Approach to Shock and Hemodynamics

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Approach to Shock and Hemodynamics

• Jeffrey E. Brauer, MD

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Outline

• Shock
• Pathophysiology
• Determinants of oxygen delivery
• Shock syndromes
• Hemodynamic monitoring
• Management of shock

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Question 1

• Which of the following is necessary in the
  definition of shock?
• (a) Hypotension
• (b) Tissue hypoxia
• (c) Use of pressors
• (d) Multiple organ dysfunction

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Question 1

• Which of the following is necessary in the
  definition of shock?
• (a) Hypotension
• (b) Tissue hypoxia
• (c) Use of pressors
• (d) Multiple organ dysfunction

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Shock

• Profound and widespread reduction in the
  effective delivery of oxygen leading to cellular
  hypoxia and injury and vital organ dysfunction
• Leads to Multiple Organ Dysfunction Syndrome
  (MODS)

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Pathophysiology

• Constant delivery of oxygen essential
• Oxygen uptake (VO2)
• Determined by metabolic demand
• Not regulated or determined by its availability
• Oxygen delivery (DO2)
• Oxygen extraction ratio
• Increases if DO2 decreases
• May not increase in critically ill
• With low DO2, VO2 can be supply-dependent

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sepsis
sepsis
sepsis
Sepsis
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Pathophysiology

• Most forms of shock
• Low cardiac output state
• Supply-dependency of systemic VO2
• Septic shock
• Systemic DO2 and VO2 are both supranormal, but an
  oxygen deficit remains
• Peripheral oxygen extraction may be deranged and
  VO2 is pathologically supply-dependent
• Possible microvascular maldistribution of
  perfusion

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Pathophysiology

• Inadequate/ineffective DO2 leads to anaerobic
  metabolism
• Large/prolonged oxygen deficit causes decrease of
  high-energy phosphates stores
• Membrane depolarization, intracellular edema,
  loss of membrane integrity and ultimately cell
  death

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Question 2

• Which is not an important determinant of oxygen
  delivery?
• (a) Hemoglobin level
• (b) Cardiac output
• (c) pO2
• (d) SaO2

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Question 2

• Which is not an important determinant of oxygen
  delivery?
• (a) Hemoglobin level
• (b) Cardiac output
• (c) pO2
• (d) SaO2

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Oxygen Delivery (DO2)

• Cardiac Output x Oxygen Content
• CO x (1.3 x Hgb x SaO2) (0.003 x PaO2)
• Hemoglobin concentration
• SaO2
• Cardiac output
• PaO2 (minimal)
• Inadequate DO2 occurs most often because of low
  cardiac output

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Cardiac Output

• Determined by
• Stroke volume
• Heart rate
• Stroke volume determined by
• Preload
• Afterload
• Contractility

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Preload

• Determined by end-diastolic volume
• Pressure and volume related by compliance of the
  ventricle
• A normal wedge measurement may reflect
  inadequate preload in some situations

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Question 3

• Which can cause low preload?
• (a) High PEEP
• (b) Tension pneumothorax
• (c) Third spacing
• (d) Positive pressure ventilation
• (e) All of the above

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Question 3

• Which can cause low preload?
• (a) High PEEP
• (b) Tension pneumothorax
• (c) Third spacing
• (d) Positive pressure ventilation
• (e) All of the above

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Preload

• Shock due to inadequate preload usually from low
  intravascular volume
• Internal or external loss of blood
• Contraction of intravascular space
• External fluid loss (GI, urinary tract)
• Internal sequestration (third spacing)
• Combination of above

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Preload

• Other causes of decreased venous return
• Increased intrathoracic pressure (tension Ptx,
  positive pressure ventilation, PEEP)
• Can decrease afterload as well
• Hypovolemia preload effects predominate
• CHF afterload beneficial effects predominate
• Markedly elevated intrapericardial pressure
  (tamponade)

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Afterload

• Less commonly the primary problem leading to
  shock
• Impedance to vascular flow is estimated by SVR
  arteriolar tone
• Primary problem in AS and PE

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Contractility

• Shock due to deterioration of intrinsic
  performance of heart
• Loss of contractile tissue
• Diminished contractility of viable myocardial
  tissue
• Regurgitant flow
• Combination of above
• Estimated by measure of ejection fraction

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Diagnosis of Shock

• Low arterial BP or a rapid, thready pulse.
• Shock may be present without hypotension
• Oliguria or AMS
• Peripheral cyanosis and pallor, cool skin temp.
• Tachycardia
• Metabolic acidosis and elevated lactate
• Hct, WBC, EKG, CXR, gram stain/Cx, etc

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Shock Syndromes

• Hypovolemic
• Cardiogenic
• Extracardiac obstructive
• Distributive

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Hypovolemic Shock

• Loss of circulating blood volume
• Signs
• Poor skin turgor
• Dry mucous membranes
• Increased Hct
• Low CVP or wedge
• Hypernatremia
• Inappropriately dilute urine

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Hypovolemic Shock

• Decrease in ventricular filling and therefore
  cardiac output
• Hemorrhagic external or internal
• Non-hemorrhagic
• Dehydration
• Third spacing

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Cardiogenic Shock

• Pump failure (systolic or diastolic) decreased
  SV and elevated PCWP
• CO can remain unchanged due to increased heart
  rate
• Later, CO falls due to decreasing SV and a heart
  rate unable to compensate
• Increased SVR compromises CO further

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Extracardiac Obstructive Shock

• Decreased diastolic filling
• Tension pneumothorax
• Pericardial tamponade
• Increased ventricular afterload
• Massive PE

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Question 4

• Which is not typical of sepsis?
• (a) Low SVR
• (b) High cardiac output
• (c) Low oxygen delivery
• (d) Low wedge pressure

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Question 4

• Which is not typical of sepsis?
• (a) Low SVR
• (b) High cardiac output
• (c) Low oxygen delivery
• (d) Low wedge pressure

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Distributive Shock

• Ex/ sepsis, anaphylaxis, adrenal crisis
• Loss of vascular tone low SVR
• Hypovolemic component - low PCWP
• High CO in early stage due to tachycardia, but
  deteriorates late
• High DO2, but maldistribution of flow and defect
  in oxygen extraction

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Sepsis - definitions

• SIRS vital sign/WBC abnormalities
• No infection pancreatitis, aspiration, trauma,
  transfusions
• Can have associated organ dysfunction
• Sepsis SIRS criteria plus infection
• Severe sepsis organ dysfunction
• Septic shock pressor-dependence

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Hemodynamic Monitoring

• Goal is to optimize tissue oxygenation
• Lactate
• CVP
• Arterial pressure
• Urine output
• Pulse oximetry

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Pulmonary Artery Catheterization

• Introduced in 1970 by Swan, et al.
• Direct measurement of determinants and
  consequences of cardiac performance
• Aids decision-making but doesnt substitute for
  clinical assessment
• No data to suggest benefit and may be harmful

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Question 5

• Which is true about the wedge?
• (a) Measures LVEDV
• (b) Falsely elevated by PEEP
• (c) Increased in pulmonary HTN
• (d) Accurately measured in mitral stenosis

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Question 5

• Which is true about the wedge?
• (a) Measures LVEDV
• (b) Falsely elevated by PEEP
• (c) Increased in pulmonary HTN
• (d) Accurately measured in mitral stenosis

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Wedge Pressure

• Correlates well with LA and LVEDP if normal
  anatomy
• Reliable measure of preload (volume) only with
  normal/stable ventricular compliance
• Falsely elevated by PEEP (and auto-PEEP)

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Cardiac Output

• Thermodilution technique allows calculation of
  net blood flow
• Mixed venous O2 can assess adequacy of CO (less
  reliable with sepsis)
• Normal SvO2 70-75
• Heart failure SvO2 lt 60
• Shock SvO2 lt 40

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Management

• Treatment of underlying cause
• Crystalloids vs. colloids
• Blood
• Vasopressors

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Vasopressin

• Relative deficiency in sepsis
• May be effective in refractory hypotension
• Direct vasoconstrictor without inotropic or
  chronotropic effects
• No studies on outcome

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Xigris

• Human activated protein C
• Anti-thrombotic, anti-inflammatory,
  pro-fibrinolytic
• Studied in patients with severe sepsis
• Known or suspected infection
• 3 of 4 criteria for SIRS
• At least one organ dysfunction
• 96-hour continuous infusion

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Xigris

• Mortality 24.7 vs. 30.8 in placebo group
  (p0.005)
• Benefit only seen in patients with highest APACHE
  scores
• Mildly increased serious bleeding rate
• Contraindicated with increased risk of bleeding
• Expensive

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• Early aggressive tx (MI, CVA, trauma)
• 263 pts presenting to ER with severe sepsis or
  septic shock
• Hypotensive after fluid challenge or lactategt4
• First 6 hrs EGDT vs. standard tx
• Optimize oxygen delivery to meet demand
• - NEJM 2001 3451368

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Early Goal-Directed Therapy
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Take Home Points

• Shock is defined by inadequate tissue
  oxygenation, not hypotension
• Oxygen delivery depends primarily on CO, Hgb and
  SaO2 (not pO2)
• Volume expand with crystalloids and blood, if
  indicated then add vasoactive drugs to improve
  vital organ perfusion
• Early treatment of shock is critical

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