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- 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