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Shock

Outline

Definition - a clinical state in which there is inadequate tissue perfusion to meet metabolic demands.

* Septic shock actually has components of several groups including distributive and cardiogenic.

General Recognition:

• hypotension is NOT a sign of shock, because of the compensatory mechanisms below. It can be present in shock
• to catch early you must have a high index of suspicion, is the patient at risk for one of the above
• History:
  • vomiting, diarrhea, decreased oral intake
  • lethargy, increased sleepiness
  • trauma
  • allergic symptoms/exposure (or rapid change in physiologic status)
  • congenital heart disease
• Physical Findings:
  • decreased CNS activity
  • abnormal color pale => gray => mottled
  • decreased urine output (sign of overall tissue hypoperfusion)
  • tachypnea, tachycardia
  • delayed capillary refill
  • others depend on etiology of shock
• Laboratory findings:
  • acidosis on ABG with a base deficit signifying tissue hypoperfusion
  • decreased mixed venous oxygen saturation on a VBG
  • electrolyte abnormalities (related to cause of shock)
• hypotension is seen only late in shock states after compensatory mechanisms are exhausted

WHY is hypotension only seen as a late sign of shock?

Compensatory mechanisms	Decompensatory effects
Baroreceptors	Cardiac Failure
Chemoreceptors	acidosis
cerebral ischemia	CNS depression
reabsorption of tissue fluids	Disseminated Intravascular Coagulation
endogenous vasoconstrictors	depression of reticuloendothelial system
Renal conservation of water

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Compensatory Mechanisms

• Baroreceptor reflexes (respond to small changes in vascular tone/pressure)
  • located in the carotid sinus and aortic arch, stimulation causes
    • decreased vagal tone, which
      • increases heart rate
      • decreases coronary resistance (improves myocardial oxygen supply)
    • increased sympathetic tone, which causes
      • venoconstriction
      • constriction of blood reservoirs (increasing circulating blood volume)
        • spleen - dogs
        • skin and skeletal muscle - humans
• Chemoreceptor
  • located locally in tissue beds
  • sense hypoxia (due to inadequate blood flow in peripheral tissues), and cause
    • further vasoconstriction
    • respiratory stimulation - improves venous return (pump model), also helps compensate for acidosis
• Cerebral Ischemia (Cerebral Perfusion Pressure<40mmHg)
  • activates sympathoadrenal system (more potent than Chemo or Baroreceptor mechanisms)
  • increased catecholamine release from both adrenal gland and sympathetic nerves (can also get vagal stimulation which is counterproductive)
• Reabsorption of tissue fluids
  • decreased mean arterial pressure
  • arteriolar constriction } All lead to decreased hydrostatic pressure
  • decreased venous pressure in capillaries, leading to increased resorption of fluid15ml/kg/hour,
  • up to 1l/hour can be reabsorbed in adult sized patients

• When Hydrostatic Pressure > Osmotic Pressure: Filtration
• Osmotic Pressure>Hydrostatic: Reabsorption
• Endogenous Vasoconstrictors
  • Epinephrine and Norepinephrine
    • released from adrenal medulla and sympathetic nerves
    • cause vasoconstriction and increased cardiac output
  • Vasopressin (Antidiuretic hormone)
    • released from posterior pituitary
    • potent vasoconstrictor
  • Renin (from decreased renal perfusion)
    • leads to angiotensinogen production eventually yielding angiotensin - a very potent vasoconstrictor
• Renal Conservation of Water
  • Aldosterone release
    • stimulated by vasopressin
    • Causes Na reabsorption in distal tubules
    • Water follows the sodium

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Decompensatory Mechanisms

• Cardiac Failure
  • many potential etiologies (i.e. actual etiology is controversial)
  • decreased circulating blood volume => decreased coronary blood flow => decreased cardiac
  • function
• Acidosis (from hypoperfusion, anaerobic metabolism => lactic acidosis)
  • depressant of myocardial function
  • decreased response to catecholamines both in myocardium and peripheral
  • vasculature
• CNS Depression
  • opioid release (enkephalins, B -endorphin)
  • Naloxone has been used as treatment in shock, with some success
• Disseminated Intravascular Coagulation
  • abnormalities of clotting system develop as a result of attempt to control hemorrhage but also dilution/loss of clotting factors
  • GI hemorrhage seen as complication in dog model of acute hemorrhage, hours after the initial event
• Reticuloendothelial System dysfunction
  • function depressed in shock
  • lose antibacterial function
  • can get endotoxin release from native bacteria
  • aggravates already compromised situation

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Recognition

Again, blood pressure is not key to deciding whether or not someone is in shock, it does help decide whether they are in compensated or decompensated shock though.

Lets think about Blood Pressure Control or production first, see the following diagram:

Recognition and Treatment of Shock Depends upon the Classification/Etiology of the Shock

The commonly used analogy of the circulatory system includes three components, a pump (the Heart), plumbing (the vascular system) and Fluid (circulating blood volume). In order to assure adequate perfusion each of these systems needs to be functioning, otherwise Shock will ensue. Consequently the three main types of shock, plus septic shock are listed below.

Hypovolemic Shock (problems with the fluid)

• loss of preload
• Clues in the History that should make you think about Hypovolemic Shock:
  • Fluid losses:
    • diarrhea
    • vomiting
    • blood loss
    • profuse and prolonged sweating
    • decreased urine output (OK, this isn't a loss, but you get the idea)
  • Decreased intake
    • vomiting
    • poor apetite
    • fluid deprivation
• Clues in the Physical Exam that should make you think about Hypovolemic Shock
  • dry mucous membranes
  • no tears
  • decreased urine output
  • others that go along with shock
    • poor perfusion
    • delayed cap refill
    • diminshed peripheral pulses
    • poor color
• Clues in laboratory or studies that should make you think about Hypovolemic Shock
  • Elevated Blood Urea Nitrogen (BUN) and to a lesser extent Creatinine
  • Small cardiac silhouette on chest X-ray
  • Low central venous pressure after a central line is placed

Cardiogenic Shock (problems with the pump)

• loss of contractility
• Clues in the History that should make you think about Cardiogenic Shock
  • history of congenital heart disease
  • recent cardiac surgery
  • other diseases associated with heart problems (e.g. Duchenne Muscular Dystrophy)
  • recent viral infection
• Clues in the Physical Exam that should make you think about Cardiogenic Shock
  • murmur, particularly if new
  • extra heart sounds (gallop)
  • friction rub
• Clues in laboratory values or studies that should make you think about Cardiogenic Shock
  • Chest X-ray findings
    • large silhouette
    • pulmonary edema
  • elevated Troponin if related to an infectious etiology
  • elevated central venous pressure after placement of a central line

Distributive Shock (problems with the plumbing)

• loss of Afterload/systemic vascular resistance
• Clues in the History that should make you think about Distributive Shock
  • recent allergic exposure (Bee Sting, peanuts, other agent with h/o severe reaction)
  • spinal cord injury
    • traumatic
    • surgical
• Clues in the Physical Exam that should make you think about Distributive Shock
  • bounding pulses
  • well perfused skin
  • very low blood pressure requiring large volumes of fluid
• Clues in laboratory values or studies that should make you think about Distributive Shock
  • high IgE levels
  • high Eosinophil count

Septic shock (a combination)

• loss of preload
• loss of afterload/SVR
• loss of contractility (to a lesser extent)
• Clues in the History that should make you think about Septic shock
  • immunosupression
  • fever
  • exposure to particular infectious agents (e.g. meningococcus)
• Clues in the Physical Exam that should make you think about Septic shock
  • initially bounding pulses
  • a rash like this (purpura fulminans - in this case from N. meningitidis)

• fever
• poor perfusion
• Clues in laboratory values or studies that should make you think about Septic shock
  • High, or very low white blood cell count
  • coagulopathy

Treatment

Always start with the ABC's

1) Airway

Needs will vary depending on etiology of shock, from no intervention to aggressive intervention (i.e. anaphylaxis)

2) Breathing

Patients need respiratory support and monitoring, consider O2 to help with oxygen delivery even though sats may be OK, patients may need intubation, or other respiratory support, particularly to help compensate for a profound metabolic acidosis.

3) Circulation

Read on.

Treatment (after ABC's)

Initial Treatment:

Volume, Volume, Volume

But after you have given volume, then what do you do? Or better yet, when is continuing to add volume not the right thing to do?

Further Treatment:

Volume (Preload)

• replacement must be made with isotonic and ideally isooncotic fluids
  • Normal Saline is the solution of first choice because it is ubiquitously available in health care settings (including ambulances) and carries minimal risk
• Initial Volume always at least 20ml/kg
  • in most cases of early shock it will take still more volume than this to correct deficits, don't be timid initially with fluid
• For later fluid, try to replace with isotonic/isooncotic fluid that is needed
  • pRBCs in hemorrhage
  • FFP also as needed
  • 5% albumin also a good choice
  • Hespan if concerned about blood products
  • plasmanate also an option (if available)
• Where ? Intravenous, which site:
  • Peripherally (saphenous, antecubital, other sites as visible/palpable) largest bore IV obtainable, but any IV will work
  • Intraosseous - proximal tibia (can also go distal femur, iliac crest, sternum) perpendicular to bone, two-three finger breadths below tibial tubercledo not have to be able to draw out marrow for it to be in correct locationcan put any IV fluid, med or colloid through IO should be considered if rapid IV access is not obtainable. (As the image below shows, AHA and others recommend angling away from knee to prevent entering the growth plate).

• Central - If skilled person is available, will most useful, allow for blood draws as well
  • More than one lumen if possible. But realize that the more lumens, the smaller the lumens you have and the slower you can give fluid
  • sites include: Femoral (safest - in the short run), Internal Jugular, Subclavian

Contractility

• The strength of contraction
• The stronger the contraction, in theory the greater the pulse pressure, and potentially greater volume pumped
• Our main course of action is through Adrenergic receptors

• The ideal agent to increase contractility would solely affect Beta - 1 receptors, listed in the table below are our most commonly used agents with inotropic properties

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Afterload/Systemic Vascular Resistance

• The 'Plumbing' of the system
• although similar these two components are not exactly the same:
• Systemic Vascular Resisitance - refers to vascular tone
• Afterload - refers to the force against which the heart must pump
  • Includes stenotic valves, or other outflow obstructions, as well as vascular tone

• To some extent they counteract each other
  • Decreasing Afterload will decrease the amount of work the heart must squeeze against
  • This should then increase Cardiac Output and therefore increase Blood Pressure
  • But commonly, afterload is decreased by causing vasodilation - this will lead to decreasing blood pressure (see the BP diagram again)

The two tables below show first the vasoconstrictive agents, then the vasodilator agents

Summary of Treatment

Hypovolemic Shock - a Preload issue, increase the Preload

• Volume, Volume, Volume, then consider more Volume

Cardiogenic Shock - a contractillity issue

• Volume first, because increasing the preload can get the heart to a better point on the Frank Starling Curve
• Do not fluid overload - risk to put into congestive heart failure
• Early use of inotropic agents to improve contactility
  • Dobutamine usual first choice
• Only after blood pressure is stabilized and patient is fluid resuscitated can you consider afterload reduction
  • vasodilator agents

Distributive Shock - a systemic vascular resistance issue

• Volume first to fill the tank
• Vasoconstrictive agents to increase vascular tone
  • Dopamine first unless anaphylaxis - then Epinephrine

Septic Shock - a combination of the three

• Volume first and frequent
• Vasocontrictive agents
  • generally start with Dopamine

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Monitoring

Remember: Shock is not something that is broke that you fix and are done. It is an evolving process that is a symptom of something else going wrong with the patient, that left untreated can result in cardiopulmonary failure and death.

Key items to monitor

• electrolytes
• glucose
• blood gases (pH and oxygenation)
• Central venous pressure
• hemodynamics
• coagulation status
• urine output
• neurologic status

Electrolytes:

• Na: can be markedly abnormal as a result of the underlying disease (hypo/hypernatremic dehydration), can get elevated during process of correcting base deficit. Goal should be to normalize Na to avoid abnormal fluid shifts, this should be done SLOWLY!
• K: in acidotic state potassium can be elevated to the point of cardiac dysrhythmias, as correction of acidosis occurs K can be driven back into cells developing severe hypokalemia in some cases. It should be monitored and treated appropriately
• Ca: in treatment of base deficit calcium can be chelated and dramatically decrease, leading to problems from seizures, hypotension and myocardial dysfunction, CaCl2 can be used acutely to correct hypocalcemia.

Glucose

• As part of response to compensatory mechanisms (epinephrine and corticosteroids) hyperglycemia is a common occurrence in stressed children. This can cause problems from osmotic diuresis and glucose intolerance. Some studies showed poor neurologic outcome could be best predicted by hyperglycemia in patients with shock. Care should be made not to overload the glucose management system in the body (i.e. no dextrose in flush solutions)

Blood Gases

• close monitoring is essential to evaluate correction of base deficit. In addition, in severe shock states respiratory compromise in common, and potential for respiratory failure is great. Patients may need intubation and mechanical ventilation. Failure to oxygenate is one sign of this. It is also important to maintain good oxygen delivery to help minimize anaerobic metabolism and worsening of acidosis.
• Venous Blood Gases are also of benefit since mixed venous oxygen saturation is a measurement of tissue perfusion and cardiac output. It needs to be from a central vein to be of use.
• Acidosis
  • Correction of the Acidosis is controversial
  • In many situations restoration of adequate perfusion will lead to a correction of the acidosis and decrease in the lactate in a few hours
  • severe acidosis can cause significant problems with cellular function and aggressive treatment should be considered
  • What level at which one should start treatment is also debatable, generally for pH < 7.1 in an unstable patient is an acceptable point
  • Formula:
    • 0.3x(weight in kg)x(base deficit) = mEq NaHCO3 to replace half of deficit
    • Should be given slowly in 1-2mEq/kg boluses
    • May need 10-20mEq/kg to correct acidosis
    • remember that this can be a large Na load leading to hyperosmolarity

Central Venous Pressure

• CVP monitoring allows close observation of hydration status and pre-load. This is essential in cardiogenic shock patients in whom too much fluid will worsen the shock state.

Hemodynamics

• good, reliable blood pressure monitoring and EKG monitoring are important. Although blood pressure is typically normal in early shock, decreasing blood pressure is a sign of someone who is decompensating

Coagulation Status

• as DIC is a common complication even early in shock, close monitoring of coagulation status will allow early correction of deficits

Urine Output

• this is representative of organ perfusion, improving urine output can be a sign of improving volume status, while worsening UO suggests more aggressive therapy

Neurologic Status

• this is also representative of organ perfusion, namely the brain.

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References

Rogers, MC Textbook of Pediatric Intensive Care. Chapter 15, p483-524. Williams and Wilkins, Baltimore, MD 1987.

• An excellent and concise overview of the etiology and management of Shock, both in general and for specific instances. There is a more recent addition than this, but the principles remain the same.

Berne RM and Levy MN. Physiology, 3rd edition. Chapter 32, pp 532-543. Mosby, St. Louis, 1993.

• Basic Physiology of all the interactions that go on to normalize circulatory function.

De Bruin WJ et. al. "Fluid Resuscitation in Pediatrics." Critical Care Clinics 8(2): 423-438. April 1992

• A nice review of everything involved in fluid resuscitaion of the Pediatric patient.

Griffel MI and Kaufman BS "Pharmacology of Colloids and Crystalloids." Critical Care Clinics 8(2): 235-253. April 1992.

• From the same Critical Care Clinics, another nice review of the fluids commonly used in resuscitation.

Textbook of Pediatric Advanced Life Support. American Heart Association.

• Stresses the basics of early management and stabilization.

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This page is meant for educational purposes only. Questions or comments regarding this page should be directed to the author at:

tegtm001@tc.umn.edu

This page last updated for content 7/14/1999

This page last updated for format 7/14/1999