SHOCK Flashcards by Shiela Micah Gascon

Most common type of shock in surgical patients

[HaNSCOT]

Hypovolemic
Neurogenic
SEPTIC
Cardiogenic
Obstructive
Traumatic

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Cause of hypovolemic shock from loss of interstitial fluid

BOWEL OBSTRUCTION

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Shock caused by decreased resistance within capacitance vessels

VASOGENIC SHOCK

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Shock from vasodilation due to acute loss of sympathetic tone

Neurogenic shock

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Shock resulting from failure of the heart as a pump

Cardiogenic shock

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Cardiogenic shock from mechanical impediment to circulation leads to depressed cardiac output rather than primary cardiac failure

Obstructive shock

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Shock from inflammation triggered by soft tissue and bone injury

Traumatic shock

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What type of shock happens during pulmonary embolism

Obstructive shock

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Core principles in the management of critically ill or injured patient

a. definitive control of airway
b. control of active hemorrhage
c. volume resuscitation
d. recognition and adequate correction of hypoperfusion
e. excessive fluid resuscitation may exacerbate bleeding

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What is the main goal of the neuroendocrine response to hemorrhage?

maintain perfusion to the heart and brain

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What is the initial stimulus for the neuroendocrine response during hemorrhagic shock?

loss of circulating blood volume

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Afferent pain signals transmit via the ______ resulting in activation of the hypothalamic-pituitary-adrenal axis as well as activation of ANS to induce direct sympathetic stimulation of the adrenal medulla to release _______

spinothalamic tract, catecholamines

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Baroreceptors are found in _____, ______ and _____

atria, aortic bodies, carotid bodies

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T/F Normally the baroreceptors inhibit the ANS (sympathetic tone). When activated, they disinhibit ANS, causing vasoconstriction

T. baroreceptor activation -> diminished baroreceptor output -> disinhibition of ANS -> increased peripheral vasoconstriction

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T/F arotic and carotid bodies do not have chemoreceptors

F. They have chemoreceptors that detect O2 concentrations

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Give 3 cardiovascular responses to diminished venous return and decreased CO due to hemorrhage

increased cardiac heart rate (1) and contractility (2), venous and arterial vasoconstriction (3)

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Heart rate and contractility are increased by which adrenergic receptors?

beta-1

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arteriolar vasoconstriction is brought about by activation of which adrenergic receptors?

alpha-1

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What is the effect of sympathetic output on the adrenal medulla?

release of catecholamines

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What is the effect of cortisol on gluconeogenesis and insulin

stimulatory to gluconeogenesis, inhibitory to insulin (insulin resistance)

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What hormones are released by the ff. organs during shock?
Hypothalamus -
Kidney -
Pituitary -

H: ACTH
K: Renin
P: ADH

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adverse effect of ADH on the intestine

intestinal ischemia

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The primary determinant of preload

venous return

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The law states that the force of ventricular contraction is a function of its preload

Frank-Starling Law

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The force that resists myocardial work during contraction

AFTERLOAD

In neurogenic shock and sepsis, the microvessels a. vasodilate b. vasoconstrict

A. VASODILATE

In hemorrhagic shock and sepsis, the microvessels a. vasodilate b. vasoconstrict

B. VASOCONSTRICT

T/F In hemorrhagic shock, correction of hemodynamic parameters and restoration of O2 delivery does not lead to restoration of tissue O2.

TRUE

Most common type of shock in surgical or trauma patient

hemorrhagic/hypovolemic

Result of acute blood loss EXCEPT a. reflexive decreased baroreceptor stimulation b. sympathetic stimulation c. increased output from atrial stretch receptors d. release of epinephrine and norepinephrine

c. increased output from atrial stretch receptors

T/F Shock in trauma patient should be presumed to be due to hemorrhage until proven otherwise

Patient A with hemorrhagic shock, stable vital signs, no CNS symptoms has a percentage blood loss of _____ and estimated volume of blood loss of _____

<15%, 750mL

Patient B with tachycardia (>120 bpm) and hypotension has approximated % blood loss of _____ and estimated volume of blood loss of _____.

30-40%, 1,500-2000mL

Patient C with tachycardia (>100bpm) and orthostatic hypotension has an approximated % blood loss of _____ and an estimated volume of blood loss of _____.

15-30%, 750-1,500mL

What is the CNS symptom of C? (tachycardia and orthostatic hypotension)

Anxiety

What is the CNS symptom of patient B? (tachycardia and hypotension )

Confusion

What is the CNS symptom of patient A ? (stable vitals)

none

Patient D Obtunded with HR >140bpm, and severe hypotension has an approximated % blood loss of _____ with an estimated volume of _____?

> 2,000

In the non-trauma patient, ______ must always be considered as a site for blood loss

GI tract

The pleural cavity can hold how many L of fluid?

2-3L

Retroperitoneal hemorrhage typically occurs in association with _______

pelvic fractures

In the resuscitation bay, what confirms retroperitoneal hemorrhage secondary to pelvic fractures?

pelvic radiography

In damage control resuscitation, initial resuscitation is limited to keep SBP around __ to __ mmHg

80 to 90

Following hemorrhage, large arterioles vasoconstrict;

Microcirculation

In Microcirculation these 3 Reserve perfusion of the myocardium and CNS to limit organ perfusion to organs such as skin, skeletal muscle, kidneys, and the GI tract

Vasopressin angiotensin II endothelin-1 (vasoconstriction)

Tissue perfusion (Adequate O2 support), need :

1. Efficient pump (Heart) 2. Good pipes (Blood vessels) 3. Well-distributed flow

PHYSIOLOGICAL RESPONSE Predominant form of response:

Increased sympathetic activity Increased catecholamine levels

These effector responses are designed to

expand plasma volume maintain peripheral perfusion maintain tissue O2 delivery restore homeostasis

Vasodilation of the coronary arteries slowing of the heart rate vasoconstriction of the splanchnic and skeletal circulation. - Its purpose is to maintain perfusion of the vital organs first usually the heart and the brain.

Chemoreceptors

Renin angiotensin system and antidiuretic hormone is stimulated in response to stress particularly in

hemorrhagic and iatrogenic shock

ACTH >> Cortisol – induce catabolic rate

o Stimulates gluconeogenesis and insulin resistance resulting in hyperglycemia as well as muscle cell protein breakdown and lipolysis to provide substrates for hepatic gluconeogenesis o Retention of sodium and water by the nephrons of the kidney and even aldosterone also

SEPTIC SHOCK NEUROGENIC SHOCK

VASODILATION -others vasoconstriction

METABOLLIC EFFECTS Impaired oxidative phosphorylation – DYSOXIA or lack of oxygen

2 moles of ATP from 1 mole of glucose - Complete oxidation of 1 mole of glucose – 38 molesof ATP

have a profound impact on cellular metabolism.

Epinephrine and norepinephrine

the deficit in tissue oxygenation overtime that occurs during shock

CELLULAR HYPOPERFUSION − O2 DEBT

Release of intracellular products from damaged and injured cells can have paracrine and endocrine-like effects on distant tissues to activate the inflammatory and immune responses, is known as

DANGER SIGNALING

Endogenous molecules are capable of signaling the presence of danger to surrounding cells and tissues. These molecules that are released from cells are known -recognized by cell surface receptors to effect intracellular signaling those primes and amplifies the immune response.

damage associated molecular patterns (DAMPs)

Recognized effectors

PRRs TLRs LPS (PAMPs) ↓ Amplification of immune response (Cytokines)

Insults: Bacteria or endotoxin, hemorrhage, ischemia produce peripheral vasodilation

TNF-a

- Febrile response to injury; anorexia - More common - Augments the secretion of ACTH, glucocorticoids, and β- endorphin

IL-1

ANTI-INFLAMMATORY

Interleukin – 4 Interleukin – 10 Interleukin – 13 Prostaglandin E2 TGFβ

Activation of the complement cascade → organ dysfunction

Activated C3a, C4a, and C5a - It acts synergistically with endotoxin – TNF-a and IL- 1 - ARDS and MODS

Neuroendocrine and Organ-Specific Responses Regulated at multiple levels of responses particularly the sympathetic system

a. Stretch receptors and baroreceptors in the heart and vasculature (Carotid sinus and aortic arch) b. Chemoreceptors, c. Cerebral ischemia responses d. Release of endogenous vasoconstrictors particularly the hormonal e. Shifting of fluid into the intravascular space f. Renal reabsorption and conservation of salt and water

The imbalance between cellular supply and demand leads to

neuroendocrine and inflammatory responses

direct effect to shock

HEMORRHAGIC NEUROGENIC CARDIOGENIC

release 1st endogenous molecules cellular activation tissue perfusion ischemia schock

TRAUMA SHOCK SEPTIC SHOCK - No direct effect

• Persistent hypoperfusion: Hemodynamic derangements and cardiovascular collapse • Extensive enough parenchymal and microvascular injury: DEATH

IRREVERSIBLE PHASE OF SHOCK

In hemorrhagic shock, the body can compensate for the initial loss of blood volume primarily through the neuroendocrine response to maintain hemodynamics. This represents the In hemorrhagic shock, the body can compensate for the initial loss of blood volume primarily through the neuroendocrine response to maintain hemodynamics. This represents the

COMPENSATED PHASE OF SHOCK.

With continued hypoperfusion, which may be unrecognized, cellular death and injury are ongoing, and the___ ensues.

DECOMPENSATION PHASE OF SHOCK

Most common cause of shock

Hypovolemia

Most common cause of hypovolemic shock

HEMORRHAGE

Physical findings of shock by class of hemorrhage

• Class I: Minimal change in vital signs • Class II: Tachycardia, a decreased pulse pressure, and delayed capillary refill mildly anxious, oliguria • Class III: Hypotension, tachycardia, tachypnea, and mental confusion progressing to lethargy • Class IV: Obtundation, profound hypotension, and anuria

Hypotension, tachycardia, tachypnea, and mental confusion progressing to lethargy

CLASS 3

Obtundation, profound hypotension, and anuria

CLASS 4

Minimal change in vital signs

CLASS 1

Tachycardia, a decreased pulse pressure, and delayed capillary refill mildly anxious, oliguria

CLASS 2

NON-HEMORRHAGIC hypovolemic shock − GI losses or Urinary tract Obstruction; Kidney dses

Extravascular fluid sequestration or “Third space” fluid loss • Peritonitis can cause a lot of fluids; (Septic shock) • Tx: Adequate fluid resuscitation, source control plus supportive measures

More than 30-40% of burn to the body surface area requires the patient to have a massive resuscitation protocol. But later on, when infected, it becomes toxic. That’s why it is considered a high index suspension.

BURNS +/- wound infections

INCREASE MYOCARDIAL CONTRACTILITY DECREASE MOVEMENT OF PLASMA INTO THE INSTERSTITIUM (change formation of albumin molecules)

MODEST HYPERCHLOREMIC ACIDEMIA

An indirect marker of tissue hypoperfusion, cellular O2 debt and the severity of hemorrhagic shock

Serum lactate and base deficit

− Minimize crystalloid solution – NSS can cause metabolic acidosis later on for massive infusion − Doctors prefer whole blood nowadays − In a patient with ongoing hemorrhage, the risk of death increases 1% for every 3 minutes in the ER

DAMAGE CONTROL

Components of Damage control or hemostatic resuscitation:

• Permissive hypotension until definitive surgical control • Minimize crystalloid use • Initial use of 5% hypertonic saline • Early use of blood products (PRBCs, FFP, platelets, cryoprecipitate) • Consider drugs to treat coagulopathy (rFVIIa, Prothrombin concentrate, TXA)

in septic schock Vasodilatory effects:

isoform of nitric oxide synthase (iNO)

IMMEDIATELY LIFE-THREATENING CAUSES OF SHOCK

• Tension pneumothorax • Massive hemothorax • Cardiac tamponade

- there is decreased breath sounds, tracheal shift to the left, and hyper resonant sound − There will be a mediastinal shift, decreased venous return, end-diastolic volume, stroke volume, and cardiac output resulting in hypotension later on. which has tympanitic (hypertympany) percussion

TENSION PNEUMOTHORAX

we have blood accumulating in the thorax. This blood can also cause problems: decreased cardiac output leading to hypotension. There is also decreased breath sounds and tracheal shift. percussion would be dull since there is fluid.

MASSIVE HEMOTHORAX

BECK’S TRIAD (CARDIAC TAMPONADE) • Distended neck veins • Muffled heart sounds • Hypotension (Most consistent)

NEUROGENIC SHOCK “Classic signs and symptoms”

-Decrease blood pressure associated with bradycardia -warm extremeties -motor and sensory, deficits -radiographic evidence

RESUSCITATION Initial approach to treatment

• A – Airway • B – Breathing, adequate ventilation • C – Circulation - Volume status – IV fluids - Pump status – Inotropic - Flow status – Vasopressors • D – Determine and treat the cause of the shock - Operating room resuscitation

CRITERIA ADEQUAE PERFUSION

− Complete when O2 debt is repaid, tissue acidosis is corrected, and aerobic metabolism is restored.