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PATHOGENESIS OF SHOCK
DEFINITION OF SHOCK
• PALS DEFINITION
Physiologic state characterized by inadeqaute
tissue perfusion to meet metabolic demand
and tissue oxygenation
Shock vs blood pressure vs cardiac output
- Shock can be present with normal, decreased
or increased BP.
Similarly shock can have low or high cardiac output
SHOCH – INADEQUATE SUPPLY OF NUTRIENTS,
INCREASED TISSUE DEMAND, OR COMBINATION
OF BOTH FACTORS.
Discussion – does not include for DKA, SAM,
dengue
Understanding Shock
• Inadequate systemic oxygen delivery activates
autonomic responses to maintain systemic
oxygen delivery
• Sympathetic nervous system
•NE, epinephrine, dopamine, and cortisol
release
•Causes vasoconstriction, increase in
HR, and increase of cardiac contractility
(cardiac output)
• Renin-angiotensin axis
•Water and sodium conservation and
vasoconstriction
•Increase in blood volume and blood pressure
• Cellular responses to decreased systemic oxygen
delivery
• ATP depletion → ion pump dysfunction
• Cellular edema
• Hydrolysis of cellular membranes and cellular
death
• Goal is to maintain cerebral and cardiac
perfusion
• Vasoconstriction of splanchnic,
musculoskeletal, and renal blood flow
• Leads to systemic metabolic lactic acidosis that
overcomes the body’s compensatory
mechanisms
Case scenario 1
1 yr old child, complaints of
• Loose stools – 8 to 10 episodes from 1 day,
• Vomiting - 3 to 4 episodes from past 4 hrs
• Decreased activity from past 4 hrs
• Decreasd urine output past 4 hrs
• ABCs
• Cardiorespiratory monitor
• Pulse oximetry
• Supplemental oxygen
• IV access
• ABG, labs
• Foley catheter
• Vital signs including rectal temperature
Approach to the Patient in Shock
Based on initial impression and primary
assessment, should be able to
• Recognise type of shock
• Stage of shock
• Intervene to halt progression of shock
Types of shock
PVR
Blood
pressure
low
Blood
pressure
normal
MODS
Repeating once again………..
• Single differentiating point
between compensated and
decompensated –
BLOOD PRESSURE
Of course, ScvO2
• Broadly classified into non hemorrhagic and
hemorrghagic
• Importance to recognise extent of volume
depletion and type to volume loss.
• Shock is usually present @ greater than 100
ml/kg of deficits.
Case scenario 2
2 yrs old with complaints of fever- 3 days
• Cough, wet type – 3 days
• Hurried breathing- 1 day
• Decreased activity- 1 day
• Decreased urine out -8 hrs
• O/E – febrile 102F, tachycaediac 140,
tachypneic 40, spo2 86, hypotension with
narrow pulse pressure
• Peripheral pulses- feeble volume,
not bounding ; central pulses – weak
• CRT- prolonged
• Extremities- pale, mottled ; central to
peripheral temp > 3 C
• RS- b/l crepts
• CNS- lethargic
What are we dealing with ????
Challenges in septic shock
1. Wide clinical spectrum – warm VS cold shock
2. Combination of hypovolemic, distributive and
cardiogenic shock
3. Early hypotension in septic shock
4. Variable degrees of inadequate perfusion and
microvascular thrombosis leading to ischemia
5. Adrenal insuffiency
Criteria for organ dysfunction
Concept of SCVO2
• Svo2 - measures venous oxygen saturation @
pulm artery.
• Scvo2 – measures venous oxygen saturation
@ superior venacava.
• Continuous ScvO2 monitoring triple-lumen
central venous catheter
Hallmark of uncompensated shock
If the body is unable to compensate
because of disease processes or
other physiologic problems, tissues
extract more than one oxygen
molecule, resulting in lower venous
oxygenation saturation as evidenced
by a decrease in ScvO2
Case scenario 3
12 yr old girl with h/o consumption of unknown
poisonous pellets, brought to ER
O/E – agitated, diaphoretic
Tachycardiac 120, hypotensive 80/62
spO2 – 86%, tachyneic with increased resp
efforts.
RS- b/l diffuse crepts; CVS- s1 and s2 normal
P/A – tender hepatomegaly
ECG – broad QRS complexes with features of
anterolateral wall MI
ABG- met acidosis with poor oxygenation
GRBS- 24, Serum Ca – 5 mg/dl, RFT – 43/1.21
S. Lactate levels- 15 mg/dl
DIAGNOSIS
Anterolateral MI with CCF with Cardiogenic
shock ?? Aluminum phosphide
Case scenario 4
4 day old term gestation male baby born to
NCM, apparently normal till 3 days, brought
with
Sudden onset resp distress- tachypneic with
retractions; Cyanotic, lethargic –from past 6
hrs
O/E- tachycardiac 180, spo2 –
CRT > 3 sec 80
86 82
78
Absence of femoral pulses, tender congested
hepatomegaly.
Metabolic acidosis with elevated lactate levels.
DIAGNOSIS-
Obstructive shock due to left ventricular
outflow obstruction ?? COA
Cardiogenic shock-
•CHD
•Myocarditis
•Cardiomyopathy
•Arrhytnmias
•Sepsis
•Myocardial injury
•Poisoning or drugs
Obstructive shock
• Cardiac tamponade
• Tension pneumothorax
• Duct dependent CHD
• Massive PE
• Abd compartment syndrome
Effusion around
the pump
Squeeze of the
pump
Strain of the
pump
Fullness of the
tank
Leakiness of the
tank
Tank compromise
Rupture of the
pipes
Clogging of the
pipes
IVC Assessment for Fluid
Responsiveness
1. Position the patient supine.
2. Obtain a subxyphoid view of the heart.
• The ultrasound indicator should be directed toward the
patient’s left flank.
3. Once identified the right atrium, turn the ultrasound
probe 90 degrees counterclockwise.
• The indicator should now be directed toward the
patient’s head.
4. Identify the IVC as it enters the right atrium.
5. Put the ultrasound into M-mode.
6. Place the M-mode cursor cross the IVC
approximately 2 cm inferior to the junction
with the RA.
7. In spontaneously breathing patients, the
following measurements suggest a patient is
likely to be fluid responsive:
• a. IVC measuring < 2 cm in diameter coupled
with IVC collapse
• > 50% with each breath or
• b. IVC collapsibility > 12%
IVC collapsibility = (max diameter – min diameter) /
(mean diameter) x 100
8. In mechanically ventilated patients who are
passive on the venti, fluid responsiveness is
likely if the IVC distensibility > 18%.
IVC distensibility = (max diameter – min
diameter) / (min diameter) x 100
Shock pathogenesis

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Shock pathogenesis

  • 2. DEFINITION OF SHOCK • PALS DEFINITION Physiologic state characterized by inadeqaute tissue perfusion to meet metabolic demand and tissue oxygenation Shock vs blood pressure vs cardiac output - Shock can be present with normal, decreased or increased BP.
  • 3. Similarly shock can have low or high cardiac output SHOCH – INADEQUATE SUPPLY OF NUTRIENTS, INCREASED TISSUE DEMAND, OR COMBINATION OF BOTH FACTORS. Discussion – does not include for DKA, SAM, dengue
  • 4. Understanding Shock • Inadequate systemic oxygen delivery activates autonomic responses to maintain systemic oxygen delivery • Sympathetic nervous system •NE, epinephrine, dopamine, and cortisol release •Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output)
  • 5. • Renin-angiotensin axis •Water and sodium conservation and vasoconstriction •Increase in blood volume and blood pressure • Cellular responses to decreased systemic oxygen delivery • ATP depletion → ion pump dysfunction • Cellular edema • Hydrolysis of cellular membranes and cellular death
  • 6.
  • 7. • Goal is to maintain cerebral and cardiac perfusion • Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow • Leads to systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms
  • 8. Case scenario 1 1 yr old child, complaints of • Loose stools – 8 to 10 episodes from 1 day, • Vomiting - 3 to 4 episodes from past 4 hrs • Decreased activity from past 4 hrs • Decreasd urine output past 4 hrs
  • 9.
  • 10. • ABCs • Cardiorespiratory monitor • Pulse oximetry • Supplemental oxygen • IV access • ABG, labs • Foley catheter • Vital signs including rectal temperature Approach to the Patient in Shock
  • 11.
  • 12.
  • 13. Based on initial impression and primary assessment, should be able to • Recognise type of shock • Stage of shock • Intervene to halt progression of shock
  • 15.
  • 16. PVR
  • 17.
  • 18.
  • 19.
  • 21.
  • 22.
  • 23.
  • 24. Repeating once again……….. • Single differentiating point between compensated and decompensated – BLOOD PRESSURE Of course, ScvO2
  • 25.
  • 26. • Broadly classified into non hemorrhagic and hemorrghagic • Importance to recognise extent of volume depletion and type to volume loss. • Shock is usually present @ greater than 100 ml/kg of deficits.
  • 27.
  • 28. Case scenario 2 2 yrs old with complaints of fever- 3 days • Cough, wet type – 3 days • Hurried breathing- 1 day • Decreased activity- 1 day • Decreased urine out -8 hrs • O/E – febrile 102F, tachycaediac 140, tachypneic 40, spo2 86, hypotension with narrow pulse pressure
  • 29. • Peripheral pulses- feeble volume, not bounding ; central pulses – weak • CRT- prolonged • Extremities- pale, mottled ; central to peripheral temp > 3 C • RS- b/l crepts • CNS- lethargic What are we dealing with ????
  • 30. Challenges in septic shock 1. Wide clinical spectrum – warm VS cold shock 2. Combination of hypovolemic, distributive and cardiogenic shock 3. Early hypotension in septic shock 4. Variable degrees of inadequate perfusion and microvascular thrombosis leading to ischemia 5. Adrenal insuffiency
  • 31.
  • 32.
  • 33.
  • 34. Criteria for organ dysfunction
  • 35.
  • 36.
  • 37.
  • 38.
  • 39. Concept of SCVO2 • Svo2 - measures venous oxygen saturation @ pulm artery. • Scvo2 – measures venous oxygen saturation @ superior venacava. • Continuous ScvO2 monitoring triple-lumen central venous catheter
  • 40. Hallmark of uncompensated shock If the body is unable to compensate because of disease processes or other physiologic problems, tissues extract more than one oxygen molecule, resulting in lower venous oxygenation saturation as evidenced by a decrease in ScvO2
  • 41. Case scenario 3 12 yr old girl with h/o consumption of unknown poisonous pellets, brought to ER O/E – agitated, diaphoretic Tachycardiac 120, hypotensive 80/62 spO2 – 86%, tachyneic with increased resp efforts. RS- b/l diffuse crepts; CVS- s1 and s2 normal P/A – tender hepatomegaly
  • 42. ECG – broad QRS complexes with features of anterolateral wall MI ABG- met acidosis with poor oxygenation GRBS- 24, Serum Ca – 5 mg/dl, RFT – 43/1.21 S. Lactate levels- 15 mg/dl DIAGNOSIS Anterolateral MI with CCF with Cardiogenic shock ?? Aluminum phosphide
  • 43. Case scenario 4 4 day old term gestation male baby born to NCM, apparently normal till 3 days, brought with Sudden onset resp distress- tachypneic with retractions; Cyanotic, lethargic –from past 6 hrs O/E- tachycardiac 180, spo2 – CRT > 3 sec 80 86 82 78
  • 44. Absence of femoral pulses, tender congested hepatomegaly. Metabolic acidosis with elevated lactate levels. DIAGNOSIS- Obstructive shock due to left ventricular outflow obstruction ?? COA
  • 46. Obstructive shock • Cardiac tamponade • Tension pneumothorax • Duct dependent CHD • Massive PE • Abd compartment syndrome
  • 47.
  • 48. Effusion around the pump Squeeze of the pump Strain of the pump
  • 49. Fullness of the tank Leakiness of the tank Tank compromise
  • 51. IVC Assessment for Fluid Responsiveness 1. Position the patient supine. 2. Obtain a subxyphoid view of the heart. • The ultrasound indicator should be directed toward the patient’s left flank. 3. Once identified the right atrium, turn the ultrasound probe 90 degrees counterclockwise. • The indicator should now be directed toward the patient’s head.
  • 52. 4. Identify the IVC as it enters the right atrium. 5. Put the ultrasound into M-mode. 6. Place the M-mode cursor cross the IVC approximately 2 cm inferior to the junction with the RA.
  • 53. 7. In spontaneously breathing patients, the following measurements suggest a patient is likely to be fluid responsive: • a. IVC measuring < 2 cm in diameter coupled with IVC collapse • > 50% with each breath or • b. IVC collapsibility > 12% IVC collapsibility = (max diameter – min diameter) / (mean diameter) x 100
  • 54. 8. In mechanically ventilated patients who are passive on the venti, fluid responsiveness is likely if the IVC distensibility > 18%. IVC distensibility = (max diameter – min diameter) / (min diameter) x 100