Ekg notes
SA node (60-100) AV node (40-60) bundle of his (40-60) bundle branches (20-40)-
Purkinjean fibers (20-40)
Normal Sinus Rhythm
EKG Readings:
 Rhythm: normal
 Rate: 60-100 beats per minute
 P-wave: rounded, small, up-right, 1:1 with QRS
 PRI: constant throughout the strip, 0.12-0.20
 QRS: 1:1 with p-wave, less than 0.12
Treatment
 None
Causes
 Healthy
Sinus Bradycardia
EKG Reading
 Rhythm: normal
 Rate: less than 60
 P-wave: upright, rounded, small, 1:1 with QRS
 PRI: constant throughout, 0.12-0.20
 QRS: 1:1 with p-wave less than 0.12
Signs and Symptoms





Hypotensive
Pale, clammy, pale
Weakness
Syncope
Angina
Treatment:
 Atropine (increases heart rate)
o Only if symptomatic (low perfusion, clammy, pale, cool)
 Pacemaker
Causes:
 Too medication (beta-blockers, calcium channel blockers, or digoxin)
 Old age
 Athletes (but this does not consider life-threatening)
 MI
 Pericarditis
 Obstructive sleep apnea
 Hypothyroidism
 Increased intracranial pressure
Sinus Tachycardia
EKG Reading
 Rhythm: normal
 Rate: greater than 101-200
 P-wave: upright, rounded, small, 1:1 with QRS
 PRI: constant throughout, 0.12-0.20
 QRS: 1:1 with p-wave less than 0.12
Signs and Symptoms
 Hypotensive
 Patient’s activity tolerance will be low
 Dizziness
 Dyspnea
 Increased myocardial oxygen consumption
 Increased heart rate
Treatment:
 Need OLDCART to rule angina (chest pain aka heart attack)
 Medication
o Beta blockers, drugs that end in “lol”
 Decreased heart rate by binding to beta receptors in the heart
o Calcium channel, drugs that end in “pine” or “zem”
 Relax the blood vessels and decrease heart workload
o Vagal maneuver
 Bare down
 Carotid massage
o
Causes:
 stress, anemia, hypotension, hypovolemia, HF, hyperthyroid, medications
Pacemaker



Pacemaker: artificial electronic device used to pace the heart
Different types
 Implanted in the chest pall
 External/transcutaneous ( epicardial pacing wires)
Different pacing
o On demand only gives a shock if an abnormal heart rate is detected and then will
shut off
o Fixed: constantly pacing with no regards to the patient’s heart rate
Atrial Fibrillation (AFib) “fibrillation flopping
Definition: un-controlled electrical; activity in the atria that causes rapid and disorganized
twitching of the atrial musculature or main pacemaker, SA node has lost control
EKG Reading
 Rhythm: irregular
 Rate: greater than 350-600
o Controlled: ventricular rate that is less than 100
o Uncontrolled: ventricular rate is more than 100
 P-wave: not present
 F-wave: not present
 PRI: not present
 QRS: normal, present, 0.06-0.12
Signs and Symptoms
 Chest pain
 Oxygen low
 Lethargic
 Low BP
 Anxiety
 Palpitations of the chest
 Shortness of breath
 Elevated ventricular activity or HR
 Dizziness
Treatment:
 Medication
o Beta blockers, drugs that end in “lol”
 Decreased heart rate by binding to beta receptors in the heart
o Calcium channel, drugs that end in “pine” or “zem”
 Relax the blood vessels and decrease heart workload
o Digoxin: increases heart’s contractility and decreases heart rate
 Be aware of toxicity levels (normal range 0.8-2.0)
 Signs of toxicity: green halo effect
 Always check heart before administration, if is less than 60 beats per min
DO NOT give
 Those with low potassium are at risk for digtoxity (3.5-5.0)
o Anticoagulants: given if in A-Fib for longer than 48 hours
 WAD
 Warfarin-Coumadian
 Vitamin K antagonist, so it can promote clotting and reduce
effectiveness of Warfarin


Tell patient to keep Potassium consumption (green leafy) intake
the same
 Check INR levels (2.5-3.5) important for patients with bleeding
disorders
 Dabigatran
 Apixaban
o Antidysrhythmic (p 3-6 months 50% have recurrance of AF)
 Amiodarone: slow the nerve impulses in the heart.
 Flecanide
 Dofetalide
Cardioversion : given if in A-Fib for less than 48 hours
o Done after TTE to rule out clots
o 200-360
o Must be synchronized with patient’s heart rate
o Nursing considerations
 Perform after TTE
 Skin integrity
 Patient’s pain tolerance
Causes:
 After heart surgery
 Heart failure
 Pulmonary issues: COPD
 HTN
 Alcohol
Atrial flutter “A FluTTer = sawtooth”
Definition: similar to A-Fib, but the electrical signals spread through atria in a fast but
regular rhythm
EKG Reading
 Rhythm: regular
 Rate: greater than 75-150
 P-wave: not present
 F-wave: present throughout (look like teeth or saws)
 PRI: not present
 QRS: normal, present, 0.06-0.12
Signs and Symptoms
 Chest pain
 Oxygen low
 Lethargic
 Low BP
 Anxiety
 Palpitations of the chest
 Shortness of breath
 Elevated ventricular activity or HR
 Dizziness
Treatment:
 Medication
o Beta blockers, drugs that end in “lol”
 Decreased heart rate by binding to beta receptors in the heart
o Calcium channel, drugs that end in “pine” or “zem”
 Relax the blood vessels and decrease heart workload
o Digoxin: increases heart’s contractility and decreases heart rate
 Be aware of toxicity levels (normal range 0.8-2.0)
 Signs of toxicity: green halo effect
 Always check heart before administration, if is less than 60 beats per min
DO NOT give
 Those with low potassium are at risk for digtoxity (3.5-5.0)
o Anticoagulants: given if in A-Fib for longer than 48 hours
 Warfarin-Coumadian
 Vitamin K antagonist, so it can promote clotting and reduce
effectiveness of Warfarin
 Tell patient to keep Potassium consumption (green leafy) intake
the same


Check INR levels (2.5-3.5) important for patients with bleeding
disorders
 Dabigatran
 Apixaban
o Antidysrhythmic (p 3-6 months 50% have recurrence of AF)
 Amiodarone: slow the nerve impulses in the heart.
 Flecanide
 Dofetalide
Cardioversion : given if in A-Fib for less than 48 hours
o Done after TTE to rule out clots
o Must be synchronized with patient’s heart rate
o Nursing considerations
 Perform after TTE
 Skin integrity
 Patient’s pain tolerance
Causes:
 Cardiomyopathy
 Atrial dilation
 Valve disease
 Thyroxicities
 Hypoxia
 CHF
 ETOH use
1st degree AV block
Definition: delay in conduction of electrical impulse, usually through the AV Node
EKG Reading
 Rhythm: Regular
 Rate: 60-100
 P-wave: present, 1:1 with QRS
 PRI: present but longer than 0.20
 QRS: normal, present, 0.06-0.12
Signs and Symptoms
 Most common Heart Block
 Patients are more likely to be asymptotic
 Some may experience:
o Chest pain
o Oxygen low
o Lethargic
o Low BP
o Anxiety
o Palpitations of the chest
o Shortness of breath
o Elevated ventricular activity or HR
o Dizziness
Treatment:
 Atropine
o Increases Heart rate
Causes:
 Hyperkalemia
 Too much medication
o Beta blockers
 Increases heart rate
o CCB
 Decreses vessel contractility and heart workload
 Acute inferior Wall MI
 Ischemic Heart Disease
 Digitalis Toxicity
Second degree AV block Type 2 “missing QRS”, more p’s than QRS
Definition: a disease of the distal conduction system (His-Purkinje system)
 In 2nd Degree, Type I, the HALLMARK IS that the PRI gets PROGRESSIVELY
PROLONGED, UNTIL THE QRS IS DROPPED, then
 the PATTERN begins again
 Very high potential to convert to Third Degree (Complete) Heart Block
 Complete block of conduction in one bundle branch and an intermittent block in the
other bundle branch
EKG Reading
 Rhythm: irregular
 Rate: atria rate faster than slower ventricular rate (more p-waves), but its slow
 P-wave: present, 2:1 OR 3:1, TOO MANY
 PRI: 0.12- 0.20, normal or prolonged
 QRS: missing, but if present is normal, but may be prolonged
Signs and Symptoms
 Patients some patients asymptotic but very rare
 Chest pain
 Oxygen low+ tachycardia
 Lethargic
 Low BP
 Anxiety
 Palpitations of the chest
 Shortness of breath
 Elevated ventricular activity or HR
 Dizziness
Treatment:
 Atropine is NOT Effective
 Stop drugs or decrease
o Beta blockers
o Calcium channels
o Digoxin
 May require Pacemaker
Causes:
 Damage to the Bundle branches
 MI
Third degree AV Block
Definition: complete absence of conduction of electrical impulse through AV node, Bundle of
His, and Bundle Branches
 Atria rhythm independent from ventricular rhythm; regular P-P and regular R-R
 Life-threatening rhythm, will lead to asystole
EKG Reading
 Rhythm: regular, but P wave and QRS contract independently
 Rate: slow 40-60
 P-wave: normal
 PRI: varies
 QRS: normal or wide
 ST segment: does a little upward “/”
Signs and Symptoms
 Chest pain
 Oxygen low
 Lethargic
 Low BP+ tachycardia
 Anxiety
 Palpitations of the chest
 Shortness of breath
 Elevated ventricular activity or HR
 Dizziness
*symptoms get progressively worst as heart block progresses*
Treatment:
 Pacing
 Stop drugs that decrease heart rate
 Atropine to increase heart rate
 Dopamine to increase blood pressure
 Epinephrine which increases heart rate, increased Blood pressure and cardiac output to
increase oxygen to the body
Causes:
 Too medication
o Beta blockers
o Calcium channel blockers
o Digoxin
 MI
 Inferior wall MI
 Ischemic heart disease
 Hyperkalemia
Bundle Branch Block “bunny ears”
Definition: irregular conduction or block of electrical pathway through bundle branches (aka.
Purkinje fibers”
 Ventricles do not contract simultaneously
EKG





Rate: depends
Rhythm: regular
P wave: normal
PR interval: normal (because atrium is not involved)
QRS: wide or appear notched (bundles lead to ventricles), larger than 0.12
o Notes to self: T-wave or impacted, appear downwards
Signs and Symptoms
 Sometimes patient does not show symptoms
 Subjective
o I feel light-headed or I might pass out”
 Objective
o Chest pain
o Oxygen low
o Lethargic
o Low BP+ tachycardia
o Anxiety
o Palpitations of the chest
o Shortness of breath
o Elevated ventricular activity or HR
o Dizziness
Treatment:
 Pacing (for extreme cases)
o Patient education
 Cardiac resynchronization: wire connected to both sides of the heart
 Fall risk interventions
 Echocardiography
Causes:
 CAD
 Anterior wall MI
 HTN
 Scar tissue
 Drug toxicity
 Congenital heart defects
PVC “Premature Ventricular Contraction” ventricular sneeze
*** may lead to V tach or V fib***
EKG Readings
 Rate: depends
 Rhythm: irregular when PVC occurs
 P-wave: none associated with PVC
 PR: not associated with PVC
 QRS: wide without a p-wave and bizarre looking
o May indicate a presence of ventricular abnormality
Cause:
 Increased catecholamine (released during stress response)
 increased sympathetic tone (related to stress)
 Stimulants
 Amphetamine and cocaine
 Myocardial ischemia or infraction
 CHF
 Hypoxia
 Acidosis
 Dig toxicity
 Hypokalemia
 Hypo magnesium
Signs and Symptoms
 Isolated PVC without history of heart disease are insignificant
 Multipliable
o Subjective: heart is pounding or skipping
o Objective: Low Blood Pressure
Treatment:



Identify causes
Medications
o Lower/ discontinue digoxin
o Amiodarone: relax heart
o CCB or BB MAYBE
Correct electrolyte imbalance
o Potassium and magnesium
V-Tach “looks like tombstones”
Definition: Dysrhythmia originating in an ectopic pacemaker in the bundle branches, purkinje
fibers, or ventricular myocardium
** More than 3 PVCs is sustained V Tach**
** Monomorphic or polymorphic(Torsades de Pointes)**
 Increased frequency can lead to Ventricular Fibrillation which is LIFETHREATENING
 PULSELESS V TACH IS TREATED THE SAME AS V FIB!
EKG Reading
 Rhythm: irregular
 Rate: 100-250
 P-wave: absent
 PRI: absent
 QRS: wide and bizarre
Causes
 Stimulants
 hypoxia
 Dig toxicity
 Electrolyte imbalance: low potassium and magnesium
 Cardiac injury: MI or heart attack
Signs and Symptoms:
 COLLSPSED
 Can be short and asymptomatic
Treatment:
 Determine onset and termination
 Pulse give them amiodarone than cardioversion

o Amiodarone to stabilize rhythm and then give cardioversion
Pulseless
o Call a code
o Defibration
V-Fib “ squggly lines”
Definition: no coordinated ventricular beats are present
EKG Reading
 Rate:300-500
 Rhythm: chaotic
 P-wave: none
 PRI: none
 QRS: none
o None because ventricles are not fully contracting and cardiac output CEASES
Causes:
 Untreated V-TACH
 Cardiac injury : post MI
 Med toxicity
 Electrical imbalances
o Untreated V-Tach, acid-base, electrolyte imbalances, electrical shock
Signs and Symptoms
 COLLSPSED if patient is conscious
 Usually, patient is not conscious!
Treatment
 Cardioversion (pulse) and Defibrillation(no pulse)
 Medical Management
 Atropine
 Vasopressors
 Anti-dysthymias
 Nursing Considerations
o Oxygen, Pain management.
 LAM drugs
Asystole or cardiac standstill “flat line”
Definition: total absence of electrical activity in the heart, patient is clinically dead
***if patient is talking they are NOT in asystole***
EKG:





Rate: none
Rhythm: none
P-wave: none
PRI: none
QRS: none
o FLATLINE
Causes
 Trauma
 Un resolved V-tachycardia
Signs and symptoms:
 None, patient is dead
Treatment
 CPR
 Epinephrine, IM or IV push 10 mL every 3 to 5 minutes
 What not to do
o Give defibrillation
 Shock needs an electrical impulse to piggyback off of
Pulseless Electrical Activity
Definition: rhythm present without a pulse
Causes:
 Hypoxemia
 Hypovolemia
Treatments:
 Call a code
 Start CPR
 ACL measures
 PEA
o ATROPINE (IF BARDYCARDIA)
o VASSOPESSIN AND EPI
 PEA
o Push epi always
o
Medications to be aware
Atropine “at the top”
 Function:
o Increases heart rate
o Blocks the parasympathetic nervous system effects of the heart
o Accelerates SA node rate
o Increases conduction velocity
 Administration
o IV bolus
 Indications
o Symptomatic bradycardia
o First degree AV block
o Second degree AV block type 1
Vasopressor
 Function: vasoconstriction of the arterioles and venous circulation
 Increases HR
 Increases the strength of contraction
 Examples of Drugs “ine:
o Vasopressin
o Dopamine
o Norepinephrine
o Dobutamine
o Isoproterenol
Anti-dysrhythmia
Adenosine: suppresses AV and SA node activity
 Indications
o SVT and tachycardia
o A-Fib and A-Flutter: but will not terminate it
Amiodarone
 Effects the NA, K, and Ca channels
 Effective for SVT, VT, V-fib
Lidocaine
 Effective for VT
 Side effects
o Altered consciousness
o Bradycardia
o Seizures
Procainamide (it’s a pro)
 Suppresses atrial and ventricular dysthymia by slowing down in conduction
 Used for VT, controls a-fib/a-flutter, PVST
Calcium Channel blockers
 Function: decreases conduction and increases conduction time in AV node
 Used with Beta-Blocker therapies
 Indications: Used in A-fib and A-flutter
 Contradictions: Second Degree AV blocks and Third Degree AV blocks
 Use with caution in those with Hypotension and CHF