Chapter 3 - Shock Flashcards by Phillip Endleman

What 3 things contribute to Stroke Volume?

Preload, Myocardial contractility, Afterload

How well did you know this?

Not at all

Perfectly

What 3 things contribute to Preload?

Venous capacitance, volume status and the diffference between systemic pressure and Right Atrial pressure.

How well did you know this?

Not at all

Perfectly

What is the earliest sign of shock?

Tachycardia

How well did you know this?

Not at all

Perfectly

What is the result of endogenous catecholamine release?

Increase in peripheral vascular resistance, leading to an increase in diastolic BP (and therefore a fall in pulse pressure), but NO increase in end-organ perfusion.

How well did you know this?

Not at all

Perfectly

Which other substances are released to cause vasoconstriction?

histamine, bradykinin, beta-endorphins, prostanoids, cytokines.

How well did you know this?

Not at all

Perfectly

What is the most effective way to restore cardiac output and end-organ perfusion?

STOP BLEEDING AND VOLUME REPLETION (venoconstriction preserves preload but its effects are limited)

How well did you know this?

Not at all

Perfectly

Which pro-inflammatory mediators cause end-organ damage?

inducible Nitric Oxide Synthase (iNOS) and Tumour Necrosis Factor (TNF), which are released after cell membranes are disruted and electric gradient is lost.

How well did you know this?

Not at all

Perfectly

Should you routiinely give vasopressors?

No. They worsen tissue perfusion. Treatment of shock is oxygenation, ventilation, stop bleeding and fluid resus.

How well did you know this?

Not at all

Perfectly

What percentage of blood volume loss can be compensated for?

Up to 30%. Check HR/RR, pulse pressure and skin circulation. ANY INJURED PATIENT WHO IS COOL AND TACHYCARDIC IS IN SHOCK UNTIL PROVED OTHERWISE.

How well did you know this?

Not at all

Perfectly

What constitutes tachycardia in different ages?

160bpm in infants, 140 in preschoolers, 120 in school age, 100 in adults.

How well did you know this?

Not at all

Perfectly

What complicating factors might mask the heart rate in elderly? What should you look at instead?

Beta-blockers, pacemakers. Look for the PULSE PRESSURE instead.

How well did you know this?

Not at all

Perfectly

How useful is checking Hb/Haematocrit? What else could be used instead?

You can get massive blood loss producing minimal Hb/Haematocrit decrease. Base deficit/Lactate levels may be more useful.

How well did you know this?

Not at all

Perfectly

What are the main sources of blood loss? Which investigations are needed?

“Blood on the Floor plus 4 more” = Chest/Abdo/Pelvis (retroperitoneum)/Thigh (also extremities).
Consider CXR/Pelvic XR/FAST/bladder catheterisation.

How well did you know this?

Not at all

Perfectly

What are the main causes of Cardiogenic shock?

MI, tamponade, air embolus, blunt cardiac injury (blunt injury especially likely if the mechanism of injury is rapid deceleration).

How well did you know this?

Not at all

Perfectly

What are the main signs of cardiac tamponade? How is it treated?

Tachycardia + muffled heart sounds + dilated JVP + hyptension (resistant to fluid resus). Needs pericardiocentesis emergently and thoracotomy definitively.

How well did you know this?

Not at all

Perfectly

What causes neurogenic shock? How is it manifested? How is it treated?

Cervical or upper thoracic injuries lead to loss of sympathetic tone, causing hypotension without tachycardia/cutaneous vasoconstriction/narrow pulse pressure. Treat with fluids. Isolated intracranial injuries do NOT cause shock.

What are the 4 types of non-haemorrrhagic shock?

1) Cardiogenic (MI, tamponade, air embolus, blunt cardiac injury)
2) Tension pneumothorax
3) Neurogenic
4) Septic

What percentage of body weight is blood?

5L in a 70kg male = 7% (it’s about 8-9% in children, about 80-90ml/kg)

What are the absolute and percentage volume losses in Class I-IV haemorrhage? What are the associated Heart rates and pulse pressures? How would you treat each?

Class I - up to 750ml, 15%. HR < 100, PP normal, give crystalloids
Class II - 750-1500ml, 15-30%, HR 100-120, PP low, give crystalloids
Class III - 1500-2000ml, 30-40%, HR 120-140, PP low, give crystalloids AND BLOOD
Class IV - >2000ml, >40%, HR >140, PP low, give crystalloids AND BLOOD.

What confounding factors alter the normal response to blood loss?

Age, Severity of injury, Time between injury and treatment, prehospital fluids given, meds (for chronic conditions)

Nonresponsiveness to fluids with ongoing blood loss means what is needed?

Surgery or angioggraphic control

Why is an NG tube often a good idea?

Gastric dilation can occur in trauma, especially in children, causing excessive vagal stimulation and unexplained hypotension/bradycardia. Risk of aspiration consequently rises.

What are the absolute contraindications to inserting a urethral catheter?

Blood at urethral meatus, mobile/non-palpable/high-riding prostate.

What is the rate of flow in a cannula proportional to?

the fourth power of the radius (and inversely proportional to the length) - so use a short, fat cannula.

What's the best first choice in children, intraosseous line or central venous catheter?

Intraosseous.

What is the protocol for initial fluid therapy? What is the complication of excessive fluids?

1-2L bolus (and 20ml/kg in children), then keep checking urine output, GCS and peripheral perfusion. Excessive fluids can worsen the lethal triad of coagulopathy, acidosis and hypothermia.

How does fluid management differ in blunt/penetrating injuries?

Fluids are very important in blunt injuries. In penetrating injuries, consider delaying fluids until bleeding is stopped, in order to prevent further bleeding (i.e. "permissive hypotension").

How might initial acid-base measurements change in hypovolaemic shock? What should not be used to correct these abnormalities?

Early on, there's respiratory alkalosis (due to tachypnoea), followed by mild metabolic acidosis. Persistent, severe acidosis is lactic in origin. Sodium Bicarbonate must NOT be used to treat the acidosis.

What are the 3 types of response to initial resus?

Rapid, Transient and Minimal responders.

What should be considered in minimal responders?

If minimal response, consider CVP monitoring or cardiac US. | Nonresponders - could be tamponade/tension pneumothorax/MI/gastric distension/DKA/Hypoadrenalism/Neurogenic shock.

What is the difference between fully crossmatched, Type-specific and Emergency blood?

TIME. Full crossmatching takes 1 hour, type-specific takes 10 minutes (ABO compatible but other antibodies may be present), emergency is immediate (RH negative to avoid sensitisation and future complications in females of childbearing age).

What other blood option is possible in haemotthorax patients?

Auto-tranfsfusion (needs anticoagulation with sodium citrate first).

What percentage of severely injured patients develop DIC on admission? How should they be investigated and managed in terms of blood loss? What type of injuries are particularly prone to coagulation abnormalities?

30%. Use platelets/cryoprecipitate/FFP, as guided by PT/APTT/platelet and fibrinogen levels. Fluids alone can dilute what little platelets and clotting factors remain. Brain injuries are particularly prone --> Give platelets/FFP early if they're known to be on antiplatelet/anticoagulation meds.

What are the 7 Special Considerations in shock?

1) BP does not = CO. [If BP = CO x SVR, using vasopressors increased SVR and therefore BP, but CO not affected, so there'll be no improvement in tissue perfusion or oxygenation]. 2) Elderly - a) There's decreased sympathetic tone and cardiac compliance, so you see less tachycardia and less contractility. b) Atherosclerosis also sensitises organs to even slight blood loss. c) Pre-existing volume depletion due to diuretics or malnutrition. d) beta-blockers can mask tachycardia 3) Athletes - 15-20% extra blood volume, up to 6x cardiac output, up to 50% increase in SV, resting HR ~50. 4) pregnancy - physiologic hypervolaemia 5) Medications - beta-blockers, CCBs, insulin overdosing, NSAIDS (affect platelet count), diuretics (hypokalaemia). 6) Hypothermia - Coagulopathy may worsen. Can irrigate peritoneal/thoracic cavity with warm crystalloids if its severe. 7) Pacemaker - Unable to change HR, so can't increase CO. CVP monitoring is invaluable in these patients to guide fluid therapy.

Why should you not be overdependent on CVP? Why might initial CVP be high? What might cause a pronounced rise in CVP?

CVP and CO are indirect estimates of the precise meassurement of cardiac function (which is the relationship between ventricular end-diastolic volume and stroke volume). Initially high = COPD or exogenous vasopressors Prnounced elevations = tamponade/tension pneumothorax/overtransfusion.