Cardiopulmonary Resuscitation ABNET

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CPR AND CARDIOVERSION

Getnet Amberber(MD)
Amir Adem(MD)
 INTRODUCTION:-
- CPR developed in the late 1950s and 1960s
-Elam and Safar described the technique and benefits of
mouth-to-mouth ventilation in 1958
-Kouwenhoven, Knickerbocker, and Jude
subsequently described the benefits of external chest
compressions.
-External defibrillation, first described in 1957 by
Kouwenhoven ,since then it has been incorporated into
resuscitation guidelines.
2006 AHA defn
 Sudden cardiac arrest is the sudden cessation of cardiac activity so that the victim
becomes
 unresponsive,
 with no normal breathing and
 no signs of circulation.
 that is reversed, usually by CPR and/or defibrillation or cardioversion, or cardiac
pacing.
 If corrective measures are not taken rapidly, this condition progresses to sudden
death. Sudden cardiac death should not be used to describe events that are not
fatal.
 Cardiovascular collapse-a sudden loss of effective blood flow due to cardiac
&/or peripheral vascular factors which may reverse spontaneously(e.g.,
neurocardiogenic syncope; vasovagal syncope) or only with intervention(e.g.,
cardiac arrest)

 Sudden Cardiac Arrest can strike anyone, anytime, anywhere...


 Sudden cardiac death (SCD) is defined as natural death due to cardiac
causes in a person who may or may not have previously recognized
heart disease but in whom the time and mode of death are unexpected.
The term “sudden,” in the context of SCD, is defined for most clinical
and epidemiologic purposes as 1 h or less between a change in clinical status
heralding the onset of the terminal clinical event and the cardiac arrest itself.
One exception is unwitnessed deaths, in which pathologists may expand the
temporal definition to 24 h after the victim was last seen to be alive and
stable
 Biological death may be delayed by interventions, but the relevant
pathophysiologic event remains the sudden and unexpected cardiac
arrest. Accordingly, for statistical purposes, deaths that occur during
hospitalization or within 30 days after resuscitated cardiac arrest are
counted as sudden deaths
Sudden Cardiac Arrest
A Heart in Distress

 Uncoordinated, very fast heart rhythm


 Ventricular fibrillation (VF)
 Some ventricular tachycardias (VT)
 Ineffective heart pump
 Unconscious, no breathing, no pulse
 Death certain without defibrillation
 In the past, the most common electrical mechanism for cardiac
arrest was ventricular fibrillation (VF) or pulseless sustained ventricular
tachycardia (PVT). These were the initial rhythms recorded
in 60–80% of cardiac arrests, with VF being the far more common of
the two. Severe persistent bradyarrhythmias, asystole, and pulseless
electrical activity (PEA; organized electrical activity, unusually slow,
without mechanical response, formerly called electromechanical
dissociation [EMD]) caused another 20–30%. Currently, asystole has
emerged as the most common mechanism recorded at initial contact
(45–50% of cases). PEA accounts for 20–25%, and VF is now present
on initial contact in 25–35%. Undoubtedly, a significant proportion
of the asystole cases began as VF and deteriorated to asystole because
of long response times, but there are data suggesting an absolute
reduction in VF as well.
Up to 80% of all SCDs in the United States are due to the consequences of
coronary atherosclerosis. The nonischemic cardiomyopathies (dilated and
hypertrophic, collectively; account for another 10–15% of SCDs, and all the
remaining diverse etiologies cause only 5–10% of all SCDs.
The inherited arrhythmia syndromes (see above and Table 327-2) are
proportionally more common causes in adolescents and young adults.
For some of these syndromes, such as hypertrophic cardiomyopathy, the risk
of SCD increases significantly after the onset of
puberty
As many as 70–75% of males
who die suddenly have preexisting healed MIs, whereas only 20–30%
have recent acute MIs, despite the prevalence of unstable plaques and
thrombi. The latter suggests transient ischemia as the mechanism of
onset. Regional or global left ventricular (LV) hypertrophy often coexists with
prior MIs
 The most powerful long-term risk factors include age, cigarette
smoking, elevated serum cholesterol, diabetes mellitus, elevated
blood pressure, LV hypertrophy, and nonspecific
electrocardiographic abnormalities. Markers of inflammation
(e.g., levels of C-reactive protein) that may predict plaque
destabilization have been added to risk classifications. The presence
of multiple risk factors progressively increases incidence, but not
sufficiently or specifically enough to warrant therapies targeted to
potentially fatal arrhythmias
 When the mechanism is pulseless VT, the outcome is best; VF is the
next most successful; and asystole an PEA, now the most common
mechanisms, generate dismal outcome statistics. Advanced age also
adversely influences the chances of successful resuscitation
 Death during the hospitalization after a successfully resuscitated
cardiac arrest relates closely to the severity of central nervous system
injury. Anoxic encephalopathy and infections subsequent to prolonged
respirator dependence account for 60% of the deaths. Another 30%
occur as a consequence of low cardiac output states that fail to
respond to interventions. Recurrent arrhythmias are the least common
cause of death, accounting for only 10% of in-hospital deaths
 Primary cardiac arrests are those that occur in the absence of
hemodynamic instability, and secondary cardiac arrests are those that
occur in patients in whom abnormal hemodynamics dominate the clinical
picture before cardiac arrest. The success rate for immediate resuscitation
in primary cardiac arrest during acute MI in a monitored setting should
exceed 90%. In contrast, as many as 70% of patients with secondary
cardiac arrest succumb immediately or during the same hospitalization.
An individual who collapses suddenly is managed in five stages:
(1) initial evaluation and basic life support if cardiac arrest is confirmed,
(2) public access defibrillation (when available), (3) advanced life
support, (4) postresuscitation care, and (5) long-term management.
The initial response, including confirmation of loss of circulation,
followed by basic life support and public access defibrillation, can
be carried out by
  SCA
usually occurs in people with some form of
underlying- structural heart disease. 
 70 % of SCAs have been attributed to CHD.

-Functional Contributing Factors


 EPIDEMIOLOGY
-Sudden cardiac arrest (SCA) -the 2nd
leading cause of death in both the United
States and Canada.
- 400,000 to 460,000 people in the United States
and 700,000 people in Europe, suffer SCA each
year.
-Risk factors include: old age ,male sex ,
Cigarette smoking,increased FFA, heavy
alchol use , increased serumCRP, family
history of SCA,stress, ?caffin use
It is estimated that more than 95% of sudden cardiac arrest victims die before
reaching a hospital, resulting in approximately 250,000 deaths each year in the U.S.
That's three lives every seven minutes - over 600 people a day! However, when all four
links of the Chain of Survival (which is a globally endorsed response model developed
by the American Heart Association) are strong, survival rates for victims of SCA can rise
from 5% to as high as 49%.
SCD risk
Eelectrical mechanism responsible for
cardiac arrest

50–80% of cardiac arrests-VF and VT


20–30%.
Severe persistent bradyarrhythmias,
asystole, and
pulseless electrical activity
-Symptoms of cardiac arrest

- absence of pulse on carotid arteries – a


pathognomonic symptom
- respiration arrest – may be in 30 seconds
after cardiac arrest
-enlargement of pupils – may be in 90
seconds after cardiac arrest
 Phases of resuscitation-
- Many researchers in resuscitation now consider
there to be three distinct phases of cardiac
arrest:
1.the electrical phase:- defined as the first 4-5
minutes of arrest due to ventricular fibrillation (VF)
- Immediate DC cardioversion is needed to optimize
survival of these patients.
2.the hemodynamic phase – consists of the
period from 4 to 10 minutes after sudden cardiac
arrest during which the patient may remain in VF
- evidence reveals that patients with low amplitude fibrillation,
due to prolonged pulselessness, may benefit from well-
performed CPR to generate adequate cerebral and
coronary perfusion, prior to initial attempts at
defibrillation.
3. metabolic phase- defined as >10 minutes of
pulselessness,
-Tx stresses post resuscitative measures,
including hypothermia therapy. If not quickly
converted into a perfusing rhythm, patients in
this phase generally do not survive.
- Resuscitation attempted in up to two-thirds of people who
sustain SCA, survival rates remain low.
- The outcome of an emergency situation and survival of the
patient are critically dependent up on the 1st few minutes of
care
- Assessments of survival from SCA have reached widely
disparate conclusions.
*In the out-of-hospital setting, studies have reported survival
rates of 1 to 6 percent.
*An analysis of a national registry of in-hospital SCA reported
a 17 percent survival to discharge .
The individual who collapses
suddenly is managed in five stages

 (1) initial assessment and summoning an


emergency response team;
 (2) basic life support (BLS);
 (3) early defibrillation by a first responder (if
available);
 (4) advanced life support; and
 (5) post-cardiac arrest care.
-Basic CPR : CPR that using “ chest wall
compression” and “ventilation”

-Advanced CPR (or ACLS) :


“basic CPR” plus advanced airway
management, defibrillation, & medications.
 If 5 min has elapsed between collapse and first contact with the
victim,there is some evidence that 60–90 s of CPR before the first
shock may improve probability of survival without neurologic
damage. If the initial shock does not successfully revert VT or VF,
chest compression at a rate of 100 per minute is resumed for 2 min
 ADVANCED CARDIAC LIFE SUPPORT (ACLS)
ACLS is intended to achieve and maintain organ perfusion and
adequate ventilation, control cardiac arrhythmias, and stabilize
blood pressure and cardiac output. The activities carried out to
achieve these goals include (1) defibrillation/cardioversion and/or
pacing, (2) intubation with an endotracheal tube, and (3) insertion
of an intravenous line
 As in basic life support, the major emphasis during ACLS is minimizing
interruptions of chest compressions until ROSC is achieved.
After two or three unsuccessful defibrillation attempts, epinephrine, 1 mg IV, is
given and attempts to defibrillate are repeated.
The dose of epinephrine may be repeated after intervals of 3–5 min. Vasopressin
(a single 40-unit dose given IV) has been
suggested as an alternative to epinephrine
 If the patient is less than fully conscious upon reversion or if two
or three attempts fail, prompt intubation, ventilation, and arterial
blood gas analysis should be carried out. Ventilation with O2 (room
air if O 2 is not immediately available) may promptly reverse hypoxemia and
acidosis. Quantitative waveform capnography is now recommended for
confirmation and monitoring of endotracheal tube
placement. A patient who is persistently acidotic after successful
defibrillation and intubation or had acidosis prior to arrest
 The four components of post-cardiac arrest syndrome include brain
injury, myocardial dysfunction, systemic ischemia/reperfusion
responses, and control of persistent precipitating factors. The
therapeutic goal is to maintain a stable electrical, hemodynamic, and
central nervous system status
 Mild therapeutic hypothermia is indicated
for resuscitated cardiac arrest victims who are hemodynamically
stable, but remain comatose. Core body temperature is decreased
to 32–34°C, by several available techniques (external and/or internal
[core]), as soon as practical after resuscitation and maintained for a
minimum of 12–24 h. By reducing metabolic demands and cerebral
edema, this intervention improves probability of survival with better
neurologic outcome
1.Basic life support

 Intended to maintain organ perfusion until definitive


intervention can be done.
 Rapid assessment for injury and responsiveness
 Head & neck trauma must be checked and pt handled
carefully if any.
• Activate EMS
• involves –air way mgmt
-breathing
-and circulation
-(defibrillation)
Airways

 Check spontaneous respiration


 Remove any visible foreign material or
vomitus.
 Head tilt –chin lift maneuver
 Jaw thrust maneuver
A (Airway)

Open the airway using a head


tilt lifting of chin. Do not tilt
the head too far back
the Heimlich maneuver,
Breathing
 Once air way is open breathing should be checked.
 Absent/insufficient respiration-absence of chest
rising and falling & no air being exhaled2 rescue
breaths given and check circulation
 Rescue breathing should be continued at 8-10/min
if adequate circulation exists.
 Chest compression should be started
immediately if circulation is absent or insufficient
 Different modalities of breathing
-Mouth to mouth
-Mouth to nose breathing
-Bag to mouth breathing
- plastic oropharyngeal airways, esophageal obturators,
masked Ambu bag
 CXNs of rescue breathing
-Gastric inflation
-Over ventilation-intrathoracic
pressurecoronary perfusion.
Circulation

 Palpation of carotid pulse is the gold standard.


( 10 seconds )
 Chest compressions should be done by
serial ,rhythmic and continuous application of
pressure over the lower half of the sternum.
 “ push hard , fast and allow adequate recoil “
 100comp/min recommended.
 The sternum should be compressed 4-5cm.
(AHA 1.5 -2 inchs)
Effective chest compression can produce arterial BP peaks of
60-80 mmhg

Idris, A. H. et al. Circulation 1996;94:2324-2336

Copyright ©1996 American Heart Association


Proper position
Emphasis on chest compressions

 Chest compressions are the most important part


of CPR
 During the initial phase of cardiac arrest when the
pulmonary vessels and heart likely contain
sufficient oxygenated blood to meet
markedly reduced demands, the importance of
compressions supersedes ventilations
 CCR vs CPR (flow is more important than content)

 Particularly early in cardiac arrest (the first 4-6


minutes)
Compression ventilation ratio (AHA)

  In all but infants and children, cardiopulmonary


resuscitation (CPR) should be performed at a rate of 100
compressions per minute with a ratio of 30
compressions to 2 ventilations until an advanced
airway has been placed.
 Following placement of an advanced airway (eg,
endotracheal tube), compressions are continuous, and
asynchronous ventilations are delivered 8 to 10
times per minute.
 In the infant or child, the healthcare provider should use
a ratio of 15 compressions to 2 ventilations
 Interruptions in compressions, no matter how brief, result in
unacceptable declines in coronary perfusion pressures and worse
outcomes
- Circulation. 2001 Nov 13;104(20):2465-70
 Rescuers must ensure that chest compressions are provided
continuously during CPR.
 When a single rescuer is providing CPR-chest compressions
should be performed continuously, without stopping to
provide ventilations. (not yet part of the AHA guidelines )
because ventilation may be important for resuscitation of
hypoxic arrest victims (eg, infants, children, and drug overdoses)
and later (after the first few minutes) in the course of any arrest.
 providers should perform five cycles of CPR over two minutes
prior to defibrillation for patients with unwitnessed cardiac arrest
whose arrest time is thought to exceed five minutes.
 Avoid operator fatigue
Alternative CPR Techniques
-Over the past 25 years a variety of alternatives to standard
manual CPR have been developed
-Compared with standard CPR, these techniques and devices
typically require more personnel, training, or equipment, or
they apply to a specific setting.
-Maximum benefits are reported when adjuncts are begun
early in the treatment of cardiac arrest, so that the use of these
alternatives to CPR is often limited to the hospital setting.
-To date no adjunct has consistently been shown to be
superior to standard manual CPR for out-of-hospital basic life
support, and no device other than a defibrillator has
consistently improved long-term survival from out-of-hospital
cardiac arrest.
Interposed Abdominal Compression
CPR (IAC-CPR)
 Abdomen compressed between xiphoid and umbilicus during
relaxation phase of chest compression(another rescuer)
 Increases forward blood flow during CPR and appears to
improve survival
 The 2005 ACLS Guidelines do not recommend the technique
 High-Frequency Chest Compressions
 High-frequency (>100 per minute) manual or
mechanical chest compressions

 The use of high-frequency chest compressions for


cardiac arrest by adequately trained rescue personnel
can be considered, but there is insufficient evidence
to recommend for or against its use.
 Open-Chest CPR
should be considered for patients with
 cardiac arrest in the early postoperative period after
cardiothoracic surgery or
 when the chest or abdomen is already open (eg, in
trauma surgery).
 "Cough" CPR
-repeated coughing every 1 to 3 seconds during
episodes of VF or rapid VT by conscious, supine,
monitored patients trained in the technique can
maintain a mean arterial pressure >100 mm Hg and
can maintain consciousness for up to 90 seconds.
-The increase in intrathoracic pressure that occurs
with coughing generates blood flow to the brain and
helps maintain consciousness.
-is not useful for the treatment of an unresponsive
victim
-should not be taught to lay rescuers
CPR Devices-
A variety of CPR techniques and devices may improve hemodynamics or
short-term survival when used by well-trained providers in selected patients.
To date no adjunct has consistently been shown to be superior to
standard manual CPR for out-of-hospital basic life support, and no device
other than a defibrillator has consistently improved long-term survival from
out-of-hospital cardiac arrest.
1. Devices to Assist Ventilation
Automatic transport ventilators (ATVs).
Manually triggered, oxygen-powered, flow-limited resuscitators.
2.Devices to Support Circulation
Active Compression-Decompression CPR
Impedance Threshold Device
Mechanical Piston Device
Load-Distributing Band CPR or Vest CPR
Phased Thoracic-Abdominal Compression-Decompression CPR With a Hand-
Held Device
Inspiratory Impedance Threshold
Valve (ITV)

 Concept: Lower intra thoracic pressure in the chest during the


decompression phase of CPR enhances venous return to the thorax.
 The ITD permits positive pressure ventilation and exhalation but
prevents the flow of air into the patient's airway during chest wall
relaxation

 Design: Each time the chest wall recoils following


a compression, the ITV transiently blocks
air/oxygen from entering the lungs, creating a
small vacuum in the chest.
 The 2005 ACLS Guidelines recommend the use of
ITDs.
Complications of Chest compression

 Rib fracture
 Hemopneumothorax
 Lung contusion
 Laceration of the liver and spleen
 Inadequate chest compression
Summary-BLS algorithm
Cont…
The probability of achieving successful
resuscitation from cardiac arrest is related to

 the interval from onset to institution of resuscitative efforts


 the setting in which the event occurss(icu vs out of hospital
setting)
 the mechanism ( best out come VT=>VF=>Asystol
=>pulseless electrical activity)
 clinical status of the patient prior to the cardiac arrest
acute cardiac event or transient metabolic disturbance
have better out come than far-advanced chronic
cardiac disease or advanced noncardiac diseases (e.g.,
renal failure, pneumonia, sepsis, diabetes, cancer)
references
 Uptodate 16.3
 Harrisons principles of int medicine 17th ed
 Braunwald's Heart Disease: A Textbook of Cardiovascular
Medicine, 8th ed.
 2005 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care

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