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Shock,
STAGES, Pathophysiology,
Classification, and
Approach to Management
ELISHA DADU FELIX
MBChB 4.1
jkuat
DEFINITION
• Shock is failure of circulatory system to maintain adequate perfusion
and oxygenation of vitals organs due to sudden severe reduction of
cardiac output and circulating blood volume.
• Kumar and Parrillo (1995) - “The state in which profound and
widespread reduction of effective tissue perfusion leads first to
reversible, and then if prolonged, to irreversible cellular injury.”
STAGES OF SHOCK.
1.Non progressive(compensated shock)- sympathetic nervous system
activated, RAS, venoconstriction.
However the cvs state is only maintained by reducing perfusion to the
skin, muscle and GIT.
2. Progressive stage- lactic acid accumulation which act as a vasodilator
3. Refractory or irreversible stage – severe deficiency of ATP, lactic
acidosis
CLASSIFICATION OF SHOCK
Hypovolemic shock - due to decreased circulating blood volume in relation to
the total vascular capacity and characterized by a reduction of diastolic filling
pressures
Cardiogenic shock - due to cardiac pump failure related to loss of myocardial
contractility/functional myocardium or structural/mechanical failure of the
cardiac anatomy and characterized by elevations of diastolic filling pressures
and volumes
Extra-cardiac obstructive shock - due to obstruction to flow in the
cardiovascular circuit and characterized by either impairment of diastolic
filling or excessive afterload
Distributive shock - caused by loss of vasomotor control resulting in
arteriolar/venular dilatation and characterized (after fluid resuscitation) by
increased cardiac output and decreased SVR
Endocrine shock-adrenal insufficiency, hypothyroidism
Classification of Circulatory Shock
HYPOVOLEMIC
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
CARDIOGENIC SHOCK
Cardiogenic shock is due to primary failure of the heart to pump blood to the
tissues. Causes include;
Myopathic
Myocardial infarction (hibernating myocardium)
Left 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
EXTRACARDIAC OBSTRUCTIVE
1. 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
2. Impaired systolic contraction (increased ventricular afterload)
• Right ventricle
- Pulmonary embolus (massive)
- Acute pulmonary hypertension
• Left ventricle
- Saddle embolus
- Aortic dissection
DISTRIBUTIVE
Septic (bacterial, fungal, viral, rickettsial)
Toxic shock syndrome
Anaphylactic, anaphylactoid
Neurogenic (spinal shock)
Endocrinologic
• Adrenal crisis
• Thyroid storm
Toxic (e.g., nitroprusside, bretylium)
Clinical Correlates of Hemorrhage
Class I ClassII Class III Class IV
Blood loss (mL) > 750 750 - 1500 1500 - 2000 > 2000
Blood loss (% total) > 15% 15 - 30% 30 - 40% > 40%
Pulse rate < 100 > 100 > 120 > 140
Blood pressure Normal Normal ↓ ↓
Pulse pressure Normal or ↑ ↓ ↓ ↓
Orthostasis Absent Minimal Marked Marked
Capillary refill Normal Delayed Delayed Delayed
Resp rate 14 - 20 20 - 30 30 - 40 > 34
UO (mL/hr) > 30 20 - 30 5 - 15 < 5
CNS mental status Slight anxiety Mild anxiety Anxious/confused Confused/lethargic
CI (L/min) ↓ 0-10% ↓ 20-50% ↓ 50-75% ↓ >75%
Diagnosis and Evaluation
Symptoms
Dizziness, anxiety, confusion, excessive sweating, fatigue, palpitations,
Clinical Signs
Primary diagnosis - tachycardia,
tachypnea, oliguria, peripheral hypoperfusion (poor capillary refill,
mottled) hypotension, cool to touch, weak pulse
Laboratory
Hgb, WBC, platelets
PT/PTT
Electrolytes, arterial blood gases
BUN, Cr
Ca, Mg
Serum lactate
ECG
Invasive Monitoring
Arterial pressure catheter
CVP monitoring
Pulmonary artery catheter (+/- RVEF, oximetry)
MVO(mixed venous oxygenation saturation) – accurate measurement is via
analysis of blood drawn from a long central line placed in the right atrium.
estimations can be made from blood drawn from lines in the superior vena cava.
50-70%- normal .
Below 50% indicate oxygen delivery and increased oxygen by the cells.
A Clinical Approach to Shock
Diagnosis and Management
Hypovolemic Shock
Identify source of blood or fluid loss and stop the loss
Rapid replacement of blood, colloid, or crystalloid
Cardiogenic Shock
LV infarction
• Intra-aortic balloon pump (IABP)
• Cardiac angiography
• Revascularization
angioplasty
coronary bypass
RV infarction
• Fluid and inotropes with PA catheter monitoring
Mechanical abnormality
• Echocardiography
• Corrective surgery
Fluid Therapy
Crystalloids
Lactated Ringer’s solution
Normal saline
Colloids
Hetastarch
Albumin
Packed red blood cells
Infuse to physiologic endpoints
Correct hypotension first (golden hour)
Correct hypoperfusion abnormalities
Monitor for deterioration of oxygenation
Complication of shock
Multiple organ failure
Lung – acute respiratory distress syndrome
Kidney – acute renal insufficiency
Clotting – coagulopathy
Cardiac – cardiovascular failure
Brain – brain injury
End points of resuscitation
Traditionally, patients have been resuscitated until they have :
1. normal pulse rate
2. normal blood pressure
3. normal urine output
However, these parameters are monitoring organs system whose blood flow is
preserved until late of shock. A patient therefore may be resuscitated to
restore central perfusion to brain, lungs and kidneys and yet continue to
underperfuse the gut and muscle bed.
Currently we use resuscitation algorithms directed at correcting global
perfusion end points : lactate levels
base deficit
mixed venous oxygen saturation
•
- end -

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SHOCK[1].pptx

  • 1. Shock, STAGES, Pathophysiology, Classification, and Approach to Management ELISHA DADU FELIX MBChB 4.1 jkuat
  • 2. DEFINITION • Shock is failure of circulatory system to maintain adequate perfusion and oxygenation of vitals organs due to sudden severe reduction of cardiac output and circulating blood volume. • Kumar and Parrillo (1995) - “The state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury.”
  • 3. STAGES OF SHOCK. 1.Non progressive(compensated shock)- sympathetic nervous system activated, RAS, venoconstriction. However the cvs state is only maintained by reducing perfusion to the skin, muscle and GIT. 2. Progressive stage- lactic acid accumulation which act as a vasodilator 3. Refractory or irreversible stage – severe deficiency of ATP, lactic acidosis
  • 4. CLASSIFICATION OF SHOCK Hypovolemic shock - due to decreased circulating blood volume in relation to the total vascular capacity and characterized by a reduction of diastolic filling pressures Cardiogenic shock - due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/mechanical failure of the cardiac anatomy and characterized by elevations of diastolic filling pressures and volumes Extra-cardiac obstructive shock - due to obstruction to flow in the cardiovascular circuit and characterized by either impairment of diastolic filling or excessive afterload Distributive shock - caused by loss of vasomotor control resulting in arteriolar/venular dilatation and characterized (after fluid resuscitation) by increased cardiac output and decreased SVR Endocrine shock-adrenal insufficiency, hypothyroidism
  • 5. Classification of Circulatory Shock HYPOVOLEMIC 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
  • 6. CARDIOGENIC SHOCK Cardiogenic shock is due to primary failure of the heart to pump blood to the tissues. Causes include; Myopathic Myocardial infarction (hibernating myocardium) Left ventricle Myocardial contusion (trauma) Myocarditis Cardiomyopathy Post-ischemic myocardial stunning Septic myocardial depression
  • 7. Pharmacologic • Anthracycline cardiotoxicity • Calcium channel blockers Mechanical • Valvular failure (stenotic or regurgitant) • Hypertropic cardiomyopathy • Ventricular septal defect Arrhythmic • Bradycardia • Tachycardia
  • 8. EXTRACARDIAC OBSTRUCTIVE 1. 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 2. Impaired systolic contraction (increased ventricular afterload) • Right ventricle - Pulmonary embolus (massive) - Acute pulmonary hypertension • Left ventricle - Saddle embolus - Aortic dissection
  • 9. DISTRIBUTIVE Septic (bacterial, fungal, viral, rickettsial) Toxic shock syndrome Anaphylactic, anaphylactoid Neurogenic (spinal shock) Endocrinologic • Adrenal crisis • Thyroid storm Toxic (e.g., nitroprusside, bretylium)
  • 10. Clinical Correlates of Hemorrhage Class I ClassII Class III Class IV Blood loss (mL) > 750 750 - 1500 1500 - 2000 > 2000 Blood loss (% total) > 15% 15 - 30% 30 - 40% > 40% Pulse rate < 100 > 100 > 120 > 140 Blood pressure Normal Normal ↓ ↓ Pulse pressure Normal or ↑ ↓ ↓ ↓ Orthostasis Absent Minimal Marked Marked Capillary refill Normal Delayed Delayed Delayed Resp rate 14 - 20 20 - 30 30 - 40 > 34 UO (mL/hr) > 30 20 - 30 5 - 15 < 5 CNS mental status Slight anxiety Mild anxiety Anxious/confused Confused/lethargic CI (L/min) ↓ 0-10% ↓ 20-50% ↓ 50-75% ↓ >75%
  • 11.
  • 12.
  • 13. Diagnosis and Evaluation Symptoms Dizziness, anxiety, confusion, excessive sweating, fatigue, palpitations, Clinical Signs Primary diagnosis - tachycardia, tachypnea, oliguria, peripheral hypoperfusion (poor capillary refill, mottled) hypotension, cool to touch, weak pulse
  • 14. Laboratory Hgb, WBC, platelets PT/PTT Electrolytes, arterial blood gases BUN, Cr Ca, Mg Serum lactate ECG
  • 15. Invasive Monitoring Arterial pressure catheter CVP monitoring Pulmonary artery catheter (+/- RVEF, oximetry) MVO(mixed venous oxygenation saturation) – accurate measurement is via analysis of blood drawn from a long central line placed in the right atrium. estimations can be made from blood drawn from lines in the superior vena cava. 50-70%- normal . Below 50% indicate oxygen delivery and increased oxygen by the cells.
  • 16. A Clinical Approach to Shock Diagnosis and Management Hypovolemic Shock Identify source of blood or fluid loss and stop the loss Rapid replacement of blood, colloid, or crystalloid
  • 17. Cardiogenic Shock LV infarction • Intra-aortic balloon pump (IABP) • Cardiac angiography • Revascularization angioplasty coronary bypass RV infarction • Fluid and inotropes with PA catheter monitoring Mechanical abnormality • Echocardiography • Corrective surgery
  • 18. Fluid Therapy Crystalloids Lactated Ringer’s solution Normal saline Colloids Hetastarch Albumin Packed red blood cells Infuse to physiologic endpoints Correct hypotension first (golden hour) Correct hypoperfusion abnormalities Monitor for deterioration of oxygenation
  • 19. Complication of shock Multiple organ failure Lung – acute respiratory distress syndrome Kidney – acute renal insufficiency Clotting – coagulopathy Cardiac – cardiovascular failure Brain – brain injury
  • 20. End points of resuscitation Traditionally, patients have been resuscitated until they have : 1. normal pulse rate 2. normal blood pressure 3. normal urine output However, these parameters are monitoring organs system whose blood flow is preserved until late of shock. A patient therefore may be resuscitated to restore central perfusion to brain, lungs and kidneys and yet continue to underperfuse the gut and muscle bed. Currently we use resuscitation algorithms directed at correcting global perfusion end points : lactate levels base deficit mixed venous oxygen saturation