Transcript Approach to the patients with shock

Approach to the patients with
shock
AA Khaleghi
Emergency medicine
specialist
PERSPECTIVE
In philosophic terms, shock can be viewed
as a transition between life and death.
Whether shock results from hemorrhage,
sepsis, or cardiac failure, mortality
rates exceed 20% .
In scientific lexicon, shock results from the
widespread failure of the circulatory
system to oxygenate and nourish the
body adequately.
Classification
For years, shock has been classified
into four broad categories based on
Blalock's 1934 description:
hematological ,neurologic,
vasogenic, and cardiogenic
Epidemiology
The epidemiology of shock in the
emergency department remains
speculative
Patients presenting with traumatic ,
cardiogenic , or septic shock
constitute about 1% of all emergency
department visits
PATHOPHYSIOLOGY
At the subcellular level, shock first affects the
mitochondria.
In the early stage of shock, the skeletal
muscle and splanchnic organs are affected
more by oxygen deprivation than by a lack
of delivery of fuel substrate
Regardless of etiology, elevated
concentrations of lactate in the blood serve
as a sentinel marker of widespread
inadequate tissue perfusion and disappear
when adequate resuscitation has been
achieved.
At the whole-body level, shock from any etiology
initiates a sequence of stress responses that are
intended to preserve flow to vital organs and to
signal cells to expend internal energy stores
Although lactic acidosis is a unifying feature of
shock, its exact source may depend on the cause
of shock.
Initiation of inflammatory events constitutes a third
unifying feature of shock.
Specific Causes
Hemorrhagic Shock
In general, hemorrhage first increases pulse and cardiac
contraction, then increases vasoconstriction.
The first clinical manifestations of hemorrhage are tachycardia,
then a slight increase in the diastolic BP, causing the pulse
pressure (difference between systolic and diastolic BP) to
narrow
Arterial hypotension is generally and arbitrarily defined as a
systolic arterial BP less than 90 mm Hg, but this threshold
should be increased to 100 mm Hg in patients with known
systemic hypertension and inpatients older than age 60 years
The second phase of organ injury from hemorrhagic shock
occurs during resuscitation.
Septic Shock
Septic shock can be produced by infection with any microbe.
gram-negative aerobic
gram-positive
In one third of cases of septic shock, no organism is identified.
Septic shock causes three major effects that must be addressed
during resuscitation: hypovolemia, cardiovascular
depression, and induction of systemic inflammation
.
Cardiogenic Shock
Cardiogenic shock results when more than
40% of the myocardium becomes necrosed
from ischemia, inflammation toxins, or
immune destruction.
Acute massive pulmonary embolism
produces circulatory shock by obstruction
of the pulmonary vasculature, which leads
to right ventricular overload and impairs left
ventricular filling
Anaphylactic Shock
Anaphylactic shock results from an IgEmediated systemic response to an
allergen.
IgE causes mast cells to release histamine,
which results invascular smooth muscle
relaxation, bronchial smooth muscle
constriction, and capillary leak of plasma
into interstitial spaces.
Platelets also participate in anaphylaxis by
secreting platelet-activating factor (PAF),
CLINICAL FEATURES
The HR-to-systolic BP ratio may provide a better marker
of shock than either measurement alone; a normal
ratio is less than 0.8,"
Measuring urine output requires at least 30 minutes,
however, to determine accurately if output is normal
(>1 mL/kg/hr), reduced (0.5 to 1 mL/kg/hr), or severely
reduced«0.5 mL/kg/hr).
An arterial lactate concentration greater than 4 mM/L or
an arterial base deficit more negativethan -4 mEq/L
predicts the presence of circulatory insufficiency
The physical examination
should be performed on an undressed patient
should begin with general inspection of the body for visual or tactile evidence of
trauma
odor of ethanol or other toxins
presence of any indwelling devices
evidence of soft tissue or bone infection, rashes, or extremity edema
Dry mucous membranes
distended jugular
heart sounds
pulmonary rales
Wheezing
Abdominal tenderness
Rectal and pelvic examinations
Recta] temperature
Laboratory, radiographic, and other
ancillary data
to assess tissue and vital organ
perfusion
to diagnose injury from trauma, find the
source of infection with sepsis, or
identify the cause of cardiac failure.
MANAGEMENT
Monitoring Perfusion Status
In all patients with shock, circulation must be
monitored by continuous ECG and pulse oximetry
BP should be measured by cuff sphygmomanometer
every 2 to 5 minutes during resuscitation
Urine output should be measured as an index of vital
organ perfusion
lactate concentration or the base deficit,
method of achieving intravenous access
Goal-Directed Therapy
refers to the practice of resuscitating patients
to a defined physiologic endpoint indicating
that systemic perfusion and vital organ
function have been restored.
lactate clearance
Mixed venous oxygen saturation (SV02)
central venous oxygen saturation (Scvo2]
Gastric or rectal tonography
Ventilation
Volume Replacement
The goal in volume replacement is
slightly elevated left ventricular enddiastolic volume