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Cardiovascular Emergencies

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Kristin Smith

on 9 September 2014

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Transcript of Cardiovascular Emergencies

Cardiovascular Emergencies
Kristin Smith, RN BSN

Chest Pain
Chest pain is one of the top chief complaints of many patients presenting to the emergency department.
Chest Pain Assessment
What things Provoke or Precipitate or Palliate or alleviate the pain or discomfort?
What is the Quality of the pain or discomfort?
Does the pain or discomfort Radiate? To what locations? What is the location or Region of the pain or discomfort?
Rate the Severity of the pain or discomfort? are there associated Symptoms?
What are the Time elements of the pain or discomfort? When did it start? How long did it last? Did the pain or discomfort begin suddenly or gradually?
Life Threatening and
Non-Life Threatening

Life Threatening Causes of Chest Pain
Acute Coronary Syndrome
Pulmonary Embolism
Aortic Dissection
Tension Pneumothorax
Acute Myocardial Infarction
Non-Life Threatening Causes of Chest Pain
Esophageal Reflux (GERD)
Spontaneous Pneumothorax
Herpes Zoster Infection
Cocain Use

Acute Coronary Syndrome
Acute Coronary Syndrome (ACS) refers to the clinical presentations of acute mycocardial ischemia
Three Types
Unstable Angina
Non ST Segment Elevation (Non-STEMI)
ST Segment Elevation Myocardial Infarction (STEMI)
Chest Pain
Unstable Angina
Change in usual pattern
More difficult to relieve
May occur at rest
More frequent and longer in duration
ST depression or T wave inversion or negative ECG Changes
****Negative Cardiac Biomarkers****
Indicates an unstable atherosclerotic plaque with potential for rupture.
Chest pain or anginal
ST Depression
Positive Cardiac Biomarkers
Indicates rupture of unstable atherosclerotic plaque and intermittent coronary occlusion
ECG shows 1 mm or more ST segment elveation in **two or more contiguous leads or new left bundle branch block pattern
Cardiac Biomarkers will be positive
Associated with complete occlusion of a coronary artery by a thrombus superimposed on a ruptured plaque.
Signs and Symptoms
Chest pain unrelieved by rest
Burning, crushing, tightness, pressure, or aching
Toothache, pain in the jaw or elbow, or indigestion like discomfort
Radiation to arm, neck, jaw, back, or shoulder
Nausea, vomiting, shortness of breath, diaphoresis, weakness, dizziness, syncope, and palpitations
Sense of impending doom
Signs of LV Failure (crackles, S3 hear sound, respiratory distress)
Tachycardia, bradycardia or varying degrees of AV block (often with inferior MI)
Diagnostic Procedures
12 Lead ECG
ST Depression
ST Segment Elevation in ***2*** or more leads
Or....LBBB presumed to be new
Differences Between Types of
Myocardial Infarction
Left Anterior Descending (LAD)
Affects the Anterior wall of the LV
See Lead Changes in V1, V2, V3, V4
Potential for Left Ventricular Failure
Affects the Lateral wall of Left Ventrical
Lead Changes in I, aVL, V5, and V6
Potential lead to Cardiogenic Shock
Right Coronary Artery (Posterior Descending)
Affects the Inferior and/or posterior Left Ventrical and AV node
Lead Changes in II, III, aVF
Can lead to Bradycardia or varying degrees of Heart Block
Right Coronary Artery (Proximal)
Affects the Right Ventrical, Inferior Left Ventrical, and Posterior Left Ventrical Wall
Lead Changes in II, III, and aVF
Can lead to Right Ventricular Failure
What Do
You Do
12 Lead EKG
Non-STEMI= ST Depression
STEMI= 1 mm or more ST Segment Elevation in two or more contiguous leads
LBBB on the 12 Lead EKG distorts the ST Segment
Presence of a "new or presumed new" LBBB and ischemic chest discomfort, manage the patient as a STEMI
If initial EKG is nondiagnostic, repeat the 12 lead ECG in 1 hour; if the patient remains symptomatic or experiences new symptoms, obtain repeat EKG at 5-10 minute intervals
Cardiac Biomarkers
Troponin I elevates 3 to 12 hours after infarct; level peaks between 10 and 24 hours
Creatine Kinase-MB elevates 4 to 12 hours after infarct; levels peaks between 10 and 24 hours
Chest X-Ray: detect pulmonary congestion or cardiac enlargement
Therapeutic Interventions
Oxygen to Keep O2 Sats
above 92%
IV Access
Aspirin 162 to 325 mg
Nitroglycerin Sublingual
Medications to limit platelet aggregation are important treatment modalities:
Clopidogrel (Plavix) loading dose 300 mg to 600 mg
Prasugrel (Effient)
The Goal
the goal for "total ischemic time" from the time of symptom onset to intervention is under 90 minutes.
Percutaneous Coronary Intervention (PCI)
Preferred method of reperfusion
Angiomax- a direct thrombi inhibitor; given to patients undergoing PCI
Glycoprotein IIb/IIIa inhibitors- antiplatelet agents that may be given
Patients who are unable to undergo PCI within 90 to 120 minutes of first medical contact, immediate fibrinolytic therapy should be administered
Medical Management
Beta Blockers
Decrease myocardial oxygen demand by decreasing HR, contractility, and BP
Angiotensin-Converting Enzyme (ACE) Inhibitors
Reduce infarct size and improve ventricular remodeling

Heart Failure
Result of inadequate cardiac output and oxygen delivery to the tissues
It can be caused by an inability of the heart to pump effectively (systolic failure) or by an inability of the heart to fill adequately (diastolic failure).
Common Precipitating Conditions
Uncontrolled Hypertension
Valvular Dysfunction
Myocarditis or endocarditis
Noncompliance with medications and diet
Signs and Symptoms of Left Sided Heart Failure
Shortness of breath
S3 Heart Sound (Kentucky)
Pulmonary Edema
Signs and Symptoms of Right Sided Heart Failure
Peripheral Edema
Jugular Venous Distension
Diagnostic Procedures
Chest X-Ray to evaluate chamber size and assess for pulmonary congestion
12-Lead EKG
Echocardiogram for EF %
Cardiac Biomarkers
Therapeutic Interventions
Airway, Breathing, and Circulation
Maintain 02
IV Access-Fluids if needed
BiPAP may improve PC by forcing fluid back
Loop Diuretics
Morphine for venous dilation and a decrease in preload
Nitroglycerin IV decrease preload
Nipride= arteriolar and venous dilation=decrease in afterload and preload
Patient's Response
Breath Sounds, RR, and O2 Sat
Shortness of Breath and work of breathing
Arterial blood pressure and HR
Level of consciousness
Jugular venous distention
Urine Output
Acute Aortic

Acute Aortic Dissection
AAD is a life threatening condition that occurs when a tear in the intimal layer of the aorta allows blood flow to endter the aortic media.
Propelled by the pulsatile flow and high pressures with the aorta, the column of blood produces a "false channel" for antegrated for retrograde blood flow.
Aortic dissections are classified based on their location and potential complications can be anticipated based on that location.
Risk Factors
Age 60 years or older
Previous cardiovascular surgery
Biscuspid aortic valve
Marfan syndrome
Iatrogenic or traumatic intimal tear
Cocaine use
Signs and Symptoms
Severe ripping, tearing pain
Difference in blood pressure of 20 mm HG b/w arms
If aortic arch is involved:
Altered LOC
S/S of Stroke
Cardiac Tamponade
Acute MI
Acute aortic valvular insufficiency
If descending aorta is involved:
Anuria and renal failure
Loss of distal pulses

Diagnostic Procedures
Chest X-Ray
12 Lead EKG
Transthoracic Echocardiogram (TTE)
What Do I Do?
Therapeutic Interventions

IV Access
BP in both arms
Vital Signs, Neuro Status, Peripheral Pulses, Movement and Sensation, and Urinary Output
Beta Blockers= labetalol, esmolol, or propanolol
Surgical Repair
Hypertensive Emergency
Hypertensive Emergency, or crisis, is present in a patient with a SBP over 180mm Hg or DBP over 120 mm Hg and evidence of impeding or progressive end-organ damage.
Signs and Symptoms
Altered LOC
Drowsiness, stupor, or coma
Chest pain, ischemic changes on EKG
Presence of s3 and s4
Retinal hemorrhage and exudates
Decreased urine output
Blurred Vision
Diagnostic Procedures
Blood urea nitrogen and creatinine
12 Lead EKG
Chest XRay= LV enlargement
CT Head= Intracranial Bleeding
Therapeutic Interventions
IV Access
Continuous BP Q5 mins
Very rapid onset
Titrate Slowly b/c risk of sudden hypotension
Rapid reduction of BP slows the progression of end-organ damage
Limit decrease in BP to 25% in the first 2 hours of treatment

IV Labetalol
The pericardium is a fibrous sac surrounding the heart, it normally contains 15 to 50 mL straw-colored fluid to "lubricate" the heart as it contracts and relaxes.
Acute pericarditis is an inflammation of the pericardium and may be an isolated condition or the result of systemic disease. Possible complications:
Cardiac Tamponade
Recurrent Pericarditis
Pericardial Constriction
Causes of Pericarditis
Infections, including TB
Acute MI
Neoplastic invasion of the pericardium
Inflammation following radiation therapy to the chest
Cardiac or Thoracic Trauma
Aortic Dissection
Uremic Syndrome in Renal Failure
Autoimmune disorders
Signs and Symptoms
Chest pain
onset is sudden
pain is severe, sharp or dull
increases with activity, lying flat, and inspiration
occasional radiation to neck, back or arm
decreased by sitting up and leaning forward
unrelieved by rest or nitro
Pericardial Friction Rub
Leathery, grating quality
may be transient
best heard on the left sternal boarder with the patient leaning forward
no associated with respiration
Tachycardia, tachypnea
Possible elevated body temp
Diagnostic Procedures
Cardiac Biomarkers
12 Lead EKG
Widespread ST segment elevation
Tall, peaked T waves
PR segment depression in Lead II
No reciprocal changes in opposite Leads
Chest X-Ray
Therapeutic Interventions
IV Access
Position of Comfort
Anti-Inflammatory Medications
Chest Trauma
Tension Pneumothorax
Occurs when air enters the pleural space during inspiration and is unable to escape during exhalation.
Air accumulates in the thoracic cavity causing life-threatening hemodynamic comprise. The increase intrathoracic pressure causes collapse of the lung on the injured side.
It can be caused by:
Blunt or penetrating trauma
Complication of mechanical ventilation
Signs and Symptoms
Severe respiratory distress: dyspnea, restlessness, and tachypnea
Poor peripheral perfusion
Jugular vein distension
Deviated Trachea
Distant HS
Diagnostic Procedures
Chest X-Ray:
Tracheal Deviation and Mediastinal shift
Therapeutic Interventions
Needle Decompression
14-16 gauge over the needle catheter
Insert above the 3rd rib into the 2nd ICS
Air under pressure released. Remove needle.
Chest Tube
Pain Control
Cardiac Tamponade
Cardiac Tamponade
The collection of blood or blood clots in the pericardial sac; accumulating blood exerts pressure on the heart, limiting ventricular filling and decreasing cardiac output.
The leading case:
Penetrating chest injuries (80-90%) such as a stab wound.
Signs and Symptoms
Chest pain
Beck's Triad
Distended neck veins
Muffled or distant HS
Altered Mental Status
Pulsus pardoxus= decrease in SBP greater than 10 mm Hg during inspiration
Diagnostic Procedures
Low voltage QRS complexes
Pulsless Electrical Activity
Electrtical Alternans= alternating amplitude of QRS complexs
Chest X-Ray
Focused Assessment with Sonography for Trauma (FAST)
Therapeutic Interventions
Rapid Infusion of IV fluids to increase cardiac filling pressure
Hemodynamically unstable= pericardiocentesis
Surgical intervention
Open Pneumothorax
Open Pneumothorax
Air enters and exits the chest cavity through the wound as the patient breathes producing a "sucking' sounds.
If the chest wounds is approximately two thirds the diameter of the trachea, air may preferentially enters the plural space with inspiration rather than the patients upper airways.
This situation results in severe hypoxia and hypercapnea.
Signs and Symptoms
History of penetrating chest trauma
visible chest wound
signs of respiratory distress
"sucking" sound with respiration
asymmetric chest expansion
bubbling of blood around a chest wound with exhalation
subcutaneous emphysema
Diagnostic Procedure
Clinical Assessment
Chest X-Ray
Therapeutic Interventions
Immediately cover wound
occlusive dressing
observe for tension penumo
chest tube insertion
The Accumulation of blood in the pleural space.
Accompanied by a pneumothorax, bleeding is the result of laceration of the intercostal vessels or internal mammary arteries, or from direct lung parenchymal damage.
Results from rapid accumulation of 1500 mL of blood in the chest cavity
Signs and Symptoms
Pain on Inspiration
Asymmetric chest wall movement
cool clammy skin
decreased capillary refill
decreased breath sounds on the affected side
dullness to percussion on the affected side
Diagnostic Procedures
decreased H/H
Chest XRay
blunting of costophrenic angle in the upright position
Therapeutic Interventions
IV Blood Products
Chest Tube Placement
36-38 French
inserted anterior to midaxillary line at the fourth or fifth ICS
CT to suction
drainage unit below level of chest
keep unit upright
assess for fluctuation, output, color, and absence of air leak (FOCA)
Consider autotransfusion
Prepare for emergent surgery if drainage is more that 1500 mL or initial drainage of 1000 mL is followed by 200 mL/hr for 2-4 hours
Flail Chest
Occurs when two or more adjacent ribs are fractured in two or more places or when the sternum is detached.
The flail segment loses continuity with the rest of the chest wall and responds to changes in intrathoratic pressure in a paradoxical manner.
Signs and Symptoms
Chest pain and bony crepitus
respiratory failure
hemothorax and pneumothorax
asymmetric or paradoxical movement of chest wall
possible subcutaneous emphysema
Diagnostic Procedures
Chest XRay
Therapeutic Interventions
Pain management with systemic narcotics, intercostal nerve block, or epidural block
O2 to maintain pO2 of 80-100 mm Hg
Chest Tube if pneumo or hemothorax is present
Correct hypovolevmia
**Do not use sandbags**
Myocardial Rupture
Traumatic myocardial rupture may involve perforation of the ventricles or atria or laceration or rupture of the ventricular septum or valvular apparatus.
Most common is from a high speed MVA
Signs and Symptoms
Severe hypotension unresponsive to fluid resuscitation
Distended neck veins
Distant HS
Loud harsh murmur
Cyanosis of upper torso, arms, and head
Evidence of thoracic trauma or massive chest injuries
Diagnostic Procedures
Chest XRay
FAST examination
Therapeutic Interventions
Minimize pre-hospital on scene time
Immediate surgical intervention
ED= with vitals, and then experiences cardiopulmonary arrest= open thoracotomy
Potentially Life Threatening Chest Trauma
Injuries to the Aorta
Blunt Cardiac Injury
Pulmonary Contusion
Tracheobronchial Disruption
Diaphragm Rupture
Esophageal Disruption
Non-Life Threatening Chest Trauma
Simple Pneumothorax
Rib Fractures
Sternal Fractures
Clavicular Fractures
Scapular Fractures

The partial or total occlusion of an artery by atherosclerosis or arteriosclerosis obliterans
Predisposing Factors:
Raynaud Disease
Thromboangilitis obliterans (Buerger disease): inflammation and blockage of sm and md sized arteries of the extremities.
Occlusion occurs at bifurcations
Damage to intima w progressive deterioration and thrombus formation
Partial or Complete occlusion:
Stage 1: pathologic changes within the artery but no clinical symptoms
Stage 2: intermittent claudication; 75% occlusion
Stage 3: pain at rest= 90% to 95% occlusion
Stage 4: necrosis= 99% to 100% occlusion
Clinical Presentation
Intermittent claudication in thigh and hip; pain increases with exercise and decreases with rest
Coolness of the lower extremities
Hair loss
Decreased or absent iliac and femoral pulses
Bruit or thrill over the iliac area
Pallor or mottling of the lower extremities
Nonhealing ulcers on the toes or points of trauma
Decreased motor strength in the lower extremities
Decreased or absent femoral and popliteal pules
Thrill or bruit over the femoral or popliteal area
Doppler or duplex
Antinuclear antibody testing
Callaborative Managment
Continue assessment
Maintain airway, oxygenation, and ventilation
Maintain adequate cirulation and perfusion
May need pharmacologic agents: fibrinolytics
Control Pain and discomfort
Monitor for complication
If evaluation criteria is met: discharge patient with follow up
If not met: admission, possible cardiac cath, or surgery for vascular bypass
Venous Thrombosis
The occlusion of a vein by a blood clot.
Predisposing factors:
Sickle cell anemia
Alterations in vessel wall:
Drug use
Venous Stasis
Bed Rest
Clinical Presentation
Pain: aching, localized pain w movement; tenderness with palpation
Unilateral edema, erythema, warmth, and dilated collateral veins on the affected extremity
Positive Homans sign
Low grade fever
Postive D Dimer
Venography and Doppler US
Impedance plethysmorgraphy
Collaborative Management
Continue Assessment
Maintain airway, oxygenation, and ventilation
Prevention of progression or dislodgement of clot
warm compresses, elevation, low molecular weigh heparin, TEDS, avoid leg massage/valsalva maneuvers, hydrate w/ oral or IV fluids
Monitor Complications
An inflammation of the endocardium that usually occurs in the membranous lining of the heart valves but that also may involve cardiac prostheses
Predisposing factors:
Congenital or acquired valvular HD
Cardiac Surgery
Invasive Tests
Skin, bone, or pulmonary infections
Poor oral hygiene
Dental procedures
IV drug use
Long term venous access devices
Body piercing
Immunosuppressed state
Causative agents:
Clinical Presentation:
Fever, chills, diaphoresis, malaise, weakness, anorexia, myalgias, arthralgias, headache, weight loss
Pleuritic chest pain
Abdominal pain
Back pain
Dyspnea, orthopnea, cough and hemoptysis
Medical History
Heart sounds change or new murmur
Confusion or delirium
Signs of embolic or allergic vasculitis: splinter hemorrahages of nail beds, petechia, roth spots, Janeway leasons, Osler nodes
Sedimentation rate=elevated
Blood cultures=persistently positive
Urine=hematuria, proteinuria
Chest XRay
Tricuspid or pulmonic valve=multiple bilateral infiltrates
Collaborative Management
Continue assessment
Maintain airway, oxygenation, and ventilation
Maintain adequate circulation and perfusion
Decrease myocardial oxygen consumption
Control and treat infection
Monitor for complications
HF, cardiogenic shock, and pulmonary edema
Extension of the infection w abscess or fistula
neurologic complications
systemic emboli
bacterial or mycotic aneurysm
dysrhythmias or blocks
spetic shock
Patients may undergo surgery for valve repair or replacement
Antibiotic use
Patient education: prophylactic antibiotics and good hygiene
Atrial Flutter

Presence of regular atrial activity with a picket fence, or sawtooth pattern
Single irritable site in atria initiates many electrical impulses at a rapid rate
Normal P wave not produced
Electrical impulses conducted throughout atria at fast rate

Rather than the presence of normally appearing P waves, flutter (or sawtooth) waves, also known as F waves, are patterned
AV node becomes “gate keeper” to ventricles
Based on number of impulses AV node accepts, ventricular response is established

Atrial Flutter Rhythm
Conduction ratio 2:1
Two atrial contractions for each ventricular contraction
Conduction ratio 4:1
Four atrial contractions for each ventricular contraction
An atrial rate of 300 beats per minute (bpm) will parallel a ventricular rate of 75 beats per minute (bpm)

Atrial flutter with a slow ventricular response
Ventricular rate of less than 60 beats per minute (bpm)
Atrial flutter with a rapid ventricular response
Ventricular rate of 100-150 beats per minute (bpm)
Atrial Flutter
Atrial Fibrillation Rhythm
One of the most common atrial dysrhythmias
Presents with three definite characteristics
1. Notable absence of P waves
2. P waves replaced by F waves
3. Ventricular response rate totally irregular or termed “irregular irregularity”
QRS complexes are usually within normal limits
Multiple ectopic foci from within atria blitzing AV node
AV node unable to handle or conduct each impulse
AV node allows impulses to enter conduction system at random
Rhythm may be chronic in nature, commonly associated with underlying heart disease, CHF, rheumatic heart disease
Also hypoxia, MI, digitalis toxicity
Slow HR < 80-100 if rapid
Done with monitoring and digitalis
Atrial Fibrillation

Encompasses all fast (tachy-) dysrhythmias in which heart rate is greater than 100 beats per minute (bpm)
Applies to any tachycardic rhythm originating above the ventricle
Paroxysmal refers to sudden onset and/or cessation

Supraventricular Tachycardia Rhythms

Beasley / Understanding EKGs, 2nd Ed.


Occurs when rapid atrial ectopic focus overrides the SA node and becomes the heart’s primary pacemaker
Can resemble a rapid sinus tachycardia
Sinus tachycardia seldom exceeds 160 to170 beats per minute at high range

Beasley / Understanding EKGs, 2nd Ed.


Beasley / Understanding EKGs, 2nd Ed.


Causes can be overexertion, stress, hypoxia, excessive use of stimulants, hypokalemia, and ASHD
Vagal maneuvers; Stimulation of the vagus nerve releases acetylcholine resulting in slowing of heart rate
Bearing down, coughing, squatting, and carotid sinus massage

Supraventricular Tachycardia

Beasley / Understanding EKGs, 2nd Ed.


Atrial flutter rhythm
Related directly to patient’s condition
Ventricular rate normal
Well tolerated
Ventricular rate fast
Decrease in cardiac output
Directed to decrease ventricular rate, either with medication (if stable) or cardioversion (if unsta

Clinical Significance of Atrial Rhythms

Beasley / Understanding EKGs, 2nd Ed.


Atrial fibrillation rhythm
Controlled atrial fib
No treatment
Rapid atrial fib
Treatment is to decrease the ventricular rate with medications (if stable) or cardioversion (if unstable)
Patients are at risk of atrial and systemic emboli due to decrease in cardiac output or loss of “atrial kick”

Clinical Significance of Atrial Rhythms

Beasley / Understanding EKGs, 2nd Ed.


Supraventricular tachycardia rhythms
May occur in healthy hearts and may be tolerated for a short while
C/O heart “racing or running away”
If symptomatic, treatment directed at slowing the heart rate by use of vagal maneuvers, drug therapy, or synchronized cardioversion

Clinical Significance of Atrial Rhythms

Beasley / Understanding EKGs, 2nd Ed.

Atrial Rhythms
Ventricular Rhythms

Also termed ventricular escape rhythms, and are considered a last-ditch effort of the ventricles to try to prevent cardiac standstill
Means SA node and AV node have failed
Rate usually less than 40 beats per minute (bpm), and cardiac output is usually compromised

Idioventricular Rhythms

Beasley / Understanding EKGs, 2nd Ed.


Agonal rhythm is when the idioventricular rhythm falls below 20 beats per minute
Frequently may be seen as the last-ordered semblance of a heart rhythm when resuscitation is either unsuccessful, or after successful defibrillation

Agonal Rhythm


Causes include extensive myocardial damage, secondary to acute myocardial infarction, or failure of higher pacemakers
Is considered a lethal rhythm and treatment must be immediate and aggressive

Idioventricular Rhythms

Beasley / Understanding EKGs, 2nd Ed.


May occur when the rate of the ectopic pacemaker exceeds 40 beats per minute
Commonly accepted rate is 40-100 beats per minute
There are no P waves or PR intervals noted

Accelerated Idioventricular Rhythm


Beasley / Understanding EKGs, 2nd Ed.


This rhythm is one in which three or more PVCs arise in sequence at a rate greater than 100 beats per minute
This rhythm commonly overrides the normal pacemaker of the heart
Often occurs rapidly and is initiated by a PVC or by PVCs occurring in rapid succession

Ventricular Tachycardia Rhythms

Beasley / Understanding EKGs, 2nd Ed.


If rhythm is sustained, patient’s clinical condition may rapidly deteriorate
A sustained rhythm is one that lasts for more than 30 seconds
If lasts for less than 30 seconds, it is a nonsustained rhythm,or simply a run of V tach


Beasley / Understanding EKGs, 2nd Ed.


Is classified (based on assessment of the patient’s clinical presentation) as either pulseless V tach or V tach with a pulse
Immediate treatment is based on the presence or absence of a palpable pulse
Pulseless V tach
Immediate defibrillation

Ventricular Tachycardia


Treatment of V tach with a pulse is based on patient’s clinical picture
Hemodynamically unstable
(Low blood pressure, shortness of breath, etc.) Immediate cardioversion is considered
Hemodynamically stable
( Normal blood pressure, absence of chest pain, and no notable change in mental status ) drug intervention is appropriate

Beasley / Understanding EKGs, 2nd Ed.


Similar to ventricular tachycardia
Morphology of QRS complexes shows variations in width and shape
Resembles a turning about or twisting motion along base line
May result from
Hypokalemia, hypomagnesemia, tricyclic antidepressant drug overdose, use of antidysrhythmic drugs, or combination of these

Torsades De Pointes


Beasley / Understanding EKGs, 2nd Ed.


Finding and treating the underlying cause of the rhythm is essential
Magnesium is the pharmacologic treatment of choice
Key to recognizing torsades is the variation of QRS morphology, or shape

Torsades De Pointes


Is a fatal dysrhythmia
Is the most frequent initial rhythm occurrence in sudden cardiac arrest
Tends to occur in the initial hours following an acute myocardial infarction
Occurs as a result of multiple weak ectopic foci in the ventricles

Ventricular Fibrillation

Beasley / Understanding EKGs, 2nd Ed.


Myocardial cells appear to quiver rather than depolarize normally
No coordinated atrial or ventricular contraction, and no palpable pulse
Electrical impulses initiated by multiple ventricular sites; Impulses are not transmitted through normal conduction pathway

Beasley / Understanding EKGs, 2nd Ed.


Waveforms appear as disorganized, rapid, irregular waves whose morphology varies vastly
No well-organized QRS complexes
Death will occur if immediate treatment is not established

Beasley / Understanding EKGs, 2nd Ed.


Classified as either
Fine ventricular fibrillation
Ventricular fibrillation waves less than 3 millimeters of amplitude
Coarse ventricular fibrillation
Ventricular fibrillation waves with amplitudes greater than 3 millimeters
Course fib is generally more irregular than fine fib

Beasley / Understanding EKGs, 2nd Ed.


Ventricular Fibrillation (Fine)

Beasley / Understanding EKGs, 2nd Ed.


Ventricular Fibrillation (Coarse)

Beasley / Understanding EKGs, 2nd Ed.

Ventricular Asystole
The absence of all ventricular activity
Also called cardiac standstill or asystole
Asystole is represented by a flat line, and is the absence of all cardiac electrical activity
It may be difficult to distinguish asystole from fine VF; you must always check two different leads to definitively identify asystole
Often follows unsuccessful resuscitation attempts
May be caused by
Massive MI, cardiac trauma, ventricular aneurysm, and complete heart blocks

Ventricular Asystole
(Cardiac Standstill, Asystole)

Pulseless Electrical Activity
The absence of a palpable pulse and myocardial muscle activity with presence of organized electrical activity on the cardiac monitor
Represents a clinical condition, the patient is clinically dead despite some type of organized rhythm on monitor
Formerly termed electromechanical dissociation, or EMD
Causes include
Profound hypovolemia, massive myocardial damage, ventricular rupture, pulmonary embolism, acidosis, cardiac tamponade, or tension pneumothorax
Clinical Significance of Ventricular Dysrhythmias
Idioventricular Rhythm
Majority are symptomatic
Due to decreased heart rate, may develop decreased cardiac output, weakness, dizziness, hypotension, and alterations in mental status
A thorough patient assessment is conducted to determine whether rhythm is perfusing
Ventricular Tachycardia
May be perfusing (producing a palpable pulse) or nonperfusing (producing no palpable pulse)
Due to rapid heart rate, ventricles do not have time to empty and refill = Cardiac output compromised
Treatment is based on the absence or presence of a palpable pulse as well as the patient’s clinical picture
If V tach is perfusing and stable
Treatment consists of oxygen administration, IV lifeline, and pharmacologic intervention
If V tach patient becomes clinically unstable (as evidenced by hypotension, SOB, and CP)
Synchronized cardioversion is indicated
If V tach is without a pulse
Treatment will require immediate unsynchronized cardioversion (defibrillation)
Remember it is treated the same as ventricular fibrillation
Treatment must be aggressive and immediate
Ventricular Fibrillation
There is no cardiac output, no perfusion
If not treated immediately, patient will not sustain life
The presence of fine V fib
Indicates rhythm has been present for extended period of time
Treatment includes
CPR, defibrillation (200, 300, 360 joules), airway control, IV lifeline, and drug intervention
Signals a complete termination of ventricular activity
Check in two leads to rule out the presence of fine V fib
Treatment includes
CPR, IV lifelines, endotracheal intubation, and pharmacologic intervention
Heart Block
Third-Degree AV Block(Complete)
Atria and ventricles are completely blocked and separated from each other electrically
They beat independently of each other
SA node fires @ 60 to 100 beats per minute
Ventricles paced by an escape pacemaker either at junctional tissues (narrow QRS complex) or ventricles (wide QRS complex) @ a rate of 20 to 40 beats per minute
Termed AV dissociation because atria and ventricles beat independently
PR intervals will be variable in length
Some P waves may be buried in QRS complex and not visible on EKG strip
Pattern illustrates regularly occurring P waves and QRS complexes; however, no relationship is noted
Third-degree (complete) heart block
Considered a lethal dysrhythmia
Signs and symptoms exhibited by patient may be indicative of severe hypoperfusion
If QRS complexes are narrow and patient is asymptomatic, AV junction is most likely the pacemaker site
If symptomatic, drug therapy (atropine) or pacing may be indicated
If the patient is exhibiting signs and symptoms, and the QRS complexes are wide, transcutaneous pacing followed by the insertion of a transvenous pacemaker may be indicated
Listen to and observe your patient, and never base your treatment decision on EKG strip analysis alone

Causes can range from the expected terminal event of chronic or acute illnesses to sudden cardiac death.
Hypoxia secondary to severe respiratory insufficiency, and traumatic cardiopulmonary arrest.

Emphasis is placed on the immediate initiation:
High quality CPR
Rapid Defibrillation
Management of Cardiopulmonary Arrest
Chest Compressions
Airway Control
Breathing and Ventilation
Obtaining Circulatory Access (IV)
Biphasic=120 to 200jouls
Monophasic=300 jouls
Epinephrine=1mg IV or IO Q3-5 mins
Vassopressin=40 units IV or IO, first or second dose of epi
Amiodarone=150-300mg/or lidocaine
IV fluid bolus
Treat Reversible Cause
Follow Current ACLS protocol ;)
Cardiopulmonary Arrest in the Pregnant Woman
Follow ACLS guidelines
Search for and treat factors with the BEAU-CHOPS mnemonic:
Anesthetic complications
Uterine atony
Cardiac Disease
Others: HIT
Placental abruption
Management following Successful Resuscitation
Early Percutaneous Coronary Intervention
Therapeutic Hypothermia
Do not forget about the family!

Remember TeamWork!!!
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