Type Causes Manifestations Diagnosis Treatment

Hypovolemic - less baroreceptor stimulation from stretch receptors = less inhibition of vasoconstriction - increased chemoreceptor stimulation of vasomotor centers CAUSES: Increase VC & peripheral arterial resistance increase SY stimulation ( NE, E, ADH, RAAS) *No SY effects on cerebral & coronary vessels

- intravascular volume depletion (haemorrhage) - extravascular sequestration of plasma volume (ascites, peritonitis) - GI, GU, sensible losses (intestinal obstruction, heat)

Hypoperfusion - low blood volume - low cardiac output - increased peripheral vasoconstriction (compensatory increase in cardiovascular adrenergic discharge) * flow to skin is sacrificed first then

kidneys & viscera, then heart & brain

Manifestations expected with 25-30% blood loss: - cool clammy extremities - tachycardia (110-120bpm) - weak or absent peripheral pulses - hypotension - oliguria??? 30% loss: - Mild tachycardia - Tachypnea - Anxiety 40% loss: - Requires immediate

operative intervention

1. Serum lactate & base

deficit - Tissue hypoperfusion - O2 debt - Severity of hemorrhagic

shock

2. ABG: measure tissue acidosis

*moderately severe & severe shock = easy to recognize, early or mild hypovolemic shock = signs

of adrenergic discharge to skin are subtle and difficult to detect - monitor urine output + serial

hematocrits + postural changes in BP

Sites that cause extravascular blood volume loss -> hypotension: - External - Intrathoracic - Intraabdominal - Retroperitoneal - Long bone fractures In nontrauma px: GI tract Pleural cavity: can hold 2-3 L of blood Intraperitioneal hemorrhage: most common source of blood loss inducing shock (dx: through ultrasound & diagnostic peritoneal lavage)

Priority: Secure airway - lower head w/ support of jaw + administration of supplemental oxygen - for those with airway obstruction: trachea should be intubated, mechanical ventilation initiated Control source of blood loss IV volume resuscitation - cannot be done until hemorrhage is controlled - initial resuscitation: administer nonsugar, nonprotein crystalloid solution w/ electrolyte composition approximating that of plasma or hypertonic saline

- Aims it to keep sys BP at 90mmHg

- if hemorrhage is severe, use blood products (fresh frozen plasma) **if patient is unresponsive to initial resuscitation, there is still ongoing active hemorrhage. **minimize heat loss & maintain normothermia - Hypothermia is associated with

acidosis, hypotension, coagulopathy

Type Causes Manifestations Diagnosis Treatment

Traumatic May be due to: - soft tissue injury - long bone fractures - burns Hypoperfusion is MAGNIFIED by proinflammatory activation!

- due to external and internal volume losses (loss of blood from wound externally and loss of blood into damaged tissues) - worsened due to plasma extravasation into tissues and organs distal from injured areas (due to a generalized systemic intravascular inflammatory response) Ex. Small volume hemorrhage + soft tissue injury or any combination of hypovolemic, neurogenic, cardiogenic, obstructive shock = precipitates proinflammatory activation

Treatment plan: - Prompt control of hemorrhage - Adequate volume resus. To correct

O2 debt - Debridement of nonviable tissue - Stabilization of bony injuries - Appropriate treatment of soft tissue

injuries Others: Administration of a balanced salt solution (several liters) - If BP does not respond promptly: Vasoconstrictors - To restore venous tone - Vasoconstriction of systemic

arterioles = increased BP *body temp must be monitored & excessive heat loss prevented

Type Causes Manifestations Diagnosis Treatment

Septic/ Vasodilatory - Final common pathway

for profound & prolonged shock

- Development of a hypermetabolic state

- dysfunction of the endothelium & vasculature secondary to circulating inflammatory mediators and cells - as a response to prolonged and severe hypoperfusion (failure of vascular smooth muscle to constrict appropriately) Causes: - systemic response to infection (by product of the bodys response to disruption of host-microbe equilibrium resulting in invasive/severe localized infection) - hypoxic lactic acidosis - CO poisoning - decompensated, irreversible hemorrhagic shock - terminal cardiogenic shock - non-infectious systemic inflammation - pancreatitis - burns - anaphylaxis - acute adrenal insufficiency

Manifestations: - Peripheral VD + resultant

hypotension + resistance to treatment with vasopressors

- Enhanced CO - Fever (due to

hypermetabolic state) - Leucocytosis - Hyperglycemia - Tachycardia VD in septic shock due to: - Upregulation of the inducible

isoform of NOS in vessel wall = increased amounts of NO for sustained periods of time

- Renders vasculature resitant to vasoconstrictors

Signs of hypoperfusion: - Confusion, malaise, oliguria,

hypotension

Sepsis: infection + inflammation Severe sepsis: hypoperfusion + signs of organ dysfunction Septic shock: above + systemic hypotension

1. Assessment of adequacy of airway and ventilation

2. Fluid resuscitation + restoration of circulatory volume w/ balanced salt solutions

3. Use catecholamines = vasopressors o Patients with SS are

resistant to catecholamines -> use Arg vasopressin

4. Manage hyperglycemia (intensive insulin therapy)

5. Corticosteroids o Improved MAP in response

to NE o Patients with SS are

believed to have adrenal insufficiencies

Type Causes Manifestations Diagnosis Treatment

Cardiogenic - Circulatory pump

failure = diminished forward flow + tissue hypoxia

Most common cause: acute, extensive MI Vicious cycle: Myocardial ischemia -> myocardial dysfunction -> more myocardial ischemia Ex. LV damage = low SV Low CO/contractility with an adequate intravascular volume will lead to underperfused vascular beds + reflexive SY discharge (increase in HR, Fc, O2 consumption)

Manifestations: - Sustained hypotension

(

Type Causes Manifestations Diagnosis Treatment

Obstructive

- Mechanical obstruction of venous return o Due to tension

pneumothorax o Cardiac tamponade:

sufficient fluid has accumulated in pericardial sac to obstruct blood flow to ventricles

- IVC obstruction o DVT o Neoplasma

- Increased intrathoracic pressure

Hemodynamic abnormalities: - Due to increased

intracardiac pressures, ventricular filling is limited = low CO

Determinants of degree of hypotension:

1. Increased intrapleural pressure due to air accumulation (TP)

2. Increased intrapericardial pressure due to blood accumulation (CT)

= low CO = increased central venous pressure

Tension pneumothorax: - Respiratory distress - Hypotension - Diminished breath

sounds - Hyperresonance - Jugular venous distention

(may be absent in hypovolemic px)

- Shift of mediastinal structures to unaffected side with tracheal deviation (usually late finding)

Cardiac tamponade: - Dyspnea - Orthopnea - Cough - Peripheral edema - Chest pain - Tachycardia - Muffled heart tones - JV distention Becks triad for CT: hypotension, muffled heart tones, neck vein distension

Type Causes Manifestations Diagnosis Treatment

Neurogenic - Diminished tissue

perfusion as a result of loss of vasomotor tone to peripheral arterial beds

o Increased vascular capacitance

o Low venous return

o Low cardiac output

- Spinal cord trauma - Spinal cord neoplasm - Spinal/epidural anesthesia

Manifestations: - Bradycardia (because there

is no SY discharge) o SY activity/input is

disrupted = prevents reflex tachycardia that occurs with hypovolemia

- Hypotension - Cardiac dysrhythmias - Low CO - Low PVR - Warm extremities (loss of

peripheral VC) - Motor and sensory deficits

- Restoration of intravascular volume alone

- Administration of vasoconstrictors (as long as hypovolemia is excluded as cause of hypotension)

o If patient is unresponsive, give dopamine.