The document defines shock and describes its various types, including hypovolemic, cardiogenic, obstructive, and distributive shock. It discusses the pathophysiology, clinical presentation, diagnosis, and general treatment approach for shock. Regarding treatment, it emphasizes early correction of pulse, ventilation, oxygenation, and fluid administration. It then provides specific protocols for resuscitation in cases of hypovolemia and septic shock.
2. DEFINITION
Acute, generalized state of inadequate
perfusion of critical organs
associated with systolic BP <90 mm Hg or
reduction of at least 40 mm Hg from baseline
• with perfusion abnormalities despite
adequate fluid resuscitation.
2
3. CONT..
Shock refers to conditions manifested by
hemodynamic alterations (e.g., hypotension,
tachycardia, low cardiac output [CO], and
oliguria)
caused by
intravascular volume deficit (hypovolemic shock),
myocardial pump failure (cardiogenic shock), or
peripheral vasodilation (septic, anaphylactic or
neurogenic shock).
The underlying problem in these situations is
inadequate tissue perfusion resulting from
3
8. PATHOPHYSIOLOGY
Shock results in failure of circulatory system to deliver
sufficient oxygen (O2) to body tissues despite normal or
reduced O2 consumption.
General pathophysiologic mechanisms of different forms
of shock are similar except for initiating events.
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9. PATHOPHYSIOLOGY….
Hypovolemic shock is characterized by:
acute intravascular volume deficiency due to
• external losses or
• internal redistribution of extracellular water.
This type of shock can be precipitated by
hemorrhage, burns, trauma, surgery, intestinal obstruction,
and dehydration from considerable insensible fluid loss,
overaggressive loop-diuretic administration, and severe
vomiting or diarrhea.
Relative hypovolemia leading to hypovolemic shock
occurs during significant vasodilation, which
accompanies anaphylaxis, sepsis, and neurogenic shock.
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10. PATHOPHYSIOLOGY….
Regardless of the etiology, fall in BP is compensated by
↑ in sympathetic outflow, activation of the RAS, and other
humoral factors that stimulate peripheral vasoconstriction.
Compensatory vasoconstriction redistributes blood away
from the skin, skeletal muscles, kidneys, and GIT toward
vital organs (e.g., heart, brain) in an attempt to maintain
oxygenation, nutrition, and organ function.
Tissue ischemia……lactic acidosis…..localized
Vd…exacerbation of CV function
Severe metabolic lactic acidosis often develops secondary to
tissue ischemia and causes localized vasodilation, which further
exacerbates the impaired cardiovascular state.
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12. CLINICAL PRESENTATION
Shock presents with a diversity of signs and
symptoms.
Hypovolemic shock: Patients may present with
Thirst.
Anxiousness.
Weakness.
Lightheadedness.
Dizziness.
Also reported reduced urine output & Dark yellow-colored
urine.
Hypotension, tachycardia, tachypnea, confusion & oliguria
are common symptoms.
Myocardial and cerebral ischemia, pulmonary edema
12
13. Clinical presentation….
Signs of volume loss:
Significant Hypotension (SBP < 90 mm Hg) &
With reflex Tachycardia (>120 beats/min) &
Tachypnea (>30 breaths/min) are often observed in
hypovolemia
Mental status changes range from subtle mood change to
agitation to unconsciousness.
Normal or low body temperature with cold extremities and a
“thready” pulse.
may be cyanotic due to hypoxemia.
Sweating results in a moist, clammy feel.
↓ed capillary refill (Digits will have severely slowed capillary
refill).
Reduced cardiac index (CI < 2.2 L/min/m2)
13
14. Clinical presentation…
Lungs:
Respiratory alkalosis secondary to hyperventilation is
usually observed
secondary to CNS stimulation of ventilatory centers due to
trauma, sepsis, or shock.
Lung auscultation may reveal
crackles (pulmonary edema) or
absence of breath sounds (pneumothorax, hemothorax).
Chest roentgenogram can confirm
early suspicions or disclose undetected abnormality such as
pneumonia (pulmonary infiltrates).
Continued insult to the lungs may result in adult
respiratory distress syndrome (RDS). 14
15. CLINICAL PRESENTATION…
Kidneys: exquisitely sensitive to changes in perfusion
pressures.
Moderate alterations can lead to significant changes in GFR.
Oliguria, progressing to anuria, occurs because of
vasoconstriction of afferent arterioles.
GIT: Redistribution of blood flow away from the GIT may
cause
stress gastritis, gut ischemia, and,
in some cases, infarction, resulting in GI bleeding.
Liver: Progressive liver damage (shock liver) manifests
as
elevated serum hepatic transaminases and unconjugated
15
16. DIAGNOSIS AND MONITORING
Noninvasive and invasive monitoring (Table 1),
medical history, clinical presentation, and
laboratory findings help to confirm diagnosis
and identify underlying cause.
Regardless of etiology, consistent findings include –
hypotension (SBP <90 mm Hg),
↓sed cardiac index (CI < 2.2 L/min/m2 ),
tachycardia (HR >100 bpm), and
low urine output (UOP<20 mL/hour).
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17. DIAGNOSIS AND MONITORING
Noninvasive assessment of BP using
sphygmomanometer and stethoscope may be
inaccurate in the shock state.
Respiratory alkalosis is associated with
low partial pressure of O2 and alkaline pH, but normal
bicarbonate.
CO (2.5 to 3 L/min) and mixed venous oxygen
saturation (70% to 75%) may be very low in a
patient with extensive myocardial damage.
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18. 18
Table 1: Hemodynamic & Oxygen-Transport Monitoring Parameters
Parameter Normal Valuea
Blood pressure (systolic/diastolic) 100–120/70–85 mm Hg
Mean arterial pressure (MAP) 80–100 mm Hg
Pulmonary artery pressure (PAP) 25/10 mm Hg
Mean pulmonary artery pressure (MPAP) 12–15 mm Hg
Pulmonary artery occlusive pressure (PAOP) 12–15 mm Hg
Central venous pressure (CVP) 8–12 mm Hg
Heart rate (HR) 60–80 beats/min
Cardiac output (CO) 4–7 L/min
Cardiac index (CI) 2.8–3.6 L/min/m2
Stroke volume index (SVI) 30–50 mL/m2
Systemic vascular resistance index (SVRI) 1,300–2,100 dyne.s/m2.cm5
Pulmonary vascular resistance index (PVRI) 45–225 dyne.s/m2.cm5
aNormal values may not be same as values needed to optimize
management of a critically ill pnt.
19. 19
Table: Hemodynamic and Oxygen-Transport Monitoring Parameters
Parameter Normal Valuea
Arterial oxygen saturation (SaO2) 97% (range, 95%–100%)
Mixed venous oxygen saturation
(SVO2)
70%–75%
Arterial oxygen content (CaO2) 20.1 vol% (range, 19–21)
Venous oxygen content (CVO2) 15.5 vol% (range, 11.5–16.5)
Oxygen content difference (C[a–v]O2) 5 vol% (range, 4–6)
Oxygen consumption index (VO2) 131 mL/min/m2 (range, 100–180)
Oxygen delivery index (DO2) 578 mL/min/m2 (range, 370–730)
Oxygen extraction ratio (O2ER) 25% (range, 22–30)
Intramucosal pH (pHi) 7.40 (range, 7.35–7.45)
Index (I) Parameter indexed to body
surface area
aNormal values may not be same as values needed to optimize
management of a critically ill pnt.
20. LABORATORY TESTS
↑ed serum sodium & chloride with acute volume
depletion.
↑ed BUN: SrCr ratio with dehydration.
↑ed SrCr with renal dysfunction.
Metabolic acidosis with elevated base deficit and
lactate concentrations and ↓ed bicarbonate and pH
CBC: Normal in absence of infection.
RBC: Reduced RBC count, Hgb, & Hct in
hemorrhagic shock.
Elevated serum transaminase levels with hepatic
dysfunction. 20
23. DESIRED OUTCOMES
Provide support for effective oxygen delivery to
tissues.
Identify and correct underlying causes.
Prevent disease progression and organ damage.
Reverse organ dysfunction if possible.
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24. General principles
Priorities for shock in general
1st correct pulse, ventilation and oxygenation
2nd provide fluids (except in cardiogenic shock)
3rd administer pressors (vasopressors and
inotropes)
Last, everything else
Exceptions
Obstructive shock: priority should be given for
removing the obstruction before fluids or pressors
This priority list should not be considered a stringent
list as there may be an emergent need for antibiotics
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25. Summary treatment principle
Primary derangements &
mgt
Iv
fluids
(↑CVP)
Vasopressors
(↑SVR)
Inotropes
(↑contractilit
y)
Hypovolemic (↓CVP) + Temporary use
only
-
Distributive (↓SVP)
+ + +/-
(individualize
d)
Cardiogenic
(↓contractility)
- - +
Obstructive (obstruction) +/- +/- +/-
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For obstructive shock the primary intervention is addressing the obstruction but
the IV fluids, vasopressors and inotropes might be used temporarily as
required.
- Tension Pneumothorax: insert chest tube to remove excess air or needle
thoracostomy (emergent decompression)
- Pericardial tamponade: pericardiocentesis
26. GENERAL APPROACH
Provide supplemental oxygen
at earliest signs of shock,
beginning with 4–6 L/min via nasal cannula or
6–10 L/min by facemask.
Ensure adequate fluid resuscitation:
to maintain circulating blood volume.
Initiate inotropic & vasoactive drug therapy.
If fluid challenge does not achieve desired end points,
26
27. Hypovolemia protocol for adults.
27
If inadequate perfusion suspected:
20ml/kg LR (or infuse as rapidly as possible if
unmeasurable pressure until response or Complication)
If + Decompensated CHF
begin dobutamine 2mcg/kg/min + pulmonary artery catheter
If+ Decompensated CHF + SBP<90/fluid related
complication
begin dopamine 5mcg/kg/min + pulmonary artery catheter
If+ no ADHF + but age>70 or interstitial fluid
accumulation give albumin based on weight
If wt <60 kg, 250 mL 5% Albumin + pulmonary artery
catheter
If wt >60 kg= 500 mL 5% Albumin + pulmonary artery
28. Hypovolemia protocol....
Normal saline (or a lower chloride-containing isotonic
crystalloid) may be used instead of lactated Ringer
solution.
surgical intervention or blood products for restoring
oxygen-carrying capacity or hemostasis may also be
considered.
For resuscitation of trauma prior to bleeding control,
usually ≤1 L of crystalloid initially used in an attempt to
maintain perfusion and not exacerbate bleeding.
Measurements, such as mean arterial pressure or
pulmonary artery catheter recordings can also be used
to monitor.
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30. Approach to resuscitation of septic shock.
30
Completed with in 1 hr, if late in 3 h of presentation
Infection source control + Antibiotics
Fluid resuscitations (Crystalloids: 30ml/Kg rapidly or Colloid:
300-500mL)
Goal: Lactate <4mmol/L, CVP 8-12mmHg, UOP≥0.5mL/Kg/h
Evaluate clinical status frequently
Completed within 6 h of presentation if MAP<65mmHg
Continue fluid administration
Repeat lactate
Pressor’s: Initiate norepinephrine 0.05-3mcg/kg/min, If
dysrhythmia, use phenylephrine 0.5mcg/kg/min
If refractory hypotension, consider Hydrocortisone
200mg/dayx7 days
31. Approach to resuscitation of septic shock…
31
Clinical signs of adequate regional or global perfusion
(lactate clearance ≥20% or ScvO2≥70% (or SvO2≥65%))
If inadequate signs of perfusion
• 1) adequate fluid administration (colloids),
• 2) Dobutamine 2-20mcg/kg/min titrated
If MAP not corrected (<65mmHg)
Initiate vasopressin 0.01-0.04 mcg/kg/min (do not
titrate), or add epinephrine 0.01-3mcg/kg/min
If Cardiac Index < 3L/min/m2 or low left ventricular EF,
Dobutamine 2-20mcg/kg/min titrated
32. Approach to resuscitation of septic shock.
32
In septic shock Colloid (albumin) may be initiated:
in patients at risk for adverse events from
redistribution of intravenous fluids to extravascular
tissues
• (eg, patients with renal dysfunction,
decompensated HF, ascites compromising
diaphragmatic function),
those that are fluid restricted, or
those not responding to crystalloid therapy.
34. Fluids for resuscitation
Fluid resuscitation for hypovolemic shock.
Crystalloid (0.9% sodium chloride or lactated Ringer’s
solution)
• Preferred over colloids as initial fluid therapy.
• Lactated Ringer’s less likely than normal saline to cause
hyperchloremic metabolic acidosis.
• Administer at 500–2000 mL/h;
• 2–4 L usually normalizes intravascular volume.
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35. Fluids for resuscitation….
Colloid (albumin 5%)
Consider use if volume resuscitation suboptimal
after several liters of crystalloid.
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36. Blood products
Blood products may be required in some patients to
ensure adequate delivery of oxygen or provide clotting
factors and platelets.
Whole blood.
Packed red blood cells.
Fresh frozen plasma.
Platelets.
Cryoprecipitate, factor VIII
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37. Pharmacotherapy for shock.
Inotropes & vasopressors may be needed for patients
who continue to have signs and symptoms of
inadequate tissue perfusion after fluids optimized.
Avoid norepinephrine & high-dose dopamine if possible
because they may ↑ BP at expense of peripheral tissue
ischemia.
Inotropes (eg, dobutamine) preferred in patients with
unstable BP despite fluid replacement if BP is adequate
(SBP ≥ 90 mm Hg).
37
38. Evaluation of therapeutic outcomes
Initial monitoring in pnts with volume depletion include:
Vital signs.
Urine output.
Mental status.
Physical examination.
CVP line placement allows estimation (although indirect
& insensitive) of relationship between ↑ed right atrial
pressure and CO.
Reserve pulmonary artery catheterization for
complicated shock cases not responding to fluids and
pharmacotherapy.
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39. Evaluation of therapeutic outcomes…
Lab tests indicated for the ongoing monitoring
of shock include
Serum electrolytes and RFTs (BUN, SrCr);
CBC to assess possible infection, O2-carrying
capacity of the blood, and ongoing bleeding;
PT and aPTT to assess clotting ability; and
lactate concentration and base deficit to detect
inadequate tissue perfusion.
39
40. Evaluation of therapeutic outcomes…
CV & respiratory parameters should be monitored
continuously (see Table above). Trends, rather than
specific CVP or PAOP numbers, should be monitored
because of interpatient variability in response.
Successful fluid resuscitation
should ↑ SBP (>90 mm Hg), CI (>2.2 L/min/m2), &
urine output (0.5 to 1 mL/kg/hour)
while decreasing SVR to the normal range.
MAP >60 mm Hg should be achieved to ensure adequate
cerebral and coronary perfusion pressure.
40
41. Evaluation of therapeutic outcomes…
Intravascular volume overload is characterized by
↑ filling pressures (CVP >12-15 mm Hg, PAOP >20-24 mm
Hg) &
↓ CO (<3.5 L/min).
If volume overload occurs,
• furosemide, 20-40 mg, should be administered by slow IV
push
• to produce rapid diuresis of intravascular volume
• and “unload” the heart through venous dilation.
41
42. Evaluation of therapeutic outcomes…
Coagulation problems are primarily associated with
low levels of clotting factors in stored blood as well as
dilution of endogenous clotting factors and platelets following
administration of blood.
As a result, a coagulation panel (PT, INR, aPTT) should
be checked
in patients undergoing replacement of 50% to 100% of
blood volume in 12 to 24 hours.
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Notes de l'éditeur
circulatory system failure
intravascular volume deficiency
significant vasodilation
Compensation (e.g ↑ HR, RAS stimulation, vasoconstriction) for significant hypotension
Compensator blood shunting initiated tissue ischemia will lead to Lactic acidosis
Impaired synthesis of clotting factors may increase prothrombin time (PT), international normalized ratio, and activated partial thromboplastin time (aPTT).
Information from noninvasive and invasive monitoring (Table 12-1) and evaluation of past medical history, clinical presentation, and laboratory findings are key components in establishing the diagnosis as well as in assessing general mechanisms responsible for shock.
Pulmonary artery (Swan-Ganz) catheter can be used to determine CVP; PAP; CO & PAOP, an approximate measure of the left ventricular end-diastolic volume and a major determinant of left ventricular preload.
arterial blood gas yields PaO2 & PH, which intern yields PCO2 and SaO2. Oximeter can measure SaO2, which is a noninvasive method that is fairly accurate and useful at the patient’s bedside.
Pulmonary artery (Swan-Ganz) catheter can be used to determine CVP; PAP; CO & PAOP, an approximate measure of the left ventricular end-diastolic volume and a major determinant of left ventricular preload.
arterial blood gas yields PaO2 & PH, which intern yields PCO2 and SaO2. Oximeter can measure SaO2, which is a noninvasive method that is fairly accurate and useful at the patient’s bedside.
Hyperdynamic circulation is abnormally increased circulatory volume. Systemic vasodilation and the associated decrease in peripheral vascular resistance results in decreased pulmonary capillary wedge pressure and decreased blood pressure, presenting usually with a collapsing pulse, but sometimes a bounding pulse
Normal saline (or a lower chloride-containing isotonic crystalloid) may be used instead of lactated Ringer solution. This protocol is not intended to replace or delay therapies such as surgical intervention or blood products for restoring oxygen-carrying capacity or hemostasis. For the resuscitation of patients with trauma prior to bleeding control, usually no more than 1 L of crystalloid should be given initially in an attempt to use the minimal amount of fluid necessary to maintain perfusion and not exacerbate bleeding. If available, some measurements can be used in addition to those listed in the algorithm, such as mean arterial pressure or pulmonary artery catheter recordings. The latter can be used to assist in medication choices (eg, agents with primary pressor effects may be desirable in patients with normal cardiac outputs, whereas dopamine or dobutamine may be indicated in patients with suboptimal cardiac outputs). Lower maximal doses of the medications in this algorithm should be considered when pulmonary artery catheterization is not available. See text for an in-depth discussion of these and other issues involved in this protocol.
Lower maximal doses of medications in this algorithm should be considered when pulmonary artery catheterization is not available. See text for an in-depth discussion of these and other issues involved in this protocol.
Normal saline (or a lower chloride-containing isotonic crystalloid) may be used instead of lactated Ringer solution. This protocol is not intended to replace or delay therapies such as surgical intervention or blood products for restoring oxygen-carrying capacity or hemostasis. For the resuscitation of patients with trauma prior to bleeding control, usually no more than 1 L of crystalloid should be given initially in an attempt to use the minimal amount of fluid necessary to maintain perfusion and not exacerbate bleeding. If available, some measurements can be used in addition to those listed in the algorithm, such as mean arterial pressure or pulmonary artery catheter recordings. The latter can be used to assist in medication choices (eg, agents with primary pressor effects may be desirable in patients with normal cardiac outputs, whereas dopamine or dobutamine may be indicated in patients with suboptimal cardiac outputs). Lower maximal doses of the medications in this algorithm should be considered when pulmonary artery catheterization is not available. See text for an in-depth discussion of these and other issues involved in this protocol.
FIGURE 3.
Algorithmic approach to resuscitative management of septic shock. Algorithmic approach is intended to be used in conjunction with clinical judgment, hemodynamic monitoring parameters, global and regional perfusion goals, and therapy end points, as discussed in the text. aColloid (albumin) may be initiated in patients at risk for adverse events from redistribution of intravenous fluids to extravascular tissues (eg, patients with renal dysfunction, decompensated heart failure, ascites compromising diaphragmatic function), those that are fluid restricted, or those not responding to crystalloid therapy. (Abbreviations: CI, cardiac index; CVP, central venous pressure; echo, echocardiography; Hct, hematocrit; MAP, mean arterial pressure; Scvo2, central venous oxygen saturation; Svo2, mixed venous oxygen saturation.)
FIGURE 3.
Algorithmic approach to resuscitative management of septic shock. Algorithmic approach is intended to be used in conjunction with clinical judgment, hemodynamic monitoring parameters, global and regional perfusion goals, and therapy end points, as discussed in the text. aColloid (albumin) may be initiated in patients at risk for adverse events from redistribution of intravenous fluids to extravascular tissues (eg, patients with renal dysfunction, decompensated heart failure, ascites compromising diaphragmatic function), those that are fluid restricted, or those not responding to crystalloid therapy. (Abbreviations: CI, cardiac index; CVP, central venous pressure; echo, echocardiography; Hct, hematocrit; MAP, mean arterial pressure; Scvo2, central venous oxygen saturation; Svo2, mixed venous oxygen saturation.)
FIGURE 3.
Algorithmic approach to resuscitative management of septic shock. Algorithmic approach is intended to be used in conjunction with clinical judgment, hemodynamic monitoring parameters, global and regional perfusion goals, and therapy end points, as discussed in the text. aColloid (albumin) may be initiated in patients at risk for adverse events from redistribution of intravenous fluids to extravascular tissues (eg, patients with renal dysfunction, decompensated heart failure, ascites compromising diaphragmatic function), those that are fluid restricted, or those not responding to crystalloid therapy. (Abbreviations: CI, cardiac index; CVP, central venous pressure; echo, echocardiography; Hct, hematocrit; MAP, mean arterial pressure; Scvo2, central venous oxygen saturation; Svo2, mixed venous oxygen saturation.)
The initial monitoring of a patient with suspected volume depletion should include vital signs, urine output, mental status, and physical examination.
Placement of a CVP line provides a useful (although indirect and insensitive) estimate of the relationship between increased right atrial pressure and CO.
The indications for pulmonary artery catheterization are controversial. Because there is a lack of a well-defined outcome of data associated with this procedure, its use is presently best reserved for complicated cases of shock not responding to conventional fluid and medication therapies.
Complications related to catheter insertion, maintenance, and removal include damage to vessels and organs during insertion, arrhythmias, infections, and thromboembolic damage.
Ongoing shock monitoring parameters include:
Serum electrolytes.
BUN
Serum creatinine.
CBC
PT
aPTT
Lactate concentration and base deficit.
