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DR DHANESH KUMAR
DNB-CTVS
 Profound hemodynamic and metabolic
disturbance characterized by failure of the
circulatory system to maintain adequate
perfusion of vital organs
 Cardiogenic (intrinsic vs compressive)
 Hypovolemic
 Distributive
◦ sepsis
◦ neurogenic (spinal shock)
◦ adrenal insufficiency
◦ anaphylaxis
 Arterial hypotension associated with signs of
altered tissue perfusion, visualized through
three windows of body :
 Peripheral window: skin that is cold, clammy
and blue ,pale or discolored.
 Renal window: decreased urine output
:<0.5ml/kg/h.
 Neurological window : Altered mental state
characterized by obtundation ,disorientation
and confusion.
 Usually not clinically apparent
 Metabolism changes from aerobic to
anaerobic.
◦ Lactic acid accumulates -must be removed by blood
and broken down by liver. usual cut-off value is
2mEq/L. but lactate level of >1.5mmol/L in patients
with septic shock are associated with increased
mortality.
 Clinically apparent –Neural, Hormonal
&Biochemical compensatory mechanisms
 Attempts aimed to overcome consequences
of anaerobic metabolism and maintaining
homeostasis.
8
•Baroreceptors in carotid and aortic bodies activate SNS in
response to ↓ BP.
•Vasoconstriction, while blood to vital organs maintained.
•↓ blood to kidneys > activates renin– angiotensin system ↑
venous return to heart, CO, BP.
•Impaired GI motility- Risk for paralytic ileus.
•Cool, clammy skin .
Except septic patient who is warm and flushed
 Shunting of blood from lungs increases
physiologic dead space.
 ↓ arterial O2 levels
 Increase in rate/depth of respirations
 V/Q mismatch
 SNS stimulation increases myocardial O2
demands.
 If perfusion deficit corrected, patient recovers
with no residual sequelae .
 If deficit not corrected, patient enters
progressive stage
 Begins when compensatory mechanisms
fail
 Aggressive interventions to prevent
multiple organ dysfunction syndrome
(MODS)
 Hallmarks -↓ cellular perfusion & altered
capillary permeability
 Leakage of protein into interstitial
space
 ↑ systemic interstitial edema
 Fluid leakage affects solid organs and
peripheral tissues.
• Anasarca
 Movement of fluid from pulmonary vasculature
to interstitium(decreased blood flow to
pulm.Cap.)
 Pulmonary edema
 Bronchoconstriction
 ↓ residual capacity
 Fluid moves into alveoli
 Edema-Red. surfactant
 Worsening V/Q mismatch
 Tachypnea, Crackles
 Incr.work of breathing
 CO begins to fall
 Red. peripheral perfusion
 Hypotension
 Weak peripheral pulses
 Ischemia of distal extremities
 Myocardial dysfunction results in
 Dysrhythmias
 Ischemia; Myocardial infarction
 End result: complete deterioration of cardiovascular
system
 Liver fails to metabolize drugs and waste.
 Jaundice; Elevated enzymes
 Loss of immune function
 Risk for DIC and significant bleeding
 Mucosal barrier of GI system becomes ischemic
 Ulcers
 Bleeding
 Risk of translocation of bacteria
 Reduced ability to absorb nutrients
 Exacerbation of anaerobic
metabolism
 Accumulation of lactic acid
 ↑ capillary permeability
 Profound hypotension and hypoxia
 Tachycardia worsens.
 Failure of one organ system
affects others.
 Recovery unlikely
 Myocardial Injury or Obstruction to Flow
◦ Arrythymias
◦ valvular lesions
◦ AMI
◦ Severe CHF
◦ VSD
◦ Hypertrophic Cardiomyopathy
 Pulmonary Edema
 Raised JVP
 Hypotension
 weak pulses
 oliguria
 Pulmonary Embolism (obstructive)
 Cardiac Tamponade
 Tension Pneumothorax
 Presentation will be according to underlying
disease process.
 Reduced circulating blood volume with
secondary decreased cardiac output
◦ Acute hemorrhage
◦ Vomiting/Diarrhea
◦ Dehydration
◦ Burns
◦ Peritonitis/Pancreatitis
 Hypotensive
 collapsed neck veins
 clear lungs
 cool, cyanotic extremities
 evidence of bleeding?
◦ Anticoagulant use
◦ trauma, bruising
 oliguria
 Peripheral Vasodilation secondary to disruption
of cellular metabolism by the effects of
inflammatory mediators.
 Gram negative or other overwhelming
infection.
 Results in decreased Peripheral Vascular
Resistance.
 Febrile
 Tachycardia
 clear lungs, evidence of pneumonia
 warm extremities
 collapsed neck veins
 oliguria
 Response to fluids
 Echo/ECG
 CXR
 Evidence of infection
Etiology CO PCWP SVR
cardiogenic decreased increased increased
hypovolemic decreased decreased increased
distributive increased decreased decreased
obstructive decreased Increased increased
 Correct underlying disorder if possible and
then direct efforts at increasing the blood
pressure to increase oxygen delivery to the
tissues.
 Maintain a mean arterial pressure of 65mmHg
(1/3 systolic + 2/3 diastolic)
 Keep O2 sats >92%, intubate if neccesary
 Normal Saline should be administered
anytime a patient is hypotensive.
 If possible give colloid.
 Vasopressors specially for septic shock .
 Inotropic agents for cardiogenic shock
 Intra-aortic Balloon Pump for cardiogenic
Drugs Indication dose MOA Principle
action
Dopamine Hypotension 5-
10mcg/k
g/min
Beta1and
dopaminergic
Inotropic(+)
Hypotension >10mcg
/kg/min
alpha1 Vasoconstri
ction
Dobutamine Cardiogenic
shock
2.5-
25mcg/k
g/min
Selective
beta1
Inotropic(+)
Norephinephrine Hypotension 2-
4mcg/kg
/min
Alpha1and
beta1
Vasoconstri
ction
Phenylephinphrine Hypotension 40-
180mcg/
kg/min
Selective
alha1
vasoconstri
ction
 Attempt to correct problem and increase
cardiac output by diuresing and providing
inotropic support.
 IABP is utilized if medical therapy is
ineffective. Cardiac Catheterization if
ongoing ischemia despite maximum medical
therapy.
 Cardiogenic shock is the exception to the rule
that NS is always given for hypotension NS
will exacerbate cardiac shock.
 Early goal directed therapy
 Identification of source of infection
 Broad Spectrum Antibiotics
 IV fluids
 Vasopressors
 Steroids ??
 Recombinant human activated protein C (
Xygris)
 Bicarbonate if pH < 7.1
 Correct bleeding abnormality
 If PT or PTT elevated then FFP
 Aggressive Fluid replacement with 2 large
bore IV’s or central line.
 Pressors are last line, but commonly required.
 HARRISON 18TH EDITION. Page no. 1689-
1695.
 Consensus on circulatory shock and
hemodynamic monitoring. Task force of
European society of Intensive care
Medicine(Intensive care Med(2014)40:1795-
1815 DOI 10.1007/s00134-014-3525-z.
 The swan –Ganz catheter: past ,present and
future(circulation .2009:119:147-152.)
Causes, Presentation and Management of Shock

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Causes, Presentation and Management of Shock

  • 2.  Profound hemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate perfusion of vital organs
  • 3.  Cardiogenic (intrinsic vs compressive)  Hypovolemic  Distributive ◦ sepsis ◦ neurogenic (spinal shock) ◦ adrenal insufficiency ◦ anaphylaxis
  • 4.
  • 5.  Arterial hypotension associated with signs of altered tissue perfusion, visualized through three windows of body :  Peripheral window: skin that is cold, clammy and blue ,pale or discolored.  Renal window: decreased urine output :<0.5ml/kg/h.  Neurological window : Altered mental state characterized by obtundation ,disorientation and confusion.
  • 6.  Usually not clinically apparent  Metabolism changes from aerobic to anaerobic. ◦ Lactic acid accumulates -must be removed by blood and broken down by liver. usual cut-off value is 2mEq/L. but lactate level of >1.5mmol/L in patients with septic shock are associated with increased mortality.
  • 7.  Clinically apparent –Neural, Hormonal &Biochemical compensatory mechanisms  Attempts aimed to overcome consequences of anaerobic metabolism and maintaining homeostasis.
  • 8. 8 •Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP. •Vasoconstriction, while blood to vital organs maintained. •↓ blood to kidneys > activates renin– angiotensin system ↑ venous return to heart, CO, BP. •Impaired GI motility- Risk for paralytic ileus. •Cool, clammy skin . Except septic patient who is warm and flushed
  • 9.  Shunting of blood from lungs increases physiologic dead space.  ↓ arterial O2 levels  Increase in rate/depth of respirations  V/Q mismatch  SNS stimulation increases myocardial O2 demands.  If perfusion deficit corrected, patient recovers with no residual sequelae .  If deficit not corrected, patient enters progressive stage
  • 10.  Begins when compensatory mechanisms fail  Aggressive interventions to prevent multiple organ dysfunction syndrome (MODS)  Hallmarks -↓ cellular perfusion & altered capillary permeability  Leakage of protein into interstitial space  ↑ systemic interstitial edema
  • 11.  Fluid leakage affects solid organs and peripheral tissues. • Anasarca  Movement of fluid from pulmonary vasculature to interstitium(decreased blood flow to pulm.Cap.)  Pulmonary edema  Bronchoconstriction  ↓ residual capacity  Fluid moves into alveoli  Edema-Red. surfactant  Worsening V/Q mismatch  Tachypnea, Crackles  Incr.work of breathing
  • 12.  CO begins to fall  Red. peripheral perfusion  Hypotension  Weak peripheral pulses  Ischemia of distal extremities  Myocardial dysfunction results in  Dysrhythmias  Ischemia; Myocardial infarction  End result: complete deterioration of cardiovascular system
  • 13.  Liver fails to metabolize drugs and waste.  Jaundice; Elevated enzymes  Loss of immune function  Risk for DIC and significant bleeding  Mucosal barrier of GI system becomes ischemic  Ulcers  Bleeding  Risk of translocation of bacteria  Reduced ability to absorb nutrients
  • 14.  Exacerbation of anaerobic metabolism  Accumulation of lactic acid  ↑ capillary permeability  Profound hypotension and hypoxia  Tachycardia worsens.  Failure of one organ system affects others.  Recovery unlikely
  • 15.  Myocardial Injury or Obstruction to Flow ◦ Arrythymias ◦ valvular lesions ◦ AMI ◦ Severe CHF ◦ VSD ◦ Hypertrophic Cardiomyopathy
  • 16.  Pulmonary Edema  Raised JVP  Hypotension  weak pulses  oliguria
  • 17.  Pulmonary Embolism (obstructive)  Cardiac Tamponade  Tension Pneumothorax  Presentation will be according to underlying disease process.
  • 18.  Reduced circulating blood volume with secondary decreased cardiac output ◦ Acute hemorrhage ◦ Vomiting/Diarrhea ◦ Dehydration ◦ Burns ◦ Peritonitis/Pancreatitis
  • 19.  Hypotensive  collapsed neck veins  clear lungs  cool, cyanotic extremities  evidence of bleeding? ◦ Anticoagulant use ◦ trauma, bruising  oliguria
  • 20.  Peripheral Vasodilation secondary to disruption of cellular metabolism by the effects of inflammatory mediators.  Gram negative or other overwhelming infection.  Results in decreased Peripheral Vascular Resistance.
  • 21.  Febrile  Tachycardia  clear lungs, evidence of pneumonia  warm extremities  collapsed neck veins  oliguria
  • 22.  Response to fluids  Echo/ECG  CXR  Evidence of infection
  • 23. Etiology CO PCWP SVR cardiogenic decreased increased increased hypovolemic decreased decreased increased distributive increased decreased decreased obstructive decreased Increased increased
  • 24.  Correct underlying disorder if possible and then direct efforts at increasing the blood pressure to increase oxygen delivery to the tissues.  Maintain a mean arterial pressure of 65mmHg (1/3 systolic + 2/3 diastolic)  Keep O2 sats >92%, intubate if neccesary
  • 25.  Normal Saline should be administered anytime a patient is hypotensive.  If possible give colloid.  Vasopressors specially for septic shock .  Inotropic agents for cardiogenic shock  Intra-aortic Balloon Pump for cardiogenic
  • 26. Drugs Indication dose MOA Principle action Dopamine Hypotension 5- 10mcg/k g/min Beta1and dopaminergic Inotropic(+) Hypotension >10mcg /kg/min alpha1 Vasoconstri ction Dobutamine Cardiogenic shock 2.5- 25mcg/k g/min Selective beta1 Inotropic(+) Norephinephrine Hypotension 2- 4mcg/kg /min Alpha1and beta1 Vasoconstri ction Phenylephinphrine Hypotension 40- 180mcg/ kg/min Selective alha1 vasoconstri ction
  • 27.  Attempt to correct problem and increase cardiac output by diuresing and providing inotropic support.  IABP is utilized if medical therapy is ineffective. Cardiac Catheterization if ongoing ischemia despite maximum medical therapy.  Cardiogenic shock is the exception to the rule that NS is always given for hypotension NS will exacerbate cardiac shock.
  • 28.  Early goal directed therapy  Identification of source of infection  Broad Spectrum Antibiotics  IV fluids  Vasopressors  Steroids ??  Recombinant human activated protein C ( Xygris)  Bicarbonate if pH < 7.1
  • 29.  Correct bleeding abnormality  If PT or PTT elevated then FFP  Aggressive Fluid replacement with 2 large bore IV’s or central line.  Pressors are last line, but commonly required.
  • 30.  HARRISON 18TH EDITION. Page no. 1689- 1695.  Consensus on circulatory shock and hemodynamic monitoring. Task force of European society of Intensive care Medicine(Intensive care Med(2014)40:1795- 1815 DOI 10.1007/s00134-014-3525-z.  The swan –Ganz catheter: past ,present and future(circulation .2009:119:147-152.)