1. SHOCK
DOOMSDAY

2. Vicken Y. Totten Shock lecture Thanks to David Cheng MD
And all who taught me

3. Definition
SHOCK: inadequate organ perfusion to meet the tissue’s oxygenation demand

4. PATHOPHYSIOLOGY OF SHOCK SYNDROME
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & cells swell
membranes becomes more permeable
electrolytes & fluids seep in & out of cell
Cells Die in Many Organs Death

5. Stages of shock Compensated /Early Shock
Vasoconstriction  (renin & carotid sinus baroceptor
Increase in HR and RR <- sympthatic activation)
Normotensive usually <- (aldosterone/ADH Na+/h20 retention)
Decompensated / late Shock
Cool, clammy , hypotenisve.
Vital organ preservation
Worsening LOC
Continued increase in HR and RR <-----(Chemreceptor respose to metabolic acidosis)
Irreversible-
HR and RR drop Multi Organ Failure Impending death)
Compensated (early shock)-Body recognizes problem and triggers mechanisms to correct BP (autotransfusion)
Vasoconstriction < (renin & carotid sinus baroceptor
Increase in HR and RR < sympthatic activation)
Normotensive usually <------(aldosterone/ADH Na+/h20 retention)
Decompensated (late shock)-Compensatory mechanisms can not keep up and begin to fail (bld moves to vital organs)
Signs and symptoms more profound (pale cool clammy hypoBP)
Worsening LOC
Continued increase in HR and RR <-----(Chemreceptor respose to
metabolic acidosis)
Irreversible-no longer be helped by compensatory mechanisms (HR and RR dropMOFImpending death)

6. Symptoms of Shock Fevers / Rigors (sepsis) SSCP (cardiogenic)
General Symptoms
Specific Symptoms
Fevers / Rigors (sepsis)
SSCP (cardiogenic)
Wheezing (anaphylaxis)
Trauma pain (hypovolemia)
Anxious
Dizziness
Weakness
Faintness
Thirsty
“I am sick”

7. Early Signs of Shock in Non Complicated Patients
WARM EARLY STAGE / PRESHOCK
Need high index of suspicion b/c lack of signs
+/- tachycardia
+/- orthostatics (HR more sensitive than BP)
+/- pulse pressure narrowing
+/-restless

8. “Hypoperfusion can be present in the absence of significant hypotension.” (Don’t only relay on BP for diagnosisng shock)
-fccs course

9. Signs of Late Shock Hypotension
COLD LATE STAGE
Cold, clammy and pale skin
Rapid, weak, thready pulse
Rapid breathing (blow off CO2 met acidosis)
Cyanotic
AMS->Coma
Anuria

10. End Stage Clinical effects
Cardiovascular
Myocardial depression
Vasogenic effects
Pulmonary
ARDS
Renal
ARF GI
Ischemic bowel
Hepatic
Increased LFT’s, liver failure
Hematologic
Neutropenia, Thrombocytopenia
DIC (Gm- > Gm+)
CNS
coma

11. Multiple Organ Dysfunction Syndrome
Number of Organs
Mortality (%)
0.8 1
6.8 2
26.2 3
48.5 4
68.8 5
83.3
*Adapted from Irwin and Rippe’s Critical Care Medicine 5th Edition, pg 1837

12. Circumferential
Subendocardial
Infarction due
to Shock

13. Shock
Lung

14. Acute congestion of liver due to shock

15. Acute tubular necrosis of the kidney due to shock

16. Intestinal mucosal hemorrhages due to shock

17. Adrenal gland hemorrhage due to shock

18. Remember History and Physical often limited by patient’s condition
Patient presentation can be variable secondary to
Severity of the perfusion defect
Underlying cause
Prior organ dysfunction
Exam should be tailored to be performed quickly with highest yield for uncovering the cause of shock.

19. Components (fluids, pump, pipes)

20. Components:
Blood (fluid)
Heart (pump)
Blood Vessels (pipes)

21. Types of Shock Hypovolemic (fluids) Cardiogenic (pump)
Redistributive (pipes)
(septic, neurogenic, anaphylactic)

22. Adequate circulating blood volume depends on 3 components; A minor impairment in one can be compensated for by the other 2 for a limited time. Prolonged or severe impairments will lead to SHOCK.

23. An Approach to Shock – Know this!
BP = SVR x CO
BP = blood pressure
CO = cardiac output (pump & fluids)
SVR = systemic vascular resistance (pipes)

24. If the blood pressure is low, then either the:
An Approach to Shock
If the blood pressure is low, then either the:
CO is low or
SVR is low
BOTH

25. Low SVR There are only a few causes of low SVR.
They ALL cause vasodilation:
Septic shock
Neurogenic (spinal cord injury) shock
Anaphylaxis Shock
Vasodilator (antihypertensive) Posioning

26. Look at and feel the patient!
How do you assess SVR?
Look at and feel the patient!
Low SVR has the features:
warm !!!
pink
Bounding pulses
hyperdynamic heart (fast and pounding)

27. Cause of shock (low BP) is then:
What if the SVR is high?
Pale
Poor cap refill (>2 seconds)
Cool arms/legs (>2 degree C difference)
Thready pulses (narrow pulse pressure (incr DBP))
Cause of shock (low BP) is then:
low CO

28. CO = HR x SV What are factors of CO? CO = cardiac output
HR = heart rate
SV = stroke volume

29. HR Problems Heart Rate problems are easy to diagnose
Rate: bradycardia versus tachycardia

30. Most difficult to diagnose and manage
Low SV (stroke volume)
Most difficult to diagnose and manage

31. Stroke Volume depends on
Preload--is the ventricle full?
Hypovolemic Shock
Obstructive Shock (ie Tension PTX, Tamponade)
Cardiac function
SqueezeContractility– can the ventricle contract?
Can blood get out?  Valve function:
normal?
regurgitation?
stenosis?

32. Perfusion (blood pressure) depends on:
BP = CO x SVR
CO = HR x SV
SV = preload & cardiac contractility-valve

33. Components of BP summary

34. Why Monitor? Essential to understanding their disease
Describe the patient’s physiologic status
Serial monitoring
Facilitates diagnosis and treatment of shock

35. Monitoring clinical shock parameter
Noninvasive：
Blood pressure (SBP, MAP)
Urine output
Heart rate
Shock index
Invasive：
Pulmonary artery catheter: CVP, PAWP, CO, SVR, DO2I, VO2I, SvO2
Arterial catheter: ABP, Serum lactate, Base deficit

36. Diagnosis of Shock MAP < 60 or decrease of 20 from baseline
systolic BP  90
 systolic BP > 40 mm Hg from the patient’s baseline pressure
Shock index (HR>SBP)
Clinical s/s of hypoperfusion of vital organs

37. Mean Arterial Pressure
MAP is the mean perfusion pressure for the tissues
Most require a MAP of 60 or greater!
Dependent only on the elastic properties of the arterial walls and the mean blood volume in the arterial tree
MAP = (2 x DBP) + SBP 3

38. Pulse Pressure=SBP-DBP
Pulse Pressure=SBP-DBP The difference between the systolic (fxn of ejection fraction) and diastolic pressures (function of SVR and distensibility (elastic recoil) of the aorta
Wide
Normal mmHg
Commonly seen with fever, anemia, exercise and hyperthyroidism
AR (aortic regurgitation) is also a cause
Narrow
May indicate an increase in vascular resistance with decreased stroke volume (ie aortic stenosis or decreased intravascular volume)

39. Invasive Markers Global Markers Regional Markers Base Deficit Lactate
Gastric pH
Sublingual CO2

40. Base Deficit Inadequate tissue perfusion leads to tissue acidosis
Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4
Normal range +3 to –3 mmol per L
Elevated base deficit correlates with the presence and severity of shock

41. Base Deficit Inadequate tissue perfusion leads to tissue acidosis
Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4
Normal range +3 to –3 mmol per L
Elevated base deficit correlates with the presence and severity of shock

42. Initial Lactate Weil and Afifi. (Circulation 1970)

43. Lactate and Outcomes Adult Patients
A peak blood lactate level
of >4.0 mmol/L
was identified as a
strong independent
predictor of mortality
and morbidity
and suggests that tissue hypoperfusion
Demmers Ann Thorac Surg 70:2082-6:2000

45. Gastric Intramucosal pH
Blood flow is not uniformly distributed to all tissue beds
Regions with inadequate tissue perfusion may exist while global markers are ‘normal’
Gut mucosa among the first to be affected during shock and the last to be restored to normal
Intramucosal pH falls when perfusion becomes inadequate

46. Sublingual capnometry:
A new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock
hypercarbia is a universal indicator of critically reduced tissue perfusion.

47. Sublingual CO2 Decrease gut perfusion Non-invasive, hand held monitor
Gastric tissue = esophagus = sublingual tissue
Non-invasive, hand held monitor
Rapid measurement
Sensitive marker of decreased blood flow

48. Sublingual capnometry:
A new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock
P SL CO2 provides a prompt indication of the reversal of tissue hypercarbia when circulatory shock is reversed

49. Direct arterial pressure A-line

50. Pulmonary Artery Catheter
INDICATIONS
volume status
cardiac status
COMPLICATIONS
technical
anatomic
physiologic

51. Swan-Ganz Catheter

52. PLACEMENT

53. Correct PA-C Position
From the RIJ approach, the RA is entered at approximately 25 cm, the RV at approximately 30 cm, and the PA at approximately 40 cm; the PCWP can be identified at approximately 45 cm.

54. Standard Parameters Measured Calculated Blood pressure
Pulmonary A. pressure
Heart rate
Cardiac Output
Stroke volume
Wedge pressure
CVP
Calculated
Mean BP
Mean PAP
Cardiac Index
Stroke volume index
SVRI
LVSWI
BSA

55. Why Index? Body habitus and size is individual
“Indexing” to patient with BSA allows for reproducible standard
PATIENT A
60 yo male
50 kg
CO = 4.0 L/min
BSA = 1.86
CI = 2.4 L/min/m2
PATIENT B
60 yo male
150 kg
CO = 4.0 L/min
BSA = 2.64
CI = 1.5 L/min/m2

57. PA Insertion 20 15 10 5
RA = 5
RV = 22/4
PA 19/10
PAOP(wedge) = 9

58. CVP CVP of SVC at level of right atrium pre-load “assessment”
normal mm Hg

59. PAOP (wedge) End expiration Wedge adjustment with positive pressure
Measured PAOP - ½ PEEP = “real PAOP”

60. Vascular Resistance PULMONARY (PVR) SYSTEMIC (SVR) MAP - CVP
MPAP - PAOP CO
PVR = constriction
PE, hypoxia
SYSTEMIC (SVR)
MAP - CVP C0
 SVR = vasoconstriction
 SVR = vasodilation
x 80
x 80
Vascular resistance = change in pressure/blood flow

61. Cardiac Cycle pulmonary Right ventricle Left ventricle systemic MPAP
PVR
MPAP
pulmonary
PCWP
RVSW
Right ventricle
Left ventricle
LVSW
MAP
CVP
systemic
SVR

62. Swan Ganz interpretation

63. Too Many Numbers

64. Definitions
O2 Delivery - volume of gaseous O2 delivered to the LV/min.
O2 Consumption - volume of gaseous O2 which is actually used by the tissue/min.
consumption > demand = anaerobic metabolism

65. Mixed venous oxygen saturation
Reflects difference between oxygen delivery and consumption
Normal – 65-75%
Measurement taken from the distal port of a PA catheter

66. SvO2: Low Values (< 60%)
 CO/CI
SV/SVI
 Hgb
 SaO2
 O2 consumption

67. SvO2: High Values (> 75%)
Sepsis
AV shunts/fistulae

68. Oxycalculations

69. Break Time…

70. Goals of Shock Resuscitation
Restore blood pressure
Normalize systemic perfusion
Preserve organ function

71. Parameters of Adequate Resuscitation
Urine output ( ml/kg/hr)
acceptable renal perfusion
Reversal of lactic acidosis (nl. pH)
improved perfusion
Normal mental status
adequate cerebral perfusion

72. Goal RAPIDLY RESTORE TISSUE PERFUSION
SHOCK: an EMERGENCY !!!
Goal RAPIDLY RESTORE TISSUE PERFUSION
Recognize it !!!
Immediate stabilization: ABC
……. SHOTGUN approach
Normalization of BP, pulse, UOP
Hemodynamic parameters
Restoration of aerobic metabolism, elimination of tissue acidosis, repayment of O2 debt
Treat the cause

73. “Shock is a symptom of its cause.”
-fccs course

74. In general, treat the cause...

75. Management Re-assess every 5-15 minutes
ABC’s
Maintain airway
Decrease work of breathing & Optimize 02
Circulation & Control Hemorrhage includes:
Direct pressure
Pressure points
Fluids & Drugs
Must address and treat:
PRELOAD
AFTERLOAD
PUMP
Re-assess every 5-15 minutes
(the sicker the patient, the shorter the interval

76. Management priorities in hypoperfused states
BP potency: Dopamine...NE…Vasopressin/Phenylephrine
When in doubt, try a little more volume

77. Hypovolemia

78. Time
Outcomes of same vol. lost over diff. periods of time. Slow losses (III, IV)
allow compensations to take effect. Rapid loss (I, II) of same vol. is fatal 5

79. Classes of Hypovolemic Shock

80. Clinical Signs of Acute Hemorrhagic Shock
% Blood loss
Clinical Signs
< 15
Slightly increased heart rate
15-30
Increased HR, increased DBP (narrow pp), prolonged capillary refill, flat neck veins
30-50
Above findings plus: hypotension, confusion, acidosis, decreased urine output
> 50
Refractory hypotension, refractory acidosis, death

81. Hypovolemic Shock Causes hemorrhage vomiting diarrhea dehydration
third-space loss
burns
Signs
 cardiac output
 PAOP/CVP
 SVR

82. Treatment - Hypovolemic
Reverse hypovolemia & hemorrhage control
Crystalloid vs. Colloid
1 L crystalloid  250 ml colloid
Watch for fluid overload by reassessing lung sounds
3:1 Rule (3cc crystalloid for 1cc bld loss)
Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infused
Best to give in 250 mL boluses in CHF followed by reassessment for another 250 cc bolus
Colloids: (ex: albumin)
Will increase osmotic pressure, watch for pulm edema
Remain in vascular space longer (several hrs)
NOT increase survival
prbc sooner than later
500 ml whole blood increases Hct 2-3%, 250ml PRBC’s increases Hct 3-4%
Increases oxygen carrying capacity
Used with acute hemorrhaging (mntn Hct 24% and Hgb 8g/dL)
NOT FOR VOLUME
FFP for coagulopathy (all factors)
Factor vii
PLT for thrombocytopenia
Pressors?

83. Resuscitation
Transport times < 15 minutes showed pre-hospital fluids were ineffective, however, if transport time > 100 minutes fluid was beneficial.
Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims.

84. Role of PASG?
Higher mortality rate in penetrating thoracic, cardiac trauma
Role undefined in rural, blunt trauma
Splinting role

85. Cardiogenic Shock Mech Signs
defect in cardiac function (lost > 40% Fxn)
Signs
 cardiac output
 PAOP/CVP
 SVR
 left ventricular stroke work (LVSW)

86. Cardiogenic Shock Myocardial failure (MI) Severe Arrhythmia
Severe Valvular dysfunction
Reduction in cardiac output:
>Decreased oxygen delivery

87. Symptoms of Cardiogenic Shock
Skin: progressive peripheral vasoconstriction results in cool, moist, pale skin with mottling
CHF Sx
JVD, HJR, APE, pedal edema
Heart:
Sounds: d/t enlargement and congestion you can hear murmurs or S3 or S4
Pulse: rapid rate and thready/weak pulse
BP: decreased BP and MAP
UO: decreases early d/t decreased renal perfusion

88. Cardiogenic Shock Assess for: Signs of heart failure
Signs of tamponade
Cardiac dysrrhythmia
Myocardial infarction
Tachycardia
Muffled heart sounds or third heart sound
Engorged neck veins with hypotension
Dyspnea
Edema in feet and ankles

89. Coronary Perfusion Pressure
Coronary PP = DBP - PAOP
coronary perfusion =  P across coronary a.
GOAL - Coronary PP > 50 mm Hg

90. Treatment of Cardiogenic Shock
Increase oxygen supply to the heart
Decrease O2 consumption (pain meds/sedation)
Increase O2 delivery (Mech vent, reperfusion of the coronary arteries)
Maximize the cardiac output
Mntn normal rhythm (dysrhythmics, pacing, cardioversion)
Diastolic Vasopressors (dopamine, epi, norepi, vasopressin)
Improve myocardial contractility--Inotropes
dobut and amrinone
Decrease the afterload (workload of the LV)
IABP
LVAD

91. The Failing Heart
Improve myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient.
Fluids first, then cautious pressors
Remember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure)
If inotropes and vasopressors fail, intra-aortic balloon pump & LV assist devices

92. Intra-Aortic Balloon Pump

93. Distributive Shock Types Signs Sepsis Anaphylactic
Acute adrenal insufficiency
Neurogenic
Signs
± cardiac output
 PAOP
SVR

94. Anaphylaxis

95. Anaphylactic Shock Rapid onset
Diffuse vasodilation mechanism from histamine & bradykinin
Edema from increased capillary permeability
Bronchoconstriction

96. Symptoms Onset within seconds and progression to death in minutes
Cutaneous manifestations
urticaria, erythema, pruritis, angioedema
Respiratory compromise
stridor, wheezing, bronchorrhea, resp. distress
Circulatory collapse
tachycardia, vasodilation, hypotension
CNS
apprehension->ams->coma

97. Diagnosis History and physical alone make the diagnosis
Lab values serve no role
Histamine levels are elevated for about 30 min, tryptase for several hours.

98. Treatment Remove the antigen ABC’s
IV Fluids, O2, cardiac monitor, pulse ox
First line Rx:
Epinephrine
For severe bronchospasm, laryngeal edema, signs of upper airway obstruction, respiratory arrest or shock: IV epi
100 micrograms of 1:100,000 (place 0.1 mL of 1:1000 in 10 mL of NS, give over 5-10 min)
If less severe, can give mL 1:1000 SC

99. Treatment 2nd line: H1 blocker: Diphenhydramine 25-50 mg IV
H2 blocker: Ranitidine 50 mg or Famotidine 20 mg IV.)
Steroids (Methylprednisolone 125 mg IV or Prednisone mg po)
Albuterol
For patients taking Beta-blockers with refractory hypotension, think about glucagon

100. Septic Shock

101. SEPSIS
Systemic Inflammatory Response (SIRS) manifested by two or > of following:
Temp > 38 or < 36 centigrade
HR > 90
RR > 20 or PaCO2 < 32
WBC > 12,000/cu mm or > 10% Bands (immature wbc)

102. Risk factors of Sepsis Extreme age: <1 and >65 years
Surgical / invasive procedures
Malnutrition
Chronic illness
DM, CRF, Hepatitis
Compromised immune status
AIDS, immunosuppressives, EtOH, malignancies
Drug resistant organisms

103. What is Sepsis? SIRS  Sepsis  Severe Sepsis  Septic Shock
Sepsis is the combination of the Systemic Inflammatory Response Syndrome (SIRS) & a confirmed or presumed infectious etiology.
Severe Sepsis: SIRS criteria, source of infection and infection-induced organ dysfunction or hypoperfusion abnormalities (sepsis + lactic acidosis/oliguria/AMS/etc.)
Septic Shock: SIRS criteria, source of infection, and hypotension not reversed with fluid resuscitation and associated with organ dysfunction or hypoperfusion abnormalities
A long line sepsis trials…but first, what is sepsis? SIRS, or Systemic Inflammatory Response Syndrome, is the overall inflammatory response of a host. We often think that “sepsis” implies that someone is close to death. This isn’t true. But they may be…Someone with sepsis can be as benign as a strep pharyngitis with a fever of 102.2, HR of 125, and WBC=16 or it can be a hypotensive patient with meningococcemia who will die in the next several hours.

104. Septic Shock Bacterial, viral, fungal infection
“Warm shock” is early stage
Fever, tachycardia, tachypnoea, leucocytosis,
inadequate oxygen extraction (High SvO2, Metabolic acidosis) in infected tissues
“Cold shock” is late stage

105. Septic/Inflammatory Shock
Signs: Early– warm w/ vasodilation, often adequate urine
output, febrile, tachypneic.
Late-- vasoconstriction, hypotension, oliguria,
altered mental status.
Monitor/findings: Early—hyperglycemia, respiratory
alkylosis, hemoconcentration,
WBC typically normal or low.
Late – Leukocytosis, lactic acidosis
Very Late– Disseminated Intravascular
Coagulation & Multi-Organ
System Failure.

106. Septic Shock TX Prompt volume replacement - fill the tank
Early antibiotic administration - treat the cause
If MAP < 60
Dopamine = g/kg/min
Norepinephrine = titrate (1-100 g/min)

107. Neurogenic shock

108. Neurogenic Shock
Essential derangement: paralysis of the sympathetic chain which controls vascular tone from injury to thoracic or cervical level spinal cord injury.
Produces decreased SVR from loss of vascular tone and bradycardia from unopposed parasympathetic input to SA node.

109. Neurogenic (Vasogenic) Shock
Caused by:
Spinal cord injury loss of SNS
Massive venous pooling & arteriolar dilatation
Signs and Symptoms:
Hypotension without tachycardia
Warm pink skin from cutaneous vasodilation
Low BP w/ minimal response to fluids
Accompanying Neurologic deficit
Spinal shock is not Neurogenic shock
Spinal Shock: the temporary loss of spinal reflex activity that occurs below a total or near total spinal cord injury

110. Treatment of Neurogenic Shock
Increase vascular tone and improve CO
Increase preload with fluids
CVP
PAWP
Increase vascular tone
Vasopressors
Maintain heart rate
Treat bradycardia if symptomatic
Maintain adequate oxygenation
Watch with SCI because of the disruption of O2 to the medulla
Initiate therapy to prevent DVT
Sluggish venous flow will increase risk factors
Steroids (Methylprednisolone 30mg/kg over 15 min in first hour, then 5.4 mg/kg/hr x 23 hours)
There are contradicting studies, all of which have flaw
The symptoms of neurogenic shock typically last 1-3 weeks

111. Obstructive Shock Causes Signs Treatment Needle decompression
Cardiac Tamponade
Tension Pneumothorax
Massive Pulmonary Embolus
Signs
 cardiac output
 PAOP/CVP
 SVR
Treatment
Needle decompression
Embolectomy / TPA

112. Adrenal Crisis Distributive Shock
Causes
Autoimmune adrenalitis
Adrenal apoplexy = B hemorrhage or infarct
This is suspected when patient is non-responsive to fluids, vasopressors and antibiotics.
Electrolytes may reveal hypoNa+ & hyperK+
Steroids may be lifesaving in patient who is unresponsive to fluids-inotropic-vasopressor (hydrocortisone 100mg IV)

113. Vasopressor Agents?
Augments contractility, after preload established, thus improving cardiac output.
Risk tachycardia and increased myocardial oxygen consumption if used too soon
Rationale, increased C.I. improves global perfusion

114. Vasopressors & Inotropic Agents
Norepinephrine
Epinephrine
Amrinone
Dopamine
Dobutamine

115. Dopamine Low dose (0.5 - 2 g/kg/min) = dopaminergic
Moderate dose (3-10 g/kg/min) = -effects
High dose (> 10 g/kg/min) = -effects
SIDE EFFECTS
tachycardia
> 20 g/kg/min  to norepinephrine

116. Dobutamine -agonist 5 - 20 g/kg/min
potent inotrope, variable chronotrope
caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension

117. Norepinephrine Potent -adrenergic vasopressor
Some -adrenergic, inotropic, chronotropic
Dose g/min
Unproven effect with low-dose dopamine to protect renal and mesenteric flow.

118. Epinephrine - and -adrenergic effects
potent inotrope and chronotrope
dose g/min
increases myocardial oxygen consumption particularly in coronary heart disease

119. Amrinone
Phosphodiesterase inhibitor, positive inotropic and vasodilatory effects
increased cardiac stroke output without an increase in cardiac stroke work
most often added with dobutamine as a second agent
load dose = mg/kg  g/kg/min drip
main side-effect - thrombocytopenia

120. vasopressin V1 vascular smooth muscle receptor vasoconstriction
units/min
Risk: coronary, mesenteric ischemia, hyponatremia, skin necrosis

121. Calcium Sensitisation by Levosimendan
Enhanced contractility of myocardial cell by amplifying trigger for contraction with no change in total intracellular Ca2+
Clinical trials status
Ultimately, the binding of levosimendan to troponin C evokes a stabilising, prolonged conformational change that occurs when calcium binds to troponin C. This is an enhancement of calcium's effects, and it thus increases the force of contraction. Sensitising the filaments to calcium rather than increasing calcium levels means that there is less potential for arrhythmia and increased contractile force with less energy consumption (i.e., myocardial oxygen demand is not increased).

122. Endpoints?
ACS / ATLS - restoration of vital signs and evidence of end-organ perfusion
Swan-guided resuscitation
C.I.  4.5, DO2I  670, VO2I  166
Lactic Acid clearance
Gastric pH

123. Shock: “rude unhinging of the machinery of life.”
Don’t forget...
Shock: “rude unhinging of the machinery of life.”
-Samuel D. Gross, 1872

124. ??????????? For the human speaker