ccmc er portfolio

8/7/2019 CCMC ER Portfolio

1/47

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%.


2/47

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.


3/47

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


4/47

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


5/47

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.


6/47


7/47

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


8/47

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


9/47

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


10/47

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


11/47

- 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


12/47

- 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.


13/47


14/47

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


15/47

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


16/47

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


17/47

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)


18/47

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


19/47

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


20/47

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


21/47


22/47

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


23/47

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.


24/47

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.


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


25/47

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.


Emergency treatment ofventricular arrhythmias

Intramuscular Adult: As hydrochloride: 300 mginjected into the deltoid muscle,repeat after 60-90 minutes ifnecessary.


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.



26/47


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.


Renal impairment: Dosagereduction or increase in dosing

intervals 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


27/47

recommended.

Max Dosage: Adult: 1 g.

Renal impairment: Dosagereduction or increase in dosingintervals 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.


Max Dosage: Adult: 1 g.

Renal impairment: Dosage

reduction or increase in dosingintervals is recommended.



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


28/47

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.


29/47


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;


30/47

CrCl(ml/min)

DosageRecommendation

30-60 Halve the usual dose.

10-30 Quarter the usual dose.


31/47

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.


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.


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


32/47


33/47

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


34/47

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.


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.


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


35/47

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.


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.


adjustments may be necessary.


Sodium bicarbonate Urine alkalinisation Oral

Adult: To prevent development of

uric-acid renal calculi in the initial


36/47

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.


adjustments may be required.



Chronic metabolic acidosis Oral

Adult: Doses providing 57 mmol

(4.8 g sodium bicarbonate) or more

daily as required.


be required.





Dyspepsia Oral

Adult: 1-5 g in water, may be takenas required.


be required.


37/47





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.


be required.






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


38/47

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



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.


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


39/47

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



5 yr: Initial: 35 mcg/kg/day in 3



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.



Emergency heart failure Intravenous

Adult: For patients who have not

received cardiac glycosides in the


40/47

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.




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.


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


Diuretics (spironolactone) Essential HTN Adult 50-100 mg/day. Severe case:

May be gradually increased at 2-


41/47

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.


42/47

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


43/47

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.


44/47

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


45/47

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


46/47

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


47/47

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

ccmc er portfolio

Documents