Transcript Approach To The Patient In Shock

Approach To The Patient In
Shock
By James Holencik, DO
Epidemiology
• More than 1 million cases of shock present
to US ED’s yearly.
• Approx. 30-45% of patient in septic shock,
and 60-90% for those with cardiogenic
shock die within 1 month of presentation.
Pathophysiology
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Shock is defined as: circulatory insufficiency
that creates an imbalance between tissue oxygen
supply and demand.
Four categories of shock:
Hypovolemic
Cardiogenic
Distributive
Obstructive
Pathophysiology Cont.
• Normally, the tissues consume
approximately 25% of the oxygen carried
on hemoglobin.
• Venous blood returning to the right heart is
approximately 75% saturated.
• When demand is insufficient the first
compensatory mechanism is increase in
cardiac output (CO).
Pathophysiology Cont.
• When compensatory mechanisms failure the
body starts anaerobic metabolism forming
lactic acid.
• Shock is usually, but not always, associated
with systemic arterial hypotension, ie SBP
<90.
Pathophysiology Cont.
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The onset of shock provokes a myriad of
autonomic responses.
Arteriolar vasoconstriction.
Increase in HR and contractility increases CO.
Constriction of venous capacitance, which
augments venous return.
Release of vasoactive hormones epi, norepi,
dopamine, and cortisol to increase arteriolar and
venous tone.
Pathophysiology Cont.
5. Release of ADH and activation of the
renin-angiotensin axis to enhance water
and sodium conservation.
• The cellular response to a decrease in
systemic O2 delivery is ATP depletion
leading to ion-pump dysfunction (influx
Na+ and efflux K+ leading to membrane
instability and cellular dysfunction.
Pathophysiology Cont.
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In early phases of shock the physiologic changes
produce a clinical syndrome called SIRS
(systemic inflammatory response syndrome).
SIRS is defined as 2 or more of the following
features.
Temp. >38 or less than 36.
HR >90 beats/min.
RR faster than 20.
WBC’s >12 or <4 or >10% bands.
Physical Examination
• No single vital sign or value is diagnostic of
shock.
• Look at the whole patient.
• Refer to all the vital signs as well as
physical signs of shock (cynosis, confusion,
restlessness, and other signs of poor
perfusion).
Diagnosis
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Ancillary Studies:
CBC, BMP with Mg and Phos.
PT, PTT, UA, lactic acid, ABG, Preg test.
CXR, EKG, Hepatic func., cortisol level.
Blood, urine, sputum, and pelvic cultures.
CT head and sinuses, lumbar puncture.
Invasive tests: filling pressures, CO, and central
venous oxygen saturation.
Diagnosis
• Also monitoring of pulse ox,
electrocardiographic, CVP, arterial line, and
end-tidal CO2.
Treatment
• The rationale for early intervention
• Application of an algorithmic approach to
optimize hemodynamic endpoints with
early goal directed therapy reduces ED
mortality by 16%.
• Also the ABCDE tenets of shock
resuscitation must be established.
Treatment Cont.
• Establishing Airway
• Airway is best controlled with endotracheal
intubation for airway protection.
• Sedatives used in intubation can worsen
hypotension, through arterial and venous dilation
as well as myocardial suppression.
• Volume resuscitation or application of vasoactive
agents may be needed before intubation.
Treatment Cont.
• Controlling Work of Breathing
• Control of breathing is required when
tachypnea accompanies shock.
• Respiratory muscles are significant
consumers of O2 during shock increasing
lactate formation.
• Mechanical ventilation and sedation has
been shown to improve survival.
Treatment Cont.
• Optimizing the Circulation
• Hemodynamic stabilization begins with IV access
through large bore peripheral lines.
• Trendelenburg positioning does not improve
cardiopulmonary performance compared with the
supine position.
• Trendelenburg position may worsen pulmonary
gas exchange and predispose to aspiration.
Treatment Cont.
• Central venous access will aid in assessing
volume status (preload) and monitoring
central venous oxygen sats (Scvo2).
• This is also the preferred route of
vassopressor therapy.
• Fluid resuscitation begins with isotonic
crystalloid, initially 20cc/kg.
Treatment Cont.
• The colloid vs crystalloid resuscitation
controversy remains despite a slight increase in
mortality when colloids are used.
• Vasopressor agents are used when an inadequate
response to volume occurs.
• Vasopressors are most effective when vascular
spaces are full and least when empty.
Treatment Cont.
• The use of vasopressors is accompanied
with pitfalls: decreasing capillary blood
flow in certain tissue beds (bowel), and
falsely elevates intracardiac filling pressures
(CVP).
Treatment Cont.
• Assuring Adequate Oxygen Delivery
• Arterial saturation should be returned to 9395% and hemoglobin above 10g/dl.
• A hyperadrenergic state results from the
compensatory response to shock,
physiologic stress, pain, and anxiety.
• Shivering frequently results so patient need
to be kept warm.
Treatment Cont.
• Achieving End Points of Resuscitation
• Traditional end points have been
normalization of blood pressure, heart rate,
and urinary output.
• A goal-directed approach at achieving urine
output >.5cc/kg/hr, CVP 8-12, MAP 65-90,
and venous oxygen sat >70% during ED
resuscitation greatly reduced mortality.
Treatment Cont.
• Bicarbonate Use in Shock
• Experimental data indicates that exogenous
bicarb can actually worsen intracellular
acidosis, and has not be shown to have a
benefit.
• Bicab also shifts the oxygen-hemoglobinbound curve to the left impairing tissue
unloading.
Treatment Cont.
• A compromise is to partially correct the acidosis.
• Bicarb deficit is determined by (normal HCO3
minus the patients HCO3) X 0.5 X body weight
(kg).
• One-half of this amount is infused slowly and the
remainder over 6-8hr.
• Bicarb should be withheld once the pH is 7.25 or
greater.
Disposition and Transition to the
Intensive Care Unit
• A system-oriented problem list with an
assessment and plan, including all
procedures and complications, should be
verbally communicated and written prior to
transfer.
• Currently outcome prediction at ED
disposition has not been fully studied.
Fluid And Blood Resuscitation
Fluid and Blood Resuscitation
• Fluid resuscitation is the initial therapy for
disorders causing intravasular volume
depletion with resulting tissue
hypoperfusion and organ dysfunction.
• Acute hemorrhage is the predominant cause
of acute intravascular volume loss requiring
aggressive fluid resuscitation.
Fluid and Blood Resuscitation
• Until recently, the widely accepted goal of
fluid resuscitation was to restore a state fo
normovolemia.
• However present laboratory and clinical
reports have raised controversy about filling
the tank in the setting of ongoing
hemorrhage.
Fluid and Blood Resuscitation
• The objective of fluid resuscitation is to
restore sufficient intravascular volume and
oxygen-carrying capacity to maintain
cellular delivery of metabolic substrates
sustaining cellular viability.
Pathophysiology
• The acute loss of intravascular volume
triggers a wide range of physiologic
regulatory responses.
• At the cellular level, hemorrhagic shock is
defined as a state of impaired oxidative
metabolism and homeostasis due to
inadequate O2 delivery and inadequate
cellular waste removal.
Pathophysiology
• Loss of circulating blood volume leads to
decreases in arterial blood pressure, venous
return, and ventricular stroke volume.
• This in turn leads to a physiologic response
by the body to increase HR, arterial and
venous constriction, increased ventricular
contractility, and extravascular to
intravascular fluid shift.
Pathophysiology
• Vagal tone is decreased
• Kidneys through the stimulation of reninangiotensin-aldosterone system and ADH retain
Na+ and H2O.
• Angiotensin II and vasopressin promote
vasoconstriction.
• Activation of the coagulation system leads to
platlet depostion and release of local mediators.
Pathophysiology
• Severe hemorrhage causes decreased CO,
and vital organs will only be perfused (brain
and heart).
• Once decompensation of the bodies natural
responses occur myocardial contractility
decreases, local tissue acidosis and hypoxia
develops resulting in loss of peripheral
vasocontriction.
Clinical Features
• The hemodynamic profile response to hemorrhage
induced hypovolemia commonly includes
tachycardia, hypotension, and signs of poor
peripheral perfusion.
• Arterial and venous constriction lead to a narrow
pulse pressure.
• Hypoalertness ensues secondary to cerebral
hypoperfusion.
Clinical Features Cont.
• The normal total circulating volume of an
adult is approx. 7% of total body weight.
• Therefore 5L for a 70kg patient divided into
3L of plasma and 2L of RBC’s.
• Class 1 shock is loss of 15% (750ml) of
circulating blood.
• Usually well tolerated in healthy patients.
Clinical Features Cont.
• Class 2 shock is loss of 15-30% (7501500ml) of circulating blood.
• Results in tachycardia and narrow pulse
pressure.
• Class 3 shock is loss of 30-40% (15002000ml) circulating blood.
• Hypotension, tachycardia, peripheral
hypoperfusion, and decline in mental status.
Clinical Features Cont.
• Class 4 shock is loss of >40% (>2000ml) of
circulating blood.
• The body has reached its limits to
compensate and therefore imminent
hemodynamic collapse.
• Be cautious with elderly due the possibility
to evoke tachycardia secondary to poor
heart function or medication.
Management
• Initial therapy should involve securing an airway,
assuring adequate ventilation and oxygenation,
controlling external bleeding, and spinal cord
protection when necessary.
• Obtain 2 large bore IV’s
• Fluid resuscitation keep 3 objectives in mind.
1. Restoring intravascular volume sufficiently to
reverse systemic hypoperfusion.
Management Cont.
2. Maintaining adequate oxygen-carrying
capacity so that tissue oxygen delivery
meets critical tissue oxygen demand.
3. Limiting ongoing loss of circulating
RBC’s.
-- Place foley cath to monitor urinary output.
Fluid Resuscitation
• Currently there is controversy concerning
normotensive vs hypotensive resuscitation.
• The goal of hypotensive resuscitation is to
provide sufficient fluid to maintain vital
organ perfusion and avoid cardiovascular
collapse while keeping arterial BP relatively
low (MAP of 60).
Fluid Resuscitation Cont.
• Currently there still is controversy
concerning crystalloids vs colloids for use
in resuscitation.
• The cost of colloids greatly out weights that
of crystalloids causing most to use the later.
Isotonic Crystalloid Solution
• Comprised mainly of normal saline and
lactated Ringer’s.
• Crystalloids are hypo-oncotic because of
there lack of protein.
• Therefore most of the fluid given will shift
into the extravascular space instead of the
intravascular or interstitial space.
Isotonic Crystalloid Solution
Cont.
• This is the physiologic basis for the 3:1
ratio for isotonic crystalloid volume
replacement.
• Therefore for every amount of blood lost 3
times that amount is needed to replace
intravascular volume using crystalloids.
Isotonic Crystalloid Solution
Cont.
• Concerns have been raised about each fluid.
1. Infusing large volumes using either causes
increased neutrophil activation.
2. LR also increases cytokine release and may
increase lactic acidosis in large amounts.
3. NS exacerbates intracellular potassium depletion
and causes hypochloremic acidosis.
Solution makeup
Osmal. Glucose
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5% D/W 278
10%D/W 556
.45% NS 154
.9% NS 308
LR
274
K+
Ca+
0
0
0
0
100g/l 0
0
0
0
0
0
77
77
0
0
0
0
154
154 0
0
0
0
130
109 4
1.5
28
50g/l
Na+
Cl-
0
Lactate
• Na, Cl, K, Ca, and lactate are measured in mmol/liter.
Colloid Resuscitation
• Colloids have larger molecular weight
particles with plasma oncotic pressures
similar to normal plasma proteins.
• With this it would be thought colloids
would be more effective at restoring
circulating blood volume compared to
crystalloid solutions.
Colloid Resuscitation Cont.
• However, in a systematic review of the use
of albumin in critically ill patients found an
increase relative risk of death, as compared
to the use of crystalloids.
• Given the much greater cost of colloid
products, there is no clear basis for the
choice of these agents over crystalloids for
resuscitation.
Blood Transfusion
• Remember there are no clear parameters for
transfusions.
• It is generally accepted that a patient in
shock not responding to 2-3 liters of
crystalloids will need a blood transfusion.
• Per American Society of Anesthesiologists
patients with an H/H of 10/30 will very
rarely need a transfusion.
Blood Transfusion Cont.
• However an H/H of 6/18 will almost always
need a transfusion.
• This however leads to a large area of
hemoglobin between 6-10.
• Many factors must be taken into account
when transfusing between the 6-10 mark.
• Remember blood is the ideal resuscitation
agent.
Hypertonic Resuscitation Fluids
• Hypertonic saline has been proposed as a potential
crystalloid solution alternative to isotonic due to
the limited tissue edema.
• Has been showed to rapidly expand intravascular
volume and enhance tissue perfusion.
• Could be a potential benefit in trauma patients by
limiting cerebral edema, lowering intracranial
pressure, and improving cerebral perfusion.
Hypertonic Resuscitation Fluids
Cont.
• Also may limit pulmonary interstitial fluid
shift.
• The volume given during resuscitation must
be monitored due to the propensity of
causing hypernatremia.
Oxygen-Carrying Resuscitation
Fluid
• Currently not being used in present day
resuscitation.
• Studies underway for use during resuscitation
efforts.
• The thought behind the idea is to have products
able to carrying O2 when loss of RBC’s occur.
• Two classes of agents, hemoglobin-based O2
carriers and fluorocarbon-based O2 carriers.
Questions
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B.
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T or F the best fluid to use during resuscitation
is colloids.
Which does not define SIRS:
WBC >12000
RR >20
SBP <90
HR >90
T or F Class 2 shock is loss of circulation blood
volume of 750-1500.
Questions Cont.
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B.
C.
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Which is not one of the categories of shock?
Obstructive
Restrictive
Distributive
Hypovolemic
T or F shock is associated with a SBP of <100
Answers: F, C, T, B, F