EKG Rhythms Part 2: Junctional Rhythms

EKG Rhythms: Part Two

• Normal conduction occurs in the SA node, AV node, Bundle of His, Bundle Branches, and Purkinje Fibers.
• Inherent rates are SA node (60-100), AV node (40-60), and Purkinje Fibers (20-40).

Pacemaker Cells and Associated Dysrhythmias

• SA node dysrhythmias include ectopic beats, SA node issues, and Atria problems.
• AV node dysrhythmias encompass ectopic beats, junctional issues, and AV blocks.
• Purkinje Fibers dysrhythmias feature ectopic beats and ventricles issues.

AV Node/Junction

• The impulse is slowed here for ventricular filling during relaxation/diastole.
• Has pacemaker properties and fires at 40-60 beats per minute.
• Conducts to the Bundle of His.

Junctional Rhythms

• Includes Junctional Rhythm, Junctional Escape Beat, Accelerated Junctional Tachycardia, Junctional Tachycardia, Supraventricular Tachycardia, and Paroxysmal Supraventricular tachycardia

Junctional Rhythm Information

• Rhythm is regular, rate typically 40-60 beats/min, and PR interval is at the low end of normal.
• P-wave changes may include being inverted, absent, or falling behind the QRS.
• QRS is narrow, less than 0.12 seconds, may have decreased cardiac output.
• Junctional Escape Beat is a late beat occurring after the next sinus beat should happen.
• Occurs when a cardiac rhythm is too slow, and a backup pacemaker site initiates an electrical impulse

Accelerated junctional

• Rate 61-100 beats per minute, regular rhythm, P wave will be inverted, absent, or fall behind the QRS complex

Junctional tachycardia

• Rate greater than 100 beats per minute, regular rhythm, P waves will be inverted, absent, or fall behind the QRS complex

Dysrhythmias of the AV Node, Part One

• Includes Supraventricular Tachycardia and Paroxysmal Supraventricular Tachycardia
• Causes may include occurring in healthy adults, increased catecholamines, stimulants, heart disease, electrolyte imbalances, and anatomic abnormality.

Supraventricular Tachycardia (SVT)

• Improper electrical activity located above the ventricles, with a rate greater than 150-250.
• Rhythm is usually regular but a P wave and a T wave can be hard to differentiate if the heart rate is high.
• If a P wave is present, the PR interval is shortened, while other intervals remain normal.
• QRS complex will be narrow and followed by a T-wave.
• Hemodynamic varies depending on pre-existing heart disease.

Treatment for SVT

• Clinical significance is a decreased cardiac output, which causes signs/symptoms of hemodynamic compromise.
• Early signs include anxiety, dizziness, fatigue, and lightheadedness.
• Late signs consist of hypotension, chest pain, shortness of breath, changes in mental status, and a decrease in urine output over several hours.

Treatment for SVT if Stable

• O2, IV, and monitor, vagal maneuvers
• Administer Adenosine 6mg rapid IVP followed by 20 ml bolus of NS, repeat with 12mg if not effective up to 1 time
• Synchronized Cardioversion

Treatment for SVT if Unstable

• Immediate synchronized Cardioversion

Atrioventricular Blocks

• Delayed electrical impulses that originate from the SA node

First Degree Atrioventricular Block

• Delayed conduction from the SA node to the AV node
• Prolonged PR interval is greater than 0.20 seconds.
• PR interval is the same for each beat.

Second Degree AV Block

• Second-degree AV block is classified as type 1, or type 2, depending on the location of the block.
• Above or type 1, and Below the bundle of His is type 2

Second Degree AV Block Type 1: Wenckebach or Mobitz 1

• Rhythm (ventricular) is often irregular, atrial rhythm is regular, and QRS is normal
• P waves look similar.
• Steadily lengthening PR intervals until one QRS fails
• PP interval is regular and RR interval is irregula, with Non-conducted p waves (dropped complex).
• QRS is usually normal, and the block rarely progresses and is self-limiting, but may decrease cardiac output

AV Block Mobitz 2

• Ventricular rhythm is irregular, with theatrial rhythm regular and PRI normal or prolonged
• Characterised by a suddenly dropped QRS
• P waves are punctual and similar, unlike a non-conducted PAC which is EARLY!
• QRS is often abnormal.
• More severe AV block, often associated with bundle branch block, with fixed PR interval.
• PP interval is regular, occasional P wave not followed by QRS, more serious than type 1 due to complete block possibility.

Third Degree AV Block Complete Block

• Conduction completely blocked between atria and ventricles
• Block may occur at the AV node, Bundle of His, and Bundle Branches.
• Atria and ventricles are depolarizing independently.
• Atrial rate is greater than the ventricular rate.
• P-P intervals and R-R intervals are regular, but unassociated.
• No PR intervals in the absence of conduction.
• QRS is often widened to greater than 0.12 seconds

Differentiation of Second-Degree AV Blocks

• Type 1 presents with irregular ventricular rhythm, lengthening PR interval, and usually narrows QRS width.
• Type 2 presents with irregular ventricular rhythm, unless every other beat is blocked, constant PR interval, and usually wide QRS width.

Key Memory Aid For Heart Blocks

• If the R is far from P, then it is a First Degree block.
• If longer, longer, longer, drop, then you have a Wenckebach block.
• If some Ps do not get through, then you have Mobitz 2 block.
• If Ps and Qs do not agree, then you have Third Degree block.

His- Purkinje System

• Made up of Right and left bundle branches, fascicles, and Purkinje fibers.

Ventricular Rhythms

• Idioventricular rhythm is a slow dysrhythmia, rate of 20 to 40 BPM, with wide QRS complexes that arise from the ventricles
• Accelerated Idioventricular rhythm is 40-100 bpm.
• Ventricular Tachycardia, or V-TACH can be Monomorphic, Polymorphic, or Torsades de pointes
• Extreme bradycardia could cause decreased cardiac output, hypotension, chest pain, shortness of breath, syncope, or altered level of consciousness if a Patient Responses to treatment

Treatment for Ventricular Rhythms

• Give oxygen, cardiac monitor, and IV access.
• Atropine 1mg IV push can be administered up to 3mg MAX.
• If needed, transcutaneous pacing (TCP)
• Dopamine or Epinephrine can also be given

Ventricular Tachycardia (V-TACH)

• A rapid, life-threatening dysrhythmia that originates in the ventricles.
• Exists when three or more PVCs occur in immediate succession at a rate higher than 100 beats/min.
• Abnormal depolarization produces a widened QRS complex >0.10 sec may or may not have a pulse and may be stable or unstable
• Two types: Monomorphic, with similar looking complexes, and Polymorphic, with complexes varying from beat to beat

Monomorphic V-Tach

• QRS complexes are the same size and shape

Polymorphic V-Tach (Torsades de pointes)

• Follows a long resting long QT interval greater than 0.44 seconds
• EKG waves are rapid and irregular while continuously changing from and upright to inverted position

V-Tach Clinical Significance & Treatment

• Decreased cardiac output can cause hypotension, chest pain, shortness of breath, Syncopeor Altered level of consciousness.
• Treat stable but symptomatic patients with oxygen therapy, IV, and monitor.
• Obtain a 12-lead EKG.
• Administer amiodarone 150mg IVP followed by 300mg IVP or lidocaine 1-1.5mg/kg, and a max dose of 3mg/kg
• Give a Synchronized cardioversion
• An unstable patient with a pulse will need immediate synchronized cardioversion

Torsades de Pointes

• A type of polymorphic V-Tach.
• Manifests as QT syndrome, with a rate of 150-300 beats per min, usually 200-250 beats per min
• The rhythm may be regular or irregular.

QRS Alterations in Torsades de Pointes

• It is greater than 0.12 seconds and has gradual alteration in amplitude and direction of QRS.
• May also have Clinical significance of a decreased cardiac output, possibly leading to V-Fib.

Stable Torsades de Pointes Management

• Oxygen therapy, IV and cardiac monitor
• Discontinue any type 1 antidysrhythmic if drug-induced.
• Perform Overdrive pacing: Pacing the heart at a higher rate than normal will shorten the QT interval.
• Medications include Magnesium and Amiodarone.

Unstable Torsades de Pointes Management

• Immediate synchronized cardioversion must be preformed

Cardiac Arrest Rhythms

• Ventricular Tachycardia (V-TACH) without a pulse
• Torsades without a pulse
• Ventricular Fibrillation (V-Fib)
• Pulseless Electrical Activity (PEA) and Asystole

Pulseless V-Tach

• The condition results in Cardiac Arrest, so call for help/initiate the code blue procedure
• Begin CPR until defibrillator is available and defibrillate as soon as possible
• Once defibrillator arrives, deliver unsynchronized shocks
• Administer Epinephrine 1mg IVP every 3 minutes (no max dose)
• Amiodarone 300mg IVP followed by 150mg IVP or lidocaine 1-1.5mg/kg up to 3mg IVP
• Prepare for intubation

Pulseless torsades

• Pulseless (Cardiac Arrest)

Responding for Code Blue

• Call for help and intiate the code blue/arrest protocol
• Begin CPR until a defibrillator is available, and defibrillate as soon as possible
• Once defibrillator arrives, deliver unsynchronized shocks.
• Administer Epinephrine 1mg IVP every 3 minutes (no max dose).
• Amiodarone 300mg IVP followed by 150mg IVP or lidocaine 1-1.5mg/kg up to 3mg IVP.
• Magnesium may be administered 1-2gms diluted in 10ml of D5W given as a bolus over 5-20mins.
• Prepare to intubate to secure airway

Ventricular Fibrillation

• Presents as a chaotic pattern, with no discernible P, Q, R, S or T waves
• May be course versus fine, causes no cardiac output and is life-threatening
• Emergent defibrillation needed

Pulseless Electrical Activity (PEA)

• PEA exists when organized electrical activity (other than VT) is present on the cardiac monitor, but the patient is pulseless
• Causes include Pulmonary embolism, Acidosis, and Tension pneumothorax
• The most common cause is Hypovolemia.
• Other causes include Heat/cold, Drug overdose/accidents, and Cardiac tamponade

Treatment for Pulseless Electrical Activity (PEA)

• Call for help-code blue
• In case the patient goes into a rhythm that can be defibrillated and the defibrillator is already present, get a crash cart/defibrillator
• Immediate CPR should be performed and Epinephrine- 1mg every 3 min NO MAX DOSE!

Asystole

• Asystole is a total absence of ventricular electrical activity and has no ventricular rate or rhythm, no pulse, and no cardiac output, however some atrial electrical activity may be evident
• Causes include a PE, Acidosis, a heat/cold event, and Hypovolemia
• Also caused by Drug overdose/accidents, Tension pneumothorax, or a Cardiac tamponade

Treatment for Asystole

• Get crash cart/defibrillator (in case the patient goes into rhythm that can be defibrillated)
• Perform immediate CPR and administer Epinephrine 1mg every 3 min (no max dose)
• Consider possible causes and never cardiovert or defibrillate asystole

Hemodynamics (HD)

• The goal of hemodynamic monitoring is to accurately assess the patient and provide therapies to optimize how oxygen is delivered into tissue
• "“Invasive and noninvasive hemodynamic monitoring is a major part of a comprehensive assessment of the critically ill patient”

Value Goals

• The goal of HD monitoring is to assess a patient's trends and the response to therapy, rather than necessarily comparing to the normal ranges
• New modalities such as bedside echocardiography, mixed venous oxygen saturation (SvO2) monitoring, and changes in the arterial pressure waveform, continually measure ever-changing bodily responses
• Traditional hemodynamic monitoring uses specific endpoints to guide therapies such pulmonary artery occlusion pressure (PAOP), and central venous pressure (CVP)

Stroke Volume (SV)

• SV = stroke volume, or the amount of blood ejected from the heart with each beat
  • Preload is how much the heart can stretch or fill before contraction
  • Afterload (arterial BP- both the aorta and pulmonary arteries and semilunar valves can impact afterload)
  • Contractility measures impact of heart contractions from inotropes

Cardiac Output (CO)

• Cardiac output is 4-8 L per min, which can be found by multiplying your HR by SV
• A slow HR means less blood pumped each minute and will decrease cardiac output, especially if the body can't somehow increase stroke volume to compensate.
• Anything that impacts the preload, afterload, and contractility will affect the cardiac output The bigger concern is always low cardiac output, which leads to shock if less than 4 L per min

Cardiac Index (CI)

• Is calculated with the patient's BMI
• When there is an index, it is a better number to look at in practice because it is more patient-specific.

Central Venous Pressure (CVP)

• Has a range of is 2-6 mmHg and tells us the VOLUME.
• 70% of blood is sitting in veins throughout the cardiac cycle

Systemic Vascular Resistance (SVR)

• SVR is normally 770-1500 dynes/sec/cm-5
• The measurement is From left ventricles, and tells us PRESSURE

Pulmonary Artery Pressure (PAP)

• PAS runs 15-25 mmHg and PAD runs 8-15 mmHg
• It measures the Pressure in pulmonary arteries, and indicates a potential presence of pulmonary HTN or congestion.

SvO2

• Measures mixed venous oxygen saturation and provides an assessment of the balance between oxygen supply and demand
• A value of less than 60% indicates low Hgb, low CO, low oxygen saturations, or increased oxygen consumption
• Trauma patients, acute respiratory distress syndrome, sepsis, and complex cardiac surgery may benefit from venous oxygen saturation monitoring

PAOP (PCWP)

• Pulmonary artery occlusion pressure and is the pressure created by the volume of blood in the left heart at end-diastole
• Normal values are 8-12 mmHg
• Also referred to clinically as pulmonary capillary wedge pressure; tells how much pressure is in the left ventricle after diastole; tells how well the left ventricle is functioning
• Fluid volume deficits, fluid volume excess, and heart dysfunctions are indicated

Pulmonary Artery Catheters

• Used to diagnose and manage a variety of conditions in critically ill patients and allows for administering meds and drawing blood samples
• Often called Swan-Ganz catheter in clinical settings after the inventors
• “The PAC is a long, flexible, multi-lumen, balloon-tipped catheter that enables measurement of several hemodynamic parameters.”

Central Venous Catheter

• Measure right heart-filling pressures, estimates fluid status and Guids volume recitation

Pulmonary artery catheter

Ο Ο -Assess left heart function with PAOP pressures

• Identify and treat the cause of hemodynamic instability Ο -Assess pulmonary artery pressure -Assess mixed venous oxygen saturation (SvO2) Ο -Directly measure cardiac output

Nursing care PAC

-Informed consent obtained -Monitor patient, vitals, and waveforms, during insertion Maintain and monitor sterility during the procedure Treat as any other central line During the insertion, monitor and record respiratory rate and effort Heart rate and rhythm O Disrhythmias (ventricular dysrhythmias may occur as the catheter passes into and then through the right ventricle into the PA)

Prioroty post PAC

• monitor blood pressure
• Visualize and record waveform while the catheter is advanced O Assist with balloon insertion during the procedure (once the balloon is deflated, the tip of the catheter settles back into the PA position
• Otherwise, it remains deflated to prevent complications such as pulmonary infarction and PA rupture.
• Accurately interpret PAC waveforms
• Recognize the effect of respiratory variations

Insertion Complications

• Hemothorax and Pneumothorax
• Perforation of the veins or cardiac chamber
• Cardiac dysrhythmias.
• Depth markings are noted on the PAC Arterial lines
• Position hand/wrist neutral
• NEVER USE FOR MEDS

Invasive Arterial Lines

• Invasive arterial pressure monitoring is the most accurate method of measuring continuous systemic blood pressure
• Arterial pressure monitoring is indicated for hemodynamic instability
• Monitor for hemodynamics and equipment
• Complications: transducerr position and bleeding

Transducer Position

• Position the zeroing stopcock of the transducer system at the level of the atria for accurate readings"
• The phlebostatic axis is identified, secure the transducer and zeroing stopcock to the chest wall or an IV pole positioned near the patient

Shock & Multiple Organ Dysfunction Syndrome (MODS)

• Shock is a clinical syndrome that results in cellular, metabolic, and hemodynamic derangements (Impaired tissue perfusion)
• shock is life threatening and MOD is caused by impaired function
• Stages include: initation, compensatorys and refractory

Stages of Shock

• Compensatory (reversible with minimal morbidity and mortality), Tachycardia & tachypnea Shock is LIFE-THREATENING response, and all body systems suffer as a
• Elevated lactate acid levels= hypoperfusion and lower of arterial PH
• Normal range <2.2 / critical >4
• If someone is acidotic, vasopressors wont lower BP

Hypovolemic Shock

• Occurs when the circulating blood volume is inadequate to fill the vascular network and can be caused by dehydration
• Hemodynamics: Pap and CVP decrease.
• Treat lost fluid with LR and 0.9% NS

Distributive Shock

• Widespread vasodilation with decreased SVR
• Neurogenic is the loss of sympathetic stimulation of nerve fibers
• Antigen starts the allergic reaction in Anaphylatic shocck

symptoms of Distributive Shock

• Septic with Sepsis, a response to infection & Anaphylatic

• Severe allergic reaction

• Common triggers

• Increased HR, Oliguria, Increased HR, elevated IgE

Septic Shock

• Symptoms- decrease SVR ( decrease CVP and PAP/PAOP- decreased)

• Treatment - Eliminste offending agent, epinephrine and anithistimes and STEROIDS

• Sepsis Life-threatening organ dysfunction caused by a dysregulated host

• Diagnoic - Suspected or known source of infection Temperature >38.3 or 36 degrees O RR >20 breaths/min (WBC >12 mm3 or <4 mm3 or 10% bands Common sepsis triggers O Antibiotics- broad(delay for cultures) Vasopressors (norepinephrine levophed first choice) And end org SBP <90 >90 beats/minmmH AND SEPSOS

Neurogenic Shock

• -Cause Spinal cord injuries is the most common cause of neurogenic shock, specifically those above the level of T4. Symptoms bradycardia Warm, dry, flushed skin Oliguria Hemodynamics O treatment - Stabilize injury, vasopressors

Cardiogenic Shock

• difficult to treat and has MI
• Symptoms include tachynea, crackles
• increased CVP, increase PAP/PAOP- increase Treatment - contractility with inotropic medications, reduceAfterload reduction may be significant, use vasodilators

Obstructive Shock

• When a blockage or compression impairs circulatory blood flow.
• Constrictive pericarditis, tension pneumo, and great vein comp Treatment O
• Preventative but can cause more harm with side effects

MODS

• Progressive dysfunction and is progressive Organ dysfunctions are fatal • Renal dysfunction & Cardiovascular dysfunc • The death of a system will cause the failure for other systems Treatement - treat with mechanical ventilation and fluids/ prevent respiratory failure

ARF

Is the inability of the respiratory system to provide oxygenation and/or remove carbon dioxide from the body.

• Two types- hypoxic and hypercapnic

Causes of ARF

COPD, VAP, and Asthma (status asthmaticus)

• Increase amoutn of blood shunted (lungs are perfusion in alveo but vent is not used)
• Fluid in avelo and a decease in pressure also have causes

ARF with COPD characteristics

Hallmark signs Dyspnea and Chronic cough Blue bloaters haev frequent epiosodes Medications and support Treat the cause and set up in unurght position

• Evaluate oxy and RR

ARDS (acute respiratory distress syndrome)

• noncardiogenic pulmonary edema
• Diagnosis is assess and recognize cues
• Whitehout on X-Ray, and ground glass on CT! Treat with vent

VAP

• New or worsening infiltrate on assessment
• Take action when intubated
• Aortic and DVT prevenetion

P.E

• Treat with 02 to correct a clot
• If a D-dimer is negative, it is NOT a PE

Status Asthmaticus

• Use a PFT and use short acting anticholinergics"
• Establish baseline PFT and teach how to self-monitor lung function using peak flow meter at home.

CF

• ARF is the primary cause of death
• Use ABGs to detect O2

Bronchoscopy

• Bedside exam with fiberoptic scope into the trachea/bronchi. (done at bedside)
• Used for Infection & Acute burn Thoracentesis Invasive procedure; done at bedside