HEART CONDUCTION/HEART RHYTHMS

VENTRICULAR ASYSTOLE

complete absence of electrical activity and ventricular movement of the heart client is in complete cardiac arrest requires implementation of BLS and ACLS protocol

VENTRICULAR FIBRILLATION (V-FIB) - PATIENT PRESENTATION

patient will be in cardiac arrest

CARDIOVERSION - NURSING CONSIDERATION

patients with atrial fibrillation of unknown duration MUST TAKE ANTICOAGULANTS for 4 to 6 weeks prior to receiving cardioversion

ADENOSINE - CONTRAINDICATIONS

poison/Rx-induced tachycardia 2nd or 3rd degree heart block

PREMATURE VENTRICULAR CONTRACTION (PVC)

premature occurrence of the QRS complex can be precursor for life-threatening arrhythmias *rhythm* irregular *rate* varies *P:QRS ratio* not visible hidden in the PVC *PR interval* not measurable *QRS complex* > 0.12 seconds wide and distorted

NON-SHOCKABLE RHYTHMS

pulseless electrical activity asystole

TWO SHOCKABLE RHYTHMS

pulseless ventricular tachycardia ventricular fibrillation

VENTRICULAR BIGEMINY

PVCs that occur every 2nd beat

VENTRICULAR TRIGEMINY

PVCs that occur every 3rd beat

SINUS TACHYCARDIA - CAUSES

fever dehydration (hypovolemia) hypotension anemia anxiety/fear/stress pain hyperthyroidism

ATROPINE - NURSING CONSIDERATIONS

0.5 mg per dose can be given every 3-5 minutes max dose 3 mg (6 doses of 0.5 mg)

EPINEPHRINE - DOSE

1 mg every 3-5 minutes

2nd DEGREE AV HEART BLOCK (TYPE 2) - THERAPEUTIC MANAGEMENT

ACLS Guidelines - atropine - prepare patient for pacemaker

VENTRICULAR FIBRILLATION (V-FIB) - THERAPEUTIC MANAGEMENT

call a code initiate CPR Follow ACLS Guidelines - CPR - defibrillate - epinephrine - amiodarone

ADENOSINE - DOSING

Initial Dose 6 mg rapid IV push followed by a fluid bolus Second Dose (if needed) 12 mg given within 1-2 minutes

PREMATURE VENTRICULAR CONTRACTIONS (PVC) - NURSING CONSIDERATION

More than 6 PVCs/min is considered serious; Nurse should notify the HCP 3 or more consecutive PVCs = ventricular tachycardia

MONOMORPHIC VENTRICULAR TACHYCARDIA

QRS complexes that are the same shape, size, and direction

POLYMORPHIC VENTRICULAR TACHYCARDIA

QRS complexes that differ in shape, size, and direction

PR INTERVAL

beginning of the P wave to the beginning of the QRS the time it takes the atria to initiate a contraction, contract, and send the impulse to the ventricles 0.12 to 0.20 seconds

QRS INTERVAL

beginning of the Q wave to the ending of the S wave time it takes for the electrical current to travel through the ventricles 0.06 to 0.12 seconds

PREMATURE VENTRICULAR CONTRACTION (PVC) - TREATMENT

Rx Therapy - beta blockers - procainamide - amiordarone Treat Underlying Cause - oxygen therapy for hypoxia - electrolyte replacement

ADENOSINE - INDICATIONS

Rx for most forms of stable narrow-complex SVT

ADENOSINE - NURSING CONSIDERATIONS

Rx is given IV rapid push

NORMAL SINUS RHYTHM

SA node generates electrical impulse; normal heart rhythm *rhythm* regular *rate* 60-100 bpm *P:QRS ratio* 1 P wave 1 QRS complex *PR interval* 0.12-0.20 seconds (3-5 small boxes) *QRS complex* 0.06-0.12 seconds

SINUS TACHYCARDIA

SA node initiates electrical conduction same as normal sinus rhythm except that the HR is greater than 100 bpm *rhythm* regular *rate* HR > 100 bpm *P:QRS ratio* 1 P wave 1 QRS complex *PR interval* 0.12-0.20 seconds *QRS complex* 0.06-0.12 seconds

SINUS BRADYCARDIA

SA node initiates electrical conduction same as normal sinus rhythm except that the HR is less than 60 bpm *rhythm* regular *rate* HR < 60 bpm *P:QRS ratio* 1 P wave 1 QRS complex *PR interval* 0.12-0.20 seconds *QRS complex* 0.06-0.12 seconds

1st DEGREE AV HEART BLOCK

SA node initiates the impulse, but there is a conduction delay in the AV; it takes a longer time for the impulse to travel prolonged PR interval - greater than 0.20 seconds - more than 5 small boxes *rhythm* regular irregular depends on underlying rhythm *rate* varies/usually slower depends on underlying rhythm *P:QRS ratio* 1 P wave 1 QRS complex *PR interval* > 0.20 seconds *QRS complex* 0.06-0.12 seconds

STEMI

ST elevation myocardial infarction (MI) full occlusion of vessel causes infarction/injury

QT INTERVAL

beginning of the QRS to the end of the T wave time it takes the ventricles to contract and relax 0.36 - 0.44 seconds

ABNORMAL WAVEFORMS DURING MYOCARDIAL INFARCTION (MI)

T wave inversion - indicates ischemia ST segment elevation - indicates injury Abnormal Q Wave - indicates necrosis

PREMATURE ATRIAL CONTRACTION (PAC)

additional stimulus in the atria that is NOT originated from the SA node; electrical impulse is produced by another cell and produces an early heartbeat P wave comes early which makes the T wave look abnormally large *rhythm* regular irregular w/PAC *rate* normal (60-100 bpm) depends on underlying rhythm *P:QRS ratio* 1 P wave 1 QRS complex *PR interval* 0.12 - 0.20 seconds depends on underlying rhythm *QRS complex* 0.06-0.12 seconds depends on underlying rhythm

HEAD TILT CHIN LIFT MANEUVER - TRAUMA SITUATIONS

airway can be opened with a modified jaw thrust maneuver

ABCDE PRINCIPLE

airway/cervical spine breathing circulation disability exposure

MEDICATIONS FOR VF OR PULSELESS VT

amiodarone hydrochloride lidocaine hydrochloride magnesium sulfate

PULSELESS VENTRICULAR TACHYCARDIA (VT)

an irritable firing of ectopic ventricular beats at a rate of 140 to 180/min over time, client will become unconscious and deteriorate into VF

BRAIN INJURY/DEATH - TIMELINE

as a result of hypoxia, brain injury/death will occur within 3 to 5 minutes if the airway is not patent

3rd DEGREE AV HEART BLOCK - THERAPEUTIC MANAGEMENT

assess patient to determine severity of symptoms prepare patient for pacemaker

HEAD TILT CHIN LIFT MANEUVER

assume a position at the head of the client place one hand on his forehead, and place the other hand underneath the client's chin head should be tilted while his chin is lifted upward and forward maneuver lifts the tongue away from the laryngopharynx and provides for a patent airway

1st DEGREE AV HEART BLOCK - PATIENT PRESENTATION

asymptomatic

2nd DEGREE AV HEART BLOCK (TYPE 1) - PATIENT PRESENTATION

asymptomatic

SINUS BRADYCARDIA - THERAPEUTIC MANAGEMENT

asymptomatic - continue to monitor symptomatic - atropine (follow ACLS guidelines) - pacemaker

SINUS BRADYCARDIA - PATIENT PRESENTATION

asymptomatic or symptomatic signs/symptoms may include: syncope - lightheadedness - vertigo decreased cardiac output - fatigue - shortness of breath - chest pain - hypotensive

P WAVE

atrial depolarization (contraction)

2nd DEGREE AV HEART BLOCK (TYPE 1)

atrial impulses have difficulty reaching the ventricles; AV node is defective progressively prolonged PR interval and dropped QRS complexes *rhythm* regular irregular *rate* varies - regular when counting R waves - irregular when QRS is dropped *P:QRS ratio* 1 P wave 1 QRS complex, except when QRS is dropped *PR interval* > 0.20 seconds progressively longer until QRS drops *QRS complex* 0.06-0.12 seconds

2nd DEGREE AV HEART BLOCK (TYPE 2)

atrial impulses have difficulty reaching the ventricles; AV node is defective; conduction in ventricles is defective normal PR interval and dropped QRS complexes *rhythm* regular (R-waves) irregular (when QRS is dropped) *rate* varies - usually slow *P:QRS ratio* 1 P wave 1 QRS complex, except when QRS is dropped *PR interval* 0.12 - 0.20 seconds normal until QRS drops *QRS complex* 0.06-0.12 seconds

3rd DEGREE AV HEART BLOCK

complete heart block atria are contracting on their own ventricles are contracting at their own pace atria and ventricles are disassociated and not communicating *rhythm* regular (atrial rate) regular/irregular (ventricular rate) *rate* varies - ventricular rate is usually slow - atrial rate is normal - lonely P wave *P:QRS ratio* not measurable no relationship between P waves and QRS *PR interval* not measurable *QRS complex* > 0.12 seconds wide

ASYSTOLE

considered the "final rhythm" if asystole persists, the HCP should consider ceasing resuscitation measures

2nd DEGREE AV HEART BLOCK (TYPE 1) - THERAPEUTIC MANAGEMENT

continue to monitor patient know underlying rhythm determine/treat the cause - electrolytes - medications - MI symptomatic bradycardia - follow ACLS guidelines

1st DEGREE AV HEART BLOCK - THERAPEUTIC MANAGEMENT

continue to monitor patient - vital signs treat underlying cause - electrolytes - medications - MI symptomatic bradycardia - follow ACLS guidelines

ATRIAL FIBRILLATION - THERAPEUTIC MANAGEMENT

determine if acute or chronic apply 12-lead EKG restore NSR assess for signs/symptoms of stroke medications - antiarrhythmics - beta blockers - calcium channel blockers - anticoagulants Transesophageal Echocardiogram (TEE) Cardioversion (CV) Ablation

VENTRICULAR TACHYCARDIA (V-TACH) - THERAPEUTIC MANAGEMENT

determine if pulse is present sustained - continuous v-tach and is not going away unsustained - patient is in normal sinus rhythm - run of v-tach - return to sinus rhythm - monomorphic (all QRS look the same) - polymorphic (all QRS look different) determine/treat cause - electrolytes - MI - abnormal heart conditions ACLS Guidelines V-Tach with Pulse - amiodarone IV - mag sulfate IV - synchronized CV ACLS Guidelines Pulseless V-Tach - CPR - defibrillation - epinephrine

PREMATURE ATRIAL CONTRACTION (PAC) - THERAPEUTIC MANAGEMENT

determine the underlying rhythm and frequency of PACs determine/treat the cause - caffeine intake - electrolyte imbalance - MI symptomatic - beta blockers asymptomatic - continue to monitor

VENTRICULAR TACHYCARDIA (V-TACH) - PATIENT PRESENTATION

does patient have a pulse? palpitations chest pain decreased CO - hypotensive - LOC changes - lightheaded/syncope pulse/pulseless - depends on severity of CO electrolytes

ST SEGMENT

end of QRS complex to beginning of T wave should be a FLAT line time between ventricular depolarization (contraction) and repolarization (relaxation)

3rd DEGREE AV HEART BLOCK - PATIENT PRESENATION

fatigue dizzy/syncope decreased CO - hypotensive - chest pain medical emergency

SINUS TACHYCARDIA - THERAPEUTIC MANAGEMENT

find/treat the underlying cause stable - continue to monitor - vagal maneuvers medications to reduce HR/O₂ consumption - metoprolol (beta blocker) - diltiazem (calcium channel blocker) - adenosine (follow ACLS guidelines) unstable - synchronized cardioversion

ADENOSINE - SIDE EFFECTS

flushing chest pain/tightness brief asystole or bradycardia

PREMATURE ATRIAL CONTRACTION (PAC) - PATIENT PRESENTATION

fluttery feeling in the chest feeling of "heart skipping" dizzy possible electrolyte imbalance

PROLONGED ("WIDE") QRS INTERVAL

greater than 0.12 seconds it's taking too long for the ventricles to contract

PROLONGED PR INTERVAL

greater than 0.20 seconds electrical current is taking too long to get to ventricles

CAUSES OF PULSELESS ACTIVITY - THE H's

hypovolemia hypoxia hydrogen ion accumulation (acidosis) hyperkalemia/hypokalemia hypothermia

SUPRAVENTRICULAR TACHYCARDIA (SVT)

increased electrical stimulation in the atria or AV node; stimulates the ventricles to contract rapidly heart is pumping so fast there is less blood going into the ventricles *rhythm* regular P waves are pointed or hidden in T wave *rate* 150 to 250 bpm *P:QRS ratio* P waves are visible = 1:1 P waves not visible = not measurable *PR interval* P waves are visible = < 0.20 seconds P waves not visible = not measurable *QRS complex* < 0.12 seconds

ADENOSINE - NURSING CONSIDERATION

injection site should be as close to heart as possible - antecubital area give IV dose rapidly followed by rapid 20 mL flush with normal saline monitor patient's ECG continuously - brief period of asystole is common observe patient for: - flushing - dizziness - chest pain - palpitations

ATRIAL FLUTTER

irritable cells produce additional electrical impulses in the atria increased risk of stroke *rhythm* irregular and sometimes regular *atrial rate* 250-300 bpm "sawtooth" pattern *ventricular rate* 60-100 bpm *P:QRS ratio* variable *PR interval* not measurable *QRS complex* 0.06-0.12 seconds

SINUS BRADYCARDIA IN PATIENT WITH HEART TRANSPLANT - Rx TREATMENT

isoproterenol (Isuprel) non-selective beta adrenoreceptor agonist

2nd DEGREE AV HEART BLOCK (TYPE 2) - PATIENT PRESENTATION

lightheadedness dizzy/syncope signs/symptoms of decreased cardiac output - dropped QRS means ventricles not pumping

ATRIAL FLUTTER - THERAPEUTIC MANAGEMENT

medications - antiarrhythmics - beta blockers - calcium channel blockers - anticoagulants (warfarin) cardioversion - synchronized ablation - destruction/removal of irritable cells

SINUS BRADYCARDIA - CAUSES

medications - digoxin toxicity - beta blockers - calcium channel blockers athletes vagus nerve stimulation SA node malfunction hyperkalemia

ATRIAL FIBRILLATION

multiple disorganized cells produce additional electrical impulses in the atria HIGH RISK FOR STROKE *rhythm* irregular *atrial rate* > 300 bpm "wavy baseline" pattern *ventricular rate* 60-100 bpm > 100 = rapid ventricular rate (RVR) *P:QRS ratio* no obvious/identifiable P waves not measurable *PR interval* not measurable *QRS complex* 0.06-0.12 seconds

VENTRICULAR FIBRILLATION (V-FIB)

multiple unorganized electrical signals in the ventricles; causes ventricles to quiver no blood going in/no blood going out life threatening emergency *rhythm* irregular *rate* not measurable *P:QRS ratio* not measurable *PR interval* not measurable *QRS complex* not measurable

VENTRICULAR TACHYCARDIA (V-TACH)

multiple unorganized electrical signals in the ventricles; ventricles do not slow down enough to allow refilling patient may/may not have a pulse significantly reduces CO and perfusion *rhythm* regular irregular *rate* 150 to 250 bpm ventricular *P:QRS ratio* no P waves not measurable *PR interval* no P waves not measurable *QRS complex* > 0.12 seconds wide

NSTEMI

non-ST elevation myocardial infarction (MI) ST depression or T inversion partial occlusion of vessel causes ischemia

ATRIAL FLUTTER - PATIENT PRESENTATION

palpitations chest pain lightheaded/syncope acute or chronic atrial and ventricular rates decreased cardiac output - syncope - hypotension PT/INR - if patient is taking Coumadin

ATRIAL FIBRILLATION - PATIENT PRESENTATION

palpitations fatigue lightheaded/syncope Chronic A-fib - monitor rate/medications Acute A-fib - convert to normal sinus rhythm atrial and ventricular rates - RVR decreased cardiac output - syncope - hypotension PT/INR - if client is taking Coumadin

SUPRAVENTRICULAR TACHYCARDIA - PATIENT PRESENTATION

palpitations fluttering in chest shortness of breath lightheaded chest pain decreased cardiac output - syncope - hypotension

PULSELESS ELECTRICAL ACTIVITY (PEA)

rhythm that appears to have electrical activity but is not sufficient to stimulate effective cardiac contractions requires implementation of BLS and ACLS protocol

SUPRAVENTRICULAR TACHYCARDIA - THERAPEUTIC MANAGEMENT

stable or unstable 12-lead EKG determine/treat the cause - increased caffeine - stress/anxiety - heart/lung problems control the heart rate - vagal maneuvers medications - beta blockers - calcium channel blockers - potassium channel blockers ACLS Guidelines - Stable - adenosine - 6 mg to start - repeat with 12 mg to slow/stop heart ACLS Guidelines - Unstable - cardioversion

SINUS TACHYCARDIA - PATIENT PRESENTATION

stable or unstable signs/symptoms may include: rapid heart beat - palpitations - lightheaded decreased cardiac output - short of breath - chest pain - hypotension

CARDIAC ARREST

sudden cessation of cardiac function caused most commonly by ventricular fibrillation or ventricular asystole

PROLONGED QT INTERVAL

takes more than 0.44 seconds for ventricle to contract and relax high risk for deadly arrhythmias

CAUSES OF PULSELESS ACTIVITY - THE T's

toxins tamponade tension pneumothorax thrombosis (coronary) thrombosis (pulmonary)

TALL OR PEAKED T WAVE

ventricles are not relaxing associated with hyperkalemia

QRS COMPLEX

ventricular depolarization (contraction) R-wave has higher amplitude and represents the force of the contraction to get the blood out

T WAVE

ventricular repolarization (relaxation) when the ventricles rest and refill with blood potassium is re-entering the cell, causing the ventricle to relax