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Shock

- Emergency
Approach -
First Part
Shock - definition,
epidemiology
 Cardiovascular insufficiency which
determines a
disturbance/imbalance between
the oxygen need and offer
 USA- one milion cases in ED/year
 Precocious intervention at the non-
traumatic patient – “the golden
hour”
Shock – classification
 Hypovolemic- decrease of the circulant
volume
 Cardiogenic- pump malfunction
 Distributive- maldistribution of the
sanguine-septic, anaphylactic, neurogene
flow
 Obstructive- obstruction of the sanguine
flow because of extra-cardiac causes
(pulmonary emboli, cardiac tamponade,
pneumothorax under tension)
Shock:
physiopathology
 CaO2- O2 arterial = O2 linked to
Hb plus a small quantity of O2
dissolved in plasma
 DO2- O2 release – it results from
CaO2 and DC (CO)
 DO2 and VO2 (release and
consumption of O2) is a sensitive
balance between offer and demand
Shock-
physiopathology
 SaO2=100%- normal 25% of the transported O2
linked to Hb is consumed by tissues – the venous
blood will have a saturation of 75%
 The offer of O2 insufficient- the first
compensatory mechanism is the increase of CO
 If the increase of CO is insufficient – the
percentage of O2 increases extracted by tissues
from HbO2 and SmVO2 decreases (the saturation
in O2of the venous blood)
Shock-physiopathology
 Demand>offer – determination of se intră în
anaerobiosis- lactic acid
 Lactic Acidosis :
due to the inadequate release of O2 (just like in the
cardiogenic shock)
Very high demand (consumption of O2 = VO2 increased)-
status epilepticus
Inadequate use of oxygen at the level of tissues (septic
shock or post-resuscitation syndrome
 Lactic acid - marker of the disturbance demand/offer
- used in the patient receiving department, diagnosis,
treatment, prognosis
 MBP=CO x peripheral vascular resistance, CO decreases-
the peripheral vascular resistance increases
MBP is not an exact marker of the tissular bipo-perfusion
Shock-
physiopathology
Compensatory mechanisms: stimulation of carotid
baro-receivers – sympathetic NS:
 Arteriolar vessel constriction – circulation
redistribution
 HR increase and miocardial contractilities –
increased DC
 Constriction on the vessels of potentia
 Release of vaso-active hormones (A,NA,D,C)-
vasoconstriction
 ADH release, activation of the renin-
angiotension-retension system of Na and water-
maintenance of the intravascular volume.
Shock- physiopathology-
cellular effects of O2
decrease
 ATP depletion- membranous pump malfunction-
Na inflow and K release
 Cellular edema, cells no longer respond to stress
hormones (insulin, cortisol, glucagon,
catecholamines)
 Intracellular destructions- cellular death
 Hyper K, hypo Na, metabolic acidosis,
hyperglicemia, lactic acidosis
Shock- symptoms
 Symptoms suggesting the volume loss:
bleeding, vomiting, diarrhea, polyuria, fever
 Symptoms suggesting: acute coronary sdr.,
congestive acute heart failure, beta-blockers
 Anaphylactic context
 Neurological disorders: vertigo, lipothymia,
alteration of the mental status-coma
Shock- physical
examination
 CV: distension of the throat veins, tachycardia,
arrhythmia, decrease of the coronary perfusion pressure,
decrease of the ventricle compliance, increase of the
diastolic pressure in LV, pulmonary edema
 Respiratory: tachypnea, increase of RF, increase of the
dead area, bronchospasm, hypocapnia, respiratory
insufficiency, distress sdr. of the adult
 Visceras: ileus, gastrointestinal bleeding, pancreatitis,
alithiasic cholecystitis, mesenteric ischemia
 Renal: decrease of the glomerulary filtering rate,
redistribution of the renal flux, oliguria
 Metabolism: respiratory alkalosis, then metabolic
acidosis, hypo/hyperglycemia, hyperK.
Shock –clinical
framework
 Temperature
– Hyperthermia or hypothermia (endogenous=hypo
metabolic shock or exogenous).
 Cardiac frequency
– Usually increased; there can also be paroxistic
bradycardia in hypovolemic shock, hypoglycemia,
beta-blockers, pre-existent cardiac affections.
 SBP
– In the precocious phase it can be increased
because it is a compensatory mechanism and
increases DC and then, it decreases.
 DBP
– Increases at the debut by arterial vessel
constriction and then it decreases.
Shock –clinical outview
 Pulse pressure
– SBP-DBP, depends on the aorta rigidity and on
the diastolic volume: it increases precociously
in shock and then decreases before SBP.
 Paradoxical pulse
– The modification of SBP with breath. The
increase and decrease of intratoracic pressure
affects the cardiac output.
– It is met in asthma, cardiac tamponade and
decompensate cardiac insufficiency.
 MBP = DBP + (MBP – DBP)/3
– Depends on DC şi RP, assures adequate
tissular perfusion, decreases in shock.
Shock – Clinical
Framework
 Shock index = HR/SBP = 0,5-0,7 (n)
– Depends on the effort of the LV in acute circulatory
insufficiency
 CNS: agitation, delirium, confusion, torpor, coma
– decrease of pressure of cerebral perfusion
 Skin: cold, wet, sweated, cyanosis
 CV, respiratory, visceral organs, renal,
metabolism – see above
Shock – paraclinic
exams
 Base evaluation: HLG, electrolytes, glycemia,
urea, creatinine, TQ, IQ, aPTT, urine summary,
ecg, thoracic Rx.
 Secondary evaluation: arterial blood gases,
lactic acid, PDF, hepatic function
 Non invasive monitoring: CO2-end tidal, DC
calculated, echocardiogram
 Invasive monitoring: capillary filling pressure,
PVC, DC, SmVO2, vascular resistance, DO2, VO2
 For etiology and complications: cultures, cranial
CT, pelvis, abdominal, lumbar puncter, cortizol
level, pelvian and abdominal echography
Shock - treatment
 A – IOT, mechanic ventilation, tracheal aspiration
 B – decrease of respiratory labor, sedation, mechanic
ventilation, decrease of oxygen demand, SaO2 > 93
%, PaCO2 < 35-40 mmHg, pH > 7,3
 C – fluid reanimation (crystalline capsule, colloid),
peripheral and central venal access, vasopressin for
MBP > 60 mmHg and SBP > 90 mmHg
 DO2 – resolving of hyperandregenic status
(analgesic, relaxation, warmth, tranquilizers), Hb >
10 g%
Shock-vasoactive
agents
 Dopamina:0-25mcg/kg/min, alfa,beta,D
 Noradrenaline:0,01-0,5mcg/kgc/min,
alfa1,beta1
 Phenyleffrine:0,15-0,75mcg/kgc/min (alfa)
 Adrenaline:0,01-0,75 mcg/kcg/min
 Dobutamine:2-20mcg/kgc/min,beta1,2, alfa
1
 Isoproterenol:0,01-0,02 mcg/kgc/min, beta
1,2
Shock – therapy
evaluation parameters
 Traditional: BP normalization, HR, urinary output,
circulator volume (intra/extra cellular)
 CVP 10-12 mmHg, PAOP 12-18 mmHg
 MBP 90-100 mmHg, RVP 800-1400 dynexs/cmp
 Contractility: DC 5 l/min, IC 2,5-4,5 l/min/mp
 HR 60-100/min
 PPC > 60 mmHg = DBP – PVC
 Tissular oxygenation: SmVO2 > 70 %, acid lactic <
2 mmoli/l
Hypovolemic shock:
causes
 Hemorrhagic shock
 Absolute hypovolemia: diarrhea, vomiting,
fever, polyuria, diuretics, burns etc.
 Relative hypovolemia: losses in III space –
intestinal occlusion, pancreatitis, entero
mesenteric attack, edema
 Traumatic shock (hemorrhagic shock,
spinal shock, obstructive shock)
Hemorrhagic shock:
causes
 Trauma: lesions of parenchymal organs, lungs,
myocardium, big vessels, retroperitoneal
hemorrhage, big bones and pelvis fractures, scalp
hemorrhages, epitasis
 Gastrointestinal: esophageal varices, hemorrhagic
ulcer, gastritis, esophagitis, Mallory-Weiss syndrome,
tumors, mesenteric ischemia
 Genitourinary: vaginal bleeding, neoplasm, abortion,
metrorrhagia, placental presentation, placental
retention, uterine rupture, ectopic pregnancy
 Vascular: aneurisms, aorta dissection, ateriovenous
malformation
Hemorrhagic shock
physiopathology
 Compensatory mechanisms: sympathetic
hyperactivity to maintain the effective
circular volume
 Vasoconstriction, circulation centralization,
diuresis decrease
 Straling forces modification by precapillar
sphincter contraction: interstitial
hydrostatic pressure increases, cell
dehydration – “transcapillar refilling”
 O2 tissular extraction increases (right
deviation of HbO dissociation curve)
Hemorrhagic shock:
decompensation
mechanisms
 Loss of precapillar sphincter
vasoconstriction– vasodilatation,
hypotension, myocardium and NCS
ischemia, transudation of interstitial liquid
 Increase of capillary permeability
 Capillary blockage by leukokeratoses micro
aggregates
 Erythrocytic deformability decrease
 Endothelian edema
Hemorrhagic shock: clinic and
paraclinic
Class I Class II ClassIII Class IV
Blood loss % < 15 15-30 30-40 40
- Volume ml 750 800-1500 1500-2000 2000

SBP Unmodified Normal Reduced Very low
DBP Unmodified Raised Reduced Very low
(immeasurable)

HR Easy 100-120 120 (weak) > 120 filiform
tachycardia
Capillary Normal Delayed Delayed Undetectable
refilling >2s >2s
RF Normal Normal Tachipnea Tachipnea
> 20/min > 20/min
Urinary output > 30 20-30 10-20 0-10
Extremities Normal colour Pale Pale Pale and cold
Conscious state Alert Anxious or Anxious, Obnubilated,
aggressive aggressive or confused or in a
obnubilated coma
Hemorrhagic shock:
Therapeutic objectives
 Adequate lung oxygenation
 Hemorrhage control
 Loss replacements
 Monitoring therapy effects
 Myocardic contractibility support
 Acido-basic and electrolytic
reequilibration
 Sustaining renal function
Hemorrhagic shock:
treatment
 ABC
 External hemorrhages control: raising
the extremities, compressive bandage,
surgery
 Loss replacement: peripheral and
central venous approach, intravascular
volume replacement, oxygen transport
replacement, coagulation anomalies
correction
Crystalline solutions
 Isotones: SF, Ringer, dairy Ringer- replace the interstitial
deficit also, rapid intra and extra vascular equilibration;
it is administrated 3:1 compared to lost blood volume
 Hyper tones: NaCl hypertonic solution- perfusion reduced
volume for a satisfactory volemic recovery, positive
intropic effect, peripheral vasodilatator; hypernatremia
danger, extreme cerebral dehydration (Na >170 mEq/l)
 Economic accessibility
Colloidal solutions
 Big intravascular remenence, small
volumes use for adequate volemic
resuscitation, maintenance of intravascular
colloidal smotic, useful in cardiac and renal
insufficiency
 Albumen, dextran 40-70, HAES, Hemacel,
plasma
 High price, anaphylactic reactions,
antiplachetary effect and of faking direct
compatibility result, histocitary system
blockage, infection transmission
Blood transfusion and
derivates
 O2 transport capacity increase
 Homologous isogroup blood, izoRh, integral,
eritrocitary mass, washed erytocytes
 Artificial blood: perflorocarbonic emulsions, Hb
pyridoxilated polymer
 Coagulation dysfunction corrections, CID
treatment: frozen fresh plasma, heparin therapy
 Contribution of citric acid (from preserved) and
of K, hypocalcaemia (1 g Ca glycolic iv for each
5U of transfused blood or plasma)
 Auto transfusion
Hemorrhagic shock:
treatment
Class I 2,5 l milky Ringer or physiological solution or 1
l colloid

Class II 1 l colloid + 1,5 l milky Ringer or physiological
solution

Class III 1 l Ringer or NaCl + 0,5 l colloid + 1-1,5 l
integral blood or an equivalent volume of
erythrocytic mass

Class IV 1 l Ringer or NaCl + 1 l colloid + 2 l integral
blood or an equivalent volume of erythrocytic
mass and colloid
Therapy efficiency
 Blood pressure
 HR, RF
 Urinary output
 CVP
 Consciousness state
 Skin coloring, capillary filling time
 Para clinic parameters (CO2, pH gastric
mucous membrane, IC, SmVO2, lactic acid)
Anaphylactic shock
 Anaphylaxis – a systemic, severe reaction
of hypersensitivity accompanied by low
blood pressure and by compromising the
airways with vital risk, determined by
anaphylaxis mediators release (IgE from
mast cells)
 Anaphylactic syndrome- the same reaction
without IgE
 Incidence: in the USA varies between
5/1000 and 2/10000
Anaphylactic shock:
causes
 Medicines
– Penicillin and other ABc
– aspirin
– trimetroprim
– AINS
 Foods and additives
– Sea fruits, fish
– Soy, nuts
– Flour, milk, eggs
– Monosodium glutamate, tartrasine
– Nitrates and nitrites
 Others
– Hymenoptera stings
– Insects
– Contrast substances from radiology
Anaphylactic shock-
physiopathology
 Hypersensitivity reaction type I-IgE
 Mast cells digranulation
 Mediators issue
 Complement activation
 Metabolism modulation arachidonic
acid
 But also hypersensitivity reaction of
type II and III
Anaphylactic shock-
clinic
 Urticaria
 Angioedema
 Non systematic abdominal pains
 Nausea, vomiting, diarrhea
 Bronchospasm
 Rhinorrhea
 Conjunctivitis
 Lipothymia or palpitations
 Anaphylaxis= any combinations of these signs and
low blood pressure or compromising of air way
Clinic signs evolution
 Pruritus
 Erythema
 Urticaria
 Dyspnea, anxiety, lipothymia, syncope
 Apparition within 60 minutes from the
exposure- gravity sign – death risk
 Symptoms recurrence - biphasic
phenomenon - 20% of patients
Positive and differential
diagnosis
Positive = historic and physical exam
Differential:
 Vague vessel reactions
 Myocardium ischemia
 Status astmaticus
 Convulsions
 Epiglottises
 Congenital angioedema
 Obstruction of air ways by foreign bodies
 Laboratory: histamine, high tryptase
Treatament
 Fluids i.v. 1-2 l or 20 ml/kg
 Corticosteroids: methylprednisolon 125 mg i.v.
 Blockings H1- diphenhydramine 25-50 mg i.v., i.m.,
p.o.
 Blockings H2- ranitidine 50 mg i.v.
 Nebulised albuterol 2,5 mg or 5 mg/kg i.v.
 Glucagon 1 mg i.v. la 5 min. then 5-15 mcg/min
 Aminophyline 5-6 mg/kg i.v.
Treatament
 Fluids i.v. 1-2 l or 20 ml/kg
 Corticosteroids: methylprednisolon 125 mg i.v.
 Blockings H1- diphenhydramine 25-50 mg i.v., i.m.,
p.o.
 Blockings H2- ranitidine 50 mg i.v.
 Nebulised albuterol 2,5 mg or 5 mg/kg i.v.
 Glucagon 1 mg i.v. la 5 min. then 5-15 mcg/min
 Aminophyline 5-6 mg/kg i.v.