1.What is preagony, terminal panse and agony?

Preagony is the mi|ifl|n.\l:\gc of dying characterised! by

severe yetreversible CNS, respiratory
and circulation disorders. This period is also accor mpanied by gradual inhibition of consciousness
and reflees, respiratory dys}unclnm (superficial
1 achypnoe or bradypnoe), hypotension and
severe
micn fon failure, which results in liml suggilations and progressive cyanosis. Preagony can
be missing if dying fast (electric injury) or slowly (bleeding).
Terminal pause is a transition period between preagony and agony, characterised
by acute
inhibition of reflexes, femporary apnoe, critical hypotension, bradycardia, further inhibition of
brain cortex andits loss of functional regulation. It’s a period of so-called “mess™ beacause upper
brain structures fail to control the vital functions and the brainstem hasn't overtaken these functions
yet. At this very moment vagus innervation is temporarily increased, which leads to apnoe and
bradycardya.
Agony is the last flash of life, characterized by short-term activation of all brain structu
res,
aimed at fighting the inhibition of the vital funcions. Apnoe period is usually followed by bradypnoe
and then tachypnoe wit the huse of additional muscles. Gasping may as well be observed (agonal
breathing pattern: brlef inspiration and expiration). This is usually followed by tachycardia and
hypertension. Such activation may result in resumption of reflectory activity and sometimes even in
the gain of consciousness. However, further inhibitions of reflexes, respiration and hemodynamics
Jeads to clinical death.

2. What is clinical death?

Clinical death is defined as the cessation of all vital functions of the body including
circulation, respiration and brain activity.

Primary (main) signs of clinical death

1. Cessation of respiration — no chest rise
2. Cessation of circulation — no pulse at magistral (carotid or femoral) arteries.

N.B.
Do not take pulse at a wrist (possible radial artery spasm with preserved cardiac pumping
function).
A rescuer can also be misled by his own finger pulsation.

3. Midriasis (pupil dilation) and negative pupillary light reflex (1 minute after cessation of
circulation).
4. Loss of consciousness.

Fig. 1. Dilated pupil 4

Negative puppilary light reflex (on the lefi) and positive pupillary light reflex (on the right)
 al death
it in nn l) si gns of clinic
ld
Secondany \m
1. Atony .
2. Areflexia ra ti on (earthy or marble-like colour,
cyanosis)
sc ol ou
% Skin di
nic seizures.
1. Clonic and to
ath signs P
postmortem lividity)
Biological de mea (also known as suggilation oror post
« dry co S S
(alsO n
« livor mortis fig’;oa hour afye
n, e na pe of th e ne ck an d in 6-12 hours all l)vcf‘l’
ssatio«n rigofor cimor io
at - app
rcultis st
fire on th T
l ante buer
dimp r)ureandandspre
laat } the bog y
edt yh
all UVgy
s ty,
humadidi
cadaver od.our - dears an pends don hothe afievirrodenmatenh ta(m
ur en
& » oUally appearg
ath
2 days after the de
)
causes of clinical death?
73, WhatCliare thsibisle@ pot
nicalthedeapos entially reversible state, which starts with cessation of
functions
e chan ges deve lop in the brai n cortex. In other words it‘,'s'lzl
and lasts until irreve
rsibl period of
tality during the state of anoxia) (oxygen concentration in brain tjissue is
reserved neurons Vil .
ute).
depleted within 1 min th is observed on the 4-5 minute afier
Under normal temperature environment the brain dea
oth
cessation of circulation. In spite of l_he ‘fac( efforts are only
changes when
that irreversible justifi ed there alli5°( er organg
in almost
resusci tation
tissues take place much later, primarily the function of brain corte: a chance
of
restoring all body organs normal functions and is limited to 4-5 minutes. Ifa patiemx' Therefore,
clinical death duration (under normal conditions) reduced and irreversible changes mkwas €xposed
erably
to hypoxia, clinical death duration is consid duration is reduced me]pzlac‘f much
clinical death
sooner. If a patient was exposed to hyperthermia, time
place at the ~ Mioutes,
of patient’s well-being or ext P:Sure
In contrast, if blood cessation took to cold,
10-12 minutes. If a patient was exposed
clinical death duration is prolonged to 0 hyperthermia,
1-2 minutes.
clinical death duration is reduced to
IfCPR starts within 5 minutes since cessation of circulation and resulted i
e Chaqces
functions wei:ihl:ult(%sp, nbiu;o]
are that a patient will make a complete recovery of upperthecortex
gain of consciousness wi{l "glcal
If CPR starts 10 minutes after clinica l death, is WSSil(;u o;:';’,
defects. after — resump tion of vegeta tive functio ns
by neurological disorders, 15 minutes
(decerebration)
(decortication ), 20 minutes after— total brain death, including brainstem
4. What is resuscitation & CPR?
Resuscitation is aimed at restoring and maintaining vital body functions.

1 stage —-BLS- basic life support (C-A-B algorithm)

Compveu‘om Alrwqy
Fig. 2. Basic life support (C-A-B algorithm)
C. Circulation - close g
yrrice /’”":l:::'l;y c;};::td-chcst cardiac massage (chest compressions)
if avalilable)
: Airway - restore nl’l’dmn'l'gil:llll::i':e and use defibri[lular/AED
- Breathing - artificial n:spiru(infla‘ency of the airways

2
 11 stage — effective ALS — advanced life support — starts when resuscitation
team a s
Ihe primary
ALS
objective is the ROSC (return of spontancous circulation) e
includes ¢ lnwaI-Llwcl cardiac massage, defibrillation drugs and fluid infusions, manual
or automatic respirators for mechanical ventilation, ECG-ver | cessation of circulation. =
Resuscitation efforts sho_uld be delivered in a fast tempo (effective closed-chest cardiac massage
ensures 30% of the cardiac output only). Afier the return of spontaneous circulation 'h’c pzticn‘lgia
admitted to 1CU
Integrated post-cardiac arrest care (cerehral resuscitation) — treatment of postresuscitation
dises e in patients with successful CPR — evaluate the patient (define the causes of clinical death.
reVe S l("(;nd;‘\r)‘ clinical death), take measures to restore brain functions and other
organs affected
cal death

5. What are the Key principles of BLS?

» The ERC and AHA Guidelines to CPR (2015) summarize key changes, additions and
specifications as \vcll as interpretation of up-to-date CPR practice:
« change in the BLS sequence of steps from A-B-C (airway - breathing- chest
compression) to C-A-B
« chest con!pmssion rate — 100-120 per minute
« compression depth ofat least 2 inches (5-6 cm) and approximately 1.5 inches (4 cm) in
newborns
» allow for complete chest recoil after each compression
+ minimizing interruptions in chest compressions
« avoid excessive ventilation
« recommended “compression to ventilation” ratio of 30:2
- give 1 rescue breath every 6-8 seconds (approximately 8-10 breaths per minute)
« recommended rescue breath volume - 6 ml/kg of BW
« recommended rescue breath duration 1 sec
« after intubation of trachea perform continuous chest compression rate at least 100 per
minute without giving rescue breaths
« each rescue breath should be followed by visible chest rise
« recommended ways of drug injection - intravenous and intraosseous (into proximal tibial
epiphysis with the help of special automatic , Bone gun” injector)
« atropine excluded from ALS irrespective of the causes of circulation cessation
« teamwork approach to CPR.

6. What is the closed-chest cardiac massage technique?

Quality and rate of chest compressions play a key role inthe ROSC and survival with preserved
cortex function. To ensure high-quality closed-chest cardiac massage follow the guidelines:
« take a side position
« find the pressure point over the middle of the chest
« locate the correct hand position by placing the heel of supporting hand on the person’s
sternum (breastbone) at the center of his or her chest
« place your other hand directly on top of the first so that they overlap and the leading hand
is on to|
“try to kel:ep your fingers off of the chest by interlacing them (“lock™) or holding them
upward
« the spot for compressions — middle third of stermum
« compression depth of at least 2 inches (5 cm)
« chest compression rate — 100-120 per minute
« after each compression relax pressure on the sternum completely
+ do not remove your hands from the person’s sternum, but do allow the chest to return to
its normal position between compressions (complete chest recoil)
« bring your shoulders directly over the person’s sternum, then press downward, keeping
your arms straight (using your BW) .
+ relaxation and compression should be of equal duration
+ avoid interruptions in chest compressions (to prevent stoppage of blood flow).
« change rescuers for chest compressions every 2 minutes; ‘ :
« monitoring the efficacy ofcardiac massage - check the pulse at the magistral arteries
(carotid, femoral) simultaneously with chest compressions. 3
 & contrain
ations cas dications,dins arres
pre cor dia l th um p? Indici cat ed in e of unv eri fie! d carardi
7. What is 8 I i tra ir adi sl
ul
i
ump 1n
th
n con
€¢ ndi t
ts
1
-ve;rif :}c,d Ouitside ¢ it
n(dial]v,\\u\nh:fl thump 15 mdu.llull patien with EC
““‘cor
||.'h"pre
: ; olivein g . unstable
V"
cstablis to deliver shock.
Precordial thur ould not lmdlta'
r|||:lh\l is not rcmi) Cause ClIaay
‘|J elcJess) when ||Cfi|1
' uls k hqy
ying shoc
in CPR o1 appl .
ttion? X )
position
What is a recovery
of enthe
is pe troneatm
Recovery positionfirst t. body, in to which an unconscious but breath;
athing casugy
3 t of aid
can be placed as par
)
sses, if present
+ remove the victim’s gla ke sure that both lus.lcgs are str
aight
« kneel beside the v ictim and ma bow bent With the
at right angles to his body, el
« place the arm nearest to you out e hand
palm-up
+ bring) the far arm across the chest, and hold the back of the hand against the vt Ictim’s
to you .
cheek near est
it up, keep;
« with your other hand, grasp the far leg just above the knee and pull P, keeping the foq
’ 4 sapint his check, pul
on the ground pull on the far le %re
his cheek,
« keeping his hand presse against € to roll the victim towards
you t:‘n l(g> his side right ang|e:
e are bent
< adjust the upper leg so that both the hip andwayknerem at
air ains open L
« 1ilt the head back to make sure that the cheek to keep the head tilted and facj
« if nece ssar y. adju st the han d und er the
n from the mouth achng
downwards to allow liquid material to drai

N.B.
Check breathing regularly. f
than 30 mi
I£the victim has to be kept in the recovery position for more min, turn him to the
the pressure on the lower arm.
opposite side to relieve

Recovery position
10. What kinds of artificial respiration are used in CPR?

Artificial respiration is performed as a part of CPR by any inflation method available. Mouth-
to-mouth and mouth-to-nose resuscitation are most widely used

rdal Mask ) to avoid

Mouth-to-mouth
« take a side position
« place one hand under the casualty’s neck
» place the palm of the other hand on the casualty’s forhead and pinch the nose with thumb
and index finger
« perform head tilt
« inhale and press your lips against the casualty’s firmly
« exhale into casualty’s airway; make sure that the chest rises
« let the casualty exhale by himself and continue (hands remain in the same position)
Mouth-to-nose
« take a side position
« place one hand on the forehead
« place the other hand on the chin bottom(from the side of neck)
« pull up the mandible and tilt the head backwards
« keep the mouth closed with your lower hand
« inhale and press your lips against the casualty’s nostrils
« exhale then do not remove your hands, but do allow the chest to rise
« continue
Visible chest rise means that the air has reached the casualty’s lungs, while the rise of
epigastrium suggests it has reached the stomach. No visible chest rise means that the air hasn’t
reached lungs, so check the airway patency and accuracy of triple airway maneuver. Sometimes,
it’s necessary to increase the inflation volume.
Inflation volume is 6 ml/kg of BW. Avoid excessive ventilation (volume over 0.5 L) as it
can increase the risk of air reaching the stomach, regurgitation and aspiration of gastric content to
the lungs. If there is a visible epigastrium rise, don’t try to eliminate air by pressing on the stomach
as this may result in regurgitation. In case of vomiting, remove the vomited content and continue
artificial ventilation. While we mock the casualty’s inspiration, the expiration is passive. During the
expiration extend his head backwards, open mouth and nose. Give 8-10 rescue breaths per minute
(1 breath every 6-8 sec).

0 per min with 500 ml volume (normal breath depth).

Head-tilt and other head movements are contraindicated in patients with suspected cervical
spine injury. The most judicious way of restoring airway patency in such patients is the jaw thrust
without head tilt (if LMA, Combitube or tracheal intubation fail).

11. How are chest compressions cycled with rescue breaths?

< before tracheal intubation
« the recommended “compression to ventilation™ ratio in adults is of 30:2
« in children this ratio depends on the number of rescuers (1 rescuer - 30: rescuers - 30:2)

< after tracheal intubation

« adults/children/newborn infants - give | recue breath every 6-8 seconds (8-10 breaths per
minute) not cycled with chest compressions
« one rescue breath duration = I second

12. How is a bystander supposed to perform CPR in case of a sudden death witnessing?
A bystander (sudden cardiac witness), being an untrained lay rescuer or trained but
inexperienced should follow the Hands Only Algorithm (chest compressions only without giving
7

s i o
 ?_
and
rescue b 15). This means ohe/she should push hard z SELF CON
3 AR, e Jost his cons eiou snes s sudd enly , | follow the voice
o
e ambulance. Theor until lay recu HCPs arrive
O e hle and ready the ambulance/other situation “l the b
n was fourdbe atchec
Climbent esounds olderWhatmaelse
i
shou ld ke
When should one start electric defib
rillation? e
13.
e' ndoaments n reflexes
possible.
as inie
the AED as soon. Cont
Khol e glectrodes and use appl comprige
chest Minim asioni W™ ,it o e
A o betore and after ying shock s (PR 2
3 D earotid areries and pupils
shock applied. 4 Blood for alcohol
5 Time
14, What is the duration of CPR? 30 minutes from circulation cessation or veri
Nomaliy CPR is performed anyat least cqpr.c "1
of spontaneous respiration /circulation, - Conti imical situation #2 yo. was unconscious
o cold exposure orof biolosigns gical death . nue et ¢ ,"::.,.:,l;',,f
‘".' 30-35
midriasis. Diagnosis
efforts to ROSC or signs reathing sounds. deat h
I Biol ogic al
15. What is the role of automatic devices in CPR? 2. Social deat death
None of the existing devices has the advantage over the manual practice of Cpj 3. Brain h
for defibrillator, can increase the e,
medical establishment and none of them, except“AutoP R outside g, 4 Clinicalstatdeat h
ulse™ automated, portable, ™ of e
Tardiac arrest cases. Some CPR devices (c.g. stuf fimm-po 5. Coma
cardiac support pump) can be used under specific conditions by highly trained
Jinical situation # 3 under water fo
16. What is the teamwork approach to CPR? i woman has been atio n with?
P should you start resu scit
In most cases teamwork CPR should be orchestrated to ensure life support. O,
e the ambulanc
sets the AED, s calls airways
emossions, while e otferperson ang eg <45 1. Closed-chest cardiac massage
ays from the mould ar
Sverfor chest compressions. The third unblock the and gives rescue ey o 2 Cleaning the airwion
teamwork algorithm may be altered due to the stuff training, specific conditions, * equimmm'm 3. Artificial respirat
e, 4. Heimlich maneuver (abdominal thrusts
5. Sellick maneuvre
Clinical situation #4
A nurse in the therapeutic unit found or
was lying on his back. no pulse at carotic
orderly heve been sent for Menawhile, ti
mistake has she made?
1. Should have called the doctor herself
2. Shouldn't have checked for pulse and
3. Should have only checked for pulse 2
4. Should have questioned relatives and
5. Should have placed the paticnt on a s
Clinical situation # 5
The fisherman fell under the ice. Whe
of water. He was diagnosed with clinica
1. Immediately start CPR and call the a
2. Too late for CPR as 15 minutes have
3 Warm the patient, then stant CPR
4 Triple airway maneuver, wait for the
- Leave the casualty and find someboc

so know? s
The AutoPulse is used by professional HCPs Distributing band (al pressions
st com
LDB) delivers che

‘L
 MONARY RESUSCITATION
(ALS)
ch arrives at
tion team, whiLk,
is ALS ? LIS ort is ens ured by a resuscitaoty
1 WhatAdv :mcc“l ife Sup Jectives are similar to that of BLS, yet specific diagnostic an}:ictrfi: s
. ) en
al death. 1he
Pumps
hieved (hmqgh the use ofmgchumcgl or electric suction 54
r,lr‘::-dum are @m Combitube), [MAs ::hclq
A. Airway pat oral airways((_mcdcl pattern airway,
s,
remove mu al obturator airway oxygen magg
endotrachea it ::‘:;glc\ entilation is achieved through the use of nasal and respiramrs)- sf
1 breathing devices, BVM device and automatic
B. Ade (BI,_S)
mechanic: oved through closed-chest gardli}c massage
ABp disordey
g' Adminislmlulm of drugs (ROSC), fluid infusion (BV replenishment and
correction)
) other
drug option among ) sympathomimetic agents
nep hri ne (ad ren : aline hydrochloride) islurthe
e.
Epi ation fai
T circules
i sfp'"‘c.‘:\\ivie’ ?r;l};cx:r;e;SCminul (may be repeated sélvcral times if necessary according 1o gp
xrrt
5-10 ml NaCl.
ction). Dissolve in
. If TV route fails, resort to IO route.
fid -r e' sp im lo ry fun
msszni
First
i dose is injected without ECG verification

Fig.4. Intraosseous (10) route

Amiodarunc(Cordarone) is given for VF or VT.

Dosing: .V./1.0. bolus 300 mg (2 ampoules) + 150 mg repeatedly (if necessary).

N.B,
Venipuncture o vein catheterization should be performed simultancously with chest pressions.
The teamwork must be orchestracted and the rescuers must not interfere with each other.

2.AlWh ;::;—E lpt:)c potentiai lly reversible

il causes of clinical
i death?
tentially reversible causes of clinical death

Memory tip 41 4T
 + Hypovolaemia
+ Hypoxin
o+ i :wo(hcm\in
Hypo-/hyperkaclemia (hypocalcaemia,
I acide
cidemia and other metabolicie disorders)
dis

« Tension pneumothorax
« Tamponade
« Toxic substances (exogenic or endogenic intoxication)
« Thromboembolism ( pulmonary embolus/ coronary thrombosis)

3. What are kinds of circulation cessation ?

asystole — flat line, which indicates cessation of heart electrical activity (Fig. 5. Asystole).
+ pulseless clectrical activity (also known as electromechanical dissociation) — organised electrical
depolarization of the heart without synchronous myocardial fiber shortening and, therefore, without
cardiac output : ]
- in PEA there is clcclnc_al activity but the heart either does not contract or there are other
reasons why this results in an insufficient cardiac output to generate a pulse and supply
blood to the organs
- ECG reveals normal or abnormal QRS complexes with regular/irregular intervals
- maybe clinically manifested through severe bradyarrythmia (heartbeat less than 45 bpm
in patients with pathology and less than 30 bpm in heaithy individuals)
- VF (tonic, atonic) is characterized by irregular, chaotic undulations of the baseline, no
recognizable P waves, QRS complexes or T waves (Fig. 6. Ventricular fibrillation)
- pulseless VT is characterized by high-rate cardiomyocyte depolarization, no recognizable
P waves and wide QRS complexes ( Fig. 7. ECG reveals VT).

Fig. 5. Asystole.

MANVVVANANAMAANNANAMRANY
Fig. 6. Ventricular fibrillation

Fig. 7. ECG reveals VT

4. What is defibrillation?
Defibrillation is a kind of electric impulse therapy used in CPR to eliminate ventricular
fibrillation and return spontaneous circulation. .
There are 2 types of defibrillation: transthoracic (external) and intrathoracic (internal). The latter is
used in cardiosurgery.
Defibrillation aims at simultaneous defibrillation of all myocardial fibres with the electric
current, which inhibits pathological foci and facilitates rhythmic heart contractions.

Possible defibrillation outcomes:

- elimination of VF and recovery of spontancous heart contractions;
- transformation of fibrillation into asystole;
- continuation of VF
SV bt equipment is used for defibrillation?
l\.-lfim\huum i petformed with the help of defibrillators
' are gy,
sic (!cfih,,”a"lr‘mI
S5
in
s (; 2 My
Ihe availability of AED is crucial as they can an, yse cardiac r, a‘('»mm:
and i case of VIEapply shock. AEDs are widely integrated ipg the (.y','h ive v, n
K‘m“ (parks, airports, train stations, stadions, casino, theat
locatey

6. How to place electrodes?

Startwith placement of dispensable electrodes or ensure ¢log
cl skin contact,
Normally the anterio-lateral electrode placement is preferre . Tw
~one is placed over the apex of heart — V intercost al sp o (lin! precopg; ial. eleg,CTectr
left of sternum, near left mammary gland)
paceace (li e, nea mcdlnclavicma:l:"( Uy
*the other -~ 1l intercostal space (linca parasternalis, 1o the 10
right of st
area ernum, su
hclzvicul.
However, any of 3 possible placements can be used (anterio-posterior, anteriog:
and posteriodexter subscapular) according to the patient condition, I‘(ecent?}s‘"‘slcr
suhsczm'
4 clectrode placements are equally effective for atrial or ventricular anhy‘hmi:la
Suggests that
7. How to perform defibrillation by biphasic
dcfihrillnlur(nonalflomlled;"
After the placement of electrodes charge the defibr
illator 10200 J (for a‘dul
off the electrocardiograph, cease artificial respiration and cardia c massage, A g 15). Then Switch
defibrillation makes everyone stay clear of the patient and the wardbed, Mode
m?"f Performing
“apply shock™ button placed on the electrode handle, which makes
defibrillation e:"c“ have g
Artificial respiration and cardiac massage are
resumed simultancously afier L]erfi -
Interruption of cardiac massage and artificial ventil
ation should not exceed 5-6 sec, [, chbrilaio,
the next shocks should be delivered with the same energy level (200 ). T hon-eflective,
8. 1 shock vs 3-shock-sequence. Whi(_:h is more effective?
2010 trials, studying the survival rate, suggest that 1 shock is more effective
simultaneous shocks delivered. If the 1st shock fails to eliminate thay
VF, he others will hardly 3
effective. In contrast, resuming cardiac massage would be mor use
e ful than applying Sho‘ct "1'.‘;'{‘
fact and also animal testing research prove that int
err
Likewise, patient trials indicate that 1 applied shockuption of chest compressions is unfay ou}mf
and resumed chest compressions are more
effective than previously recommended 3 successive shocks,

9. How to perform defibrillation in children?

Optimal shock value applied in children remains unknown.
According to the current guidelines: first shock applied
- 2-4 J/kg, the next ones - 4 J/kg and more
(do not exceed 10 J/kg or max adult level).
* defibrillation in children aged 1 up to 8 years is performed
with alleviated shocks; ifno
AED with alleviated shocks is available, use simple AED.
« defibrillation in children up to 1 year is performed by nonautomated
(manual)
defibrillation; if there is no manual defibrillator, use AED with alleviated shocks or
simple
AED.

10. What is the max quantity of shocks applied and are there any restrictions to it? s
There are no restrictions to the number of shocks applied. This number equals the ‘numberof
ECG-verified VFs (in case of relapsing VF, defibrillation can be performed 10 - 100 times a day).
To avoid skin burns, apply electrically conductive gel and ensure close skin contact.

11. How to perform defibrillation in patients with cardioverter-defibrillator? FE

Therer is a possibility
p of damaging
4 a pacemaker¢ or cardioverter-defibrillator. Therefore,
should avoid placing the electrodes right on the device projerd10
ction. Place the electrodes 5 accordi
accordin;
né
to anterio-lateral or anterio-posterior position.

e placement of electrodes must not cause delays in defibrillation!

 12. When should one stop doing CPR?
1. ROSC pulse wave palpated at y ral arteries;
5 30 minutes of non-effective CPR;
7 Exceptions (when CPR should be prolonge
d):
- exposure to cold (hypothermia)
- drugs overdosage
- electric injury.lightning strike
- last stages of exhausting diseasas (cancer,
= DNR —do not resuscitate ( a person dementia)
leagally does not want to be resuscitated)

3. Biological death signs.

13. What are the clinical and investigational (additional) signs of brain death?

Clinical signs
« coma state
- complete muscle atony
« unresponsive to pain stimulation in the trigeminal area
« no reflexes above the cervical spine
« negative pupillary light reflex (rule out pupil dilation drugs intake)
+ no corneal/oculocephalic/oculovestibular reflexes
« no pharyngeal and tracheal reflexes (during endotracheal intubation or bronchi
catheterizaion for secretion aspiration)
« no spontaneous breathing

Investigation (additional) signs:

« EEG in case of brain death (no brain activity)
* ABG tests (PCO2 test)
« angiography of the common carotid arteries and vertebral arteries with no longer than
half and hour interval (no brain circulation)
Brain death is diagnosed by a group of doctors: intensivist and neurologist with at least 5
years experience. - .
To diagnose brain death, one should rule out intoxication, drugs intake, hypovolemic
shock, endocrine emergency (coma).

14. What is PRD? )

Postresuscitation disease is a condition after successful CPR, caused by whole-body ischemia
and reperfusion syndrome, which triggers a systemic inflammatory response. It also involves
homeostasis disorder and integrative CNS failure.

PRD dynamics
I'stage (6-8 hours after CPR) functional instability 4 (o
+4-5 times decrease in tissue perfusion, in spite of hemodynamics stability.
* circulatory hypoxia
13
 « lactate acidosis
*inc ed levels of “1DP and fibrin-monomers, which are norm; ally not g,
11 stage (10-12 hours after CPR) functional stability and general imprc IVemeny
+ significant perfusion disorders
« lactate acidosis
+ increased levels of FDP o
« redu ced fibri nolyt ic plas ma activ ity
+ so-called “metabolic mess™ and enzymemia
111 stage. (12-24 hours after CPR) repeal ted exacerbation accordin g to clinica
ini A|l
and g,
findings . . Tal ory

« hypoxemia with decrease in Pa02 (60-70 mm Hg)

« tachypnoe (30 permin), tachycardia, hypertension
« acute lung injury syndrome
*DIC
« 1V stage (3-4 day after CPR) either stabilisation and recove TY Or exacerba
multiple organ failure) tioy, (SIRs,
V stage (5-7 day after CPR) unfavourable
« inflammatory suppurative process with further generalisation
« destructive changes in the organ parynchema
« posthypoxic encephalopathy

15. What are the stages of recovering from coma?

Recovering From Coma

Neurophysiological
Phase characteristics Clinical manifestat
ion
comple! te areflexiX143, a, y;
hypotens
Extreme coma irreversible loss of brain activity respiratory and cardio ior
vasmla:L
disorders,
Acute coma with respiratory disorders, hy;
potensi
severe vegetative severe disorder of brain activity loss of cough reflex. musclcm'
l
diorders hypotony
. X resumption of breathing ang
Coma with partial p 2
11 ¢ :
vegetative function
recovery of pontobulbary struct cough reflex,increased muscl
oL s tone, resumed tendon r:fl:v.-:,
symptoms of focal brain injury
4 X general condition improves, eyes
Apglllc syndrom_e recovery of asc:ndu,g reticular open spontancously, eccentric
IV | (persistent vegetative | activating system and improvement | pupils, unresponsive, sleepless
state) of the descending reticular system period changes with sleeping one, |
positive light pupillary reflex
recovery of reticular formation, 5 ¥
thalamic system and nonspecific still unresponsive, fixed pupils, s
A Akinetic mutism thalamocortical projection system, w:l.'f};:"g moving Ohjmmmmmg
diencephalic and structures and Is head to “.m“d Sl."“ oy
inhibition systems prolonged sleepless pered
first signs of neocortical functions responsive to commands,
Vi Recovery recovery with inadequate level of | articulates some words, prolonged
nonspecific activation sleepless period
Severe dementia with | in2dequate recovery of limbic prolonged sleepless period.
Vil hypothalamic and and neocortical system, adequate improvement of speech
Xdre 5
limbic prevalence
reintegration
& )
of nonspecific
pe
emotional response, memory 204
activation disorder
Recovery of recovery and interaction of cortex,
Vil psychological and neocortex and other functional
somatic functions systems

_—4
 16. What it the management of PRID?

A. Maintenance of extracranial homeostasis

1. SRP monitoring. BV replenishment, plasm
a volume expanders (10 ml/kg)
a) short-term mild hypertension (SBP 120140 mmilg
) for 15 minutes after the return
of circulation )
e b) normotensie on (SBP 90 mmiig) or mild hy) P pertension n (SBP
(SBP
(S 100120 mmHg) for coma
¢) central venous and arterial lines, pulmonary artery balloon cathe
terization
lzr‘w'::::‘:;‘.‘}:l::“"
ilisation by small doses
oses of MRs § (pancuronium),
N i ifi necessary — mechanical ventilation
3. 1.V, painkillers, antiscizure medications: sodium
dose 30 mg/kg) or diazepam (sibazon), propofol topental (5 mg/kg + 2 mg/kg. per hour /max
n pm‘fl7 1‘.348 mmHg through mechanical ventilation
s pH =737,
6. Maintain adequate oxygen concentration in the breathing mixture (Fi0,) so that SpO, = 94-99%
7.- ee + 0.2 mg/kg LV.
Corticosteroids: per methylprednisolone
6 hours for 2.5 daye)(5 mg/kg
2/kg +1
+1 mg/kg Y per hour ) ' or I.V. dexamethasone
S whpr(1

8. Laboratory values correction

« HT 30—35%
« electrolytes WNL
« colloid and osmotic pressure >15 mmHg
« plasma osmolarity 280—300 mosmol/I

9, 'rhcmmulic_h_\"polhemia (30-32"C) equals T in the external auditory meatus.

10. Donotadminister glucose solution in the first 3 days after clinical death (exception: hypoglycemia,
amiodarone injections). .
Administer 0.9 % NaCl solution. Dosing: 30-50 mI/kg(children 100 m/kr) per 24 hours. If necessary
administer potassium solutions.
11. Clinical nutrition (parenteral and enteral routes) e.g. Cabiven 2 L/24 hours + V. Dipepti
100-150 ml/24hours +Fresubin 1 L/24 hours via G-tubeg) pepsves
B. Maintenance of intracranial homeostasis

1. Examine a patient for for multiple brain injuries ( take medical history, assess clinical presentation,
cerebral angiography or CT scans).
2. Intracranial pressure monitoring (use safe equipment) is justified immediately afier the return of
circulation.
Intracranial pressure (upper limit 15 mmHg) can be maintained through:
a) 2-hour hyperventilation with PetC02 reduction to 20-25 mmHg
b) drainage of brain ventricles
¢) mannitol — IV 0,5 gr/kg IV
(if intracranial pressure monitoring is impossible mannitol I.V. 1g/kg;
HyperHAES, Sorbilact, Reosorbilact have similar effects )
d) furosemide (lasix) - 0,5-1 mg/kg IV;
¢) sodium thiopental - 2-5 mg/kg IV- twice if necessary (A.3)
) corticosteroids (A.7)
3. EEG
4. Further investigation for treatment and prophylaxis of multiple organ failure.
5. Assess the severity of brain injury (coma state|)

15