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II. Basic Life Support (BLS)
It is a level of medical care which is used for patients with life-threatening illness or injury until thepatient can be given full medical care. It can be provided by trained medical personnel, includingemergency medical technicians, and by laypersons who have received BLS training. BLS is generallyused in the pre-hospital setting, and can be provided without medical equipment.
BLS generally does not include the use of drugs or invasive skills, and can be contrasted with theprovision of Advanced Life Support (ALS). Most laypersons can master BLS skills after attending a shortcourse. Firefighters and police officers are often required to be BLS certified. BLS is also immenselyuseful for many other professions, such as daycare providers, teachers and security personnel.
CPR provided in the field buys time for higher medical responders to arrive and provide ALS care.For this reason it is essential that any person starting CPR also obtains ALS support by calling for helpvia radio using agency policies and procedures and/or using an appropriate emergency telephonenumber.
An important advance in providing BLS is the availability of the automated external defibrillator orAED, which can be used to defibrillation or delivery. This improves survival outcomes in cardiac arrestcases.
Basic life support consists of a number of life-saving techniques focused on the medicine "ABC"sof pre-hospital emergency care:
- Airway: the protection and maintenance of a clear passageway for gases (principally oxygen andcarbon dioxide) to pass between the lungs and the outside of the body- Breathing: inflation and deflation of the lungs (respiration) via the airway- Circulation: providing an adequate blood supply to the body, especially critical organs, so as todeliver oxygen to all cells and remove carbon dioxide, via the perfusion of blood throughout the body.
1) BLS Algorithm
- Check for Response- Activate the EMS System
-Open the Airway and Check Breathing.
- Give 2 Rescue Breaths that make the chest rise.- Pulse Check (for Healthcare Providers)
- If theres a pulse, give 1 breath every 5-6 seconds. Then, recheck pulse every 2 minutes.- If theres no pulse, give cycles of 30 compressions and 2 breaths until AED/defibrillator
arrives, ALS providers take over, or victim starts to move. Push hard and fast (100/min) andrelease completely. Minimize interruptions in compressions.
- AED/ Defibrillator arrives
- Check rhythm if its shockable or not.- If its shockable, give 1 shock. Resume CPR immediately for 5 cycles.- If its not shockable, resume CPR immediately for 5 cycles. Check rhythm every 5 cycles;
continue until ALS providers take over or victim starts to move.
a) Witnessed Arrest- presence of primary PEA, and return of spontaneous circulation. The most accurate decision
rule to recognize MPE consisted of witnessed arrest+primary PEA. This rule generatedsensitivity=67.6% and specificity=94.5% and yielded a posttest probability of MPE of 57%.
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b) Unwitnessed Arrest
- is unlikely with an initial response of basic life support alone. Withdrawal of resuscitationshould be considered if an adult victim of unwitnessed cardiac arrest is found in asystole andthe arrest is of obvious cardiac origin.
c) Cricoid pressure
- Pressure applied to the victims cricoid cartilage pushesthe trachea posteriorly, compresses
the esophagus against thecervical vertebrae, and can prevent gastric inflation and reducetherisk of regurgitation and aspiration. Application
of cricoid pressure usually requires a third
rescuer, one whois not responsible for chest compressions or ventilations. Cricoid
pressure
should be used only if the victim is deeply unconscious(ie, has no cough or gag reflex).
d) Pulse Check- Lay rescuers fail to recognize the absence of a pulse in 10%
of pulseless victims (poor
sensitivity for cardiac arrest) andfail to detect a pulse in 40% of victims with a pulse
(poorspecificity). In the ECC Guidelines 2000
the pulse check
was deleted from training for
lay rescuers and deemphasizedin training for healthcare providers. There is no
evidence,however, that checking for breathing, coughing, or movement
is superior for
detection of circulation.For ease of training,
the lay rescuer will be taught to assume that
cardiac arrestis present if the unresponsive victim is not breathing.
Healthcare providers also may take too long to check for a pulseand have difficulty
determining if a pulse is present or absent.The healthcare provider should take no more than
10 secondsto check for a pulse (Class IIa). If a pulse is not definitely
felt within 10 seconds,
proceed with chest compressions
How to do a Pulse Check
y Don a watch (or look at a clock) with a sweep second hand.
y Run your index and middle fingers along your thumb line until you reach the
bend in your wrist.
y Gently press down until you feel your pulse.
y Begin counting pulsations and continue to count for one full minute. Yourpulse should feel strong and regular and have a steady beat (rhythm).
e) Chest Compression
- Chest compressions consist of rhythmic applications of pressureover the lower half of the
sternum. These compressions create
blood flow by increasing intrathoracic pressure anddirectly
compressing the heart. Although properly performed chest compressions
can produce
systolic arterial pressure peaks of 60 to 80 mmHg, diastolic pressure is low and mean arterial
pressurein the carotid artery seldom exceeds 40 mm Hg.
Blood flow generated by chest compressions delivers a smallbut critical amount of oxygen
and substrate to the brain andmyocardium. In victims of VF SCA, chest compressions
increasethe likelihood that a shock (ie, attempted defibrillation) will
be successful. Chest
compressions are especially important ifthe first shock is delivered 4 minutes after collapse.
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Much of the information about the physiology of chest compressionsand the effect of varying
compression rates, compression-ventilationratios, and duty cycles (percent of time the chest
is compressed
versus time allowed for chest recoil) is derived from animal
models.Researchers at the 2005 Consensus Conference,
however,
reached several conclusions
about chest compressions:
-
"Effective" chest compressions are essential for providing blood
flow during CPR (ClassI).
- To give "effective" chest compressions,"push hard and push
fast." Compress the adult
chest at a rateof about 100 compressions
per minute, with a compression depth
of 1 to 2
inches (approximately4 to 5 cm). Allow the chest
to recoil completelyafter each
compression,
and allow approximatelyequal compression and relaxation
times.
- Minimize interruptionsin chest compressions.
- Further studies are needed to definethe best method for coordinating
ventilations and
chest compressionsand to identify the best
compression-ventilation ratio in terms
of survival
and neurologicoutcome.
f) Compression Ventilation Ratio
- A compression-ventilation ratio of 30:2 is recommended and furthervalidation of this
guideline is needed (Class IIa).In infants and children (see Part 11: "Pediatric Basic
LifeSupport"), 2 rescuers should use a ratio of 15:2 (Class IIb).
This 30:2 ratio is based on a consensus of experts rather thanclear evidence. It is designed
to increase the number of compressions,reduce the likelihood of hyperventilation, minimize
interruptionsin chest compressions for ventilation, and simplify instruction
for teaching and
skills retention. A manikin study suggeststhat rescuers may find a compression-ventilation
ratio of 30:2more tiring than a ratio of 15:2. Further studies are needed
to define the best
method for coordinating chest compressionsand ventilations during CPR and to define the
best compression-ventilationratio in terms of survival and neurologic outcome in patients
with
or without an advanced airway in place.
Once an advanced airway is in place, 2 rescuers no longer delivercycles of CPR (ie,
compressions interrupted by pauses for ventilation).Instead, the compressing rescuer should
give continuous chestcompressions at a rate of 100 per minute without pauses for
ventilation.
The rescuer delivering ventilation provides 8 to10 breaths per minute. The 2 rescuers should
change compressorand ventilator roles approximately every 2 minutes to prevent
compressor
fatigue and deterioration in quality and rate ofchest compressions. When multiple rescuers
are present, theyshould rotate the compressor role about every 2 minutes.
The compression rate refers to the speedof compressions, notthe actual numberof
compressions delivered per minute. Theactual number of chest compressions delivered per
minute isdetermined by the rate of chest compressions and the number
and duration of
interruptions to open the airway, deliver rescuebreaths, and allow AED analysis.
Rescuers
must make every
effort to minimize these interruptions in chest compressions. In 1 out-of-hospital study rescuers intermittently achieved
compression rates of 100 to 121 compressions
per minute, butthe mean number of compressions delivered per minute was reduced
to 64
compressions per minute by frequent interruptions.
g) Compression-OnlyCPR
The willingness to actA few simple skills
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Warning: Whenever possible, be sure to use personal protective equipment such asdisposable gloves when providing emergency care.
Step 1: Act immediately!
If you see an adult or adolescent suddenly collapse, check the scene for safety and then seeif the person responds to you by tapping them on the shoulder and shouting, "Are you okay?"
Step 2: Call Emergency Hotline
If they don't respond, call or send someone to call the local emergency number right away.
Step 3: Check for normal breathing
Open the airway by tilting their head back and lifting the chin up, and briefly check for normalbreathing. Look to see if the chest rises and falls, listen for breathing, and feel for breathingon the side of your face.
Step 4: Get into position
If the person is not breathing, prepare to give them chest compressions: Kneel beside themand put the heel of one hand on the center of their chest. Place your other hand over thathand, lacing your fingers together. Position your shoulders directly over your hands, keepingyour arms straight and your fingers off the chest.
Tip: Loosen or remove clothing if it gets in the way of giving deep compressions in the middleof the chest.
Step 5: Begin chest compressions
Push down on the chest fast and deep -- about two inches -- then let the chest risecompletely before pressing down again. Don't take your hands off the chest, just your weight.
Tip: Chest compressions keep blood containing vital oxygen flowing throughout the body.
Step 6: Keep going!
Keep going. Do not stop or interrupt compressions until the person shows an obvious sign oflife, like normal breathing; the scene becomes unsafe; an automated external defibrillator, or
AED, is ready; you're too exhausted to continue; or a trained responder arrives and takesover.
Step 7: Take a class
Get training -- and encourage others to do so. Knowing full CPR -- chest compressions and
breaths -- will enable you to help in other emergencies, such as those that involve infants andchildren. Every household should have at least one person trained in lifesaving skills.
ACLS (Advanced cardiac life supportorAdvanced Cardiovascular Life Support)
Refers to a set of clinical interventions for the urgent treatment of cardiac arrest and other lifethreatening medical emergencies, as well as the knowledge and skills to deploy those interventions.
[1]
Extensive medical knowledge and rigorous hands-on training and practice are required to master ACLS.Only qualified health care providers (e.g. physicians, paramedics, nurses, respiratory therapists,clinical
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pharmacists, physician assistants, nurse practitioners and other specially trained health care providers)can provide ACLS, as it requires the ability to manage the patient's airway, initiate IV access, read andinterpret electrocardiograms, and understand emergency pharmacology. Some health professionals, oreven lay rescuers, may be trained in basic life support (BLS), especially cardiopulmonary resuscitation orCPR. When a sudden cardiac arrest occurs, immediate CPR is a vital link in the chain of survival. Anotherimportant link is early defibrillation, which has improved greatly with the widespread availability of AEDs.
ACLS is an extension of BLS. It often starts with analysing patient's heart rhythms with a manualdefibrillator. In contrast to an AED in BLS, where the machine decides when and how to shock a patient,the ACLS team leader makes those decisions based on rhythms on the monitor and patient's vital signs.The next steps in ACLS are insertion of intravenous (IV) lines and placement of various airway devices.Commonly used ACLS drugs, such as epinephrine, atropine
[2]and amiodarone, are then administered. At
this time, the ACLS personnel quickly search for possible causes of cardiac arrest (e.g., a heart attack,drug overdose, or trauma). Based on their diagnosis, more specific treatments are given. Thesetreatments may be medical such as IV injection of an antidote for drug overdose, or surgical such asinsertion of a chest tube for those with tension pneumothoraces or hemothoraces. While the abovementioned ACLS steps are being carried out, it is crucial to continue chest compression with minimalinterruptions. This point is emphasized repeatedly in the new ACLS guidelines.
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III. ECG Interpretation
Electrical System of the heart
y Electrocardiogram (ECG/EKG)
y A fundamental part of cardiovascular assessment
y Records the depolarization and repolarization of the myocardial cells via
electrodes placed on limbs and chest wall and then transcribes on to graph paper
y Is recorded to a standard paper traveling at a rate of 25 mm/s
The paper is divided into large squares, each measuring 5 mm wide and
equivalent to 0.2 secondsy Large squares are divided into five small squares, 1 mm in width and
equivalent to 0.04 seconds
y Lead Placements
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Locations:V1 Right 4
thIntercostal Space, Parasternal Border
V2 Left 4th
Intercostal Space, Parasternal BorderV3 Between V2 and V4V4 Left 5
thIntercostal Space, Midclavicular Line
V5 Left 5th
Intercostal Space, Anterior Axillary Line
V6 Left 5th Intercostal Space, Mid-axillary Line
Sinus Rhythm
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A 6 second strip on the ECGo Normal Sinus Rhythm
A. Electrocardiogram Interpretation
A. ECG Waves and Intervals:
y P wave: the sequentialactivation (depolarization) of the right and leftatria
y QRS complex: right and left ventricular depolarization (normally the
ventricles are activated simultaneously)
y U wave: origin for this wave is not clear - but probably represents "afterdepolarizations" in the ventricles
y PR interval: time interval from onset of atrial depolarization (P wave) toonset of ventricular depolarization (QRS complex)
y QRS duration: duration of ventricular muscle depolarization
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y QT interval: duration of ventricular depolarization and repolarization
y RR interval: duration of ventricular cardiac cycle (an indicator ofventricular rate)
y PP interval: duration of atrial cycle (an indicator or atrial rate)
B. Determine the rhythm.
a. Atrial rhythm: P P Regular / Irregular
b. Ventricular rhythm: R R
***Measure using a paper or a microcaliper.
C. Compute the rate.
** 1 small square 0.04 seconds
** 1 big square 0.2 seconds
FOR REGULAR RHYTHM
a. Atrial rate
- the number of P waves in a 6 second strip multiplied by 10
eg. 7 P waves x 10 = 70 bpm
b. Ventricular rate
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- count the number of QRS complexes multiplied by 10
eg. 8 QRS complex x 10 = 80 bpm
- Normal Duration: 60 100bpm
FOR IRREG
ULA
R RHYT
HM
- count the number of small complexes between 2 P waves (Atrial) /2 R waves (Ventricular) and divide to 1500.
eg. 1500 / 25 small squares = 60 bpm
- Normal Duration: 60 100bpm
D. Identify the P- wave.
- It can be upright or biphasic
- Normal Duration: 0.04 0.125 seconds ( 1-3 small squares)
E. Determine the P R interval.
- Time between atrial contraction before ventricular contraction
- Count the number of small squares between beginning of P tobeginning of QRS multiplied by 0.04.
- Normal Duration: 0.12 0.20 seconds (3-5 small squares)
F. Identify theQRS complex.
- May be narrowed or widened
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- Number of small square comprising a QRS complex
- Normal Duration: 0.04 0.12 seconds (1 3 small squares)
G. Measure theQ T interval.
- Number of small square start of QRS to end of T multiplied by 0.04seconds.
- Normal Duration: 0.36 0.44 seconds (9 11 small squares)
H. Identify S T segment.
- Line between S-T wave
- Isoelectric
- Results: elevatedor depressed
I. Identify T wave.
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The ECG shows a normal P wave, P-R interval, QRS complex; the only abnormality is an irregular P-P
interval. Sinus arrhythmia is a normal finding in children and young adults and tends to diminish or
disappear with age. Sinus arrhythmia is often somewhat more prominent with fluctuation in the respiratory
cycle as heart rate accelerates with inspiration and slows with expiration. The alternating acceleration and
deceleration of heart rate with respiration is mainly the result of fluctuations in vagal tone. Sinus
arrhythmia may be aggravated by any factor that increases vagal tone.
SINUS BRADYCARDIA is the term for a sinus rate of less than 60 beats/min and may be seen in the
normal adult population. Sinus bradycardia during exercise, fever or congestive heart failure is abnormal.
Persistent rates of less than 45 beats/min are also considered abnormal, and in the absence of drugs
such as digitalis, beta-blockers and calcium channel blockers, reflect abnormality in the sinus node. Sinus
bradycardia can be present in otherwise normal individuals and is common in well-trained athletes and in
most people during deep sleep. It is part of the normal reaction to vagal stimulation. Sinus bradycardia
may also be related to metabolic abnormalities, including hypothermia and myxedema. Nonvagally
mediated sinus bradycardia also may occur as a manifestation of organic heart disease, including
ischemic heart disease, particularly when the SA node is damaged, as with certain types of acute MI and
in association with severe chest pain of acute MI. Sinus bradycardia may also be a complication of
myocardial disease in which the SA node is damaged by scarring or infiltrative processes associated with
aging as part of a degenerative conduction system process.
Summary of ECG criteria
y Normal-looking QRS
y Rate: Less than 60 beats/min
y Rhythm: Regular
y P waves: Upright in leads I, II and aVF
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SINUS TACHYCARDIA is defined as sinus rhythm with a rate of greater than 100 beats/min. To be
certain that sinus tachycardia is the etiology for a supraventricular tachycardia (tachycardia with its origin
in the AV junction, atria or SA node), one must identify a constant single P wave for every QRS complex.
Sinus tachycardia usually represents a physiologic response to fever, intravascular volume depletion,hypermetabolism, anxiety or the administration of pharmacologic agents that dramatically increase sinus
rate, such as catecholamines. Sinus tachycardia may also be a response to severe emotional distress,
fright and strenuous exercise. Other causes may include a response to anemia, CHF, hemorrhage,
extensive heart muscle damage associated with a reduction in cardiac output and pulmonary embolism.
Physiologically, sinus tachycardia results from either vagal withdrawal and/or endogenous release of
catecholamines.
Summary of ECG criteria
y Identify a constant single P wave for every QRS complex
y Normal-looking QRS
y Rate: Greater than 100 beats/min
y Rhythm: Regular
y P waves: Upright in leads I, II and Avf
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Sinus Arrest is where there is no conduction through the SA node, the result is a minimum of 3seconds. Possible causes include increase in vagal tone, damage to the SA node, hypoxia,hyperkalemia, digitalis,beta blockers, calcium channelblockers, decreased PB, shock, andcongestive heart failure.
EKG Characteristics: Rate: The rate of the intrinsic rhythm. Irregular rhythm during sinus arrest. P
Wave is not present during sinus arrest. PR Interval not present when sinus arrest occurs.QRSComplex is usually normal for the intrinsic rhythm and absent during the sinus arrest.
Sinus exit block/sinoatrial blockThis results when the impulse from the sinoatrial(SA) node is block and does not depolarizes the atrium.
Although there SA node is firing at the usual rate, the impulses are not passed on. There will be pausesequivalent to multiple P-P intervals.
Premature Atrial Contraction
A type of cardiac arrhythmia with premature atrial contractions or beats caused by signals originating from
ectopic atrial sites. The ectopic signals may or may not conduct to the HEART VENTRICLES. Atrial
premature complexes are characterized by premature P waves on ECG which are different in
configuration from the P waves generated by the normal pacemaker complex in the SINOATRIAL NODE.
Atrial Tachycardia
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Atrial tachycardia is one of several heart problems which can cause heart arrhythmia. The problem stems
from an abnormal cardiac rhythm which occurs when the electrical impulses which regulate the heartbeat
originate in the wrong area of the heart. It does have a low morbidity rate, but in children who are born
with this heart abnormality the death risk is somewhat higher.
Atrial Flutter
Atrial flutter is an abnormality of the heart rhythm, resulting in a rapid and sometimes irregular heartbeat.
Atrial Fibrillation
Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the
upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the
lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.
Wolff-Parkinson-White Syndrome
Wolff-Parkinson-White syndrome is a pre-excitation occurrence enabled by an accessory pathway
(Bundle of Kent) that connects the atria to the ventricles. The slurring of the beginning of the QRS
called a Delta wave - results from part of the ventricles depolarizing early (preexcitation) before being met
by the normal depolarization of ventricles ( from the bundle branches). A short PR interval is also
expected.
Premature Junctional Complex (PJC)
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A PJC arises from an irritable focus within the AV junction. Characteristics of a PJC include: 1) an absent
or inverted P wave in lead II; 2) a shortened PR interval less than .12 seconds; and 3) the complex
comes early or premature
Junctional Rhythm
Junctional rhythm or junction escape rhythm originates from the AV junction AV node and Bundle of
His. The expected pacemaker rate of the AV junction is 40-60/minute. In lead II, inverted or absent P
waves are expected usually with a narrow QRS. An absent P wave in junctional rhythm is also associated
with loss of atrial kick.
Accelerated JunctionalRhythm
Accelerated junctional rhythm occurs as a result of enhanced automaticity, due to increased sympathetic
activity (catecholamines) and/or hypoxia. Key features of this rhythm include a rate between 60-100/minute, inverted or absent P waves (in lead II), shortened PR interval, and most often narrow QRS
complexes.
JunctionalTachycardia
Junctional tachycardia occurs due to the enhanced automaticity, possibly from increased sympathetic
activity (catecholamines) and/or hypoxia. Key features of this rhythm include a rate over 100/minute,
inverted or absent P waves (in lead II), shortened PR interval, and most often narrow QRS complexes
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Premature VentricularComplexes
Premature ventricular complexes (PVC) often represent ventricular automaticity and/or reentry
phenomenon. The presence of PVC may be benign but can indicate irritable ventricles. The PVC arrives
earlier than epected and is usually wide (.12 seconds or more) and bizarre. Note that the T wave will
often point in an opposite direction from the QRS complex. A PVC every second complex is called
ventricular bigemy, every third is ventricular trigeminy.
1. Bigeminy1. Extrasystole follows every sinus beat
2. Trigeminy
1. Extrasystole follows every other sinus beat2. Every third beat is ectopic
3. Couplet1. Extrasystole and preceding beat
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Idioventricular Rhythm (IVR)
Idioventricular rhythm (IVR) occurs when the SA and AV nodes are either not firing or firing slower than
the ventricular pacemaker rate. A common ventricular pacemaker rate is 20-40/minute, a rate that is often
not sufficient to sustain an adequate cardiac output.
Accelerated Idioventricular Rhythm (AIVR)
Accelerated idioventricular rhythm (AIVR) is not yet a tachycardia but is occurring at a rate greater than
what is expected of the ventricles. AIVR is found with a rate 40-100/minute. Enhanced automaticity
possibly due to hypoxia or abundant sympathetic stimulation increases the ventricular firing. Note that
this rhythm is not usually stable and can move quickly to either asystole or ventricular tachycardia.
VentricularTachycardia
Ventricular tachycardia is a pulse rate of more than 100 beats per minute, with at least three irregular
heartbeats in a row. It is characterized by absence of P and T waves.
Ventricular Fibrillation
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In this type (also known as Wenckebach's block), the electrical signals are delayed more and more with
each heartbeat, until the heart skips a beat. On the EKG, the delay is shown as a line (called the PR
interval) between the P and QRS waves. The line gets longer and longer until the QRS waves don't follow
the next P wave.
Second Degree Heart Block Mobitz II
In second-degree Mobitz type II heart block, some of the electrical signals don't reach the ventricles.
However, the pattern is less regular than it is in Mobitz type I. Some signals move between the atria and
ventricles normally, while others are blocked. On an EKG, the QRS wave follows the P wave at a normal
speed. Sometimes, though, the QRS wave is missing (when a signal is blocked).
Third Degree Heart Block
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In this type of heart block, none of the electrical signals reach the ventricles. This type also is called
complete heart block or complete AV block.
When complete heart block occurs, special areas in the ventricles may create electrical signals to cause
the ventricles to contract. This natural backup system is slower than the normal heart rate and isn't
coordinated with the contraction of the atria. On an EKG, the normal pattern is disrupted. The P waves
occur at a faster rate that isn't coordinated with the QRS waves.
Torsades de Pointes
Torsade de pointes, literally meaning twisting of points, is a distinctive form of polymorphic ventricular
tachycardia (VT) characterized by a gradual change in the amplitude and twisting of the QRS complexes
around the isoelectric line. Torsade de pointes (torsade) is associated with a prolonged QT interval, which
may be congenital or acquired. Torsade (not long QT) usually terminates spontaneously but frequently
recurs and may degenerate into ventricular fibrillation.
IV. A. Pharmacologic Agents forArrhythmias
Drug Indication Dosage Atropine sulfate Bradycardia Intravenous
Adult: 500 mcg every 3-5minutes. Total: 3 mg.Max Dosage: 0.04 mg/kg bodyweight.
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Drug Indication Dosage
Adenosine Differential diagnosis ofsupraventricular tachycardias
Intravenous Adult: Initially, 3 mg by rapid IVinj into a central or large
peripheral vein over 2 sec withcardiac monitoring; 6 mg may begiven after 1-2 minutes ifnecessary, then 12 mg after afurther 1-2 minutes. Avoidincrements if high level AV blockoccurs at any particular dose.
Child: Initially, 50-100 mcg/kg; ifnecessary, may increase dose by50-100 mcg/kg increments at 1-2minute intervals or untilarrhythmia is controlled. Maxdose: 300 mcg/kg.
Paroxysmal supraventriculartachycardia
Intravenous Adult: Initially, 3 mg by rapid IVinj into a central or largeperipheral vein over 2 sec withcardiac monitoring; 6 mg may begiven after 1-2 minutes ifnecessary, then 12 mg after afurther 1-2 minutes. Avoidincrements if high level AV blockoccurs at any particular dose.
Child: Initially, 50-100 mcg/kg; ifnecessary, may increase dose by
50-100 mcg/kg increments at 1-2minute intervals or untilarrhythmia is controlled. Maxdose: 300 mcg/kg.
Myocardial imaging Intravenous Adult: 140 mcg/kg/minute byinfusion for 6 minutes. Injectradionuclide 3 minute afterinfusion.
Drug Indication Dosage
Lidocaine Pulseless ventricular fibrillation or
ventricular tachycardia
Intravenous
Adult: As hydrochloride: 1-1.5mg/kg repeated as necessary.Max total: 3 mg/kg. Forventricular arrhythmias in morestable patients: Usual loadingdose: 50-100 mg as an IV inj at25-50 mg/minute, may repeatonce or twice up to a max of 200-300 mg in 1 hr, followed by 1-4
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mg/minute via continuous IVinfusion. May need to reducedose if the infusion is longer than24 hr.
Hepatic impairment: Reducedose by 50% in acute hepatitisand decompensated cirrhosis.
Sympathetic nerve block ParenteralAdult: As hydrochloride: 50 mg (5ml) of a 1% solution for cervicalblock or 50-100 mg (5-10 ml) of a1% solution for lumbar block.
Hepatic impairment: Reducedose by 50% in acute hepatitisand decompensated cirrhosis.
Emergency treatment ofventricular arrhythmias
Intramuscular Adult: As hydrochloride: 300 mginjected into the deltoid muscle,repeat after 60-90 minutes ifnecessary.
Hepatic impairment: Reducedose by 50% in acute hepatitisand decompensated cirrhosis.
Peripheral nerve block Parenteral Adult: As hydrochloride: Forbrachial plexus block: 225-300mg (15-20 ml) of a 1.5% solution;for intercostal nerve block: 30 mg(3 ml) of a 1% solution; forparacervical block: 100 mg (10
ml) of a 1% solution on eachside, repeated not morefrequently than every 90 minutes;for paravertebral block: 30-50 mg(3-5 ml) of a 1% solution; forpudendal block: 100 mg (10 ml)as a 1% solution on each side;for retrobulbar block: 120-200 mg(3-5 ml) of a 4% solution.
Hepatic impairment: Reducedose by 50% in acute hepatitisand decompensated cirrhosis.
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Drug Indication Dosage
Procainamide Ventricular arrhythmias Oral Adult: 50 mg/kg daily in divideddoses every 3-6 hr.
Child: 15-50 mg/kg daily in 4divided doses.
Elderly: Dosage reduction orincrease in dosing intervals isrecommended.
Renal impairment: Dosagereduction or increase in dosingintervals is recommended.
Hepatic impairment: Dosagereduction is recommended.
Short-term management ofsevere or symptomaticarrhythmias
Oral Adult: 50 mg/kg daily in divideddoses every 3-6 hr.
Child: 15-50 mg/kg daily in 4divided doses.
Elderly: Dosage reduction orincrease in dosing intervals isrecommended.
Renal impairment: Dosagereduction or increase in dosing
intervals is recommended.
Hepatic impairment: Dosagereduction is recommended.
Ventricular arrhythmias IntravenousAdult: Dilute in 5% glucose solnand given in doses of 100 mgevery 5 min at a rate notexceeding 50 mg/min untilarrhythmia has been suppressedor a max of 1 g has beenreached. Alternatively admin bycontinuous infusion of 500-600
mg over 25-30 min with ECGmonitoring followed by infusion ata rate of 2-6 mg/min.
Child: Loading dose of 10-12mg/kg, followed by continuousinfusion of 20-75 mcg/kg/min.
Elderly: Dosage reduction orincrease in dosing intervals is
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recommended.
Max Dosage: Adult: 1 g.
Renal impairment: Dosagereduction or increase in dosingintervals is recommended.
Hepatic impairment: Dosagereduction is recommended.
Short-term management ofsevere or symptomaticarrhythmias
IntravenousAdult: Dilute in 5% glucose solnand given in doses of 100 mgevery 5 min at a rate notexceeding 50 mg/min untilarrhythmia has been suppressedor a max of 1 g has beenreached. Alternatively admin bycontinuous infusion of 500-600mg over 25-30 min with ECG
monitoring followed by infusion ata rate of 2-6 mg/min.Child: Loading dose of 10-12mg/kg, followed by continuousinfusion of 20-75 mcg/kg/min.
Elderly: Dosage reduction orincrease in dosing intervals isrecommended.
Max Dosage: Adult: 1 g.
Renal impairment: Dosage
reduction or increase in dosingintervals is recommended.
Hepatic impairment: Dosagereduction is recommended.
Drug Indication Dosage
Amiodarone Ventricular arrhythmias Oral Adult: 800-1,600 mg/day in 1-2divided doses for 1-3 wk untilinitial therapeutic response isachieved, then reduce dose to
600-800 mg/day in 1-2 divideddoses for 1 mth. Maintenance:400 mg/day; lower doses may beused for supraventriculararrhythmias. Daily doses may bedivided. Close monitoring of thepatient is recommended. Use theminimum effective dose.
Hepatic impairment: Dosage
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reduction may be necessary.
Life-threatening ventriculararrhythmias
Intravenous Adult: Recommended startingdose: About 1 g over 1st 24 hr.Dose is given in a 3-phasesequence. Initial rapid loading
dose: Infuse 150 mg at a rate of15 mg/minute (initial infusion rateshould not exceed 30mg/minute); followed by the slowloading phase: Infuse 360 mg ata rate of 1 mg/minute; followedby the first maintenance phase:Infuse 540 mg at a rate of 0.5mg/minute. After the 1st 24 hr,maintain infusion rate at 0.5mg/minute (i.e. 720 mg over 24hr); rate may be increased toachieve effective suppression ofarrhythmia. For breakthrough
episodes, supplemental doses of150 mg may be given at 15mg/minute; may repeatsupplemental doses up to a maxIV dose of 2.2 g/24 hr.Maintenance infusion at up to 0.5mg/minute may be continued forup to 2-3 wk with caution.Concentrate for inj should bediluted prior to admin.Conversion to oral therapy willdepend on the administered doseof the IV therapy and the
bioavailability of the oral drug.Hepatic impairment: Dosagereduction may be necessary.
Pulseless ventricular fibrillation orventricular tachycardia
Intravenous Adult: Initial: 300 mg (diluted in20-30 ml dextrose 5% or normalsaline) if VF or VT recurs, to begiven as a single dose by rapidIV inj. Supplemental dose: 150mg followed by an infusion of 1mg/minute for 6 hr, then 0.5mg/minute. Max: 2.1 g daily.
Hepatic impairment: Dosagereduction may be necessary.
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Drug Indication Dosage
Sotalol Supraventricular and ventricular
arrhythmias
Oral
Adult: Initially, 80 mg daily as a
single or in 2 divided doses,
increased gradually every 2-3days. Usual dose: 160-320 mg
daily in 2 divided doses. Max:
640 mg daily.
Child: Neonates: Initially, 1
mg/kg bid, increased every 3-4
days, if necessary. Max: 4
mg/kg bid. 1 mth-12 yr: Initially,
1 mg/kg bid, increased as
necessary every 2-3 days. Max:
4 mg/kg bid, not exceeding 80mg bid. For refractory
supraventricular tachycardia,
sotalol may be given with
flecainide;
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CrCl(ml/min)
DosageRecommendation
30-60 Halve the usual dose.
10-30 Quarter the usual dose.
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Stable symptomatic heart failure Oral
Adult: As a modified-release
preparation of metoprolol
succinate: Initially, 12.5-25 mg of
equivalent metoprolol tartrate
dose. Increase, as tolerated, at 2-
wk intervals to a max of 20 mg
once daily.
Hepatic impairment: Reduce
dose.
Emergency treatment of cardiac
arrhythmias
Intravenous
Adult: Initially, up to 5 mg at a rate
of 1-2 mg/min; may repeat at 5-
minute intervals if needed up to a
total dose of 10-15 mg. When
acute arrhythmias are controlled,
initiate maintenance therapy 4-6
hr after IV therapy using oral
therapy not exceeding 50 mg tid.
Hepatic impairment: Reduce
dose.
Prophylaxis or control of
arrhythmias on induction of
anaesthesia
Intravenous
Adult: 2-4 mg as slow inj; may
repeat injections of 2 mg as
necessary up to a max total dose
of 10 mg.
Hepatic impairment: Reduce
dose.
Adjunct in the early management
of acute myocardial infarction
Intravenous
Adult: Admin within 12 hr of the
onset of chest pain, 5 mg at 2-
minute intervals to a total of 15mg, if tolerated. After 15 minutes,
for patients who have received
full IV dose: Initiate oral therapy
of 50 mg every 6 hr for 2 days; for
patients who did not tolerate the
full IV dose: Reduced oral dose
should be given as and when
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adjustment may be needed.
Initial dose of 120 mg daily, as a
single dose or in 2 divided doses
depending on the formulation and
titrated carefully as required. Do
not increase dose if the heart rate
drops
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Dopamine Acute heart failure Intravenous
Adult: As hydrochloride: Initially, 1-5
mcg/kg/min increased gradually by
up to 5-10 mcg/kg/min according to
the patient's BP, cardiac output and
urine output. Up to 20-50
mcg/kg/min may be required in
seriously ill patients.
Drug Indication Dosage
Dobutamine Acute heart failure Intravenous
Adult: 2.5-10 mcg/kg, up to 0.5-40
mcg/kg according to patient's heartrate, cardiac output, BP and urine
output.
Cardiac stress test Intravenous
Adult: 5 mcg/kg/min for 8 min using
a 1 mg/ml solution, dose is then
increased at 5 mcg/kg/min until 20
mcg/kg/min, with each dose being
infused for 8 min before the next
increase. Monitor ECG and stop
infusion if arrhythmias, marked STsegment depression or other
adverse effects occur.
Drug Indication Dosage
Sodium nitroprusside Hypertensive crisis Intravenous
Adult: For patients not receiving any
antihypertensives, initially 0.3-1.5
mcg/kg/min, adjust gradually
according to response. Usual range
0.5-6 mcg/kg/min. Lower doses
should be used in patients receiving
antihypertensives. Max rate: 8
mcg/kg/min, discontinue infusion if
there is no response after 10 min.
May continue for a few hr if there is
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response. Introduce oral
antihypertensive as soon as
possible.
Child: Initially, 250-500nanograms/kg/min, rate may be
repeatedly doubled at intervals of
15-20 min until the desired effect is
achieved or treatment is judged
ineffective. Max rate: 6 mcg/kg/min.
Elderly: Lower doses may be
required.
Renal impairment: Dosageadjustments may be necessary.
Induction of hypotension during
anaesthesia
Intravenous
Adult: Recommended max dose:
1.5 mcg/kg/min.
Renal impairment: Dosage
adjustments may be necessary.
Heart failure Intravenous
Adult: Intially 10-15 mcg/min, may
increase by 10-15 mcg/min every 5-
10 min according to response; usual
range 10-200 mcg/min. Max: 280
mcg/min.
Renal impairment: Dosage
adjustments may be necessary.
Drug Indication Dosage
Sodium bicarbonate Urine alkalinisation Oral
Adult: To prevent development of
uric-acid renal calculi in the initial
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stages of uricosuric therapy for
hyperuricaemia in chronic gout: Up
to 10 g daily in divided doses, to be
taken with a liberal amount of fluid.
Elderly: Dosage adjustments may
be required.
Renal impairment: Dosage
adjustments may be required.
Hepatic impairment: Dosage
adjustments may be required.
Chronic metabolic acidosis Oral
Adult: Doses providing 57 mmol
(4.8 g sodium bicarbonate) or more
daily as required.
Elderly: Dosage adjustments may
be required.
Renal impairment: Dosage
adjustments may be required.
Hepatic impairment: Dosage
adjustments may be required.
Dyspepsia Oral
Adult: 1-5 g in water, may be takenas required.
Elderly: Dosage adjustments may
be required.
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Renal impairment: Dosage
adjustments may be required.
Hepatic impairment: Dosage
adjustments may be required.
Severe metabolic acidosis Intravenous
Adult: By slow inj of a hypertonic
solution of up to 8.4% (1000
mmol/L), or by continuous infusion
of a weaker solution, usually 1.26%
(150 mmol/L). For correction of
acidosis during advanced cardiac
life support procedures, 50 ml of an8.4% solution may be given.
Elderly: Dosage adjustments may
be required.
Renal impairment: Dosage
adjustments may be required.
Hepatic impairment: Dosage
adjustments may be required.
Drug Indication Dosage
Digitalis (Digoxin) Heart failure Oral
Adult: Rapid digitalisation: Loading
dose of 0.75-1.5 mg during the first
24-hr period as a single dose or in
divided doses every 6 hr for less
urgent or greater risk cases. For
mild heart failure: Loading dose
may not be required, 250 mcg 1-2
times daily. For patients with normal
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renal function, steady-state plasma
concentrations are usually achieved
in about 7 days. Usual
maintenance: 125-250 mcg daily
but may range from 62.5-500 mcg
daily.
Child: Neonate 2.5 kg and child 1 mth-2
yr: Initial: 45 mcg/kg/day in 3
divided doses for 24 hr, then 10
mcg/kg/day in 1-2 divided doses. 2-
5 yr: Initial: 35 mcg/kg/day in 3
divided doses for 24 hr, then 10
mcg/kg/day in 1-2 divided doses. 5-
10 yr: Initial: 25 mcg/kg/day (max:
750 mcg/day) in 3 divided doses for
24 hr, then 6 mcg/kg/day (max: 250
mcg/day) in 1-2 divided doses. 10-
18 yr: Initial: 0.75-1.5 mg/day in 3
divided doses for 24 hr, then 62.5-
750 mcg/day in 1-2 divided doses.Reduce doses if patient has been
given cardiac glycoside in the
preceding 2 wk.
Elderly: Lower doses are given.
Renal impairment: Dosage
reductions may be needed.
Supraventricular arrhythmias Oral
Adult: Rapid digitalisation: Loading
dose of 0.75-1.5 mg during the first
24-hr period as a single dose or in
divided doses every 6 hr for less
urgent or greater risk cases. For
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mild heart failure: Loading dose
may not be required, 250 mcg 1-2
times daily. For patients with normal
renal function, steady-state plasma
concentrations are usually achieved
in about 7 days. Usual
maintenance: 125-250 mcg daily
but may range from 62.5-500 mcg
daily.
Child: Neonate 2.5 kg and child 1 mth-2
yr: Initial: 45 mcg/kg/day in 3
divided doses for 24 hr, then 10
mcg/kg/day in 1-2 divided doses. 2-
5 yr: Initial: 35 mcg/kg/day in 3
divided doses for 24 hr, then 10
mcg/kg/day in 1-2 divided doses. 5-
10 yr: Initial: 25 mcg/kg/day (max:
750 mcg/day) in 3 divided doses for
24 hr, then 6 mcg/kg/day (max: 250
mcg/day) in 1-2 divided doses. 10-18 yr: Initial: 0.75-1.5 mg/day in 3
divided doses for 24 hr, then 62.5-
750 mcg/day in 1-2 divided doses.
Reduce doses if patient has been
given cardiac glycoside in the
preceding 2 wk.
Elderly: Lower doses are given.
Renal impairment: Dosage
reductions may be needed.
Emergency heart failure Intravenous
Adult: For patients who have not
received cardiac glycosides in the
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previous 2 wk. 0.5-1 mg by IV
infusion as a single dose over at
least 2 hr or in divided doses with
each dose given over 10-20
minutes. Maintenance dose is
usually given orally.
Renal impairment: Dosage
reductions may be needed.
Drug Indication Dosage
Inodilators (amrinone) Heart failure Intravenous
Adult: Loading dose: 750 mcg/kg by
slow inj over 2-3 min (may be
repeated after 30 minutes if
necessary). Maintenance: 5-10
mcg/kg/min by infusion. Max
cumulative dose: 10 mg/kg in 24 hr.
Drug Indication Dosage
Nitrates (isosorbide dinitrate) Relief of acute angina pectoris or forprophylactic management in
situations likely to provoke angina
attacks
2.5-10 mg sublingually. If relief isnot attained after a single dose
during an acute attack, additional
dose may be given at 5-10 min
interval: No more than 3 doses
should be given in a 15-30 min
period.
Long-term prophylactic
management of angina pectoris
10-20 mg tid-qid
Treatment of heart failure 5-10 mg orally tid-qid
Drug Indication Dosage
Diuretics (spironolactone) Essential HTN Adult 50-100 mg/day. Severe case:
May be gradually increased at 2-
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wkly intervals up to 200 mg/day.
CHF Adult 100 mg/day, maintenance: 25-
200 mg/day
Malignant hypertension Adjunctive therapy. Initially 100mg/day, increased as necessary at
2-wkly intervals to 400 mg/day
Edematous disorders Total daily dose may be given either
in divided doses or as single daily
dose.
V. Endotracheal Tube Preparation
The patient is placed on the operating table lying on the back with a pillow under the head. The
anesthesiologist wears gloves, a gown and goggles. General anesthesia is administered to the patient
before starting intubation.
Endotracheal Tube Insertion
y To begin the procedure, an anesthesiologist opens the patient's mouth by separating the lips and
pulling on the upper jaw with the index finger.
y Holding a laryngoscope in the left hand, he or she inserts it into the mouth of the patient with the
blade directed to the right tonsil.
y Once the right tonsil is reached, the laryngoscope is swept to the midline, keeping the tongue on
the left to bring the epiglottis into view.
y The laryngoscope blade is then advanced until it reaches the angle between the base of the
tongue and the epiglottis.
y Next, the laryngoscope is lifted upwards towards the chest and away from the nose to bring the
vocal cords into view. Often an assistant has to press on the trachea to provide a direct view of
the larynx.
y The anesthesiologist then takes the endotracheal tube, made of flexible plastic, in the right handand starts inserting it through the mouth opening. The tube is inserted through the cords to the
point that the cuff rests just below the cords.
y Finally, the cuff is inflated to provide a minimal leak when the bag is squeezed.
y Using a stethoscope, the anesthesiologist listens for breathing sounds to ensure correct
placement of the tube.
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Source: http://www.surgeryencyclopedia.com/Ce-Fi/Endotracheal-Intubation.html
SUCTIONING ENDOTRACHEAL TUBE
y Wash your hands.
Rationale: Handwashing prevents transmission of microorganisms.
y Explain procedure and purpose to client.
Rationale: Explanations reduce anxiety and encourage cooperation with procedure.
y Position the conscious client with an intact gag reflex in a semi-Fowler's position.
Rationale: The semi-Fowler's position helps prevent aspiration of secretions.
y Position the unconscious client in a side-lying position facing you.
Rationale: A side-lying position facilitates drainage of secretions by gravity and prevents aspiration.
y Turn on suction device and adjust pressure: infants and children, 50 to 75 mm Hg; adults, 100 to
120 mm Hg
Rationale: Excessive negative pressure traumatizes mucosa and can induce hypoxia.
y Open and prepare sterile suction catheter kit
Rationale: Tube occlusion tests suction apparatus; higher pressures cause excessive trauma without
enhancing secretion removal.
y Unfold sterile cup, touching only the outside. Place on bedside table.
Pour sterile saline into cup.
y Preoxygenate client with 100% oxygen. Hyperinflate with manual resuscitation bag.
Rationale: Preoxygenation helps prevent hypoxia; hyperinflation decreases atelectasis caused by
suctioning.
y Use sterile gloves. If kit provides only one glove, place on dominant hand.
Rationale: Dominant hand will remain sterile. You may use a clean disposable glove on the nondominanthand to protect yourself from exposure to mucous membranes and sputum.
y Pick up catheter with dominant hand. Pick up connecting tubing with nondominant hand. The
nondominant hand is now considered clean rather than sterile. Attach catheter to tubing without
contaminating sterile hand
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y Place catheter end into cup of saline. Test functioning of equipment by applying thumb from
nondominant hand over open port to create suction .
Rationale: Lubrication makes catheter insertion easier and ensures proper functioning of suction
equipment.
y Insert catheter into trachea through artificial airway during inspiration.
Rationale: Inspiration opens epiglottis and facilitates catheter the side of the mouth prevents
stimulation of the gag reflex.
y Advance catheter until you feel resistance. Retract catheter 1 cm before applying suction. Note:
Client usually will cough when catheter enters trachea.
Rationale: Retracting catheter slightly prevents mucosal damage.
y Apply suction by placing thumb of nondominant hand over open port. Rotate the catheter with
your dominant hand as you withdraw the catheter. This should take 5 to 10 seconds.
Rationale: Rotation of catheter prevents trauma to mucous membrane from prolonged suctioning of one
area. Limiting the suction time to 10 seconds or less prevents hypoxia.
y Hyperoxygenate and hyperinflate using manual resuscitation bag for a full minute between
subsequent suction passes. Encourage deep breathing.
Rationale: Prolonged suctioning can induce hypoxia.
y Rinse catheter and tubing by suctioning saline through.
Rationale: Rinsing clears secretions from catheter.
y Repeat Steps 10 to 14 until airway is clear, limiting each suctioning to three passes.
Without applying suction, insert the catheter gently along one side of the mouth. Advance to the
oropharynx.
Rationale: Suction the oropharynx after trachea because the mouth is less clean than the trachea.
Directing the catheter along the side of the mouth prevents stimulation of the gag reflex.
y Apply suction for 5 to 10 seconds as you rotate and withdraw catheter.
Rationale: Rotation of the catheter prevents trauma to the mucous membrane. Be sure to remove
secretions that pool beneath the tongue and in the vestibule of the mouth.
y Allow 1 to 2 minutes between passes for the client to ventilate. Encourage deep breathing.
Replace oxygen if applicable.
y Repeat Steps 16 and 17 as necessary to clear oropharynx.
y Rinse catheter and tubing by suctioning saline through.
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y Remove gloves by holding catheter with dominant hand and pulling glove off inside-out. Catheter
will remain coiled inside the glove. Pull other glove off inside-out (Fig. 8). Dispose of in trash
receptacle.
Rationale: Contain client secretions inside gloves to reduce transmission of microorganisms.
y Turn off suction device.
y Assist client to comfortable position. Offer assistance with oral and nasal hygiene. Replace
oxygen device if used.
y Wash your hands.
Source:http://downloads.lww.com/wolterskluwer_vitalstream_com/sample-
content/9780781788786_Craven/samples/mod09/topic8a/text.html
Assisting NasogastricTube Insertion
y Check physicians order for insertion of nasogastric tube.
y Explain procedure to patient.
y Gather equipment.
y If nasogastric tube is rubber, place it in a basin with ice for 5 to 10 minutes or place a plastic tube
in a basin of warm water if needed.
y Assess patients abdomen.
y Perform hand hygiene. Don disposable gloves.
y Assist patient to high Fowlers position or to 45 degrees if unable to maintain upright position and
drape his or her chest with bath towel or disposable pad. Have emesis basin and tissues handy.
y Check nares for patency by asking patient to occlude one nostril and breathe normally through
the other. Select nostril through which air passes more easily.
y Measure distance to insert the tube by placing tip of tube at patients nostril and extending to tip
of earlobe and then to tip of xiphoid process. Mark tube with a piece of tape.
y Lubricate tip of tube (at least 1-2 inches) with water-soluble lubricant. Apply topical analgesic to
nostril and oropharynx or ask patient to hold ice chips in his or her mouth for several minutes
(according to physicians preference).
y After having the patient lift his or her head, insert tube into nostril while directing tube downward
and backward. Patient may gag when tube reaches the pharynx.
y Instruct patient to touch his or her chin to chest. Encourage him or her to swallow ever if no fluids
are permitted. Advance tube in a downward-and-backward direction when patient swallows. Stop
when patient breathes. Provide tissues for tearing or watering eyes. If gagging and coughing
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persist, check placement of tube with a tongue blade and flashlight. Keep advancing tube until
tape marking is reached. Do not use force. Rotate tube if it meets resistance.
y Discontinue procedure and remove tube if there are signs of distress, such as gasping, coughing,
cyanosis, and inability to speak or hum.
y Determine that tube is in patients stomach. Hold tube in place to keep it from withdrawing while
placement is checked.
VI. Recovery Position
HOW TO MOVE A BABY INTO THE RECOVERY POSITION
1. Understand that an infant is anyone under the age of 1.
For victims over the age of 1, use the adult recovery
position described in Section 1. Do not use this on anyone
under 1. Death could result.
2. Hold the infant stomach down on your forearm so that
his head is cradled in the palm of your hand.
3. Tilt the infant so that his head is slightly lower than his
buttocks to prevent choking.
4. Keep the infant's mouth and nose clear of fluids until
help arrives.
HOW TO MOVE ACHILD INTO THE RECOVERY POSITION
1. Kneel beside the child. Remove glasses and anybulky objects from the pockets. Ensure the airway isopen by lifting the chin and tilting the head. Make sureboth legs are straight, then place the arm nearest toyou to straight out from the childs body, with the elbowbent and the palm placing upward.
2. Bring the arm furthest away from you across thechilds chest and hold the back of the hand against the
cheek nearest you.
3. With your other hand, grasp the childs far leg justabove the knee and pull it up, keeping the foot flat onthe ground.
4. Keeping the childs hand pressed against her cheek,pull on the far leg and roll the child toward you and to
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her side. Adjust the upper leg so that both the hip and knee are bent in right angles.
5. Tilt the head back so that the airway remains open. If necessary, adjust the hand under the
cheek to make sure the childs head remains tilted and the airways stays open. Call for
emergency help if this has not already been done. Check the breathing regularly, and check the
lower arm for any loss of color or warmth. If it turns white or blue, or if it becomes cold, gently
move it until the color or warmth returns.
HOW TO MOVE AN ADULT INTO THE RECOVERY POSITION
1. Kneel beside the victim. Remove glasses and any bulky objects from the pockets. Ensure the
airway is open by lifting the chin and tilting the head. Make sure both legs are straight, then place
the arm nearest to you straight from the victims
body, with the palm facing upward.
2. Bring the arm furthest away from you across
the victims chest and hold the back of the hand
against the cheek nearest to you.
3. With your other hand, grasp the far leg just
above the knee and pull it up, keeping the foot flat
on the ground.
4. Keeping the victims hand pressed against his
or her cheek, pull on the far leg and roll the victim
toward you and on to his or her side. Adjust the
upper leg so that both the hip and knee are bent
at right angles.
5. Tilt the head back so that the airway remains open. If necessary, adjust the hand under the
cheek to make sure the victims head remains tilted and the airways stays open. Call for
emergency help if this has not already been done. Check the breathing regularly, and check the
lower arm for any loss of color or warmth. If it turns white or blue, or if it gets cold gently move it
until the color or warmth returns.
SOURCES:
y http://www.womensheart.org/content/Stroke/pulse_check.asp
y https://www.erc.edu/forum/index.php?showtopic=868
y http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-19
y http://www.youtube.com/watch?v=2n3ahmJzH_E
y http://en.wikipedia.org/wiki/Advanced_cardiac_life_support
y http://www.actnt.com/images/2005%20guidelines/Algorithms/ACLS/ACLS%20Pulseless%20Arre
st%20algorithm.pdf
y http://nursingcrib.com/demo-checklist/inserting-a-nasogastric-tube/
y http://www.ehow.com/how_2089839_use-recovery-position.htmly http://www.firstaid.ph/first-aid-techniques/the-recovery-position-for-children-and-babies.html
y http://www.firstaid.ph/first-aid-techniques/the-recovery-position-for-adults.html
y http://www.fpnotebook.com/cv/EKG/PrmtrAtrlCntrctn.htm
y http://www.fpnotebook.com/cv/EKG/AtrlFbrltn.htm
y http://www.wisegeek.com/what-is-atrial-tachycardia.htm
y http://www.emedicinehealth.com/atrial_flutter/article_em.htm#Atrial Flutter Overview
y http://emedicine.medscape.com/article/158243-overview
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y http://www.nhlbi.nih.gov/health/dci/Diseases/hb/hb_types.html
y http://medical-dictionary.thefreedictionary.com/cricoid+pressure
y http://www.nursingtimes.net/nursing-practice-clinical-research/cricoid-pressure/201259.article
y http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-19
y http://docs.google.com/viewer?a=v&q=cache:xsl1o7M-Ol0J:www.starcpr.com/blsalgorithm.pdf+basic+life+support+algorithm&hl=en&gl=ph&pid=bl&srcid
=ADGEEShw3WZuGo1cFDM4KL4bR7jItyBjhTcnHO_bCKCCh-mBN-pkaPzWII7DKCJWRRrtxbEVGVPLCHk8ofi3cc_6rKXV8-T8CYHTBLKg89yt69z-GOObEwmZ1q1pxXnQ25SXmZi5dgK-&sig=AHIEtbTTSCLyqLDSYQpcoyg8PQ4iAO89Hw
y http://en.wikipedia.org/wiki/Basic_life_support
y http://www.annemergmed.com/article/S0196-0644%2897%2970114-8/abstract
y http://www.ncbi.nlm.nih.gov/pubmed/11719120
y http://richardang0418.blogspot.com/2009_07_01_archive.html
y http://www.google.com.ph/imglanding?q=accelerated+junctional+rhythm&um=1&hl=en&biw=102
4&bih=673&tbs=isch:1&tbnid=BUVBBZZV1B8
y http://www.google.com.ph/imglanding?q=accelerated+idioventricular+rhythm&um=1&hl=en&biw=
1024&bih=673&tbs=isch:1&tbnid=NXSOc6l89
y http://www.fpnotebook.com/cv/EKG/PrmtrVntrclrCntrctn.htm
y http://www.google.com.ph/imglanding?q=junctional+tachycardia&um=1&hl=en&biw=1024&bih=673&tbs=isch:1&tbnid=b1ryUWm_xjIzhM:&imgrefurl=ht
y http://www.google.com.ph/imglanding?q=PVC+trigeminy&um=1&hl=en&biw=1024&bih=673&tbs=
isch:1&tbnid=kZDgRHC__Ff8PM:&imgrefurl=http://emedicine.medscape.com/article/158939-
media&imgurl=http://img.medscape.com/pi/emed/ckb/cardiology/150072-158939-
4351.jpg&zoom=1&w=960&h=140&ei=gvjdTJ_8KsWXcdmP0ZcM&iact=hc&oei=EfjdTMzRJoHyv
wOf2qXIDg&esq=6&page=3&tbnh=38&tbnw=263&start=32&ndsp=17&ved=1t:429,r:0,s:32
y http://www.google.com.ph/imglanding?q=PVC+couplet&um=1&hl=en&biw=1024&bih=673&tbs=is
ch:1&tbnid=IJyBskYPzesryM:&imgrefurl=http://physchem.ox.ac.uk/~wayne/ECG%252520etc/Mar
k%252520Hammerschmidt%252520-
%252520Arrythmia%252520FAQ.htm&imgurl=http://rpw.chem.ox.ac.uk/ECG%252520etc/Mark%
252520Hammerschmidt%252520-
%252520Arrythmia%252520FAQ_files/fig24.gif&zoom=1&w=378&h=73&iact=hc&ei=r_jdTKvaBo
HuvQO9v53WDg&oei=r_jdTKvaBoHuvQO9v53WDg&esq=1&page=1&tbnh=34&tbnw=176&start
=0&ndsp=20&ved=1t:429,r:13,s:0
y http://www.skillstat.com/Flash/ECGSim531.html
y http://library.med.utah.edu/kw/ecg/ecg_outline/Lesson2/index.html
y https://reader009.{domain}/reader009/html5/0520/5b00804f1e256/5b00807188ad2.jpgy http://knol.google.com/k/atrial-fibrillation#
y http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/images/sinus_rhythm.gif
y http://sprojects.mmi.mcgill.ca/cardiophysio/NormalEKG.htm
y http://www.preventing-a-heart-attack.com/images/SinusRhythmLabels.jpg
y http://static.howstuffworks.com/gif/adam/images/en/19195-normal-sinus-rhythm-picture.jpg
y http://www.bem.fi/book/19/fi/1902a.gif
y http://www.ambulancetechnicianstudy.co.uk/images/NSR.gif
E-book:
y Morris Francis Brady William J Camm John (2008) ABC of Clinical Electrocardiography 2nd