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BASIC LIFE SUPPORT

GUIDELINES IN GIVING EMERGENCY CARE
GETTING STARTED
1. Plan of Action
Emergency plans should be established based on anticipated needs and available resources
2. Gathering of Needed Materials
The emergency response begins with the preparation of equipment and a personnel before any emergency occurs.
3. Initial Response
• Ask for HELP.
• Intervene
• Do no further harm
4. Instruction to Helper/s
Proper information and instruction to a helper/s would provide organized first aid care.
EMERGENCY ACTION PRINCIPLES
Activate Medical Assistance
In some emergency, you will have enough time to call for specific medical advice before administering first aid. But in some situations, you will
need to attend to the victim first.
Call First and Care first
adult victim = “call first”.
infants and children = “care first”
Do a Primary Survey
In every emergency situation, you must first find out if there are conditions that are an immediate threat to the victim’s life
1. Check for Consciousness
2. Check for Airway
3. Check for Breathing
4. Check for Circulation
A. INTERVIEW THE VICTIM • RESPIRATION - Respiration = 1
• Victim’s name inhalation & 1 exhalation
• Address • SKIN APPEARANCE -
• Phone number Temperature, color & capillary
• Ask what happen refill
• S A M P L E history • PUPILS - PERRLA
• Signs & symptoms • BLOOD PRESSURE
• Allergies C. PERFORM HEAD-TO-TOE EXAMINATION
• Medications • Deformities
• Past medical history • Contusions
• Last oral intake • Abrasions
• Events prior to the episode • Punctures/penetrations
B. CHECK VITAL SIGNS • Burns
• PULSE - Rate, Strength & • Tenderness
Rhythm • Lacerations
• Swelling
Basic Precautions and Practices
• Personal Hygiene
• Protective Equipment
• Equipment Cleaning & Disinfecting
Review on breathing and circulation
• Air that enters the lungs contains about _____% oxygen and only a trace of carbon dioxide.
• Air that is exhaled from the lungs contains about ______% oxygen and ______% carbon dioxide.
BASIC LIFE SUPPORT
An emergency procedure that consists of recognizing respiratory or cardiac arrest or both and the proper application of CPR to maintain life until a victim
recovers or advanced life support is available.
Guidelines
 The American Heart Association’s Guidelines for CPR and ECC provide science-based recommendations for treating cardiovascular emergencies,
particularly sudden cardiac arrest in adults, children, infants and newborns.
 Every five years, hundreds of leading resuscitation experts from around the world review all new and existing research as part of an international
consensus process. This is the basis for any revisions to the American Heart Association’s Guidelines for CPR and ECC.
History of CPR
 In 1960, researchers combined breaths and compressions to create CPR as we know it today.
 CPR training has been recommended for healthcare professionals and for the general public for more than 40 years.
 2010 marks a change in the sequence of CPR from Airway-Breaths-Compressions (A-B-C) to Compressions-Airway-Breaths (C-A-B) sequence.
Sudden Cardiac Arrest
 EMS treats nearly 300,000 victims of out-of-hospital cardiac arrest each year in the U.S.
 Less than eight percent of people who suffer cardiac arrest outside the hospital survive to make it home from the hospital.
 Sudden cardiac arrest can happen to anyone at any time. Many victims appear healthy with no known heart disease or other risk factors.
 Sudden cardiac arrest is not the same as a heart attack.
Strengthening the Links in the Chain of Survival
 Immediate recognition of cardiac arrest and activation of the emergency response system
 Early CPR with an emphasis on chest compressions
 Rapid defibrillation
 Effective advanced life support
 Integrated post– cardiac arrest care
Respiratory Arrest - the condition in which the breathing stops or inadequate
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Causes: 3. Other causes of Respiratory Arrest

1. Obstruction Electrocution
Anatomical Circulatory collapse
Mechanical External strangulation
2. Diseases Chest compression (by physical forces)
Bronchitis Drowning
Pneumonia Poisoning
COPD Suffocation
Rescue Breathing - a technique of breathing air into a person’s lungs to supply him / her with the oxygen needed to survive
Cardiopulmonary-cerebro Resuscitation (CPCR)
 Less than one-third of out-of-hospital sudden cardiac arrest victims receive bystander CPR.
 Effective bystander CPR, provided immediately after sudden cardiac arrest, can double or triple a victim’s chance of survival.
 Chest compressions should be provided at a rate of at least 100 compressions per minute – the same rhythm as the beat of the Bee Gee’s song, “Stayin’
Alive.”
 Compressions of adequate rate and depth
 allowing complete chest recoil between compressions
 minimizing interruptions in compressions
 avoiding excessive ventilation
Building Blocks of CPR Simplified Adult BLS Algorithm.

YOUR ROLE IN A CODE BLUE

PHASE I: Putting the code in motion
NURSE 1 NURSE2 NURSE 3 / 4
- LOC - make sure the code has been called according to - Connect the patient to a monitor
- Call for help hospital procedure - Set up AED or defibrillator, oxygen, and
- Check circulation - Obtain emergency equipment (Crash cart) suction equipment
- Initiate CPCR - Begin 2-responder CPCR with nurse 1 - Get intubation equipment ready
- Set up IV equipment

Phase II: Drugs and Defibrillation

Initiate ACLS protocols and evaluation of the patient’s response to therapy
CODE TEAM
Team Leader - Usually a physician directs and coordinates the resuscitation effort, but a nurse who’s trained in ACLS
may direct the code until a physician arrives
- The team leader usually stands at the foot or head of the bed: she needs a clear view of the patient
to ensure that procedures and patient assessments are performed rapidly and correctly

Defibrillator Operator - A physician or a specially prepared nurse actually delivers the shock
Rapid defibrillation is the key to survival from ventricular fibrillation, so the team must be prepared
to defibrillate immediately.
Recorder - At the start of the code, one nurse should begin recording the events and interventions
- Document all events and interventions, including the type and time of arrest, respiratory
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management, procedures, medication administration, Iv fluids, VS, cardiac rythms, defibrillations,

patient response to treatment, patient outcome, and termination of code.
- The role of a recorder is vital. She should’nt be asked to participate in any other way that distracts
her from this responsibility.
- An important duty of a recorder is to announce when a medication maybe due
- Identify which clock should be the official code clock and be precise about the timing on the
resuscitation record.
Intubationist - A physician (anaesthesiologist), respiratory therapist, nuse anesthetist, or other specially prepared
nurse may do so.
- Prepare: Laryngoscope
: endotracheal tube and a stylet
: 10 ml syringe
: Lubricating gel
: Suction to remove oral secretions
and improve visualization of
anatomical landmarks
: Stethoscope
- If patient can’t be intubated within 30 seconds, stop and hyperventilate and hyperoxygenate
IV nurse - Solutions typically used during resuscitation efforts include .9% sodium chloride and lactated ringers
solution

Medication nurse - Familiarize self with the drugs used during codes
- As you prepare a drug, repeat the drug name and dosage order out loud, so no one’s confused about
what you’re drawing up. Again, announce the drug and dosage prior to administration

Floor nurse - Throughout the entire code, the other patients in the unit must be cared for

Phase III: Winding down

 Typically begins after initial ACLS measures have been instituted and their effectiveness evaluated.
 In this phase, the team leader continues to coordinate all the medical therapies, vital signs, cardiac rhythm, and patient response must be assessed
frequently throughout the code.
Efforts are now aimed at one of the following:
- Maintaining the patient in stable condition until he can be transported to a critical care bed
- Attempting other strategies to restore cardiac function
- Deciding to terminate the code

Key Challenges to Improve CPR Quality for Adults, Children, and Infants
 Recognition ● Failure to recognize gasping as sign of cardiac arrest
● Unreliable pulse detection
 Initiation of CPR ● Low bystander CPR response rates
● Incorrect dispatch instructions
 Compression rate ● Slow compression rate
 Compression depth ● Shallow compression depth
 Chest wall recoil ● Rescuer leaning on the chest
 Compression Interruptions
● Excessive interruptions for
– rhythm/pulse checks
– ventilations
– defibrillation
– intubation
– intravenous (IV) access
– other
 Ventilation ● Ineffective ventilations
● Prolonged interruptions in compressions to deliver breaths
● Excessive ventilation (especially with advanced airway)
 Defibrillation ● Prolonged time to defibrillator availability
● Prolonged interruptions in chest compressions pre- and post-shocks
 Team Performance ● Delayed rotation, leading to rescuer fatigue and decay in compression quality
● Poor communication among rescuers, leading to unnecessary interruptions in compressions
Being prepared
 Each code situation is unique.
 Knowing that a code usually progresses through three phases will help you feel more confident when the actual event occurs.
Tips to fine-tune your skills
 Keep your CPCR skills up-to-date and review hospital policy on code procedures and documentation
 Know current BLS guidelines
 If rule permit, open your crash cart and medication box every 1 to 2 months and review where supplies and medications are located.
 Review the drugs used most frequently during a code and their indications, usual dosages, dilutions, and administration times.
 Know how to operate the cardiac monitor and AED in you unit.
 Make sure you know how to change batteries in the laryngoscope handle and the lightbulb in the blade. Practice connecting the handle to the blade
 These preparations will help you stay calm and focused during a code – and may make the difference between chaos and a smooth-running, well-
organized code.!!
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CARDIAC ARREST
DEFINITION
 It is the cessation of effective pumping action of the heart wherein the electro-conduction of the heart suddenly stops due to cardiac related
disorders.
 When this happens, blood stops flowing into the brain and vitals organs which in turn will cause death to a person within minutes if untreated.
 Irreversible brain damage can occur within ten minutes if arrest is not treated.
 About 95% of people who experiences cardiac arrest die, most within minutes
CAUSES
• Most cases of cardiac arrest are due to ventricular fibrillation and other electrical related problems of the heart such as CAD and MI.
• Other causes may include the following:
• Physical stress
• Inherited problems (LQTS)
• Structural changes in the heart (cardiomegaly)

• • Physical Stress
• Certain types of physical stress can cause the heart's electrical system to fail. Examples include:
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 Intense physical activity. The hormone adrenaline is released during intense physical activity. This hormone can trigger CA in people who have
other heart problems.
 Very low blood levels of potassium or magnesium. (These minerals play an important role in your heart's electrical signaling).
 Major blood loss. (surgical operations)
 Severe lack of oxygen.
• Inherited Disorders
• LQTS (Long QT syndrome)
 is a disorder of the heart's electrical activity due to problems with tiny pores on the surface of heart muscle cells. LQTS can cause sudden,
uncontrollable, dangerous heart rhythms.
• Septal Defects
 Patent ductus arteriosus
 Atrial septal defect
 Ventricular septal defect
 Many cases of CA in children are due to these problems.
 Non cardiac causes
 35% of SCDs are related to non cardiac causes. The most common non–cardiac causes were: trauma, non-trauma related bleeding (such as
gastrointestinal bleeding, aortic rupture, and intracranial hemorrhage), overdose, drowning and pulmonary embolism.
 Non cardiac causes the “ H’s”  Non cardiac causes the “ T’s”
 Hypovolemia - A lack of blood volume  Tablets or Toxins
 Hypoxia - A lack of oxygen  Cardiac Tamponade - Fluid building around the heart
 Hydrogen ions (Acidosis) - An abnormal pH in the body  Tension pneumothorax - A collapsed lung
 Hyperkalemia or Hypokalemia - Both excess and inadequate  Thrombosis (CVA) - stroke
potassium can be life-threatening.  Thromboembolism (Pulmonary embolism) - A blood clot in
 Hypothermia - A low core body temperature the lung
 Hypoglycemia or Hyperglycemia - Low or high blood glucose  Trauma
• Risk Factors
• Persons with heart problems
 CAD
 CHF
 Hypertension
• Obesity
• Cigarette smoking
• Drug abusers and excessive alcohol intoxication
• Affects men twice as often as women and those aging 35-45 years old.
 CA in children is rare unless they have inherited heart conditions.
• Signs and Symptoms
• Usually, the first sign of cardiac arrest is loss of consciousness (fainting). At the same time, no heartbeat (or pulse) can be felt.
• Some people may experience the following prior to loss of consciousness:
 a racing heartbeat (tachycardia)
 feeling dizzy or lightheadedness
 chest pain
 shortness of breath
 nausea and vomiting.
• Diagnosis
• Cardiac arrest is rarely diagnosed before it can happen or as it is happening due to the fact that it can occur without warning.
• Instead it is diagnosed after the incident through series of laboratory exams and by ruling out other causes of a person’s sudden collapse.
• Diagnostic Test
 EKG
 Painless procedure that records the electrical activity of the heart, used to detect and locate the source of several heart problems.
 It also shows the rhythm and strength of the heart to pump blood.
 Echocardiogram
 is a painless test that uses sound waves to create pictures of the heart. It provides the doctor with information about the size and
shape of the heart and how well the heart's chambers and valves are working.
 The test also can find areas of heart muscle that aren't contracting normally due to poor blood flow or injury from a previous heart
attack.
 Cardiac magnetic resonance imaging (MRI)
 is a safe procedure that uses radio waves and magnets to create detailed pictures of the heart. The test creates images of the heart
as it is beating, producing both still and moving pictures of the heart and major blood vessels.
 Cardiac catheterization
o is a procedure used to diagnose and treat certain heart conditions. A long, thin, flexible tube (catheter) is put into a blood vessel in an
arm, groin or neck and threaded to the heart. Through the catheter, the doctor can do diagnostic tests and treatments on the heart.
 Sometimes a special dye is put into the catheter to make the inside of the heart and blood vessels show up on x rays. The dye can show whether
plaque has narrowed or blocked any coronary artery.
 In addition the patient may have blood tests to check the levels of potassium, magnesium, and other chemicals in the blood that play an important
role in the heart's electrical signaling.
o CBC
o Troponin T/I Used to diagnose MI
o CPK-MB
Treatment
 Emergency Treatment includes the following:
o Use of defibrilator (AED)
 AEDs unlike the conventional defibrilator, are programmed devices with command features that tells the rescuer what to do,
thereby reducing the risk of giving too much electric shock.
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o CPR- cardio pulmonary rescusitation

o Emergency drugs e.g. epinephrine
 Treatment in the hospital depends on the cause of cardiac arrest but generally will include the following:
o Cardiac drugs- beta blockers
o Sympathomimetic drugs- dobutamine
o Catecholamines- dopamine
o The latter two drugs are used to control hypertension and may be given as adjuncts via continuous intravenous drip.
 Prevention is better than CURE
o Lifestyle changes
 Daily regular exercise
 Avoidance of foods high in sodium, trans fat, & sugar
 Stay within your caloric levels and increase intake of fruits and vegetables.
 Maintain appropriate weight by balancing intake and activity levels
 Quit smoking and excessive alcohol consumption.

MYOCARDIAL INFARCTION
Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, is the interruption of blood supply to
a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable
atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting
ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death ( infarction) of heart muscle
tissue (myocardium).

TYPES OF MI
• A transmural MI is characterized by ischemic necrosis of the full thickness of the affected muscle segment(s), extending from the endocardium through the
myocardium to the epicardium.
• A nontransmural MI is defined as an area of ischemic necrosis that does not extend through the full thickness of myocardial wall segment(s). In a
nontransmural MI, the area of ischemic necrosis is limited to the endocardium or to the endocardium and myocardium.
• It is the endocardial and subendocardial zones of the myocardial wall segment that are the least perfused regions of the heart and the most vulnerable to
conditions of ischemia
• 1. Q wave infarction, which is diagnosed by the presence of pathological Q waves and is also called transmural infarction. However, transmural infarction is
not always present; hence, the term Q-wave infarction may be preferable for ECG description
• 2. Non-Q wave infarction, which is diagnosed in the presence of ST depression and T wave abnormalities.
Symptoms of acute myocardial infarction
• sudden chest pain (typically radiating to the left arm or left side of the neck)
• shortness of breath
• nausea& vomiting
• Palpitations
• sweating
• anxiety (often described as a sense of impending doom)
• Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue.
• Approximately one quarter of all myocardial infarctions are "silent", without chest pain or other symptoms.
Diagnostic tests
• electrocardiogram (ECG)
• Echocardiography
• blood tests The most often used markers are the creatine kinase-MB (CK-MB) fraction and the troponin levels.
Treatment
• Immediate treatment is to give oxygen, aspirin, and sublingual nitroglycerin.
• Most cases of STEMI (ST elevation MI) are treated with thrombolysis or percutaneous coronary intervention (PCI). NSTEMI (non-ST elevation MI) should be
managed with medication, although PCI is often performed during hospital admission. In people who have multiple blockages and who are relatively
stable, or in a few emergency cases, bypass surgery may be an option.
• *Nitroglycerin – 3 tabs 5 mins apart

ELECTROCARDIOGRAM
• a diagnostic tool that measures and records the electrical activity of the heart in exquisite detail. Interpretation of these details allows diagnosis of a wide
range of heart conditions. These conditions can vary from minor to life threatening.
• The term electrocardiogram was introduced by Willem Einthoven in 1893 at a meeting of the Dutch Medical Society. In 1924, Einthoven received the
Nobel Prize for his life's work in developing the ECG.
• The 12- lead ECG that is used throughout the world was introduced in 1942.
• Reasons to Have an ECG
Heart problems can produce a wide array of symptoms.
• Without the benefit of an ECG, it may be impossible to tell whether these symptoms are being caused by a heart problem or just mimicking one.
Common symptoms that frequently require an ECG include the following:
• Chest pain or discomfort
• Shortness of breath
• Nausea
• Weakness
• Palpitations (rapid or pounding heartbeats or increased awareness of heart beating)
• Anxiety
• Abdominal pain
• Fainting (syncope)
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The Heart
• The heart itself is made up of 4 chambers, 2 atria and 2 ventricles. De-oxygenated blood returns to the right side of the heart via the venous circulation. It
is pumped into the right ventricle and then to the lungs where carbon dioxide is released and oxygen is absorbed. The oxygenated blood then travels back
to the left side of the heart into the left atria, then into the left ventricle from where it is pumped into the aorta and arterial circulation.
• Systolic blood pressure:
• Is the pressure created in the arteries when the ventricles contract
• Diastolic blood pressure:
• When the ventricles starts to refill, the pressure from the arteries falls simultaneously the atriums contract creating pressure known as the
diastolic pressure.
Role of the ECG Machine
 The ECG machine is designed to recognise and record any electrical activity within the heart. It prints out this information on ECG paper made up of small
squares 1mm squared.

• Each electrical stimulus takes the form of a wave and so patterns emerge made up of a number of connected waves. A standard ECG is printed at 25mm
per second or 25 small squares per second (see above). In this way it is possible to calculate the duration of individual waves.
• 10 small squares vertically is equal to 1 millivolt. So it is possible to calculate the amount of voltage being released within the heart. If the line is flat at any
time in the duration of a series of waves, it indicates no electrical activity at that particular moment.
• The direction in which the waves point indicates whether electricity is moving towards or away from a particular lead.
Sinus Rhythm
• Sinus rhythm is the name given to the normal rhythm of the heart where electrical stimuli are initiated in the SA node, and are then conducted through
the AV node and bundle of His, bundle branches and Purkinje fibres.
• Depolarisation and repolarisation of the atria and ventricles show up as 3 distinct waves on ECG. A unique labelling system is used to identify each wave.
• Less muscle means less cells which means less voltage.

The QRS

Complex

• After the first wave there follows a short period where the line is flat. This is the point at which the stimulus is delayed in the bundle of His to allow the
atria enough time to pump all the blood into the ventricles.
• As the ventricles fill, the growing pressure causes the valves between the atria and ventricles to close. At this point the electrical stimulus passes from the
bundle of His into the bundle branches and Purkinje fibres. The amount of electrical energy generated is recorded as a complex of 3 waves known
collectively as the QRS complex. Measuring the waves vertically shows voltage. More voltage is required to cause ventricular contraction and therefore the
wave is much bigger.
• Q wave and represents depolarisation in the septum.

The R Wave
• R wave represents the ventricular depolarisation

The S Wave
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• S wave represents depolarisation of the Purkinje fibres.

The T Wave
• T wave represents ventricular repolarisation.

The ST Segment
• There is a brief period between the end of the QRS complex and the beginning of the T wave where there is no conduction and the line is flat. This is
known as the ST segment and it is a key indicator for both myocardial ischemia and necrosis if it goes up or down.

• V1: 4th intercostal space right sternal border

• V2: 4th intercostal space left sternal border
• V3: halfway between V2 and V4
• V4: left 5th intercostal space,mid-clavicular line
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• V5: horizontal to V4, anterior axillary line

• V6: horizontal to V5, mid-axillary line

Points To Remember:
• Ask the patient to remove all metalic objects including watches, rings, neclaces, pocketed coins and phones etc…
• Let the patient relax before the procedure starts and ask them to lay still for a minute during the procedure.
• Explain the procedure and reassure them that no pain will be felt during the procedure.
Emergency DRUGS
Epinephrine  Follow dose with a 20 ml PNSS flush
 Indication  If methylxanthines, dipyridamole and
 VF, pulseless VT, or asystole carbamazepine are present higher dose may be
 1 mg I.V push every 3-5 min needed
 Intermediate dosing: 2-5 mg IV push over 3-  A brief period of Asystole is common after
5 min administration
 Escalating dosing: 1mg, 3mg, 5 mg IV push 3 Bretylium
min apart  VF/ pulseless VT unresponsive to defibrilation, epi and lido
 High dosing: ,1 mg/kg IV push every 3 – 5  5mg/kg iv push; if arhythmia persists, increase to
min 10 mg/kg q 5-10 min, to a max dose of 35 mg/kg
 Symptomatic Bradycardia: continous infusion at 2-10  Stable VT or Stable wide-complex tachycardia:
mcg/min; titrate to hemodynamic response  5-10 mg/kg over 8-10 min, to max 35 mg/kg over
 Nsg. consideration 24 hrs, if loading dose converts arhythmia start
 Each dose is followed by 20 mL iv fluid flush. infusion of 2 mg/min.
 Can be given via ET tube 2-2.5 x the IV dose, followed Dobutamine
with 10 mL Flush PNSS  Heart Failure
 IC when no other route is available  2-20 mcg/kg/min
 It increases systemic vascular resistance, BP, Cardiac  Nsg considerations
elec. Activity, strenth of contraction, automaticity, and  May cause tachycardia and other arhythmias, BP
myocardial O2 requirement fluctuations, nausea and hypokalemia
Lidocaine  Monitor heart closely; increases in heart heart
 Indication rate more than 10% may induce or exacerbate
 VF or Pulseless VT: Initially 1-1.5 mg/kg IV push: every 3-5 Myocardial Ischemia
mins, max of 3mg/kg Dopamine
 Stable VT or Stable wide-complex tachycardia: repeat doses  Hypotension with symptomatic bradycardia, heart failure or
half the original dose. after spontaneous return of circulation
 If lidocaine succesfully converts the VF/VT: begin continous  Initially, 1-5 mcg/kg/min; max is 20 mcg/kg/min
infusion at 2-4 mg/min  Enhances renal blood flow – 1-2 mcg/kg/min
 Nsg consideration  Nsg consideration
 Toxicity( Slurred speech, altertered LOC, Muscle twitching,  May induce tachycardia, - dose
and seizures), stop the drug/reduce dose reduction/withdrawal
 Via ET: 2-2.5 times the iv dose, flush with 10 ml PNSS  Extravasation may cause severe tissue necrosis
 Don’t give if PVC occurs with bradycardia or escape rhythm.  Norepinephrine should be added is more than
 No longer recommended for VT/VF prophylaxis in acute MI max dose is needed to maintain BP
Atropine  Use slowest infusion first
 Symptomatic Bradycardia  Can exacerbate pulmonary congestion and
 .5-1 mg iv push q 3-5 min, not to exceed .04 compromise cardiac output
mg/kg  Eliminate hypovolemia as a cause of hypotension
 Asystole before treating
 1 mg iv push q 3-5 min, not to exceed a total dose Magnesium
of .04mg/kg  VF/VT with hypomagnesemia
 Nsg consideration  1-2 grams diluted in 10 mL D5W given IV push
 Don’t give less than .5 mg dose – may further over 1-2 min
slow heart rate  Torsades de pointes: 5-10 grams iv
 Via ET: dilute 1-2 mg in 10 mL sterile water of  Torsades de pointes, or simply torsades is a
PNSS, flush with 10 mL PNSS French term that literally means "twisting of the
Adenosine points". It was first described by Dessertenne in
 wide-complex tachycardia: 1966 and refers to a specific, rare variety of
 Initially 6 mg rapid iv push; if no response in 1-2 ventricular tachycardia that exhibits distinct
min, give 12 mg iv push; may be followed by a characteristics on the electrocardiogram (ECG).
third 12 mg dose given in 1-2 min.  Characteristics
 Nsg consideration  Rotation of the heart's electrical axis
 Given rapidly over 1-3 sec by at least 180º
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 Prolonged QT interval (LQTS)

 Preceded by long and short RR-
intervals
 Triggered by an early premature
ventricular contraction

 Acute MI with hypomagnesemia

 Intermitent of continous infusions
 Nsg consideration

 Flushing, sweating, mild bradycardia, and hypotension

may develop from rapid administration in non arrest
situations
Procainamide

 PVCs or recurrent VT with pulse

 Initially, 20 mg/min until
 Hypotension occurs
 QRS complex
 PR interval
 QT interval is widened by 50 %
 Total of 17mg/kg of the drug was
administered
 Maintenance infusion 1-4 mg/min
 Nsg consideration
 Monitor BP closely during administration; may cause
precipitous hypotension, infuse cautiously in patients
with acute MI
 Contraindicated in patients with preexisting long QT
intervals and torsades de pointes