Uploaded by Mohammed Sebayel


Shock in the ICU
Definition: circulatory failure that results in inadequate
cellular oxygen utilization.
Definition and
• First: systemic arterial hypotension (systolic below 90 and mean
below 70) with Tachycardia (Pulse rate above 100
• Second: signs of tissue hypoperfusion, which are apparent through
the three “windows” of the body:
• Cutaneous: skin is cold and clammy, with vasoconstriction and
• Renal: urine output of <0.5 ml per kilogram of body weight per
• Neurologic: altered mental state, which typically includes
obtundation, disorientation, and confusion.
• Third: hyperlactatemia indicating abnormal cellular oxygen
metabolism. The normal blood lactate level 1 mmol per liter,
increased (>1.5 mmol per liter) in acute circulatory failure.
Four potential (Non-Exclusive), pathophysiological
hypovolemia (from internal or external fluid loss),
cardiogenic factors (e.g., acute myocardial infarction, endstage cardiomyopathy, advanced valvular heart disease,
myocarditis, or cardiac arrhythmias),
obstruction (e.g., pulmonary embolism, cardiac tamponade,
or tension pneumothorax),
or distributive factors (e.g., severe sepsis or anaphylaxis
from the release of inflammatory mediators).
Nonexclusive means combination:
Example: Hypovolemic shock due to trauma and hemorrhage
may be associated with spinal shock (distributive) or cardiac
tamponade (obstructive). Septic shock (distributive) with
cardiac depression (cardiogenic)…..etc
Type of
ion of the
four types
of shock
The most common in ICU is septic shock
(distributive) followed by cardiogenic and
hypovolemic. Obstructive is rare.
The type and cause of shock may be obvious from:
the medical history,
physical examination.
or clinical investigations.
Point-of-care echocardiographic evaluation:
Assessment for pericardial
Measurement of left and
right ventricular size and
Assessment for respiratory
variations in vena cava
Calculation of the aortic
velocity–time integral
(measures of stroke
Initial Approach:
Resuscitation should be started even while investigation of the cause Iis ongoing.
Identify the cause and correct rapidly examples:
control of bleeding,
percutaneous coronary intervention for coronary syndromes
thrombolysis or embolectomy for massive pulmonary embolism,
administration of antibiotics and source control for septic shock).
◦ arterial catheter to monitor arterial blood pressure and blood sampling.
◦ a central venous catheter for the infusion of fluids and vasoactive agents and to guide fluid therapy.
Since the goal of management of shock is the same (achieve adequate tissue
perfusion regardless of the case) management is similar and should be problem
oriented although the exact treatments that are used to reach those goals may
A useful mnemonic (memory aid) to describe the
important components of resuscitation is the VIP rule:
V: ventilation (oxygen administration)
I: infusion (fluid resuscitation)
P: pump (administration of vasoactive agents).
oxygen should be started immediately to increase oxygen delivery and prevent
pulmonary hypertension.
Pulse oximetry unreliable (Peripheral vasoconstriction)
Blood gas monitoring (ABG).
• Mechanical ventilation with endotracheal intubation
• patients with severe dyspnea,
• hypoxemia,
• or persistent or worsening acidemia (pH, <7.30). Invasive mechanical
Additional benefits
• of reducing the oxygen demand of respiratory muscles.
• decreasing left ventricular afterload by increasing intrathoracic pressure.
An abrupt decrease in arterial pressure after the initiation of invasive mechanical
ventilation strongly suggests hypovolemia and a decrease in venous return.
Sedative agents should be kept to a minimum to avoid further decreases in arterial
pressure and cardiac output.
Infusion (fluid
Fluid challenge observe four elements in advance:
◦ First, the type of fluid: Crystalloid solutions are the first choice followed by
◦ Second, the rate of fluid administration Fluids should be infused rapidly to
induce a quick response typically, an infusion of 300 to 500 ml of fluid during
a period of 20 to 30 minutes.
◦ Third, the objective of the fluid challenge must be defined. In shock, the
objective is usually an increase in systemic arterial pressure,
◦ Fourth the safety limits must be defined. Pulmonary edema is the most
serious complication of fluid infusion. Central venous pressure of a few
millimeters of mercury above the baseline value is usually set to prevent fluid
overload (not always accurate).
Fluid challenges can be repeated as required but must be stopped rapidly in case
of nonresponse in order to avoid fluid overload.
Adrenergic agents (adrenergic agonists):
of vasoactive
β-adrenergic: increase blood flow but also increases the risk of myocardial
ischemia as a result of increased heart rate and contractility e.g. isoproterenol
(only in bradycardia).
α-adrenergic increase vascular tone and blood pressure but can also decrease
cardiac output and impair tissue blood flow, especially in the hepatosplanchnic
region for this reason, phenylephrine, an almost pure α-adrenergic agent, is
rarely indicated.
Norepinephrine to be the vasopressor of first choice; it has predominantlyαadrenergic properties, but its modest β-adrenergic effects help to maintain
cardiac output. Administration generally results in a clinically significant increase
in mean arterial pressure, with little change in heart rate or cardiac output. The
usual dose is 0.1 to 2.0 μg per kilogram of body weight per minute.
Dopamine has predominantly βadrenergic effects at lower doses
and α-adrenergic effects at
higher doses:
very low doses (<3 μg
perkilogram per minute, given
intravenously) may selectively
dilate the hepatosplanchnic and
renal circulations, but controlled
trials have not shown a
protective effect on renal
function,14 and its routine use
for this purpose is no longer
undesired endocrine effects on
the hypothalamic–pituitary
system, resulting in
immunosuppression, primarily
through a reduction inthe release
of prolactin.
In a recent randomized,
controlled, double blind trial,
dopamine had no advantage over
norepinephrineas the first-line
vasopressor agent; moreover, it
induced more arrhythmias and
was associated with an increased
28-day rate of death among
patients with cardiogenic shock..
Epinephrine, which is a stronger agent, has predominantly βadrenergic effects at low doses, with α-adrenergic effects
becoming more clinically significant at higher doses. However,
epinephrine administration can be associated with an increased
rate of Arrhythmia. Reserve for refractory cases.
Vasopressin: deficiency can develop in patients with very
hyperkinetic forms of distributive shock, low-dose vasopressin
may result in substantial increases in arterial pressure.
Dobutamine: predominantly β-adrenergic properties. Inotropic
cardiac support. Increase cardiac output.
Arterial blood pressure: Mean arterial pressure of 65 to 70 to achieve
adequate tissue perfusion (skin, metal status, urine output).
Oxygen Delivery, SvO2 and ScvO2.
Goals and
Monitoring of
Lactate to Guide Treatment of Shock:
• Lactate is produced during tissue hypoxemia and hypoperfusion.
• In cardiogenic and hypovolemic shock, lactate rises as tissue hypoxemia results in
increased anaerobic metabolism.
• In distributive (usually septic) shock, mechanisms other than pure tissue ischemia
(anaerobic metabolism) may contribute to elevated lactate levels.
• Impaired liver function (either pre-existing or due to shock) may reduce lactate
clearance in any patient with shock, resulting in persistently high lactate values even
after perfusion is restored and lactate production normalizes.
Microcirculatory Variables.
Side stream Dark-Field
Image of Sublingual
Microcirculation in
Healthy Volunteer and
Patient with Septic
handheld devices for orthogonal
polarization spectral (OPS) imaging and its successor, sidestream dark-field
The four phase of shock treatment:
First (salvage) phase,
◦ the goal of therapy is to achieve a minimum blood pressure and cardiac output compatible with immediate survival.
◦ Minimal monitoring is needed; arterial and central venous catheters.
◦ Lifesaving procedures to treat cause (e.g., surgery for trauma, pericardial drainage, revascularization for acute
myocardial infarction, and antibiotics for sepsis)
Second (optimization)phase:
◦ The goal is to increase cellular oxygen availability
◦ Adequate hemodynamic resuscitation.
◦ Measurements of SvO2 and lactate guide therapy and monitoring of cardiac output cardiac output should be
Third (stabilization) phase:
◦ the goal is to prevent organ dysfunction,
◦ Oxygen supply to the tissues is no longer the key problem, and organ support becomes more relevant.
Fourth (de-scalation) phase:
◦ the goal is to wean the patient from vasoactive agents
◦ promote spontaneous polyuria or provoke fluid elimination using diuretics or ultrafiltration to achieve a negative
fluid balance.
Circulatory shock is associated with high morbidity and
Appropriate treatment is based on a good understanding of
the underlying pathophysiological mechanisms.
Treatment should include correction of the cause of shock
and hemodynamic stabilization, primarily through fluid
infusion and administration of vasoactive agents.
The patient’s response can be monitored by means of careful
clinical evaluation and blood lactate measurements;
microvascular evaluation may be feasible in the future.
Hemorrhagic Shock
Definition and Causes
hypovolemic shock. (examples: of Hypovolemic non-Hemorrhagic) ?
inadequate oxygen delivery at the cellular level.
Death quickly follows if bleeding not stopped (2 million/year/globally)!
Common causes:
Trauma ( Death 1.5 million annually)
maternal hemorrhage.
gastrointestinal hemorrhage.
Rupture Aortic Aneurysm.
Perioperative hemorrhage
Oxygen delivery is
Cells transition to
anaerobic metabolism.
Lactic acid, inorganic
Oxygen debt .
Accumulation of lactic
acid, Inorganic phosphate
free radicles.
Release of damageassociated molecular
patterns (known as
DAMPs or alarmins) leads
to systemic inflammation.
ATP deficiency leads to
failure of homeostasis,
membranes disruption
Necrosis and celldeath
Shock at
Cellular level:
Shock at Tissue level
hypovolemia and vasoconstriction cause hypoperfusion.
End-organ damage in the kidneys, liver, intestine, and skeletal muscle and multiorgan failure in
Extreme hemorrhage (exsanguination) pulselessness results in hypoperfusion of the brain and
◦ cerebral anoxia
◦ fatal arrhythmias within minutes.
Blood vessels:
◦ Endotheliopathy systemic shedding of the protective glycocalyx barrier.
◦ Clot formation at the site of injury and fibrinolysis at distant area (plasminogen activation and glycocalyx
shedding .
◦ Profound coagulopathy , plantlets dysfunction and loss. Iatrogenic factors.
◦ Pressure, Tourniquet, hemostatic dressing.
◦ Large pore IV administration (minimal to keep palpable pulse and patient awake)
◦ Avoid dilutional coagulopathy.
Rapid transport to Hospital.
◦ s/s subtle.
◦ BP low when loss of more than 30%.
◦ anxiety, tachypnea, a weak peripheral pulse, and cool extremities with pale or mottled skin.
Classification of Hemorrhagic Shock
Initial Evaluation:
Source…Hidden or obvious….Intracavity in trauma (chest, abdomen and pelvis)
Radiograph and US (pelvis chest and abdomen)
Blood gas and lactate
CBC, INR and Electrolytes.
◦ Find and control source of bleeding
◦ Restore intravascular volume
Transfusion: Massive-transfusion protocols mobilize universal donor blood products (e.g.,
packed red cells, plasma, platelets, and cryoprecipitate) to the patient’s bedside in prespecified
ratios (1:1:1 (i.e., 6 units of plasma and 1 unit of apheresis platelets [equivalent to approximately
6 units of pooled platelets] for every 6 units of red cells)
1 g of intravenous calcium chloride after transfusion of the first 4 units of any blood product)
limiting crystalloid infusions to 3 liters in the first 6 hours after arrival at the hospital
Phramcology: many …factors VII ?? Tranexamic acid
Management ….4:
Achieving definitive hemostasis:
Acute torso trauma… less than 10 minutes in ER.
Limbs….Tourniquet…… OR
Priorities the site of severe bleeding.
GI bleed…. Endoscopy.
Endovascular occlusion: resuscitative endovascular
balloon occlusion of the aorta (REBOA).
assessed for evidence of:
◦ ongoing hemorrhage,
◦ unpaid oxygendebt,
◦ anemia, coagulopathy,
◦ electrolyte derangements,
◦ other sequelae of over- or under-resuscitation
Septic Shock
Warm and Cold Shock
Sepsis: systemic inflammatory response to infection.
Severe Sepsis: when sepsis is complicated by acute organ dysfunction.
Septic Shock: sepsis complicated by either hypotension that is refractory to fluid resuscitation or
by hyperlactatemia.
Organ dysfunction: need for supportive therapy (mechanical ventilation, dialysis….)
Incidence: 2% of all hospital admissions and 10% of ICU admission, ¾ million per year in USA, 19
million per year worldwide.
Mortality : 80% 30 years ago now 20-30%.
Community acquired (pneumonia) or Hospital acquired.
Pneumonia, abdominal sepsis and UTI.
Blood culture positive in only 1/3 of cases.
In 1/3 culture from all sites are negative.
Causative organism:
◦ Gram negative in 62%
◦ Gram positive in 47%
◦ Fungi in 19%
Predisposing factors: Age, sex, chronic disease, immunological status and genetics
Clinical features: General Variables.
Fever (core temperature, >38.3°C)
Hypothermia (core temperature, <36°C)
Elevated heart rate (>90 beats per min or >2 SD above the upper limit of the normal range for
Altered mental status
Substantial edema or positive fluid balance (>20 ml/kg of body weight over a 24-hr period)
Hyperglycemia (plasma glucose, >120 mg/dl [6.7 mmol/liter]) in the absence of diabetes
Clinical Features: Inflammatory Variable
Leukocytosis (white-cell count, >12,000/mm3)
Leukopenia (white-cell count, <4000/mm3)
Normal white-cell count with >10% immature forms
Elevated plasma C-reactive protein (>2 SD above the upper limit of the normal range)
Elevated plasma procalcitonin (>2 SD above the upper limit of the normal range)
Clinical features: Organ dysfunction
Arterial hypoxemia (ratio
of the partial pressure of
arterial oxygen to the
fraction of inspired
oxygen, <300)
Acute oliguria (urine
output, <0.5 ml/kg/hr or
45 ml/hr for at least 2 hr)
Paralytic ileus (absence of
bowel sounds)
Increase in creatinine level
of >0.5 mg/dl (>44
(platelet count,
Coagulation abnormalities
(international normalized
ratio, >1.5; or activated
time, >60 sec)
(plasma total bilirubin, >4
mg/dl [68 μmol/liter])
Clinical Features: Tissue
perfusion Variables.
Hyperlactatemia (lactate, >1 mmol/liter)
Decreased capillary refill or mottling
Severe sepsis (sepsis plus organ dysfunction)
Septic shock (sepsis plus either hypotension [refractory to
intravenous fluids] or hyperlactatemia)
Acute organ dysfunction:
Respiratory: acute respiratory distress syndrome (ARDS) defined as hypoxemia with bilateral
infiltrates of noncardiac origin.
Cardiovascular: hypotension or an elevated serum lactate level after adequate volume
expansion, requiring the use of vasopressors’ myocardial dysfunction.
Brain: obtundation or delirium.
Kidney: Acute kidney injury, decreasing urine output, increasing serum creatinine level , may
requires treatment with renal-replacement therapy.
Others: Paralytic ileus, elevated aminotransferase levels, altered glycemic control,
thrombocytopenia and disseminated intravascular coagulation,adrenal dysfunction, and the
euthyroid sick syndrome
Guidelines are
organized into two
“bundles” of care:
Initial management:
• initial management
bundle to be
accomplished within 6
• management bundle
to be accomplished in
the ICU.
• Resuscitation: fluid
and vasoactive agents
and respiratory
• Forming probable Dx,
culture, drainage and
Antibiotic therapy.
ICU management:
• monitoring and
support of organ
• avoidance of
• de-escalation of care
when possible.