Transcript Shock - Mecriticalcare.net

Approach and Hemodynamic
Evaluation of Shocks
Mazen Kherallah, MD, FCCP
King Faisal Specialist Hospital & Research Center
Shock Definition
Question #0
Which of the following is necessary in the definition
of shock?
• (a) A drop in the systolic blood pressure of less
than 90 mm Hg
• (b) A drop in the mean arterial pressure of less
than 60 mm Hg
• (c) A drop in the SBP of 40 mm Hg or 20% from
baseline
• (d) An elevated lactic acid of ≥ 4 mmoL/L
• (e) Any of the above
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
Shock
• Profound and widespread reduction in the
effective delivery of oxygen leading to first
to reversible, and then if prolonged, to
irreversible cellular hypoxia and organ
dysfunction” Kumar and Parrillo
• Leads to Multiple Organ Dysfunction
Syndrome (MODS)
Pathophysiology
Pathophysiology
Oxygen delivery
Oxygen uptake
DO2
VO2
Oxygen extraction ratio
Oxygen Consumption
Physiologic Oxygen Supply Dependency
Critical Delivery
Threshold
Oxygen Delivery
Mizock BA. Crit Care Med. 1992;20:80-93.
sepsis
sepsis
Sepsis
Oxygen Consumption
Pathologic Oxygen Supply Dependency
Pathologic
Physiologic
Oxygen Delivery
Mizock BA. Crit Care Med. 1992;20:80-93.
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
Question #2
• Which is not an important determinant of
oxygen delivery?
• (a) Hemoglobin level
• (b) Cardiac output
• (c) pO2
• (d) SaO2
Oxygen Delivery (DO2)
Cardiac Output x Oxygen Content
CO x [(1.3 x Hgb x SaO2) + (0.003 x PaO )]
2
– Hemoglobin concentration
– SaO2
– Cardiac output
– PaO2 (minimal)
Cardiac Output
CO  SV  HR
Preload
Afterload
Contractility
Preload
• Determined by end-diastolic volume
• Pressure and volume related by compliance
of the ventricle
Left ventricular end-diastolic pressure versus
left ventricular end-diastolic volume
35
LVEDP (mm HG)
30
25
20
15
10
5
0
25
50
75
100
125
150
LVEDV (ml/m2)
Decreased compliance
Normal compliance
175
200
Cardiac Output
Cardiac output
• Sterling relationship
Volume loading
Clinical Adaptation of the Sterling
Myocardial Function Curves
80
LVSWI (g.m/m2)
70
60
50
40
30
20
10
0
5
10
15
20
PAOP (mmHg)
Hypodynamic
Normal
Hyperdynamic
25
30
Global Hemodynamic
Relationships
MAP  CO  SVR
HR  SV
Preload
Afterload
Contractility
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
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
Effects of Shock at Cellular Level
Common Histopathology Associated
with
Tissue Hypoperfusion and Shock?
Histopathology of Tissue Hypoperfusion
Associated with Shock
Myocardium
Lung
Coagulative necrosis
Diffuse alveolar damage
Contraction bands
Exudate, atelectasis
Edema
Edema
Neutrophil infiltrate
Hyaline membrane
Robbins & Cotran Pathologic Basis of Disease: 2005
Histopathology of Tissue Hypoperfusion
Associated with Shock
Small Intestine
Liver
Mucosal infarction
Centrilobular hemorrhagic necrosis
Hemorrhagic mucosa
Nutmeg appearance
Epithelium absent
Robbins & Cotran Pathologic Basis of Disease: 2005
Histopathology of Tissue Hypoperfusion
Associated with Shock
Brain
Bland infarct
Punctate hemorrhages
Brain
Eosinophilia and shrinkage of
neurons
Neutrophil infiltration
Robbins & Cotran Pathologic Basis of Disease: 2005
Histopathology of Tissue Hypoperfusion
Associated with Shock
Kidney
Pancreas
Tubular cells, necrotic
Fat necrosis
Detached from basement membrane
Parenchymal necrosis
Swollen, vacuolated
Robbins & Cotran Pathologic Basis of Disease: 2005
Incidence of Ischemic Histopathology
in Patients Dying with Shock
Hypovolemic
Septic
Cardiogenic
n = 102 (%)
n = 93 (%)
n = 197 (%)
Heart
37
17
100
Lung
55
65
10
Kidney
25
18
11
Liver
46
30
56
Intestine
9
26
16
Pancreas
7
6
3
Brain
6
3
4
McGovern VJ, Pathol Annu 1984;19:15
Shock Syndromes
Shock
Cardiogenic shock - a major component of the the
mortality associated with cardiovascular disease (the #1
cause of U.S. deaths)
Hypovolemic shock - the major contributor to early
mortality from trauma (the #1 cause of death in those < 45
years of age)
Septic shock - the most common cause of death in
American ICUs (the 13th leading cause of death overall in
US)
Cardiac Performance
Preload
Left
ventricular
size
Peripheral
resistance
Stroke
volume
Contractility
Myocardial
fiber
shortening
Cardiac
output
Heart
rate
Afterload
Arterial
pressure
Compensatory Mechanisms
Case 1
• 34 year old involved in a motor vehicle
accident arrived to emergency room with
blood pressure of 70/30 and heart rate of
140/min
Question #5
•
•
•
•
•
Which is typical of hypovolemic shock?
(a) High SVR
(b) High cardiac output
(c) High oxygen delivery
(d) Normal wedge pressure
Hypovolemic Shock
Preload
Left
ventricular
size
Peripheral
resistance
Stroke
volume
Contractility
Myocardial
fiber
shortening
Arterial
pressure
Cardiac
output
Heart
rate
Afterload
Compensatory Mechanism
Adrenaline
Hypovolemic Shock Hemodynamics
CO
Hypovolemic
Cardiogenic
Obstructive
afterload
preload
Distributive
pre-resusc
post-resusc
SVR
PWP
EDV
Hypovolemic Shock
Hemorrhagic
•
•
•
Trauma
Gastrointestinal
Retroperitoneal
Fluid depletion (nonhemorrhagic)
•
External fluid loss
-
•
Dehydration
Vomiting
Diarrhea
Polyuria
Interstitial fluid redistribution
-
Thermal injury
Trauma
Anaphylaxis
Increased vascular capacitance (venodilatation)
•
•
•
Sepsis
Anaphylaxis
Toxins/drugs
Kumar and Parrillo, 2001
Case 2
• 54 year old with acute onset chest pain
arrived to emergency room with blood
pressure of 70/30 and heart rate of 140/min
Question #5
•
•
•
•
•
Which is typical of cardiogenic shock?
(a) Low SVR
(b) High cardiac output
(c) Low oxygen delivery
(d) Low wedge pressure
Cardiogenic Shock
Preload
Left
ventricular
size
Peripheral
resistance
Stroke
volume
Contractility
Myocardial
fiber
shortening
Arterial
pressure
Cardiac
output
Heart
rate
Afterload
Compensatory Mechanism
Adrenaline
Cardiogenic Shock Hemodynamics
CO
Hypovolemic
Cardiogenic
Obstructive
afterload
preload
Distributive
pre-resusc
post-resusc
SVR
PWP
EDV
Cardiogenic Shock
Myopathic
•
•
Myocardial infarction (hibernating myocardium)
Left ventricle
Right ventricle
Myocardial contusion (trauma)
Myocarditis
Cardiomyopathy
Post-ischemic myocardial stunning
Septic myocardial depression
Pharmacologic
•
•
Anthracycline cardiotoxicity
Calcium channel blockers
Mechanical
•
•
•
Valvular failure (stenotic or regurgitant)
Hypertropic cardiomyopathy
Ventricular septal defect
Arrhythmic
•
•
Bradycardia
Tachycardia
Kumar and Parrillo, 2001
Case 3
• 67 year old with fever,
chills, SOB, and ugly
looking abdominal
wound arrived to
emergency room with
blood pressure of
70/30 and heart rate of
140/min
Question #6
•
•
•
•
•
Which is not typical of sepsis?
(a) Low SVR
(b) High cardiac output
(c) Low oxygen delivery
(d) Low wedge pressure
Distributive Shock
Preload
Left
ventricular
size
Peripheral
resistance
Stroke
volume
Contractility
Myocardial
fiber
shortening
Arterial
pressure
Cardiac
output
Heart
rate
Afterload
Compensatory Mechanism
Adrenaline
Distributive Hemodynamics
CO
Hypovolemic
Cardiogenic
Obstructive
afterload
preload
Distributive
pre-resusc
post-resusc
SVR
PWP
EDV
Distributive Shock
Septic (bacterial, fungal, viral, rickettsial)
Toxic shock syndrome
Anaphylactic, anaphylactoid
Neurogenic (spinal shock)
Endocrinologic
• Adrenal crisis
• Thyroid storm
Toxic (e.g., nitroprusside, bretylium)
Kumar and Parrillo, 2001
Obstructive Shock
Preload
Left
ventricular
size
Peripheral
resistance
Stroke
volume
Contractility
Myocardial
fiber
shortening
Arterial
pressure
Cardiac
output
Heart
rate
Afterload
Compensatory Mechanism
Adrenaline
Obstructive Shock Hemodynamics
CO
Hypovolemic
Cardiogenic
Obstructive
afterload
preload
Distributive
pre-resusc
post-resusc
SVR
PWP
EDV
Extracardiac Obstructive Shock
Impaired diastolic filling (decreased ventricular preload)
•
Direct venous obstruction (vena cava)
-
•
Intrathoracic obstructive tumors
Increased intrathoracic pressure
- Tension pneumothorax
- Mechanical ventilation (with excessive pressure or volume depletion)
- Asthma
•
Decreased cardiac compliance
- Constrictive pericarditis
- Cardiac tamponade
Impaired systolic contraction (increased ventricular afterload)
•
Right ventricle
- Pulmonary embolus (massive)
- Acute pulmonary hypertension
•
Left ventricle
- Saddle embolus
- Aortic dissection
Kumar and Parrillo, 2001
Clinical Features
Symptoms of Shock
General Symptoms
•
•
•
•
•
•
•
•
Anxiety /Nervousness
Dizziness
Weakness
Faintness
Nausea & Vomiting
Thirst
Confusion
Decreased UO
Specific Symptoms
• Hx of Trauma / other
illness
• Vomiting &
Diarrhoea
• Chest Pain
• Fevers / Rigors
• SOB
Signs of Shock
Pale
Cold & Clammy
Sweating
Cyanosis
Tachycardia
Tachypnoea
Confused / Aggiatated
Unconscious
Hypotensive/Oliguric
Stridor / SOB
Capillary Refill
Skin Mottling
Skin Mottling
Diagnosis and Evaluation
• 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
Poor skin turgor and dry mucous membranes: hypovolemic
Unable to produce Tachycardia
• Limited cardiac response to catecholamine
stimulation: elderly
• Autonomic dysfunction: DM
• Concurrent use of beta-adrenergic blocking
agents
• The presence of a pacemaker
Severity of Hemorrhage
Comparison of Adult vs Child
Classification of Hemorrhagic Shock
Class I
Class II
Class III
Class IV
Blood loss (ml)
Up to 750
750-1500
1500-2000
>2000
Blood loss (%)
Up to 15%
15-30%
30-40%
>40%
Pulse rate
<100
>100
>120
>140
Normal
Decreased
Decreased
Blood pressure Normal
Pulse pressure
Normal
Decreased
Decreased
Decreased
Respiratory
rate
Urine output
(ml/h)
CNS/mental
status
Fluid
replacement
14-20
20-30
30-40
>35
>30
20-30
5-15
Negligible
Slightly
anxious
Crystalloid
Mildly
Anxious/
anxious
confused
Crystalloid Crystalloid/
blood
Confused/
lethargic
Crystalloid/
Blood
Shock Evaluation and
Monitoring
A Clinical Approach to Shock
Diagnosis and Management
Initial Therapeutic Steps
Admit to intensive care unit (ICU)
Venous access (1 or 2 large-bore catheters)
Central venous catheter
Arterial catheter
EKG monitoring
Pulse oximetry
Urine output monitoring
Hemodynamic support (MAP < 60 mmHg)
• Fluid challenge
• Vasopressors for severe shock unresponsive to fluids
Diagnosis and Evaluation
Laboratory
•
•
•
•
•
Hgb, WBC, platelets
PT/PTT
Electrolytes, arterial blood gases
BUN, Cr
Ca, Mg
• Serum lactate
• ECG
A Clinical Approach to Shock
Diagnosis and Management
Initial Diagnostic Steps
•
•
•
•
•
CXR
Abdominal views*
CT scan abdomen or chest*
Echocardiogram*
Pulmonary perfusion scan*
* When indicated
A Clinical Approach to Shock
Diagnosis and Management
Diagnosis Remains Undefined or
Hemodynamic Status Requires Repeated Fluid Challenges or
Vasopressors
Pulmonary Artery Catheterization
•
•
–
–
•
Cardiac output
Oxygen delivery
MVO2
DO and VO
Filling pressures
Echocardiography
• Pericardial fluid
• Cardiac function
• Valve or shunt abnormalities
Hemodynamic Monitoring
Measurement of PCWP
Components of the Atrial Waves
The difference between CVP and
PCWP waves
The mean of the A wave approximates
ventricular end-diastolic pressure
Reading CVP
A
V
c
Reading PCWP
AV
A
V
Reading the mean of an A wave
22+10/2=16
Question #7
•
•
•
•
•
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
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)
Shock Management
Management
• Treatment of underlying cause
• Volume
• Vasopressors
A Clinical Approach to Shock
Diagnosis and Management
Identify source of blood or fluid loss in hypovolemic shock
Intra-aortic balloon pump (IABP), cardiac angiography, and
revascularization for LV infarction
Echocardiography, cardiac cath and corrective surgery for
mechanical abnormality
Pericardiocentesis surgical drainage for pericardial
tamponade
Thrombolytic therapy, embolectomy for pulmonary
embolism
Source control and early broad antibiotics for septic shock
Perfusion Goals in Patients with Septic
Shock
HEMODYNAMCS
ORGAN PERFUSION
MAP > 60 mm Hg
PAOP = 12 - 18 mmHg
Cardiac Index > 2.2
L/min/m2
CNS - improved sensorium
Skin - warm, well perfused
Renal - UOP > 0.5 cc/kg/hr
Decreasing lactate (<2.2 mM/L)
Improved renal, liver fucntion
O2 DELIVERY ADEQUACY
Arterial Hgb SpO2 > 92%
Hgb concentration > 9 gm/dL
SVO2 > 65%
Blood Lactate Conc < 2
mM/L
Volume Therapy
Crystalloids
• Lactated Ringer’s solution
• Normal saline
Colloids
• Hetastarch
• Albumin
Packed red blood cells
Infuse to physiologic endpoints
Early Goal Directed Therapy
89
Rivers E, Nguyen B, Havstad S, et al 2001;345:1368-1377.
Early Goal-Directed Therapy Results:
28 Day Mortality
60
50
49.2%
Vascular
Collapse
P = 0.01*
40
Mortality %
33.3%
p=0.02
30
MODS
20
22% vs 16%
10
0
21% vs 10%
P=0.27
Standard Therapy
N=133
*Key difference was in sudden CV collapse, not MODS
EGDT
N=130
NEJM 2001;345:1368-77.
The Importance of 92Early Goal-Directed
Therapy for Sepsis-induced Hypoperfusion
NNT to prevent 1 event (death) = 6 - 8
60
Mortality (%)
50
Standard therapy
EGDT
40
30
20
10
0
In-hospital
mortality
(all patients)
28-day
mortality
Rivers E, Nguyen B, Havstad S, et al. 2001;345:1368-1377.
60-day
mortality
Therapies Across The Sepsis
Continuum
Infection
SIRS
Sepsis
Severe Sepsis
Septic Shock
 CVP > 8-12 mm Hg
 MAP > 65 mm Hg
 Urine Output > 0.5 ml/kg/hr
 ScvO2 > 70%
 SaO2 > 93%
 Hct > 30%
*
Early Goal Directed Therapy
Early Goal-Directed Therapy (EGDT): involves adjustments of cardiac preload, afterload, and contractility to
balance O2 delivery with O2 demand: Fluids, Blood, and Inotropes
Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. NEJM 2001;345:1368.
Type of Fluids
Therapy: Resuscitation Fluids
• Crystalloid vs. colloid
• Optimal PWP 10 - 12 vs. 15 - 18 mm Hg
• 20-40 mL/kg fluid challenge in
hypovolemic or septic shock with
• Re-challenges of 5 - 10 mL/kg
• 100 - 200 mL challenges in cardiogenic
Vasoactive Agent Receptor Activity
Agent
a1
a2
+
+
++++
++
0
Dopamine
++/+++
?
++++
++
++++
Epinephrine
++++
++++
++++
+++
0
+++
+/++
0
0
+
?
0
0
Dobutamine
Norepinephrine +++
Phenylephrine ++/+++
b1
b2
Dopa
Vasopressors/Inotrops
0
Dopamine
Norepinephrine
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
Thank You