1. Internal Medicine/Critical Care Medicine
Shock
Jose Emmanuel M Palo, MD
Internal Medicine/Critical Care Medicine

2. In critical illness, heart and lung must be considered as one organ system.
Adapted from Weibel ER: The Pathway for Oxygen: Structure and Function in the Mammalian Respiratory System. Cambridge, MA, Harvard University Press, 1984

3. Mechanical events always preceded by electrical events.
Cardiac Cycle
Mechanical events always preceded by electrical events.

4. Shock
clinical syndrome of organ dysfunction due to cellular hypoxia from hypoperfusion

5. Definitions
unrelated to “emotional shock” or the acute stress reaction

6. Inflammatory mediators
Hypoperfusion
Cellular injury
Microvascular/
endothelial
dysfunction
Cellular Death
Inflammatory mediators

7. Multiple organ failure
Cellular Death
Multiple organ failure
Death

8. Determinants of Effective Tissue Perfusion
Cardiovascular Performance
Cardiac Function
Venous Return
Vascular Performance
Oxygen Transport
Cardiopulmonary level
Cellular level
Microvascular Function
Cellular Energy Metabolism
Determinants of Effective Tissue Perfusion in Shock
1) Cardiovascular Performance (total systemic perfusion/cardiac output)
Cardiac Function
Preload
Afterload
Contractility
Heart rate
Venous Return
Right atrial pressure (dependent on cardiac function)
Mean circulatory pressure
Stressed vascular volume
Mean vascular compliance
Venous vascular resistance
Distribution of blood flow
2) Distribution of Cardiac Output
Intrinsic regulatory systems (local tissue factors)
Extrinsic regulatory systems (sympathetic/adrenal activity)
Anatomic vascular disease
Exogenous vasoactive agents (inotropes, vasopressors, vasodilators)
3) Microvascular Function
Pre- and postcapillary sphincter function
Capillary endothelial integrity
Microvascular obstruction (fibrin, platelets, WBC, RBC)
4) Local Oxygen Unloading and Diffusion
Oxyhemoglobin Affinity
RBC 2,3 DPG
Blood pH
Temperature
5) Cellular Energy Generation/Utilization Capability
Citric acid (Kreb's) cycle
Oxidative phosphorylation pathway
Other energy metabolism pathways (e.g. ATP utilization)

9. Cardiovascular Function
In humans, most critical organ perfusion is auto-regulated at MAP between mmHg

10. Cardiovascular Function
Perfusion pressure ~ MAP

11. SV x HR MAP = CO x SVR SNS and PNS balance
catecholamine levels/responsiveness
ACTH and cortisol
R-A-A
Vasopressin
prostacycline
Nitric Oxide
Adenosine
Drugs
Preload
Afterload
Contractility
SV x HR
MAP = CO x SVR

12. amount of oxygen leaving
Oxygen Transport
DO2 =
1.39 x CO x Hb x saO2
amount of oxygen leaving
the heart per unit time

13. amount of oxygen being consumed per unit time
Oxygen Transport
VO2 =
1.39 x CO x Hb x (saO2-svO2)
amount of oxygen being consumed per unit time

14. Physiologic Oxygen Supply Dependency
Critical Delivery
Threshold
Lactic Acidosis
VO2
DO2
Mizock BA. Crit Care Med. 1992;20:80-93.

15. Pathologic Oxygen Supply Dependency
Physiologic
VO2
DO2
Mizock BA. Crit Care Med. 1992;20:80-93.

16. Arterial Desaturation
Compensation
VO2 =
1.39 x CO x Hb x (saO2-svO2)
Arterial Desaturation

17. Compensation
VO2 =
1.39 x CO x Hb x (saO2-svO2)
Anemia

18. Compensation
VO2 =
1.39 x CO x Hb x (saO2-svO2)
Decreased CO

19. Oxygen Unloading
Association
Segment

20. Oxygen Unloading
Dissociation
Segment

21. Oxygen Unloading

22. Shock Types Hypovolemic Distributive Cardiogenic Obstructive afterload
preload

23. Hypovolemic Shock decreased effective blood volume
decreased end- diastolic filling pressures
trauma, diarrheal illness
relative hypovolemic state in septic shock
volume is key

24. Stages of Hypovolemic Shock
Mild
(<20% EBV)
Moderate
(20-40%)
Severe
(>40%)
cool ext
inc capillary refill time
diaphoresis
collapsed veins
anxiety
(plus)
tachycardia
tachypnea
oliguria
postural changes
marked tachycardia
hypotension
coma

25. Distributive Shock decreased SVR due to loss of vasomotor control
frequently, need volume to unmask a distributive shock state
sepsis, anaphylaxis, anaphylactoid reactions, neurogenic shock, hypoadrenalism

26. Distributive Shock Anaphylactoid shock Anaphylactic shock
insect envenomations
antibiotics (beta-lactams, vancomycin, sulfonamides)
heterologous serum (anti-toxin, anti-sera)
blood transfusion
immunoglobulins (esp IgA deficient)
Egg-based vaccines
latex
Anaphylactoid shock
ionic contrast media
protamine
opiates
polysaccharide volume expanders (dextran, hydroxyethyl starch)
muscle relaxants
anesthetics

27. Cardiogenic Shock loss of cardiac pump function (intrinsic)
due to myocardial damage, loss of contractility
Special: valvular dysfunction
characterized by elevations of both diastolic volumes and pressures

28. Extra-Cardiac Obstructive
due to obstruction of flow in the cardiovascular circuit
preload obstruction: cardiac tamponade, constrictive pericarditis, other intrathoracic processes
afterload obstruction: pulmonary embolism

29. Hemodynamics of Shock Types
CO SVR PWP EDV
Hypovolemic
Distributive
Cardiogenic
Obstructive
afterload
preload

32. Management Principles
frequently reversible in early stages
early recognition and emergent intervention are key
clinical signs and symptoms may be due to the primary shock state, compensatory mechanisms or end- organ effects

33. Clinical Signs
Primary diagnosis - tachycardia, tachypnea, oliguria, encephalopathy (confusion), peripheral hypoperfusion (mottled, poor capillary refill vs. hyperemic and warm), hypotension
Differential DX:
JVP - hypovolemic vs. cardiogenic
Left S3, S4, new murmurs - cardiogenic
Right heart failure - PE, tamponade
Pulsus paradoxus, Kussmaul’s sign - tamponade
Fever, rigors, infection focus - septic

35. The Swan-Ganz Catheter
Proximal (CVP)
CO Thermistor
Balloon port
Distal (PCWP)
Pulmo Artery
Sup Vena Cava
R Atrium
R Ventricle

36. Diagnosis and Evaluation
Invasive Monitoring
Arterial pressure catheter
CVP monitoring
Pulmonary artery catheter (+/- RVEF, oximetry)
MVO2
DO2 and VO2 2 2

37. Static and dynamic volume assessment
CVP
PCWP
Straight leg raising
Intrathoracic fluid index
Pulse pressure variability
Pre-ejection period variability
Pulse contour analysis

38. Advanced Concepts: PPVar
resp fluctuations during positive pressure ventilation cause decreased R-sided preload and increased R-sided afterload during inspiration, leading to decreased CO on the R, followed by decreased CO on the L a few beats later. This shows up as a decrease in pulse pressure. Wide variation in pulse pressure due to positive pressure ventilation denotes preload dependence. PEEP moves it to the L. Spec 100%, sensitivity 68%. SV
PEEP
RAP

39. Advanced Concepts: Straight Leg Raising
concept is that of a reversible fluid load.
Michard, 2008

40. Advanced Concepts: Microvascular Function
sublingual sidestream darkfield imaging

41. Advanced Concepts: Cellular Energetics

42. A Clinical Approach to Shock Diagnosis and Management
Initial Therapeutic Steps
Admit to ICU
Venous access (1 or 2 wide-bore catheters)
Central venous catheter
Arterial catheter
ECG monitoring
Pulse oximetry
Hemodynamic support (MAP < 60 mmHg)
Fluid challenge
Vasopressors for severe shock unresponsive to fluids

43. A Clinical Approach to Shock Diagnosis and Management
When Diagnosis Remains Undefined or Initial Management Fails
Pulmonary Artery Catheterization
Cardiac output
Oxygen delivery
Filling pressures
Echocardiography
Pericardial fluid
Cardiac function
Valve or shunt abnormalities

44. A Clinical Approach to Shock Diagnosis and Management
Immediate Goals in Shock
Hemodynamic support MAP > 60mmHg PAOP = mmHg Cardiac Index > 2.2 L/min/m Maintain oxygen delivery Hemoglobin > 9 g/dL Arterial saturation > 92% Supplemental oxygen/mechanical ventilation Reversal of oxygen dysfunction Decreasing lactate (< 2.2 mM/L) Maintain urine output Reverse encephalopathy Improving renal, liver fxn tests
MAP = mean arterial pressure; PAOP = pulmonary artery occlusion pressure.

45. SV x HR MAP = CO x SVR SNS and PNS balance
catecholamine levels/responsiveness
ACTH and cortisol
R-A-A
Vasopressin
prostacycline
Nitric Oxide
Adenosine
Drugs
Preload
Afterload
Contractility
SV x HR
MAP = CO x SVR

47. Case #1
90/M inpatient for cholecystitis, treated now for 11 days with antibiotics and fluid
Pacemaker 2 yrs ago for symptomatic bradycardia
PAC placed for peri-operative management
BP 189/86 PAWP 23 (6-12) HR 80
CO 3 L/min (4-8) SVR 6600 ( )
lactate 5 mmol/L (<2.2)

48. Case #2
50/M brought to ER unresponsive, arrested and had ACLS/CPR for 12 minutes
Comatose now and on norepinephrine
Urine output 0
BP 55/40 HR 45 PACW 8 (6-12) RA 0 (2-6)
CO 3.6 (4-8) SVR 1000 ( )
lactate 12 mmol/L (<2.2) )

49. Case #3 59/M 2 days after STEMI, not on mechanical ventilator
BP 55/40 HR 110 RR 26
PA 35/18 CVP 18
PPV 8%

50. End(points) shock is common and life-threatening
differentiating diagnoses frequently requires invasive procedures
management is time dependent
use therapy with the highest physiologic benefit at the lowest physiologic cost