1. Hemodynamic monitoring and Shock
Dr. Mohammad Aljawadi PharmD, Msc, PhD
PHCL 477
Clinical Pharmacy Department
College of Pharmacy
King Saud University
April 2015

3. Inadequate tissue perfusion
What is Shock?
Inadequate tissue perfusion
Cellular Injury
Organ Dysfunction

4. To understand the hemodynamics of shock we need:
To understand the basics of hemodynamics
What is a pulmonary artery catheter and how it is used
Let us start with the latter and go
back to the former later

5. Pulmonary Artery Catheter
Swan-Ganz Catheter
110 cm long
Up to 5 ports
Tip encloses a balloon  1.5 mL
Ports at 19cm and cm for the infusion of drugs.

6. Pulmonary Artery Catheter
Indications
Myocardial infarction with shock/hypotension.
Intraoperative cardiac or vascular surgery patients.
Severe trauma.
Relative Indications
CHF
Pulmonary hypertension
Neurosurgical procedures
Sepsis/septic shock
Respiratory failure
Uses
Establish Diagnosis
Guide therapies
Monitor Treatment
Assess O2 delivery

7. Central Venous Access Complications
Line sepsis
Thrombosis
Pneumothorax
Hemothorax
Arrhythmias (Swan-Ganz)
Air Embolus
Infarction
Catheter Knotting (Swan-Ganz)

8. How it is inserted?
During diastole while mitral valve is open, left ventricle, left atrium and pulmonary capillary become one chamber.

9. The Basics of Hemodynamics
Blood Pressure
Cardiac Output
Systemic vascular resistance
Stroke Volume
Heart rate
Pre-load
After-load
Contractility

10. The Basics of Hemodynamics
BLOOD
PRESSURE CO
SVR = X SV HR X

11. The Basics of Hemodynamics
Cardiac Output (CO)
Amount of blood that is pumped out of the heart in one minute.
5.6 L/min for a human male and 4.9 L/min for a female
Stroke Volume
The quantity of blood pumped out of the ventricles with every heart beat.
~ 70 mL in a healthy 70-kg man

12. Determinants of stroke volume
PRELOAD
AFTERLOAD
CONTRACTILITY

14. DEFINITIONS
Pre-Load
Force on ventricles during relaxation phase (diastole)
Measured at end-diastole (just before ejection) SV

15. DEFINITIONS Afterload
Load on the ventricle during ejection (in systolic phase)

16. DEFINITIONS
Contractility
Force of ejection
INOTROPE

17. MEASURES OF PRE-LOAD Right ventricular pre-load
Central Venous Pressure (CVP)
0-4 mmHg
Left ventricular pre-load
Pulmonary Artery Occlusion Pressure (PAOP)
(8-12 mmHg)
Measured during diastole when the MV is open
When mitral valve is open we assume
PAEDP ~ PVEDP ~ LAEDP ~ LVEDP
Pulmonary Artery End-diastolic Pressure

18. MEASURES OF PRE-LOAD
Normally, PAOP approximates left atrial pressure, which in turn approximates left ventricular end-diastolic pressure (LVEDP).
LVEDP reflects left ventricular end-diastolic volume (LVEDV).
LVEDV is the actual target

19. MEASURES OF AFTERLOAD Afterload on Right Ventricle
Pulmonary Vascular Resistance
PVR =MPAP – PAWP x 80 ( dyne x sec / cm-5) CO
Afterload on Left Ventricle
Systemic Vascular Resistance
SVR = MAP – CVP x 80 ( dyne x sec / cm-5)
MAP = SBP + 2(DBP) 3

20. CONTRACTILITY CO = SV x HR CARDIAC OUTPUT (4-7 L/min)
Thermodilution: a thermistor near the end of the catheter injects cold saline into the bloodstream and the temperature change determines CO
CARDIAC INDEX = CO/BSA ( L/min/m2)

22. OXYGEN SUPPLY
OXYGEN DEMAND

23. OXYGEN SUPPLY DO2 = CO X CaO2 (arterial O2 content) CO = SV x HR
CaO2 determined by:
HgB
SaO2

24. OXYGEN DEMAND Determined by metabolic activity of tissues
O2 extraction
Usually about 25% for the entire body
CvO2 determined by:
HgB
SvO2 (60-75%)
 SvO2 = increased oxygen consumption
Either decreased delivery, or increased demands
Examples???

25. A word about O2 monitoring
Oxygen Saturation
(SpO2)
normal > 90%
Non-invasive
Mixed venous oxygen saturation
(SvO2)
Normal 65%-75%
invasive

26. RECAP PA catheter measurements RA or CVP (0-4 mmHg) PAP (25/10 mmHg)
PAOP (8-12 mmHg)
CO / CI (4-7 L/min,
L/min/m2)
SVR ( dyne x sec / cm-5)
SvO2 (65-75%)
RIGHT HEART PRE-LOAD
LEFT HEART PRE-LOAD
BLOOD FLOW / PUMP PERFORMANCE
LEFT HEART AFTERLOAD
OXYGEN SUPPLY /DEMAND

27. Shock in the ICU

28. What is Shock?
Inadequate tissue perfusion resulting in cellular injury.
This causes the release of inflammatory mediators that further compromise tissue perfusion, resulting in organ failure and death unless quickly corrected
Circulating volume must be identified and expanded quickly, and the underlying pathological process must be controlled.

29. Classification of Shock
Hypovolemic Shock
Cardiogenic Shock
Distributive Shock
Extra-cardiac Obstructive Shock

30. Organ dysfunction is the threat of shock

31. Hypovolemic Shock Loss of blood or fluid.
Results from
Loss of blood or fluid.
Decreased circulating blood volume
decrease in diastolic filling pressure and volume
 inadequate CO, hypotension, and shock

32. Hypovolemic Shock Causes:
dehydration, hemorrhage, gastrointestinal fluid losses, urinary losses, or decreased vascular permeability from sepsis
hypotension with signs of shock indicating tissue hypo-perfusion, activation of the inflammatory cascade, and widespread cellular damage

33. Hypovolemic Shock 10% Tachycardia, ↑ SVR , ↔ BP 20% to 25%
Acute Loss in circulating Blood Volume
Consequences
10%
Tachycardia, ↑ SVR , ↔ BP
20% to 25%
Mild hypotension, ↓CO, ↑lactate
40%
Moderate-severe hypotension with signs of shock indicating tissue hypo-perfusion, activation of the inflammatory cascade, and widespread cellular damage

34. Cardiogenic Shock Myocardial damage or cardiac mechanical abnormality
Reduced cardiac function
Decrease in cardiac output and blood pressure  Shock

35. Cardiogenic Shock Causes: Special signs:
Q-wave myocardial infarctions.
Special signs:
Patients have signs of heart failure, an S3, elevated neck veins, and peripheral hypo-perfusion

36. Cardiogenic Shock (most frequent in-hospital cause) Q-wave MI
↑Ventricular volume
↑PAOP
↑ Preload
↑CVP
↓MAP
↓SV
↓CI
an S3, elevated neck veins, and peripheral hypo-perfusion
Signs of heart failure:

37. Distributive Shock
Loss of peripheral resistance fluid leak to extracellular space
Vasodilation  Decrease in preload  Hypotension  Normal or increased CO
Myocardial depression frequently accompanies distributive shock.
Decrease in SVR  inadequate blood pressure  shock and multi-organ dysfunction

38. Distributive Shock Causes: Sepsis
Anaphylaxis, drug overdose, neurogenic causes, and Addisonian crisis

39. Extra-cardiac obstructive
Obstruction to flow in the cardiovascular circuit. inadequate diastolic filling or decreased systolic function secondary to an increase in afterload and a drop in CO and blood pressure

40. Extra-cardiac obstructive
Causes
cardiac tamponade, constrictive pericarditis, pneumothorax, mediastinal tumors and pulmonary embolus

41. Tip of the mountain

42. Causes:

43. Pathophysiology

44. Auto-regulation

45. Body auto-regulation during shock

46. Manifestations of shock
CNS:
Alerted level of consciousness from confusion to coma
Ischemia

47. Manifestations of shock
CVS:
Hypotension
Decreased coronary artery perfusion pressure
Ischemia in patients with coronary artery disease
Tachycardia. (which type of shock is not associated with it?) 
Contractility will increase in most types
Cardiogenic

48. Manifestations of shock
Respiratory:
Increase in minute ventilation
 Hypocapnia 
Severe hypo-perfusion  Respiratory muscle weakness 
Respiratory alkalosis
Respiratory Failure

49. Manifestations of shock
Renal:
Because of auto-regulation glomerular filtration is maintained by efferent arteriole constriction
Late in shock:
Cortical and medullary ischemia  tubular necrosis
↓ urine output followed by ↑ BUN and SCr

50. Manifestations of shock
GI:
Very sensitive to sympathetic vasoconstriction:
Ileus
Gastritis
Pancreatitis
Acalculous cholecystitis (not due to stone gallbladder inflammation)
Colonic submucosal hemorrhage
Ischemia of the gut can lead to translocation of bacteria from the gut to the circulation

51. Manifestations of shock
Liver:
LFTs elevations
Hematological:
Disseminated intravascular coagulation
Dilutional thrombocytopenia due resuscitation
Metabolic:
Hyperglycemia due ↓ insulin production
Protein catabolism negative nitrogen balance

52. Manifestations of shock
Cardiogenic shock: jugular venous distension, an S3 and S4, and regurgitation murmurs.
Pulmonary embolus: patients present with hypoxia, dyspnea, and elevated right heart pressures.
Septic shock patients may have fevers, chills, and usually a nidus of infection ( a source of infection)

53. Labs: Low or high WBC count with a left shift and bands
High or normal hemoglobin levels
High to low platelets
Low serum bicarbonate
High anion gap
High or normal creatinine
High lactate
(unless hemorrhagic
shock)
Why?

54. Hemodynamic monitoring:
Arterial pressure and CVP  monitor vasopressors effect
Mixed venous oxygen saturation (Svo2)
Normal 65%-75%
Inversely proportional to perfusion level
Pulmonary artery catheter  no evidence of decreased mortality

55. Shock Hemodynamics CO SVR PAOP CVP pre-resusc Hypovolemic Cardiogenic
Distributive
pre-resusc
post-resusc
Extra-cardiac obstructive
Shock (pulmonary embolism)
or normal

56. Goals of therapy: Prevent target organ damage
Achieve adequate CO and MAP
Treat underlying cause

57. Therapy Adequate oxygenation (mechanical ventilation)
Goal: Oxygen saturation 90% or greater
Volume resuscitation
Mainly crystalloids (NaCl 0.9%)
Colloids
(Albumin)
Good in severe sepsis
Hetastarch
Limited use in renal failure
Other colloids include: dextrane , hetastarch and pentastarch
Other crystalloids include: dextrose, ringer’s lactate

58. Therapy
Once volume resuscitation is optimized  vasopressors and inotropes
What happened if you start with a vasopressor before fluid resuscitation?

59. Vasopressors: Norepinephrine: Dopamine:
Reliable increase in blood pressure and inotrope
Dopamine:
Low dose: mild inotropic effect as well as some renal effects.
high dose: vasoconstriction
Higher incidence of mesenteric ischemia than norepinephrine

60. Vasopressors: Epinephrine: Phenylephrine:
1st choice in anaphylactic shock
Watch for:
Tachycardia and arrhythmia
Mesenteric ischemia
Phenylephrine:
Pure α-agonist
Good for patients with underlying tachycardia

61. Vasopressors: Vasopressin:
In refractory cases not responding to previous vasopressors
↓ heart rate and cardiac output
↑ blood pressure and pulmonary artery pressure
May lead to myocardial ischemia due a decrease in coronary artery blood flow

62. Inotropes: Dobutamine: Milrinone: β1 and β2 agonistsCO
SVR
Milrinone:
phosphodiesterase inhibitor
It is a potent vasodilator
Decreases both pulmonary vascular resistance and SVR.

65. Therapy Hypovolemic Shock: Cardiogenic:
Rapid reversal with blood, colloid, or crystalloid
Cardiogenic:
Left ventricular MI:
Intra-aortic balloon pump, cardiac angiography, and revascularization
Right ventricular MI:
Fluids and inotrops

66. Therapy Extra-cardiac obstructive shock: Cardiac tamponade:
Pericardiocentesis or surgical drainage
Pulmonary embolism:
Thrombolytics, Heparin and embolectomy

67. Therapy Distributive shock: Septic: Anaphylactic:
Antibiotics + fluid resuscitation+ vasopressors or inotropes
Anaphylactic:
Steroids, diphenhydramine, H1 and H2 blockers, and epinephrine

68. Questions