nd Degree Type II AVBBradydysrhythmias

Nausea, vomiting Papillary muscle dysfunction Mitral regurgitation

Right Circumflex Artery (RCA) (proximal)

RA, RV Inferior LV Posterior LV SA, AV nodes

ST é : II, III, aVF, V4R

T wave é II, III, aVF

Q waves:II, III, aVF

1st degree AVB 2nd degree type I AVBIncomplete right BBB Transient complete heart blockAtrial fibrillation Ventricular tachycardia, fibrillation

Kussmaul sign* Jugular vein distension Hypotension é SVR, é CVP Clear breath sounds initially Hepatomegaly Cool, clammy, pale skin

Abbreviations:AV: atrioventricular AVB: atrioventricular block BBB: bundle branch blockBP: blood pressure CO: cardiac output CVP: central venous pressureHF: heart failure LA: left atrium LV: left ventricleRA: right atrium RV: right ventricle SA: sinoatrialSVR: system vascular resistance


*Note: In this eLearning course, ENA is following the AMA’s guidelines in the use of eponyms in their nonpossessive form (e.g., Beck triad, Kehr sign, Cushing syndrome).


Right-Sided 12-Lead Electrocardiogram � Indications

§ Acute myocardial infarction (AMI) of the right ventricle or posterior wall § Especially for adult and geriatric populations

Figure 13: ECG Placement

Acute Coronary Syndrome (ACS)Presents with signs and symptoms of acute myocardial ischemia

� Caused by imbalance of myocardial oxygen supply and demand � Four stages of myocardial ischemia

§ Stable angina (angina pectoris) · Chest pain that occurs with physical exertion, short in duration · Relieved by rest or medication

§ Unstable angina · Chest pain that occurs with little or no physical exertion (e.g., while at rest), longer in duration than stable angina, unrelieved by rest or medication

· Indicative of unstable atherosclerotic plaque, may lead to acute myocardial infarction (AMI) · Interventions

� 12-lead ECG § May be non-specific or show transient ST depression or T wave inversion

� Cardiac enzymes § Negative troponin levels

§ Non-ST elevation myocardial infarction (Non-STEMI) · AMI that results in ischemic chest pain · Indicative of rupture of unstable plaque that results in intermittent coronary occlusion



· Interventions � 12-lead ECG

§ Absent ST elevation § ST depression may be present

� Cardiac enzymes § Positive troponin levels

§ ST elevation myocardial infarction (STEMI) · AMI with a complete obstruction of one or more coronary arteries with thrombosis

� Interventions § 12-lead ECG

· ST elevation in at least 2 contiguous leads · Reciprocal changes may be present · Possible new left bundle branch block

§ Cardiac enzymes · Positive troponin levels

Figure 14: Continuum of Cardiac Conditions

By User:Stevenfruitsmaak (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html), CC-BY-SA-3.0 http://creativecommons.org/licenses/by-sa/3.0/) or CC BY-SA 2.5-2.0-1.0 (http://creativecommons.org/licenses/by-sa/2.5-2.0-1.0)], via Wikimedia Commons; https://commons.wikimedia.org/wiki/File%3AACS_scheme.jpg

� Clinical manifestations § Chest pain or discomfort may be categorized as burning, crushing, tightness, pressure, and aching

· May radiate to arm, neck, jawline, back, or shoulder · Toothache or elbow pain may also occur · Pain or discomfort is unrelieved by rest or medication

§ Nausea/vomiting § Shortness of breath, dyspnea § Diaphoresis § Weakness § Dizziness § Syncope § Palpitations § Indigestion-like discomfort § Report of sense of impending doom may occur § Anterior left ventricle infarct-specific



· Signs of left ventricle failure (crackles upon lung auscultation, presence of S3 heart sound, respiratory distress due to pulmonary edema)

§ Right ventricle infarct-specific · Signs of right ventricle failure (severe hypotension, increased central venous pressure, jugular venous distention; absent crackles upon lung auscultation)

§ Tachycardia · Result of sympathetic nervous system stimulation and catecholamine release

§ Bradycardia · Often result of AV block

Table 9: Acute Coronary Syndrome

Stable Angina Unstable Angina Non-STEMI STEMI

Pain Relieved by rest or nitroglycerin (NTG)

Over 20 min duration Unrelieved by rest, NTG

Continuous chest pain/discomfort

Pain often described as worse than angina

ECG changes Transient ST depression

Transient ST depression T wave inversion

ST segment depression T wave abnormalities

ST elevation greater than 2 mm in V1, V2, V3 and greater than 1 mm in other leads

Troponin Normal Normal Elevated Elevated

� Interventions § 12-lead ECG § Treat ischemic chest discomfort as a STEMI § Nondiagnostic ECGs

· Repeat the 12-lead ECG in one hour and every 5–10 minutes thereafter if still symptomatic · Consider continuous ST monitoring

§ Inferior wall findings · ST elevation in at least 2 contiguous leads (II, III, aVF) · ST depression in V2 and R is greater than S in V1, V2

§ Obtain right-sided 12-lead ECG to identify possible right ventricular infarct � Cardiac enzymes

§ Values vary by time and type of cardiac enzyme

Table 10: Cardiac Enzymes

Cardiac Enzyme Elevation with Infarct Peak Elevation

Troponin I 3–12 hours 10–24 hours

CK-MB 4–12 hours 10–24 hours

� Chest X-ray, laboratory studies

§ Complete blood count, chemistry, coagulation studies � Pharmacologic interventions

§ moNA administration · Note: Recent evidenced-based findings have led to changes in 2015 AHA guidelines that decrease the role of morphine and oxygen administration



· Morphine � Can decrease associated pain and reduce anxiety � Should generally be reserved for patients with persistent cardiac chest pain that is not relieved by nitroglycerin

· Oxygen � Supplemental administration may still be used for patients with pulse oximetry levels at or below 94% or those with severe respiratory symptoms or signs of shock

· Nitroglycerin � Initial administration via sublingual spray or tablets to reduce myocardial oxygen demand, cause coronary vessel dilation, improve collateral blood flow to ischemic myocardial tissue, dilate peripheral vasculature, and reduce preload and, to some extent, afterload

� Further administration may be needed via transdermal or continuous IV infusion � Contraindications include severe hypotension (systolic below 90 mm Hg), profound bradycardia (below 50 beats/min), and recent use of phosphodiesterase inhibitors

� Relative contraindication with inferior wall infarcts which can profoundly potentiate diminished cardiac output

� Use extreme caution with nitroglycerin administration to avoid profound hypotension · Aspirin

� Of greatest benefit when taken as soon as symptoms identified � Dose: 160–324 mg in chewable form � Antiplatelet with few contraindications; during third trimester of pregnancy, labeled category D by the FDA (evidence of risk to fetus, but potential benefits may warrant use of drug in pregnant women)

· Clopidogrel administration � Antiplatelet effects

� STEMI interventions § Early reperfusion § Percutaneous coronary intervention (PCI)

· Gold standard · Goal for PCI: less than 90 minutes of total ischemic time

§ Fibrinolytic therapy · Consider if PCI is unavailable within 90–120 minutes from onset of ischemic symptoms · Possible agents for administration include unfractionated heparin, low molecular weight heparins, and factor Xa inhibitors

� Post-infarct interventions § Pharmacologic

· Beta-blockers � For all ACS patients, unless contraindicated � Consider early for hypertensive STEMI patients

· ACE inhibitors � Initiate after reperfusion therapy is complete to reduce infarct size and improve ventricular remodeling � Angiotensin receptor blockers (ARBs) are an alternative for patients who cannot tolerate ACE inhibitors

§ Transfer · STEMI patients with large anterior MI, heart failure, or pulmonary edema should be transferred to higher level cardiac care facility for possible PCI therapy

· Goal for door-to-transfer: less than 30 minutes



CHAPTER 6Heart Failure

� Definition § Inadequate cardiac output and oxygen delivery to tissues § Left ventricular ejection fraction (EF) is typically below 40%

� Causes § Systolic heart failure: inability to pump effectively § Diastolic heart failure: inability to adequately fill

Table 11: Heart Failure Clinical Presentation

Right-sided Failure Left-sided Failure

Peripheral edema Shortness of breathJVD DyspneaAscites CracklesHepatomegaly S3 heart soundIncreased CVP Pulmonary edema

� Assessment § Chest X-ray § 12-lead ECG § Obtain laboratory studies

· Brain natriuretic peptide (BNP) over 100 pg/mL · Complete blood count · Metabolic panel · Cardiac enzymes

� Interventions § Support ABCs § Initiate continuous cardiac monitoring § Titrate supplemental oxygen administration to a pulse oximetry greater than 90% § Consider BiPAP as appropriate § Initiate IV access § Administer IV fluids with caution § Administer loop diuretics, vasodilators (morphine, nitroprusside, nesiritide, ACE inhibitors) as needed § If presence of cardiogenic shock, administer positive inotropes

Aortic Dissection � Definition

§ Tear in intimal layer of aorta, which exposes medial layer to the forces of the blood pressure § Results in dissection of the two layers of the arterial wall

� Risk factors § Hypertension § Atherosclerosis § Age 60 years and above § Previous cardiovascular surgery § Connective tissue disease § Cocaine use § Trauma



Figure 15: Types of Aortic Dissection

Creative Commons Attribution-Share Alike graphic: By J. Heuser JHeuser [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC-BY-SA-3.0 ? (http://creativecommons.org/licenses/by-sa/3.0/)], via Wikimedia Commons

� Clinical manifestations § Pain to chest, back, flank, shoulders

· Sudden onset · Tearing, ripping, sharp, stabbing · Not relieved by analgesics

§ Difference of 20 mm Hg in systolic blood pressure between arms may be present § Ascending

· Altered level of consciousness · Signs and symptoms of stroke, AMI, cardiac tamponade, aortic valvular insufficiency

§ Descending · Renal failure · Paraplegia · Loss of distal pulses

§ Assessment · Obtain chest X-ray · 12-lead ECG · Obtain transthoracic echocardiogram (TTE) or transesophageal echocardiogram (TEE) · Obtain chest CT or MRI · Angiography

§ Interventions · Support ABCs

� Anticipate rapid deterioration � Administer supplemental oxygen � Obtain vascular access with two large bore catheters

· Maintain systolic blood pressure of 100–120 mm Hg � Administer IV nitroprusside, nitroglycerine, or beta-blockers as appropriate

· Administer analgesics as needed · Prepare for surgical repair

Types 1. Ascending (most common, lethal)2. Descending3. Descending into Ascending4. Abdominal



Hypertension � Hypertensive urgency

§ Definition · Substantial elevation in blood pressure · Should be treated within 24 hours of presentation

� Hypertensive emergency/crisis � Definition

§ Significant elevation in blood pressure · Systolic BP greater than 180 mm Hg OR · Diastolic BP greater than 120 mm Hg PLUS

� Evidence of (impending) end-organ damage: § AMI § Aortic dissection § Heart failure § Pulmonary edema § Cerebral infarction, intracranial hemorrhage

� Hypertensive encephalopathy � Eclampsia

§ Must be treated within one hour to prevent end-organ damage � Clinical manifestations

§ Altered level of consciousness § Chest pain § Dizziness § Epistaxis § Headache § Heart failure § Hematuria or oliguria § Presence of S3 or S4 heart sounds § Seizures § Visual disturbances

� Assessment § 12-lead ECG § Chest X-ray § Head CT § Urinalysis § Blood urea nitrogen (BUN), creatinine

� Interventions § Administer supplemental oxygen titrated to patient’s response § Initiate vascular access § Initiate continuous blood pressure monitoring

· Consider arterial line § Pharmacologic intervention

· Administration of nitroglycerin or nitroprusside via infusion to slowly decrease blood pressure by a maximum of 25% in the first two hours of treatment

· Labetalol is an alternative, but has a slower onset; safe and effective during pregnancy § Prepare for ICU admission



CHAPTER 7Endocarditis

� Definition § Inflammation of the endocardium, which includes cardiac valves

� Clinical manifestations § Signs of infection (e.g., fever, anorexia, weight loss, night sweats, myalgia, fatigue, malaise) § Pleuritic chest pain § Abdominal or back pain § Signs of embolization (e.g., stroke-like presentation, hemoptysis, conjunctival petechiae)

� Complications § Myocardial infarction § Pericarditis § Cardiac arrhythmias § Valvular insufficiency § Congestive heart failure § Stroke § Arthritis § Aneurysm § Abscesses

� Assessment § Laboratory studies

· White blood cell count (WBC) · Erythrocyte sedimentation rate (ESR) · Blood cultures

§ 12-lead ECG � Interventions

§ Administration of IV antibiotics § Prepare for surgical valvular repair or admission

Pericarditis � Definition

§ Acute or chronic inflammation of pericardial sac � Common causes

§ Viruses § Bacterial infections § Acute myocardial infarction § Aortic dissection § Cancer, radiation therapy § Renal failure § Mediastinal injury § Connective tissue disorders



Figure 16: Pericarditis

National Heart, Lung, and Blood Institute. (n.d.). Pericarditis. https://www.nhlbi.nih.gov/health/health-topics/topics/peri

� Clinical manifestations § Chest pain that usually has sudden onset, exacerbated by inspiration, activity, and supine position; relieved by leaning forward or sitting up

§ Pericardial friction rub § Tachycardia, tachypnea § Signs of infection (e.g., low-grade fever, dry cough)

� Assessment § Cardiac enzymes § 12-lead ECG

· Acute pericarditis common changes � ST elevation in most or all leads � Absent reciprocal changes � Tall, peaked T waves in all leads except aVR, V2 � PR segment depression in lead II

§ Chest X-ray § Echocardiogram

� Interventions § Administer supplemental oxygen § Initiate IV access § Initiate cardiac monitoring § Place the patient in position of comfort § Pharmacologic

· Anti-inflammatory agents (e.g., ibuprofen, aspirin, indomethacin, colchicine) · Corticosteroids if refractory to standard treatment · If pericarditis occurs with heart failure, administer high-dose NSAIDs, colchicine, antibiotics or antifungals (depending on cause), and corticosteroids or diuretics



Blunt Cardiac Injury � Definition

§ Blunt force to the chest that may result in damage to the myocardium, coronary arteries, or other structures of heart

� Causes § Most commonly from motor vehicle collision in which thorax strikes steering wheel § Falls, crush injuries, acts of violence, and sporting injuries

� Mechanism of injury § Rapid deceleration § Shearing forces § Compression against points of fixation cause damage to the heart

� Effects § Right ventricle and right atrium are most frequently associated due to the positioning of the heart in the thorax § Coronary arteries § Other structures (e.g., pericardium, thoracic aorta)

� Clinical manifestations § Vary significantly depending on underlying damage § May be asymptomatic § Chest pain § Dysrhythmias and ectopy are common, including sinus tachycardia, atrial fibrillation, and PVCs; ventricular tachycardia or fibrillation may occur if damage extensive

§ Signs and symptoms of cardiac tamponade, great vessel rupture, shock, thorax or thoracic spine fractures, change in pulses (i.e., differences in upper extremity pulses, loss of upper or lower extremity pulses)

§ Cardiac failure � Interventions

§ Based on history, physical examination findings, and specific traumatic injuries sustained § Initiate continuous cardiac monitoring § 12-lead ECG § Initiate vascular access and provide for fluid replacement as appropriate; use caution to avoid fluid overload § Cardiac biomarkers § Administer analgesics for pain § Obtain chest X-ray or other diagnostic imaging § Initiate appropriate interventions for heart failure, dysrhythmias as appropriate § Prepare for admission for patients requiring surgical repair or ongoing monitoring

Pericardial Tamponade � Definition

§ Potentially life-threatening condition in which pericardial sac, which normally contains 20–50 mL of fluid, accumulates additional fluid, resulting in pericardial or cardiac effusion

§ Resulting increased pressure causes compression of the heart and inability to effectively pump � Precipitating factors

§ Dissecting aortic aneurysm § End-stage lung cancer, other cancers as well breast and esophageal cancer, melanoma, lymphoma, and leukemia § Myocardial infarction § Cardiac surgery § Pericarditis § Trauma



� Complications § Pulmonary edema § Shock § Rapidly fatal if not treated

Figure 17: Cardiac Tamponade

https://commons.wikimedia.org/wiki/File%3ABlausen_0164_CardiacTamponade_02.png By BruceBlaus. When using this image in external sources it can be cited as: Blausen.com staff. “Blausen gallery 2014”. Wikiversity Journal of Medicine. DOI:10.15347/wjm/2014.010. ISSN 20018762. (Own work) [CC BY 3.0 http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons

Table 12: Beck Triad*

Beck’s Triad: 3 Ds

Distant (muffled) heart soundsDistended jugular veins (JVD)Decreased blood pressure (hypotension)

� Clinical manifestations § Beck triad § Kussmaul sign

· Paradoxical increase in jugular venous distention and jugular venous pressure on inspiration § Obstructive shock

· Narrowing pulse pressure · Cool, moist skin · Decreased urinary output

� Assessment § 12-lead ECG § Chest X-ray, CT § Echocardiogram § Laboratory studies

· Chemistry · CBC · Coagulation studies · CK-MB


*Note: In this eLearning course, ENA is following the AMA’s guidelines in the use of eponyms in their nonpossessive form (e.g., Beck triad, Kehr sign, Cushing syndrome).


� Interventions § Prepare for pericardiocentesis or pericardial window § Support blood pressure

· IV fluid administration; use caution to avoid fluid overload · Consider vasopressors (dobutamine), which increase cardiac output without increasing systemic vascular resistance

§ If advanced airway management is required, use caution as endotracheal intubation will decrease venous return to the right side of the heart, and changing ventilation from negative pressure to positive pressure will often exacerbate the tamponade

§ Prepare for surgery and/or admission

2015 AHA Guidelines UpdateRecently released and may or may not be reflected in the CEN exam.

� Major changes § Chest compressions rate

· Now 100–120 per minute (was at least 100 per minute) · Upper limit added to ensure adequate time for chest recoil, which assists with refilling of the heart with blood

§ Ventilation frequency · All patient populations should now be ventilated at a rate of 1 breath every 6 seconds · Standardized rate, regardless of patient population, will be easier to teach, learn, and recall and therefore more likely to benefit patients

§ Vasopressin · Removed from the adult ACLS algorithms as alternative to the first or second dose of epinephrine · No difference in the efficacy of vasopressin or epinephrine during cardiac arrest · Only epinephrine is now recommended

§ Targeted temperature management (therapeutic hypothermia) · Initiation of this treatment for the patient with ROSC and persisting neurologic deficit is no longer recommended in the pre-hospital setting

· Targeted temperature is 32–36°C for at least 24 hours § Fluid administration in septic pediatrics

· PALS guideline for pediatric shock now states that in the absence of critical care resources, extreme caution should be used when administering IV fluid boluses to the pediatric patient with suspected septic shock to avoid harmful adverse effects

§ Atropine administration in pediatric intubation · Atropine is no longer recommended for routine use to prevent bradycardia during pediatric intubation · May still be used in certain circumstances

§ Routine intubation for meconium-staining · Routine intubation to suction the airway of the newborn with meconium-staining and respiratory distress or arrest is no longer recommended

· Basic life support maneuvers should be used instead · Intubation should only be performed by highly experienced and qualified providers

§ Delayed cord clamping · New recommendation of 30-second delay in umbilical cord clamping for the newborn who does not require resuscitation at birth

Refer to the 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care for details and all changes.



CHAPTER 8Peripheral Vascular Disease

� Definition § Slow and progressive circulation disorder that may affect arteries, veins, or the lymphatic system § Directly affects each system

· Secondary effects on organs � Primarily caused by atherosclerosis � Multiple types

§ Peripheral artery disease § Peripheral venous disease § Peripheral lymphatic disease

Atherosclerosis � Definition

§ “Hardening of the arteries” that results from an accumulation of plaque on the arterial wall § Arterial wall becomes narrowed and stiff § Leg muscles must work harder to get more oxygenated blood since they are the farthest extremities from the heart and are therefore commonly affected

Figure 18: Atherosclerosis

National Heart, Lung, and Blood Institute. (n.d.). Atherosclerosis. https://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis



Peripheral Artery Disease � Definition

§ Narrowing or hardening of arteries outside of the heart, in which blood flow is compromised due to compromised vessels

� Complications § Organs that are supplied by these arteries are damaged due to decreased blood flow, oxygen, and other nutrients

Figure 19: Peripheral Artery Disease

National Heart, Lung, and Blood Institute. (n.d.). Peripheral artery disease. https://www.nhlbi.nih.gov/health/health-topics/topics/pad

� Clinical manifestations § May be asymptomatic § Weakness or numbness § Sores with delayed healing § Shiny skin § Decreased pedal pulses § Hair loss § Intermittent claudication

Peripheral Venous Disease � Definition

§ Chronic venous insufficiency § Form of peripheral venous disease § One or more veins do not adequately return blood flow from the lower extremities back to the heart due to damaged venous valves

� Complications § Pulmonary embolism § Dilated veins § Edema § Leg pain § Cutaneous changes (e.g., skin fibrosis, venous ulcers) § Venous claudication (intermittent cramping with ambulation) § Cellulitis § Ulcers § Delayed wound healing



� Clinical manifestations § Vary significantly § Varicose veins § Edema of the lower extremities § Hair loss § Cutaneous changes (redness, bruising) § Delayed wound healing

Deep Vein Thrombosis � Definition

§ Type of thromboembolic disease § Blood clots that develop in deep peripheral veins

� Risk factors § Injuries resulting in damage to veins in pelvis, thigh, or lower leg § Slow blood flow caused by lack of activity, limited movement, or paralysis § Increased estrogen due to oral contraceptive use, hormone replacement therapy, pregnancy, or recently having given birth

§ Chronic conditions such as heart or lung disease, cancer, or bleeding disorders § Genetics, age § Obesity

� Complications § Venous stasis ulcers § Delayed healing § Dislodging or traveling of the clot to the lungs, resulting in pulmonary embolism

� Clinical manifestations § Cutaneous changes in color § Edema § Venous status ulcer formation § Delayed wound healing

Thrombophlebitis � Definition

§ Form of peripheral venous disease § Blood clot in a superficial or deep vein that is inflamed, most commonly in the legs

� Risk factors § Varicose veins § Recent surgery or trauma § Prolonged period of inactivity

� Complications § Limb ischemia § Pulmonary embolism § Varicose veins

� Clinical manifestations § Edema § Skin discoloration (erythema) § Persisting symptoms (e.g., pain, swelling, feeling of heaviness in affected extremity)



Peripheral Lymphatic DiseaseLymphedema

� Definition § Most common type of peripheral lymphatic disease § Edema caused by blockage to the normal drainage pattern of lymph nodes

� Causes § Surgery § Cancer § Radiation treatment for cancer § Infection of lymph nodes § Inherited conditions

� Clinical manifestations § Asymmetry or increased circumference of affected extremity § Progressive, painless swelling § Leg heaviness

Thromboembolic Disease � Definition

§ Blood clots can travel through the bloodstream and become lodged in end organs where they cause significant damage

§ Typically occurs in legs, but also occurs in arms § Deep vein thrombosis is a type of thromboembolic disease

Table 13: PVD Symptoms

Symptoms Arterial Occlusion (PAD) Venous Occlusion (PVD, DVT)

Provocation, PalliationPain is constant, worsens with movement and exercise Improves with rest

Pain is more common with standing Diminishes with rest, elevation

Quality Burning discomfort Deep ache or throbbing

Region, Radiation Area of occlusion distally Localized to area of occlusion

Severity Excruciating Aching or throbbing

Timing Pain begins as occlusion develops Not easily relieved Pain that evolves

Objective findings Cold extremity, decreased pulses that may progress to paralysis

Swelling of extremity with deep muscle tenderness, darkened color and possible fever



Table 14: PVD Interventions

Interventions Arterial Occlusion (PAD) Venous Occlusion (PVD, DVT)

Positioning Elevate HOB but not extremity Elevate affected extremity

Activity Encourage activity Absolute bed rest

Complications

Emboli, thrombi CAD, MI, stroke Ischemic ulcers, gangrene Critical limb ischemia

Emboli PE Stroke

Treatment

Thrombolytic infusion Embolectomy Balloon catheter extraction or bypass grafting Surgery for critical limb ischemia

Anticoagulants or thrombolytics Vena cava filter Compression socks

ResourcesAmerican Association of Critical-Care Nurses. (2015). AACN cardiac medications pocket reference card. Aliso Viejo, CA: Author.

American Heart Association. (2015). Highlights of the 2015 American Heart Association guidelines update for CPR and ECC. Retrieved from https://eccguidelines.heart.org/wp-content/uploads/2015/10/2015-AHA-Guidelines-Highlights-English.pdf

Burns, S. M. (Ed.). (2014). AACN essentials of critical care nursing (3rd ed.). New York, NY: McGraw Hill Education.

Chameides, L., Samson, R. A., Schexnayder, S. M., & Hazinski, M. F. (Eds.). (2012). Pediatric advanced life support provider manual. Dallas, TX: American Heart Association.

Emergency Nurses Association. (2012). Emergency nursing pediatric course (ENPC) provider manual (4th ed.). Des Plaines, IL: Emergency Nurses Association.

Emergency Nurses Association. (2014). Trauma nursing core course (TNCC) provider manual (7th ed.). Des Plaines, IL: Emergency Nurses Association.

Hammond, B. B., & Zimmermann, P. G. (Eds.). (2013). Sheehy’s manual of emergency care (7th ed.). St. Louis, MO: Mosby Elsevier.

Hazinski, M. F., Samson, R., & Schexnayder, S. (Eds.). (2010). 2010 handbook of emergency cardiovascular care for healthcare providers. Dallas, TX: American Heart Association.

Hoyt, K. S., & Selfridge-Thomas, J. (Eds.). (2007). Emergency nursing core curriculum (6th ed.). St. Louis, MO: Saunders Elsevier.

Provinse, J. F., Harris, C., Stauss, M., Gallagher, K., & Evangelista-Hoffman, E. (2013). ENA’s translation into practice: Right-sided and posterior electrocardiograms (ECGs). Retrieved from the Emergency Nurses Association website: https://www.ena.org/practice-research/Practice/Documents/RightSideECG.pdf

Schwartz, B. G., & Kloner, R. A. (2010). Drug interactions with phosphodiesterase-5 inhibitors used for the treatment of erectile dysfunction or pulmonary hypertension. Circulation, 122(1), 88–95. doi:10.1161/CIRCULATIONAHA.110.944603

Sinz, E, & Navarro, K. (Eds.). (2011). Advanced cardiac life support provider manual. Dallas, TX: American Heart Association.

Sudden Cardiac Arrest Association. (n.d.). Fact sheet: Sudden cardiac arrest. Retrieved from http://www.suddencardiacarrest.org/aws/SCAA/asset_manager/get_file/43858?ver=17985

CEN Online Review: Cardiovascular Emergencies — Chapter 8 & Resources 39


Image ResourcesBlausen.com staff. (2014). Wikiveresity Journal of Medicine. doi:10.15347/wjm/2014.010. ISSN 20018762. (Own work) [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)] , via Wikipedia Commons

Bouma, W., Klinkenberg, T. J., van der Horst, I. C., Wijdh-den Hamer, I. J., Erasmus, M. E., Bijl, M., … Mariani, M. A. (2010). Mitral valve surgery for mitral regurgitation caused by Libman-Sacks endocarditis: A report of four cases and a systematic review of the literature. Journal of Cardiothoracic Surgery, 5, 13. doi:10.1186/1749-8090-5-13

Budzyń, M., Iskra, M., Krasiński, Z., Dzieciuchowicz, Ł., Kasprzak, M., & Gryszczyńska, B. (2011). Serum iron concentration and plasma oxidant-antioxidant balance in patients with chronic venous insufficiency. Medical Science Monitor, 17(12), CR719–727. doi:10.12659/MSM.882132

Cannon, S. (2009). Pneumatic compression devices for in-home management of lymphedema: Two case reports. Cases Journal, 2, 6625. doi:10.1186/1757-1626-2-6625

Cho, K. H. (2012). Inflammatory nodules of the leg. Annals of Dermatology, 24(4), 383–392. doi:10.5021/ad.2012.24.4.383

Fuertes, B., Toquero, J., Arroyo-Espliguero, R., & Lozano, I. F. (2003). Pacemaker lead displacement: Mechanisms and management. Indian Pacing and Electrophysiology Journal, 3(4), 231–238. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513524/

Heilman, J. (Own work) [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikipedia Commons. Retrieved from https://commons.wikipedia.org/wiki/File%3ADeltaWave09.JPG

Heuser, J. (2006). [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikipedia Commons. Retrieved from https://upload.wikimedia.org/wikipedia/commons/9/94/Aortic_dissection_%281%29_Victoria_blue-HE.jpg

Heuser, J. (2007). [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikipedia Commons. Retrieved from https://upload.wikimedia.org/wikipedia/commons/d/d4/AoDissekt_scheme_StanfordB_en.png

Koo, E. H., Kim, S. M., Park, S. M., Park, J. W., Kim, E. K., Lee, G. Y., ... Choe, Y. H. (2012). Acute recurrent pericarditis accompanied by Graves’ disease. Korean Circulation Journal, 42(6), 419–422. doi:10.4070/kcj.2012.42.6.419

Lück, Tom (Own work) [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikipedia Commons. Retrieved from https://commons.wikimedia.org/wiki/File%2AWPW.jpeg

Mantziari, A-A., Vassilikos, V. P., Chatzizisis, Y. S., Dakos, G., Stavropoulos, G., Paraskevaidis, S., Styliadis, I. H. (2011). Cardiac arrest caused by torsades de pointes tachycardia after successful atrial flutter radiofrequency catheter ablation. The Open Cardiovascular Medicine Journal, 5, 1–3. doi:10.2174/1874192401105010001

National Heart, Lung, and Blood Institute. (2014). What is atherosclerosis? Retrieved from https://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis

National Heart, Lung, and Blood Institute. (2012). What is pericarditis? Retrieved from https://www.nhlbi.nih.gov/health/health-topics/topics/peri

National Heart, Lung, and Blood Institute. (n.d.). What is peripheral artery disease? Retrieved from https://www.nhlbi.nih.gov/health/health-topics/topics/pad

Patil, V. C., Patil, H. V., Agrawal, V., & Patil, S. (2011). Cardiac tamponade in a patient with primary hypothyroidism. Indian Journal of Endocrinology and Metabolism, 15(Suppl2), S144–S146. doi:10.4103/2230-8210.83358

Seyahi, E., & Yurdakul, S. (2011). Behçet’s syndrome and thrombosis. Mediterranean Journal of Hematology and Infectious Diseases, 3(1), e2011026. doi:10.4084/MJHID.2011.026

Sohn, D. W. (2012). Constrictive pericarditis as a never ending story: What’s new? Korean Journal of Circulation, 42(3), 143–150. doi:10.4070/kcj.2012.42.3.143

Stevenfruitsmaak (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html), CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0/) or CC BY-SA 2.5-2.0-1.0 (http://creativecommons.org/licenses/by-sa/2.5-2.0-1.0)], via Wikipedia Commons. Retrieved from https://commons.wikimedia.org/wiki/File%3AACS_scheme.jpg

Yates, C., & Manini, F. (2012). Utility of the electrocardiogram in drug overdose and poisoning: Theoretical considerations and clinical implications. Current Cardiology Reviews, 8(2), 137–151. doi:10.2174/157340312801784961

CEN Online Review: Cardiovascular Emergencies - Image Resources 40