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Type

 

Causes

 

Manifestations

 

Diagnosis

 

Treatment

Hypovolemic

-

intravascular volume depletion

Hypoperfusion

1.

Serum lactate & base

Priority:

-

less baroreceptor

(haemorrhage)

- low blood volume

deficit

Secure airway

stimulation from stretch receptors = less inhibition of vasoconstriction

-

extravascular sequestration of

- low cardiac output

-

Tissue hypoperfusion

-

lower head w/ support of jaw +

plasma volume (ascites, peritonitis)

- increased peripheral

-

O2 debt

administration of supplemental oxygen

-

GI, GU, sensible losses (intestinal

vasoconstriction (compensatory increase in cardiovascular adrenergic discharge)

-

Severity of hemorrhagic shock

-

for those with airway obstruction:

-

increased chemoreceptor

obstruction, heat)

trachea should be intubated, mechanical ventilation initiated

stimulation of vasomotor

 

centers

CAUSES:

* flow to skin is sacrificed first then kidneys & viscera, then heart & brain

2.

ABG: measure tissue acidosis

Control source of blood loss

Increase VC & peripheral arterial resistance increase SY stimulation

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

IV volume resuscitation

Manifestations expected with 25- 30% blood loss:

cannot be done until hemorrhage is controlled

-

(

( NE, E, ADH, RAAS) - cool clammy extremities of adrenergic discharge to skin are -

NE, E, ADH, RAAS)

- cool clammy extremities

of adrenergic discharge to skin are

-

initial resuscitation: administer

- tachycardia (110-120bpm)

weak or absent peripheral pulses

- hypotension

-

subtle and difficult to detect

- monitor urine output + serial

nonsugar, nonprotein crystalloid solution w/ electrolyte composition approximating that of plasma or hypertonic saline

-

Aims it to keep sys BP at

*No SY effects on cerebral & coronary vessels

hematocrits + postural changes in BP

- oliguria???

Sites that cause extravascular blood volume loss ->

hypotension:

- External

 

90mmHg

if hemorrhage is severe, use blood products (fresh frozen plasma)

-

30% loss:

- Mild tachycardia

- Tachypnea

- Intrathoracic

 

- Anxiety

40% loss:

- Intraabdominal

- Retroperitoneal

**if patient is unresponsive to initial

resuscitation, there is still ongoing active

-

Requires immediate operative intervention

- Long bone fractures

hemorrhage.

In nontrauma px: GI tract Pleural cavity: can hold 2-3 L

**minimize heat loss & maintain normothermia

-

Hypothermia is associated with acidosis, hypotension, coagulopathy

 

of blood Intraperitioneal hemorrhage:

most common source of blood loss inducing shock (dx:

through ultrasound & diagnostic peritoneal lavage)

 
 

Type

 

Causes

Manifestations

Diagnosis

 

Treatment

Traumatic

-

due to external and internal

   

Treatment plan:

May be due to:

- soft tissue injury

- long bone fractures

volume losses (loss of blood from

wound externally and loss of blood

into damaged tissues)

- Prompt control of hemorrhage

- Adequate volume resus. To correct O2 debt

-

burns

-

worsened due to plasma

-

Debridement of nonviable tissue

 

extravasation into tissues and organs distal from injured areas (due to a generalized systemic intravascular inflammatory

response)

- Stabilization of bony injuries

Hypoperfusion is MAGNIFIED by proinflammatory activation!

- Appropriate treatment of soft tissue injuries

   

Others:

Ex. Small volume hemorrhage + soft tissue injury or any combination of hypovolemic, neurogenic, cardiogenic, obstructive shock = precipitates proinflammatory activation

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

-

dysfunction of the endothelium &

Manifestations:

Sepsis: infection +

1. Assessment of adequacy of airway and ventilation

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

- Final common pathway for profound & prolonged shock

- Development of a hypermetabolic state

vasculature secondary to

circulating inflammatory mediators and cells

- Peripheral VD + resultant hypotension + resistance to treatment with vasopressors

inflammation Severe sepsis: hypoperfusion + signs of organ dysfunction

-

as a response to prolonged and

- Enhanced CO

Septic shock: above +

severe hypoperfusion (failure of vascular smooth muscle to constrict appropriately)

- Fever (due to hypermetabolic state)

systemic hypotension

3. Use catecholamines = vasopressors

 

- Leucocytosis

o

Patients with SS are resistant to catecholamines -> use Arg vasopressin

 

- Hyperglycemia

Causes:

- Tachycardia

-

systemic response to infection

4. Manage hyperglycemia (intensive insulin therapy)

(by product of the body’s response

VD in septic shock due to:

to disruption of host-microbe equilibrium resulting in

- Upregulation of the inducible isoform of NOS in vessel wall = increased amounts of NO for sustained periods of time

5. Corticosteroids

o

Improved MAP in response to NE

invasive/severe localized infection)

- hypoxic lactic acidosis

o

Patients with SS are believed to have adrenal insufficiencies

- CO poisoning

decompensated, irreversible hemorrhagic shock

-

- Renders vasculature resitant to vasoconstrictors

- terminal cardiogenic shock

 

Signs of hypoperfusion:

- non-infectious systemic

-

Confusion, malaise, oliguria, hypotension

inflammation

- pancreatitis

 

- burns

- anaphylaxis

- acute adrenal insufficiency

 

Type

Causes

Manifestations

 

Diagnosis

 

Treatment

Cardiogenic

-

Most common cause: acute,

Manifestations:

- Present with clinical

1. Airway and ventilation

extensive MI

- Sustained hypotension (<90mmHg for at least

findings associated with discharge of the adrenergic nervous

2. Support of circulation

 

Circulatory pump failure = diminished forward flow + tissue hypoxia

3. Treatment of cardiac dysfunction

Vicious cycle:

30mins)

o

Maintenance of adequate oxygenation = ensure myocardial O2 delivery

Myocardial ischemia -> myocardial dysfunction -> more myocardial ischemia

- Elevated pulmonary artery wedge pressure

system and release of angiotensin and

 

- Cool & mottled skin

vasopressin

o

Judicious fluid administration = avoid fluid overload & cardiogenic

 

- Tachycardia

- If caused by R vent

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)

- Diminished pulses

dysfunction:

o

pulmonary edema

Neck veins are distended

- If caused by L vent dysfunction:

o

Treat dysrhythmias & cardiac block

o

Inotropic support

o

Px has rales + 3 rd heart sound or ventricular gallop rhythm (usually heard at the end of diastolic vent filling)

(more on p.106)

 

- If dysfunction is chronic/severe, px may present with the ff:

 

enlarged heart, distended neck veins, etc

Type

 

Causes

 

Manifestations

 

Diagnosis

Treatment

Obstructive

- Mechanical obstruction of venous return

Hemodynamic abnormalities:

Tension pneumothorax:

 

-

Due to increased

- Respiratory distress

o

Due to tension pneumothorax

intracardiac pressures, ventricular filling is limited =

- Hypotension

-

Diminished breath sounds

o

Cardiac tamponade:

low CO

sufficient fluid has

 

-

Hyperresonance

accumulated in pericardial sac to obstruct blood flow to ventricles

Determinants of degree of hypotension:

-

Jugular venous distention (may be absent in

 

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

hypovolemic px)

-

Shift of mediastinal structures to unaffected

- IVC obstruction

 

o

DVT

2. Increased

side with tracheal deviation (usually late finding)

o

Neoplasma

intrapericardial pressure due to blood accumulation (CT)

- Increased intrathoracic

pressure

 
 

Cardiac tamponade:

= low CO = increased central venous pressure

- Dyspnea

- Orthopnea

 

- Cough

- Peripheral edema

- Chest pain

- Tachycardia

- Muffled heart tones

- JV distention

Beck’s triad for CT:

hypotension, muffled heart tones, neck vein distension

 

Type

Causes

 

Manifestations

Diagnosis

 

Treatment

Neurogenic

 

- Spinal cord trauma

Manifestations:

 

- Restoration of intravascular volume alone

-

Diminished tissue

- Spinal cord neoplasm

- Bradycardia (because there is no SY discharge)

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

- Spinal/epidural anesthesia

- Administration of vasoconstrictors

o

SY activity/input is disrupted = prevents reflex tachycardia that occurs with hypovolemia

(as long as hypovolemia is excluded as cause of hypotension)

o

If patient is unresponsive, give dopamine.

 

o

Increased

 

vascular

 

capacitance

- Hypotension

 

o

Low venous

- Cardiac dysrhythmias

 

return

- Low CO

 

o

Low cardiac

- Low PVR

 

output

- Warm extremities (loss of peripheral VC)

 

- Motor and sensory deficits