SHOCK – SURGERY A - What does plasma have that is disadvantage to the recipient?

Dagani, MD Antibody, Waste product

References: Dany Targ trans, PPT 2019, 2B recording
HISTORICAL BACKGROUND
Alfred Blalock
- Stated that shock in hemorrhage was associated with reduced
cardiac output due to volume loss and not by a toxic factor
Shock
- The failure to meet the metabolic needs of the cell and the
consequences that ensues
- Basically, if there will be a problem with the circulation the oxygen
and nutrition would not reach the cell or tissue for homeostasis to
ensue
- Decreased tissue perfusion - is the central component of shock
Four categories of shock (by Alfred Blalock)
1. Hypovolemic Shock
- Most common type
- Results from loss of circulating blood volume
- Result of bleeding leading to hypotension
• Hemorrhagic / Whole blood loss (trauma, gunshot wound), Non
hemorrhagic / Plasma loss (due to third space loss like dehydration or
diarrhea), Interstitial fluid (bowel obstruction), or a combination
2. Vasogenic (Septic) Shock
- Results from decreased resistance (increase vasodilation and
space) within a capacitance vessel, seen in sepsis hence at
the end insufficient circulation.
3. Neurogenic Shock
- Form of vasogenic shock
- Spinal cord injury or spinal anesthesia causes vasodilation
due to acute loss of sympathetic vascular tone
4. Cardiogenic Shock
- Results from failure of the heart as a pump, seen in arrythmias
(uncoordinated contraction hence no effective cardiac output or
ejection) or acute myocardial infarction (the myocardial cells are
dead)
- Instead of giving WB, we give pRBC for volume
D. Unrecognized or inadequately corrected hypoperfusion
increases morbidity and mortality
• Patient optimization for faster recovery
E. Excessive fluid resuscitation may exacerbate bleeding
• Related to principles of damage control surgery
PRIMARY SURVEY
A – Airway
• Control the airway, if not breathing secure and intubate the patient
B – Breathing
- Look if there is any obstruction
C – Circulation
- Check for blood pressure, use fluids
D – Deficit / Disability (Neurologic)
- Glasgow coma scale (highest-15, lowest-3)
E – Exposure
PATHOPHYSIOLOGY OF SHOCK
PHASES:
Compensatory Phase
- The body compensate for the initial loss of blood volume through
the neuroendocrine response to maintain hemodynamics (such
as in hemorrhagic shock)
- The body will try to compensate so that the blood pressure will
normalize due to the initial blood loss

Overtime, 2 additional shocks were added

5. Obstructive Shock
- Form of cardiogenic shock
- Results from mechanical impediment to circulation leading
to depressed cardiac output rather than primary cardiac failure
(pulmonary embolism or tension pneumothorax)
- In reality the heart has no problem it is the expansion of the heart Decompensatory Phase
- Physiology: in preload the volume of blood coming from the - Continued hypoperfusion, which may be unrecognized, ongoing
venous return will go to the heart hence more blood going to the cellular death and injury
heart the better the pump BUT in cases such as tension - Microcirculatory dysfunction, parenchymal tissue damage and
pneumothorax or cardiac tamponade the heart cannot expand inflammatory cell activation can perpetuate hypoperfusion
thus lower blood amount going to the heart. - Ischemia or reperfusion injury often exacerbates the initial result
6. Traumatic Shock o If it is an anaerobic condition and you give oxygenated
- Soft tissue and bony injury leads to the activation of inflammatory blood the patient will have free radicals, thus there will
cells and the release of circulating factors (cytokines & be a compromise of the function of the organ. (Tissue
intracellular molecules that modulate the immune response. cycle of shock)
- The effects of tissue injury are combined with the effects of - Vicious cycle of shock: compromise function at the organ system
hemorrhage creating a more complex and amplified deviation level due to untreated damage at the cellular level
from homeostasis.
-
Core Principles in the Management of the Critically ill / Injured patient
A. Definitive control of the airway must be secured
B. Control of active hemorrhage
- Paramount priority especially for hemorrhagic shock
- WHY? If for example there was a patient with blood loss (neck
wound) in the emergency room and you took his BP and the
result was hypotensive or palpatory (can’t detect BP)-
Management: give electrolytes and fluid (replace)
- However, even if you infuse fluid to normalize the bp that would
not happen until the patient is bleeding, so what is important is
to control the bleeding by pressing or any other mechanical ways
- If in another part like the abdomen or stomach which is hard to
control a different type of management is used.
C. Volume resuscitation with blood products with limited volume of Irreversible Phase
crystalloid must occur while operative control of bleeding is - Persistent hypoperfusion results in further hemodynamic
achieved. derangements and cardiovascular collapse
- There are different types of blood products: WB, pRBC, platelet - Develop quite insidiously and may only be obvious in retrospect
conc. FFP - Expensive parenchymal and microvasculature injury that volume
- What does WB have that pRBC doesn't have? Plasma resuscitation fails to reverse process and will eventually lead to
death
Modified Wiggers model in animals representing the phases of
compensation, decompensation and irreversible phases of
hemorrhagic shock:
• 0% - 100% recovery
• 50% - death
How many blood volume
does a person have? 5L
Neuroendocrine and Organ - Specific Response to Hemorrhage
- Goal: maintain perfusion to the heart and brain, even at
the expense of the other organs systems (EXCEPT: coronary
artery and circle of willis)
- Peripheral vasoconstriction occurs and fluid excretion is
inhibited.
o Hence those with prolonged hypovolemia or
hypotension it will lead to acute renal failure because
it isn't the priority.
- Mechanisms:
1. Autonomic control of peripheral vascular tone and
cardiac contractility
2. Hormonal response to stress and volume depletion
3. Local microcirculatory mechanism
o organ specific
o regulate regional blood flow
- Initial stimulus: loss of circulating blood
- Magnitude of the response is based on:
o the volume of blood lost
o rate at which it is lost (hemorrhagic)
Afferent Signals
- Impulses transmitted from the periphery and processed
within the CNS and activates reflexive efferent impulses
- Role of Effector:
1. Expand plasma volume
2. Maintain peripheral perfusion, and tissue O2 deliver
3. Restore homeostasis
- Other stimuli: pain, hypoxemia, hypercarbia, acidosis,
infection, change in temperature, emotional arousal or
hypoglycemia
A. Spinothalamic Tracts
- Transmits the sensation of pain
- Resulting in activation of the hypothalamic – pituitary -
adrenal axis and autonomic nervous system including
direct sympathetic stimulation of the adrenal medulla to
release catecholamines (epinephrine and norepinephrine)
B. Baroreceptors
- Volume receptors sensitives to changes in both chamber
pressure and wall stretch present within the atria of the
heart, activated with low volume hemorrhage or mild
reductions in right atrial pressure
- Receptors in the aortic arch and carotid bodies respond to
alterations in pressure or stretch of the arterial wall
responding to larger reductions in intravascular
volume or pressure
- Normally inhibits induction of the ANS, but when activated
these receptors diminish their output, disinhibiting the
ANS, increasing output via sympathetic activation at the
vasomotor centers producing centrally mediated
constriction of peripheral vessels
C. Chemoreceptors
- Found in the aorta and carotid bodies
- Sensitive to changes in O2 tension, H+ ion concentration
and CO2 levels
- Stimulation ->
1. Coronary Vasodilation
2. Bradycardia
3. Splanchnic & skeletal circulation vasoconstriction
D. Variety of protein and nonprotein mediators
- Histamine, cytokines, eicosanoids and endothelins
- Produced at the site of injury as part of the inflammatory
response, acts as afferent impulse to induce a host response
Efferent Signals
1. Cardiovascular Response
- Results from neuroendocrine and ANS response to shock and
constitute a prominent feature of the body’s adaptive response
mechanism and clinical signs and symptoms of the patient in
shock
- Hemorrhage results in diminished venous return and decreased
cardiac output (B1 adrenergic)
o Compensated by (tachycardia) increase cardiac
heart rate and contractility and venous and arterial
vasoconstriction (via a1-adrenergic)
o Increased myocardial O2 consumption occurs due to
increased workload, thus O2 supply must be
maintained to prevent development of myocardial
dysfunction
- Increased sympathetic output induces catecholamine release
from the adrenal medulla and peaks within 24-48 hours of
injury then return to baseline
o Stimulate of hepatic glycogenolysis and
gluconeogenesis
o Increase skeletal muscle glycogenolysis
o Suppression of insulin release
o Increased glucagon release
2. Hormonal Response
- activation of the ANS and the hypothalamic-pituitary-
adrenocorticotropic-axis
ACTH and Cortisol
- Shock stimulates the hypothalamus to release corticotrophin
releasing hormone resulting to the release of ACTH by the
pituitary
- ACTH stimulates the adrenal cortex to release cortisol (primary
stress hormone)
- Functions of Cortisol:
o Acts synergistically with epinephrine and glucagon to
induce catabolic state
o Stimulates gluconeogenesis and insulin resistance
resulting in hyperglycemia as well as muscle cell
protein breakdown (proteolysis) and lipolysis to
provide substrates for hepatic gluconeogenesis
o Retention of sodium and water by the nephrons of the
kidney
RAAS
- Renin is released from the juxtaglomerular cells and the release
is caused by:
o Decreased renal artery perfusion
o Beta adrenergic stimulation
o Increased renal tubular sodium concentration
- Renin catalyzes the conversion of angiotensinogen (from the
liver) to angiotensin I which is then converted to angiotensin II
by ACE (produced by the lungs)
- Angiotensin I: NO significant functional activity
- Angiotensin II: potent vasoconstrictor of both splanchnic and
peripheral vascular beds.
- It also stimulates secretion of aldosterone, ACTH and ADH
- Aldosterone: a mineralcorticoid that acts on nephron to
promote reabsorption of sodium and (as a consequence) water
o Potassium and hydrogen ions are lost in the urine in
exchange for sodium
ADH or Arginine Vasopressin
- Released by the pituitary in response to:
o Hypovolemia
o Changes in circulating blood volume sensed by
baroreceptors and left atrial stretch receptors
o Increased plasma osmolality detected by hypothalamic
osmoreceptors
- Epinephrine, angiotensin II, pain and hypergylcemia increases
production of ADH
- Acts on distal tubule and collecting duct of the nephrons to
o Increase water permeability
o Decreased water and sodium losses
o Preserve intravascular volume
- In hypovolemic state, acts as a potent mesenteric
vasoconstrictor, shunting circulating blood away from
splanchnic organs
- In shock state, may contribute to intestinal ischemia and
predispose to intestinal mucosal barrier dysfunction
- Increases hepatic gluconeogenesis and increases hepatic
glycolysis
- In septic states, endotoxin directly stimulates arginine
vasopressin (independent of blood pressure, osmotic or
intravascular volume changes)
- Proinflammatory cytokines also contribute to release of
vasopressin
Circulatory Homeostasis
A. Preload
B. Ventricular Contraction
- Franks Starlings Curve: strength of force of ventricular
contraction as a function of preload.
- If there are a lot of preload - the heart stretches more-
stronger contraction of ventricles
C. Afterload
- Force that resists myocardial work during contraction
- Arterial pressure is a major component and influences the
ejection fraction
D. Microcirculation
- Microvasculature bed is innervated by the sympathetic
nervous system and has a profound effect on the larger
arterioles
- In hemorrhage, this vessel constricts but on septic or
neurogenic, they dilate
- Other vasoconstrictors: vasopressin, angiotensin II and
endothelin 1
- Pathophysiologic response of microcirculation in shock:
o Failure of integrity of the endothelium of the
microcirculation - due to dysfunction of energy-
dependent mechanisms
o Intracellular swelling - multifactorial
o Recruitment of segmenters and platelet - higher
resistance of microcirculation
o Extracellular fluid deficit - due to decreased
capillary hydrostatic pressure secondary to changes
in blood flow and increased cellular uptake of fluid
o Capillary leak - dysfunction in secondary to
activation of endothelial cells by circulating
inflammatory mediators generated in septic or
traumatic shock
- Lead to diminished capillary perfusion:
o Endothelial cell swelling
o Dysfunction
o Recruitment of PMN and platelets
Metabolic Effects
- Cellular metabolism is based on the hydrolysis of ATP
o Splitting of the phosphoanhydride bond of the
terminal or gamma-phosphate from ATP is the
source of energy for most processes
o Majority of ATP is generated in our bodies through
aerobic metabolism in the process of oxidative
phosphorylation in the mitochondria
o Process is dependent on O2 availability which serves
as final electron acceptor in the ETC
- As O2 tension decreased, oxidative phosphorylation decreases,
and generation of ATP is slowed down
o (+) anaerobic metabolism & glycolysis
- Glycolysis (is not an efficient process) only 2 mol of ATP is
produced from 1 mol of glucose
- Complete oxidation produces 38 mol of ATP per 1 mol of glucose
- Under hypoxic conditions, in anaerobic metabolism, pyruvate is
converted to lactate leading to intracellular metabolic
acidosis (if it is in a local area: spasm, pain)
Consequences that are secondary to Metabolic Changes:
- Depletion of ATP potentially influence all ATP-dependent
cellular processes:
o Maintenance of cellular membrane potential (no
traveling of impulse)
o Synthesis of enzymes and proteins
o Cell signaling
o DNA repair mechanisms (paracrine function)
- Decreased intracellular pH influences vital cellular functions
- Changes will lead to changes in gene expression within the
cell
o Normal enzyme activity
o Cell membrane ion exchange
o Cellular metabolic signaling
- Acidosis leads to changes in calcium metabolism and
signaling
-
Effects of Catecholamines:
- Processes increased by catecholamines:
o Hepatic glycogenolysis
o Gluconeogenesis
o Ketogenesis
o Skeletal muscle protein breakdown
o Adipose tissue lipolysis
- Cortisol, glucagon and ADH also contribute to the catabolism
during shock
- Epinephrine induces further release of glucagon and
inhibits release of insulin resulting to:
o Catabolic state with glucose mobilization
o Hyperglycemia
o Protein breakdown
o Negative nitrogen balance
o Lipolysis
o Insulin resistance during shock and injury
- The underuse of glucose by peripheral tissue preserve it for
the glucose-dependent organs such as heart and brain
Cellular Hypoperfusion
- Crowell, 1961- hypoperfused cells and tissue experience
what has been termed “oxygen debt”
- O2 debt - deficit in tissue oxygenation over time
o normal circumstances cells can “repay” the O2
debt during reperfusion
- Magnitude of the O2 debt correlates with the severity and
duration of hypoperfusion
o The more severe the hypoperfusion and longer the
condition the more O2 debt will happen hence more
compensation. It is a need for the oxygen demand
to catch up in order for homeostasis to happen
- Changes in Cellular Gene Expression
o The DNA binding activity of a number of nuclear
transcription factors is altered by hypoxia and
production of O2 or nitrogen radicals which are
produced by shock ((+) ROS, RNS)
o Other gene products increased by shock
§ Heat shock proteins
§ Vascular endothelial growth factor
(VEGF)
§ inducible Nitric Oxide Synthase (iNOS)
§ Cytokines
Immune and Inflammatory Response
Danger Signaling
- Damage-associated molecular patterns (DAMPs)
o endogenous molecules are capable of signaling the
presence of danger to surrounding cells and tissues
(proposed by Matzinger)
o recognized by cells surface receptors to effect
intracellular signaling that primes and amplifies the
immune response (2 effects good or bad)
Cytokines / Chemokines
- Substances released very early during changes in the body
specifically inflammation (innate immune response)
- Innate immune response can help restore homeostasis, or if
excessive, it can promote cellular organ dysfunction
 4. IL-6
- Elevated levels correspond with mortality in shock states
- Contributes to lung, liver, and gut injury after hemorrhagic
shock
- Play a role in development of diffuse alveolar damage and
ARDS (acute respiratory distress syndrome)
- Along with IL-1, they are:
o Mediators of hepatic acute phase response to
injury
o Enhance the expression and activity of
complement,C-reactive protein, fibrinogen,
1. Tumor Necrosis Factor Alpha (THF-alpha) haptoglobin, amyloid A and a1-antitrypsin
- One of the earliest potent proinflammatory cytokines o Promote neutrophil activation
released in response to injurious stimuli 5. IL-10
- Released by: - Anti-inflammatory cytokine that may have
o Monocytes immunosuppressive properties
o Macrophages - Associated with depressed immune function and
o T-cells increased susceptibility to infections
- Peaks within 90 minutes of stimulation and returns to - Secreted by T-cells, monocytes and macrophages
baseline by 4 hours - IL-10 inhibits:
- Induced by: o Pro-inflammatory cytokine secretion
o Bacteria or endotoxin and leads to development o O2 radical production by phagocytes
of shock and hypoperfusion (most commonly o Adhesion molecule expression
observed in septic shock) o Lymphocyte activation
o Hemorrhage 6. Chemokines
o Ischemia - Specific set of cytokines that have the ability to induce
- Functions of TNF-a: chemotaxis of leukocytes
o Produce peripheral vasodilation - Chemotaxis- is the property to let the immune cells migrate
o Activate release of other cytokines to the sight of injury
o Induce procoagulant activity - Involved in:
o Stimulate a wide array of cellular metabolic o Immune system development
changes o Immune surveillance
- TNF-a (deadly!) levels correlate with mortality in models of o Immune priming
hemorrhage o Effector response
- Increase in serum TNF-a levels in trauma patients is less o Immune regulation
than in septic patients
- During stress response, it contributes to muscle protein Complement
breakdown and cachexia (Cancer patient have increase - Marker of severity and injury
TNF-alpha) - Activated complement factors (C3a, C4a, C5a) are potent
mediators of
2. Interleukin - 1 (IL-1) o Increased vascular permeability
- Actions similar to TNF-a o Smooth muscle contraction
- Short half life of 6 minutes o Histamine and arachidonic acid by product release
- Primarily acts in paracrine fashion to modulate local cellular o Adherence of neutrophils to vascular endothelium
responses vs TNF which is more generalized - Acts synergistically with endotoxin top induce the release of
- Produces a febrile response to injury by activating the TNF-a and IL-1
prostaglandins and causes anorexia by activating the - Development of ARDS and MODS in trauma patients
satiety center correlates with intensity of complement activation
- Augments the secretion of:
o ACTH (related to stress) Neutrophils
o Glucocorticoids - First cells to be recruited at the site of injury
o B-endorphins - PMNs remove infectious agents, foreign substance and
- Stimulate the release of other cytokines (together with TNF- nonviable tissue through phagocytosis
alpha): - Activated PMNs and their products may produce cell injury
o IL-2 and organ dysfunction
o IL-4 - Generate and release a number of substances that may
o IL-6 induce cell or tissue injury, such as:
o IL-8 o Reactive O2 species
o Granulocyte-macrophage colony stimulating o Lipid peroxidation products
factor (increase macrophage) o Proteolytic enzymes (lysosome)
o Interferon-y o Vasoactive mediators
3. Interleukin – 2 (IL-2) - Oxygen free radicals induce lipid peroxidation, inactivate
- Produced by activated T-cells in response to variety of enzymes and consume antioxidants
stimuli and activates other lymphocytes subpopulations
and natural killer cells. Cell Signaling
- Role is still not confirmed in shock, current postulates - Signaling pathways are altered by changes in:
include: - Intracellular calcium (Ca2+) concentrations regulate many
o Increased IL-2 secretion promotes shock- aspects of cellular metabolism and changes of Ca2+ levels
induced tissue injury and the development of and Ca2+ transport is seen in shock
shock - Alteration of Ca2+ regulation to:
o Depressed IL-2 contributes to depression in o Direct cellular injury
immune function after hemorrhage that o Changes in transcription factor activation
increased the susceptibility of patients who o Alteration in the expression of genes important
develop shock to suffer infections in homeostasis
o Overly exuberant pro-inflammatory activation, o Modulation of the activation of cells by shock-
promotes tissue injury, organ dysfunction, & induced hormones or mediators
immune suppression
Effects of Oxygen Radicals on the Intracellular Signaling Cascade
- Intracellular signaling cascade consists of a series of kinase
that transmit and amplify the signal through phosphorylation
of target proteins
- The O2 radicals produced during shock and intracellular
redox state are known to influence the activity of components
of the intracellular cascade, such as:
o Protein tyrosine kinase
o Mitogen activated kinase
o Protein kinase C
FORMS OF SHOCK
HYPOVOLEMIC / HEMORRHAGIC SHOCK
- Most common cause of shock is loss of circulating
volume from hemorrhage (due to surgery/trauma)
- Response of the body to acute blood loss → decreased
baroreceptor stimulation → decreased inhibition of
vasoconstrictor centers, increased chemoreceptor
stimulation of vasomotor centers, diminished output from
atrial stretch receptors → increases vasoconstriction and
peripheral arterial resistance
- Hypovolemia induces sympathetic stimulation leading to:
o Epinephrine and Norepinephrine release
o Activation of the renin-angiotensin cascade
o Increased vasopressin release
- Peripheral vasoconstriction + lack of sympathetic effects
on cerebral and coronary vessels + local autoregulation →
maintenance of cardiac and CNS blood flow
- Initially, treatment is empiric (ABCDE)
o Secure airway
o Volume infusion initiated while the search for the
cause
o Shock in trauma or post-op patients is presumed
to be due to hemorrhage until proven otherwise
- Clinical signs of shock:
o Agitation
o Cool clammy extremities
o Tachycardia
o Week or absent peripheral pulses
o Hypotension (atleast 25% of blood loss)
- Elderly not very tolerant to hemorrhage:
o Maintenance meds promote bleeding (aspirin,
clopidogrel)
o Atherosclerotic vascular disease
o Diminishing cardiac compliance
o Inability to elevate HR or cardiac contractility in
response to hemorrhage
o Overall decline in physiologic reserve
- Sites of blood loss sufficient to cause shock:
o External: carotid
o Intrathoracic: pulmonary vessels
o Intraabdominal: mesenteric vessels
o Retroperitoneal: renal vein/artery
o Long bone fractures: femur
- Each pleural cavity can hold 2-3L of blood and can be a
site of significant blood loss (HEMOTHORAX)
o Unstable patients - tube thoracostomy
§ to drain the blood, because when lung
expands, it may cause cardiac
tamponade
o Stable patients- chest radiograph
- Pelvic fracture: major retroperitoneal hemorrhage
- Intraperitoneal hemorrhage: most common source
inducing shock
- Non-trauma: GIT must always be considered
o Upper or Lower GIT bleeding
o With hematemesis or bleeding
o Hx & PE is important
- Direct pressure must be applied and sustained to minimize
ongoing blood loss
TREATMENT: Control ongoing hemorrhage
o Treatment instituted concurrently with diagnostic
evaluation
o Patients who fail to respond to initial
resuscitation should be assumed to have
ongoing active hemorrhage from large
vessels and require prompt operative
intervention → bring patient to OR immediately
- Appropriate priorities in patients:
o Secure the airway
o Control the source of blood loss
o Intravenous volume resuscitation
- Active bleeding patient cannot be resuscitated until control
of ongoing hemorrhage is achieved
TREAMTMENT: Damage control resuscitation
- begins in the emergency department and continues into
the OR up to the ICU
o Initial resuscitation: limit systolic BP (SBP)
around 80-90 mmHg
o Prevent renewed bleeding from recently clotting
vessels
o Warm the patient & prevent coagulopathy
§ Development of hypothermia in the
bleeding patient is associated with
acidosis, hypotension and
coagulopathy
§ Hypothermia is an independent risk
factor for bleeding and death 2° to
impaired platelet function and
impairments in coagulation cascades
o Resuscitation and intravascular volume
resuscitation are accomplished with blood
products (RBC, FFP, PLTs in equal numbers)
and limited crystalloids
- For patients with blunt injury (car crash, usually head
trauma), an SBP of 110 mmHg is more appropriate
- For patients with penetrating injury (stab wound, gunshot
wound), a goal of SBP 80-90 mmHg may be adequate
TREATMENT: Irreversible Shock
- Patients who fail to respond to resuscitative efforts but with
control of hemorrhage have deteriorated to decompensate or
irreversible shock with peripheral vasodilation and resistance
to vasopressor infusion
- Ongoing fluid requirements despite adequate control of
hemorrhage
- Persistent hypotension despite restoration of intravascular
volume necessitating vasopressor support
- Exhibit of futile cycle of acidosis, hypotension, and
coagulopathy
- Fluid resuscitation → major adjunct to hemorrhage control
o Crystalloids: mainstay of fluid of choice
o Increased risk of death treated with colloid vs
crystalloid (Colloid → requires crossmatch and
blood products that are not readily available)
o Severe hemorrhage: restoration of intravascular
volume should be achieved with blood products
TREATMENT: Fluid resuscitation
- Hypertonic saline is evaluated as a resuscitative adjunct in
bleeding patients, & as the benefit of being immunomodulatory,
and may contribute to the decreases of incidence of perfusion-
mediated injury, less impairment of immune function, less brain
swelling in multi-injured patients, contribute to decrease ARDS
and MOF (multiple organ failure)
o PRBC: target Hgb of 7-9 g/dL
o Damage control resuscitation: transfuse with pRBC,
FFP, platelet concentrate given in equal number
o Increased platelet: appears to improve outcome
§ Most pronounced in trauma patients with
brain injury
§ Maintain counts above 50x109 /L (<50,
spontaneous bleeding)
o Minimization of heat loss and maintaining
normothermia --- Hypothermia → acidosis,
hypotension, and coagulopathy → give warmers
§ Independent risk factor for bleeding and
death
 TRAUMATIC SHOCK
- Systemic response after trauma, combining the effects of soft
tissue injury, long bone fractures, and blood loss
- MOF, including ARDS develop often in trauma patient, rarely
in pure hemorrhagic shock patient
- Hypoperfusion deficit is magnified by the pro-inflammatory
activation that occurs following the induction of shock
- At the cellular level, releases of DAMPs (RNA, Uric acid) →
(+) Pattern recognition receptors (PRRs) & TLR family of
proteins
- Examples of traumatic shock include:
o Small-volume hemorrhage with by soft tissue
injury
o Any combination of hypovolemic, neurogenic,
cardiogenic, and obstructive shock that
precipitates rapidly progressive
proinflammatory action
TREATMENT:
- Focused on correction of the individual elements to
diminish the cascade of pro-inflammatory activation
- Prompt control of hemorrhage, adequate volume
resuscitation to correct O2 debt
- Debridement of non-viable tissue
- Stabilization of bone injures
- Appropriate treatment of soft tissue injuries
SEPTIC / VASODILATORY SHOCK
- Result of the dysfunction of the endothelium and
vasculature
- Secondary to circulating inflammatory mediators and cells
or as a response to prolonged and severe hypoperfusion
- Hypotension and resistant to treatment with vasopressors
result from failure of the vascular smooth muscle to
constrict appropriately
- Catecholamine and RAAS are activated
- Septic shock: Most frequently encountered vasodilatory
shock
- Vasodilatory shock: final common pathway for profound
and prolonged shock of any etiology
o Other vasodilatory shock:
ü Hypoxic lactic acidosis
ü Carbon monoxide poisoning
ü Decompensated & irreversible
hemorrhagic shock
ü Terminal cardiogenic shock
ü Post-cardiotomy shock
DIAGNOSIS:
Septic shock is a by-product of the body’s response to disruption
of the host-microbe equilibrium, resulting in invasive or severe
localized infection
- Manifestation of sepsis (host response)
o Fever
o Leukocytosis
o Hyperglycemia
o Enhanced cardiac output
o Peripheral vasoconstriction
o Tachycardia
- Diagnostic criteria: manifestation of host response +
identification of offending organism
o Identify offending organism through blood
culture: extract from at least 3 sites
ü (+) isolated in at least 2
- Patients with sepsis have evidence of an infection, as well
as signs of systemic inflammation
- Severe sepsis is hypoperfusion with signs of organ
dysfunction
- Septic shock requires presence of severe sepsis,
associated with more significant hypoperfusion and
systemic hypotension (circulatory failure)
TREATMENT:
- Beings with the assessment of airway and ventilation
- Severely obtunded patients require intubation and ventilation
to prevent respiratory collapse
- Fluid resuscitation and restoration of circulatory volume with
balanced salt solutions is essential (at least 30 mL/kg with the
first 4-6 hrs)
- Starch-based colloid solutions should be avoided
- Antibiotics should be tailored to cover the responsible
organism (give broad-spectrum, empiric even if you have not
yet isolated bacteria)
- Role of surgery - source control
- Catecholamines are used more often with norepinephrine
being the first line agent followed by epinephrine
- Arginine vasopressin is often added with norepinephrine for
patients that develop resistance to catecholamines
- Dobutamine therapy is recommended for patients with
cardiac dysfunction as evidenced by high filling pressures and
low CO
CARDIOGENIC SHOCK
- Circulatory pump failure leading to diminished forward flow
and subsequent tissue hypoxia, in the setting of adequate
intravascular volume
- Hemodynamic criteria:
o Sustained hypotension (SBP <90 mmHg for at least
30 mins)
o Reduced cardiac index (<2.2L/min per square meter)
o Elevated pulmonary artery wedge pressure (>15
mmHg)
- Mortality rate: 50-80% (ex. massive MI)
o Left anterior descending coronary art. supplies a big
part of the heart, if this is obstructed, 2/3 of heart will
be infarcted
- Acute, extensive MI is the most common cause and a
smaller infarction in a patient with existing left ventricular
dysfunction also may precipitate this type of shock
o Develops signs of cardiogenic shock within 24h after
onset of infarction, average within 7h
DIAGNOSIS:
- Cardiac exam: dysrhythmia, precordial heave, distal heart
tones
- Confirmation requires ECG and urgent echocardiography
- Blood chemistry- Troponins, CK-MB
TREATMENT:
- Intubation and mechanical ventilation often are required, to
decrease work of breathing and facilitate sedation of the
patient
- Treatment of cardiac dysfunction:
o Maintenance of adequate oxygenation
o Judicious fluid administration to avoid fluid overload
and development of cardiogenic pulmonary edema
- Correct electrolyte abnormalities
- Pain is treated with IV morphine sulfate or fentanyl
- Dysrhythmias and heart block must be treated with anti-
arrhythmic drugs (amiodarone), pacing or cardioversion
(shock)
- If profound cardiac dysfunction exists, inotropic support may
be indicated to improve cardiac contractility and cardiac
output
o Dobutamine: stimulates cardiac β1 receptors to
increase CO, but may:
§ Vasodilate peripheral vascular beds
§ Lower total peripheral resistance
§ Lower systemic blood pressure through
effects of β2 receptors
§ Adequate preload (measure via CVP
N=8-10 cmH20) is essential prior to
giving dobutamine
o Dopamine stimulates vasoconstriction, β1
receptors (cardiac stimulation) and β2 receptors
(vasodilation) at low doses
§ Preferred treatment for cardiac
dysfunction in hypotensive patients
§ Tachycardia and increased peripheral
resistance from dopamine infusion may
worsen myocardial ischemia
o Epinephrine stimulates α and β receptors and may
increase cardiac contractility & HR, may also have
intense peripheral vasoconstrictor effects that can
impair cardiac performance
o Phosphodiesterase inhibitors (amrinone and
milrinone) may be required on occasion in patients
with resistant cardiogenic shock
 - Intra-aortic balloon pump: mechanical circulatory for those
with resistant cardiotonic and increased CO and improved
coronary blood flow
- Percutaneous transluminal coronary angiography is
recommended for patients with: (treatment of choice)
o Cardiogenic shock
o ST elevation
o Left bundle branch block
o Less than 75 years old
- Coronary artery bypass grafting (CABG) seems to be more
appropriate for patients with multiple vessel diseases or left
main coronary artery diseases
OBSTRUCTIVE SHOCK
- Heart cannot pump or expand effectively
- Most commonly due to presence of tension pneumothorax
o Increased intrapleural pressure secondary to air
accumulation, pushes mediastinum to side and
affects the heart
- Cardiac tamponade occurs when sufficient fluid has
accumulated in the pericardial sac to obstruct blood flow to
the ventricles (limited ventricular filling in diastole)
- Pericardial pressure is the major determinant of degree
of hypotension
DIAGNOSIS:
- Diagnosis of tension pneumothorax should be made on
clinical examination
- Findings include:
o Respiratory distress
o Hypotension
o Diminished breath sounds over one hemithorax
o Hyperresonance to percussion
o Jugular venous distention
o X-ray: Shift of mediastinal structures to the
unaffected side with tracheal deviation
- FOR CARDIAC TAMPONADE
o CXR: provide trajectory information
o ECG: preferred test for diagnosis of cardiac
tamponade
o UTZ: detect myocardial status if there is fluid
§ Large volume of fluid, right atrial
collapse, distensibility of right ventricle
TREATMENT:
- Needling: pleural space can be decompressed with a
large caliber needle (gauge 14,15) at mid-clavicular line 2nd
ICS
- Chest tube thoracotomy (CTT) is the definitive treatment
for tension pneumothorax placed at the 4th ICS at the
anterior axillary line
- Pericardiocentesis to diagnose pericardial blood and
potentially relieve tamponade may be used
o Potential to produce cardiac injury
o Mapoke yung heart <3
- Diagnostic pericardial window
o Most direct method to determine the presence of
blood within the pericardium, performed through
either subxiphoid or transdiaphragmatic
approach
o Best performed at the operating room under GA
- Diagnosis of cardiac tamponade
o Beck’s triad - collection of signs associated with
acute cardiac tamponade
§ Hypotension (low arterial BP)
§ Distant, Muffled heart sounds
§ Neck vein distention (NV: 6 - 8cm
H2O)
o Narrowed pulse pressure
o Pulsus paradoxus
§ Heart sounds disappear when px
inhales, heard only on exhalation
(when lung pressure is released)
§ Cardiac rate varies during
inhale/exhale
NEUROGENIC SHOCK
- Diminished tissue perfusion as a result of loss of vasomotor
tone to peripheral arterial beds → increase vascular
capacitance → decreased venous return → decreased
cardiac output
- Usually secondary to spinal injuries (cervical or high thoracic
region)
o Disrupt sympathetic regulation of peripheral vascular
tone
- Causes: spinal cord trauma, neoplasm, spinal / epidural
anesthesia
- Acute spinal cord injury results in activation of multiple
secondary injury mechanisms:
o Vascular compromise to the spinal cord with loss
of autoregulation, vasospasm and thrombosis
o Loss of cellular membrane integrity and impaired
energy metabolism
o Neurotransmitter accumulation and release of free
radicals
DIAGNOSIS:
- Classic description of neurogenic shock:
o Hypotension with bradycardia
§ Hypotension is usually with
tachycardia to compromise cardiac
output (absence of reflexive
tachycardia)
o Warm extremities (loss of peripheral
vasoconstriction)
o Motor and sensory deficits indicative of a spinal
cord injury
o Radiographic evidence of a vertebral column
fracture
o Cardiac dysrhythmias, hypotension may occur
up to 14days after SC injury (monitoring is
required)
TREATMENT:
- Airway, ventilation, Fluid resuscitation
o Often respond
- Vasoconstrictor to improve peripheral vascular tone,
decrease vascular capacitance, and increase venous
return
o Should only be considered once hypovolemia is
excluded
- Vasoconstrictors:
o 1st line of medication: Dopamine
o Phenylephrine (α agonist) is used in patients
who are not responsive to dopamine
o Typically lasts 24 to 48 hours
o Cardiac dysrhythmias and hypotension may
occur up to 14 days after spinal cord injury
 ENDPOINT IN RESUSCITATION
Goal of treatment: to restore adequate organ perfusion
- Resuscitation is complete when:
o O2 debt is repaid
o Tissue acidosis is corrected
o Aerobic metabolism is restored
- Optimizing outcome in bleeding patients
o Early control of hemorrhage
o Adequate volume resuscitation (RBC & crystalloid)
- Expedient operative resuscitation - mandatory
- Attempts to stabilize an actively bleeding patient not in OR are
inappropriate
- Compensated shock: normal BP, HR, UO
o Inadequate tissue perfusion
§ Increase lactate or decrease mixed venous
O2 saturation
§ 3x infection than normal lactate (12hr)
§ Mortality – 4x if with infection
§ Injury severity score, occult hypotension
(lactic acidosis) >12 hrs are independent
predictors of infection
- Divisions:
o Systemic or global parameters:
§ Vital signs
§ Cardiac output
§ Pulmonary artery wedge pressure
§ O2 delivery and consumption
§ Lactate and base deficit
o Tissue-specific parameters
§ Gastric tonometry
§ Tissue pH, O2, CO2 levels
§ Near infrared spectrometry
o Cellular parameters
§ Membrane potential
§ ATP
- Assessment of Endpoints in Resuscitation
o Inability to repay O2 debt
§ Predictor of mortality and organ failure
§ Directly correlated to probability of death
§ Direct measurement is difficult
• BP, HR, UO, CVP, Pulmonary
artery occlusion pressure – poor
indicators
§ Serum lactate, base deficit – correlate with O2
debt
o Lactate
§ Generated in insufficient O2 setting
§ Metabolized by liver (50%), kidneys (30%)
§ Admission lactate level, highest lactate level,
& time to normalized – important prognostic
indicators for survival
§ Survival normalization of lactate:
100% within 24H
78% between 24-48H
14% > 48H
o Base deficit and volume of blood transfusion required in
the first 24 hours – better predictors of mortality than
plasma lactate
o Base deficit: amount of base in millimoles required to
titrate 1L of whole blood to a pH of 7.40 with the sample
fully saturated with O2 at 37oC (98.6oC) and a partial
pressure of CO2 of 40 mmHg
– measure by ABG
o Base deficit in the first 24 hours:
§ Mild (3-5 mmol/L)
§ Moderate (6-14 mmol/L)
§ Severe (15mmol/L) – 70% mortality
✓ Require 2x volume of fluid infusion &
6x more BT in 1st 24hrs
§ Directly correlated with mortality, organ failure
o Factors may compromise utility of base deficit
§ IV bicarbonate, hypothermia, hypocapnia,
heparin, ethanol, ketoacidosis
o Lactate and base deficit – indicate global tissue acidosis.
Focus on systemic endpoints.
o Gastric tonometry – focus on tissue specific endpoints
§ Assess GIT perfusion
§ CO2 in gastric mucosa sampled via NGT
§ Assume gastric HCO3 = serum level
§ pHi (gastric intramucosal pH)
✓ should be > 7.3
✓ good prognostic indicator
o NIR – Near Infrared Spectroscopy
§ Measure tissue O2
§ Measure redox state of cytochrome A, A3
✓ Correlated with tissue lactate
elevation
o Decoupled oxyhemoglobin and cytochrome A, A3 =
redox dysfunction = higher organ failure
o Tissue pH, O2, and CO2 concentration
§ Subcutaneous sites, muscle, and bladder
o Right Ventricular End – Diastolic Volume (RVEDVI)
§ Accurate prediction of preload for cardiac
index than does pulmonary artery wedge
pressure
o Left Ventricular Power Output (LVP)
§ >320 mmHg L/min/m2 – with improved
clearance of base deficit
FNMV