MS WK9

Sinus rhythms: sinus bradycardia, normal sinus, sinus tachycardia

Atrial rhythms: atrial fibrillation

Ventricular rhythms: premature ventricular contractions, ventricular fibrillation

Asystole


DYSRHYTHMIA - abnl heart rhythm of hearts electrical system

  • Affects CO and perfusion thru body

  • Are a result in a disturbance in electrical impulse formation, conduction or both

  • Any electrical dysfunction impacts cardiac output, which affects blood getting to brain and body

How heart conducts electricity

  • SA node: pacemaker of heart 60-100 bpm

    • P wave

  • AV junction

    • PR segment

    • Contraction called ‘atrial kick’

  • Bundle of His

    • Right and left bundle branch

SA node sends signal to av node, where signal is delayed (pauses for just a moment and then resumes) to allow ventricles to fill, and then its sent to the bundle of His, into the right and left bundle branches, and into the Purkinje fibers


ELECTROPHYSIOLOGIC PROPERTIES

  • Automaticity: ability to generate an electrical impulse

  • Excitability: ability to respond to stimulus

  • Conductivity: ability to pass signal to neighboring cells

  • Contractility: ability to contract (squeeze) after stimulation

^^unique to cardiac cells


ECG LEAD SYSTEM: views hearts electrical activity

  • Standard 12-lead ECG: 

    • Limb leads: 6 total placed on 4 extremities (take the vertical electricity)

    • Chest (precordial) leads (6 total): V1-V6 (takes the horizontal electricity)

  • 18-lead ECG (Right-sided ECG) ← not as ordered. Would only if MD sus’d smth w rt side or posterior side of heart that they want to view)


CONTINUOUS ECG MONITORING

  • Rt arm electrode = below rt clavicle

  • Lt arm electrode = below lt clavicle

  • Rt leg electrode = lowest palpable rib, rt midclavicular line

  • 5th electrode placed to obtain one of six chest leads

ECG Lead 2 is the most ideal and most viewed on the monitors for continuous EKG (basiclly only one lead is showing, but you can switch the monitor to view another lead)

Continuous monitoring can have 5 leads and 3 leads



READING STRIPS

  • Vertical axis: voltage

  • Horizontal axis: time

  • Standard strip = 6 seconds (30 large boxes)

  • Ea large box = 0.20 sec (5 small boxes)

  • Ea small box = 0.04 sec



NORMAL EKG

  • P wave: atrial depolarization (contraction)

    • Nml: <0.12 seconds (3 small boxes)

  • PR interval: time it takes for electrical impulse to travel from SA node thru AV node to ventricles

    • Nml: 0.12-20 sec (3 small boxes)

  • QRS complex: ventricular depolarization (contraction)

    • Nml: 0.06-0.10 sec (1.5-2.5 small boxes)

  • T wave: ventricular repolarization (relaxation)

  • QT interval: total time for ventricle to depolarize and repolarize (contract and reset)

  • ST Segment: time between ventricular depolarization and repolarization (resting phase before reset)


ST elevation on 2 or more different leads = STEMI


ECG RHYTHM ANALYSIS

  • Step 1: Is it regular? – look at R-R intervals and see if spaces between R waves is consistent

    • Yes = regular

      • Seen in NSR, SB, ST, A-flutter, SVT

    • No = irregular

      • Seen in Afib, sinus arrythmia

  • Step 2: Whats the HR? – count R waves in 6 sec strip (30 large boxes) and multiply by 10

    • Slow: <60 bpm (SB, 2nd degree, 3rd degree)

    • Regular: 60-100bpm (NSR, A-flutter, controlled afib, 1st degree block)

    • Fast: >100 bpm (ST, Afib RVR, A-flutter, SVT, V-tach, torsades de pontes

  • Step 3: Is there a P wave before every QRS?

    • Yes?  

    • No? 

  • Step 4: Measure QRS duration (start of Q, end of S)

    • Nml: <0.12 seconds (<3 small boxes) ← also called narrow QRS

    • Wide: >0.12 seconds

  • Step 5: Measure PR interval (start of P wave to start of QRS)

    • Nml: 0.12-0.20 seconds (3-5 boxes)

    • Too long = heart blocks


S I N U S  R H Y T H M S

  • Upright, consistent p-waves. P waves are identical

  • PRI constant ((0.12-20)

  • 1:1 ratio, pwave to ea QRS

  • R-R is regular


NORMAL SINUS: Rate: 60-100bpm

  • Regular rhythm

  • Pwaves present, one pwave before ea QRS complex

  • PR interval: 0.12-0.20 second and constant

  • QRS duration: 0.06-0.10 second and constant


SINUS TACHYCARDIA rate: >100bpm

  • Sympathetic nervous system stimulated or vagal (parasympathetic) inhibition results in increased rate of SA node discharge, increasing HR

  • Tx underlying cause

ST causes: anxiety, hypovolemia, exercise, fever, sepsis, hypoxemia; drugs can cause sympathetic stimulation too


SINUS BRADYCARDIA rate: <60bpm

  • Excessive vagal (parasympathetic) stimulation

  • Syncope (blackouts or fainting)

  • Dizziness, weakness, confusion

  • Hypotension, Diaphosesis, SOB

  • Chest pain

Can be caused by meds such as BETA BLOCKERS, CALCIUM CHANNEL BLOCKERS, DIGOXIN. Any drug that could potentially 

Treatment: 

  • Stable: (not symptomatic)

    • Treat underlying cause (ie did they throw up and that stimulated the vagal nerve→ just look for a reason) but also consider what their baseline is

    • If Betablocker overdose sus’d, give GLUCAGON (its an IM inj for hypoglycemia that can help to increase the HR too)

  • Unstable: (symptomatic)

    • First line is usually to order EKG if they are unstable

    • Atropine 0.5 mg IV push

    • Transcutaneous Pacing (TCP)

      • External, uses defibrillator pads (has a pacing option where if a pt goes below certain bpm, it shocks them to maintain perfusion)

      • Used in emergencies and is painful

    • Transvenous pacing: internal pacing method using catheter w pacing wire inserted into vein (usualy subclavian/internal jugular) and threaded into heart. Pt will have a wire handing out from them 

    • Permanent pacemaker

    • Will start w TCP, if that fails it goes to Transvenous pacing. If that fails they get perm pacemaker

PACEMAKERS: small devices placed under skin to help control abnl heart rhythms

  • Avg lifespan: 10 years (may need another one or a battery replacement)

  • Combo pacemaker/defibrillator devices are also available (ICD) (ICD is dffnt from just a pacemaker)

  • Avoid sources of strong electromagnetic fields, ie magnets and telecommunications transmitters, Shouldnt lift arm, lift up more than 10 lbs ← NOT ALL PACEMAKERS ARE MRI SAFE

  • Carry pacemaker ID card; wear med alert bracelet ALWAYS

  • Single chamber pacemaker and dual chamber (A-pace and V-pace)



A T R I A L  R H Y T H M S

  • Rhythms that originate from w/in atria. NOT SA NODE

  • Not ‘classic’ p-waves (if they are easy to ID, theyre not atrial)

  • Typically fast, can be controlled (<100bpm or uncontrolled >100bpm)

  • QRS complexes can be narrow or wide


ATRIAL FIBRILLATION

  • Supraventricular arrhythmia

  • Atrium is fibrillating → it is quivering and has abunch of electrical firing thats erratic

  • Completely irregular

  • No distinct P waves

  • Variable R-R intervals

  • Narrow QRS complexes (which is nml)

High stroke risk

Etiology and incidence: most common dyrhythmia in developed world

  • Affects 12.1 million ppl in US

  • RISK FACTORS: HTN, CAD, HF, Vavular disease, Hyperthyroidism, post cardiac sx, >65yo

  • More women affected than men

  • Chaotic rhythm decreases ventricular filling, decreasing cardiac output and as it progresses it can affect CO by 20%

  • Alteration allows blood to pool and increases risk for clotting concerns

  • Assct w atrial fibrosis and loss of muscle mass (bc its basically overworking itself and its not actually even doing its job right)

Treatment: 

  • Goal is to convert from AF to SR, but it maynot be poss for many older adults

Meds: 

  • Rate control: slow ventricular response so heart can fill more effectively and s/s are reduced

    • Beta blockers: metoprolol, atenolol

    • CCB: diltiazem, verapamil

    • Digoxin

  • Rhythm control: restore and maintain NSR

    • Potassium channel blockers: amiodarone, sotalol

    • Sodium channel blockers: flecainide, propafenone

  • Anticoagulation: prevent clot formation d/t stasis of blood in atria

    • DOAC: apixiban, dabigatran

    • Vit K antagonist ie warfarin

Amiodarone is probably most common one


Procedural intervention: 

  • Electrical cardioversion: converts Afib back to NSR using synchronized electric shocks

  • Catheter ablation: destroys small areas of heart tissue where abnl electrical signals are triggering A-Fib

  • MAZE: creates ‘maze’ of scar tissue in atria to block abnl impulses and direct nml conduction

  • Left Atrial Appendage Occlusion ‘Watchman Device’: closes off Lt atrial appendage, where most A-fib related clots form



V E N T R I C U L A R  R H Y T H M S

Potentially more life threatening than atrial dysrhythmias bc the left ventricle pumps o2 blood thruout body to perfuse vital organs and other tissue

  • Regular or irregular

  • Pwaves absent

  • Can be fast or slow dpdnig on location of impuses

  • Main thing is QRS complexes are wide (>0.12 sec)


PREMATURE VENTRICULAR COMPLEXES (PVCs)

  • Result of increased irritability of ventricular cells

  • Seen as earl yventricular complexes followed by a pause

  • Common, frequency increases w age

  • Not really a problem if its here or there, but more concerned if they start to occur more often

  • If pt is post MI and start developing PCVs, it could be a warning sign that pt is entering life threatening rhythm ie Vfib


VENTRICULAR FIBRILLATION

Ventricles are quivering which musst be rapidlycorrected to reset electrical activity and restore perfusion

  • Result of electrical chaos in ventricles bc ventricles are NOT CONTRACTING

  • LIFE THREATENING! Bc theres No refilling, no perfusion

  • If you come into the room and see this→ Call a CODE, start CPR until we get a defibrillator


ASYSTOLE

  • No electrical impulses in ventricles

  • No ventricular depolarization, no QRS complex, No contraction, no CO ← all of this to say: NO PERFUSION TO REST OF THE BODY

  • Requires ACLS/CPR

  • Dont shock asystole


CPR 

  • When pt is unresponsive and not breathing normall, and no pulse is felt w/in 10 seconds:

    • Rate: 100-120 compressions/min

    • Depth: 2-2.4 in (5-6 cm)

    • Ratio: 30:2 (compressions:breaths)

  • Cardiac arrest rhythms that need CPR:

    • Ventricular fibrillation (VF) → shockable

    • Pulseless ventricular tachycardia (VT) → shockable

    • Asystole → not shockable

    • Pulseless Electrical Activity (PEA) → not shockable

  • Advanced cardiac life support (includes epinephrine, amiodarone, dopamine, etc)



CARDIOPULMONARY DEFIBRILLATION

  • Defibrillation: asynchronous countershock that depolarizes critical mass of myocardium simultaneously to stop re-entry circuit, allowing sinus node to regain control of heart

    • Ventricular Fibrillation (VF): shockable

    • Pulseless Ventricular Tachycardia (VT): shockable


Automated external defibrillation: 

  • Allows for earlier defibrillation.

  • When used there is a greater chance of successful rhythm conversion and pt survival


Implantable cardioverter/defibrillator: indicated for pts who have experienced one or more episodes of spontaneous sustained VT or VF not caused by MI

  • Transvenous = most common type

  • Subcutaneous types = for ppl who are typically younger or those w congenital heart defects

  • External vest-like device worn 24 hours a day except when showering or bathing. Ppl get these bc after a MI,  pt has to wait a certain amount of time before getting ICD. Or if pt is waiting for heart transplant, this is like a bridge to that


RHYTHM EXAMPLES


SINUS RHYTHMS

  NORMAL SINUS RHYTHM

SINUS TACHYCARDIA

SINUS BRADYCARDIA

  ‘A-pace’ and ‘V-pace’ ← occur when pacemaker delivers electrical impulses to atrium (apace) and ventricle (vpace) to control rhythm. Line before pwave is A-pace, line after pwave is V-pace

ATRIAL RHYTHMS

ATRIAL FIBRILLATION


VENTRICULAR RHYTHMS

PVCs

VENTRICULAR FIBRILLATION

ASYSTOLE