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SHOCK
7TH YEAR MEDICAL STUDENTS
PRESENTED BY DR MULENGA MULEWA
Definition
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.”
Hypovolemic shock- inadequate fluid for vascular
system
Distributive shock- increased size of vascular system
Cardiogenic shock- inadequate pumping action
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course
• Obstructive- obstruction of blood flow in lungs or heart
Basic Physiology
• BP = CO x PR
• CO = SV x HR
4900ml =70ml x 70bpm
• Stroke Volume is a function
• Preload
• Afterload
• Myocardial Contractility
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course
COMPENSATORY MECHANISMS
• Baroreceptors
• Renin Angiotensin Aldosterone System
• ANP
• ADH
• Activation of thirst centres
• Chemoreceptors and respiratory centres
What is Unique about Children
• Poor ability to concentrate urine
• Neonates & infants urine output 1 – 2ml/Kg/hr
• Compare elderly urine outuput <0.5ml/Kg/hr
• Blood vol 8 – 9% of ideal body weight
• Children have more insensible losses compared to adults
CLASSIFICATION OF CIRCULATORY SHOCK
• 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
CONT’N OF CARDIOGENIC SHOCK
CARDIOGENIC
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
OBSTRUCTIVE SHOCK
• Extra-cardiac obstructive shock - due to obstruction to flow in the
cardiovascular circuit and characterized by either impairment of
diastolic filling or excessive afterload
EXTRACARDIAC OBSTRUCTIVE
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
• Distributive shock - caused by loss of vasomotor control resulting in
arteriolar/venular dilatation and characterized (after fluid
resuscitation) by increased cardiac output and decreased VR
DISTRIBUTIVE
Septic (bacterial, fungal, viral, rickettsial)
Toxic shock syndrome
Anaphylactic, anaphylactoid
Neurogenic (spinal shock)
Endocrinologic
• Adrenal crisis
• Thyroid storm
Toxic (e.g., nitroprusside, bretylium)
• Hypovolemic shock - due to decreased circulating blood volume in
relation to the total vascular capacity and characterized by a
reduction of diastolic filling pressures
HYPOVOLEMIC
Hemorrhagic
• Trauma
• Gastrointestinal
• Retroperitoneal
Fluid depletion (non haemorrhagic)
• External fluid loss
- Dehydration
- Vomiting
- Diarrhea
- Polyuria
• Interstitial fluid redistribution
- Trauma
- Anaphylaxis
CLINICAL CORRELATES OF HAEMORRHAGE
CLASS I CLASS II CLASS III CLASS IV
BLOOD LOSS
(ml)
= 750 750-1500 1500-2000 >2000
BLOOD LOSS % =15 15-30 30-40 >40
PULSE RATE <100 >100 >120 >140
BP NORMAL NORMAL DECREASED DECREASED
PULSE
PRESSURE
NORMAL/
INCREASED
DECREASED DECREASED DECREASED
ORTHOSTASIS ABSENT MINIMAL MARKED MARKED
CAP REFILL NORMAL DELAYED DELAYED DELAYED
RR 14-20 20-30 30-40 >34
UO (ml/hr) >30 20-30 5-15 <5
CNS MSE SLIGHT ANXIETY MILD ANXIETY ANXIOUS/
CONFUSED
CONFUSED/
LETHARGY
PHASES OF SHOCK
• Discrete phases based on physiological changes
• PHASES: (1) compensated phase (2) decompensated phase (3)
terminal shock
• Clinical signs vary with phases
• Prognosis depend on phase
Initial Patient Assessment
• Recognition of Shock
• Clinical signs and symptoms depends on the severity of
the shock
• Early manifestations include tachycardia and cutaneous
vasoconstriction
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course
CLINICAL FEATURES
• Hypotension
• Rapid Pulse
• Cold skin and extremities
• Pale skin
• Intense thirst
• Rapid respirations
• Restlessness and coma
• History related to the cause
TREATMENT
• According to available protocols
• Pt prep is important
• Need to plan our surgery
• Need good pre op, intra op and post op care
• Anticipate haemorrhage in certain cases
• WHAT IF PATIENT COMES BLEEDING
• WHAT IF PATIENT COMES WITH BURNS
• WHAT IF PATIENT COMES WITH IO
Treating Hypovolemic Shock
• In SGY we have what we call the golden hour
ABCDEs + call for help
• Airway and Breathing
• Would prefer O2 sat greater than 95%
• Placing O2 on the patient
• Circulation
• Hemorrhage Control
• Vascular Access, Large bore IV x 2
• Xmatch
• IVF
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course
Monitoring
Continuous monitoring
• Oxygen Saturation
• Urine output
LR Hopson, 2005
Source Undetermined
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course
Treating Hemorrhagic Shock
•Identify & reverse the cause
•Restore tissue perfusion
•Restore organ function
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course
Initial Fluid Therapy
• Adult with normal Cardiac Function
• 1 to 2 Liters of LR or NS rapidly
• Pediatric
• 20ml/kg of LR or NS rapidly
• Evaluate patients response to fluid
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course
THE CRYSTAL RANDOMISED TRIAL
• JAMA: effects of fluid resuscitation with colloids Vs crystalloids on
mortality in critically ill patients with hypovolaemic shock
• 359 (25.4%) deaths Colloids Vs 390 (27.0%) deaths in crystalloids. This
outcome was 28 day period mortality
• 434 (30.7%) colloid mortality over 90 days period Vs 493 (34.2%)
crystalloid mortality
Evaluation of Treatment
•Assess organ perfusion
•Urinary output
•Mental Status
•Skin exam
•Vitals
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course
MECHANISMS OF CELLULAR INJURY IN SHOCK
1) Cellular ischemia
2) Free radical reperfusion injury
3) Inflammatory mediators (local and circulating)
NOTE
• Children have their own major haemorrhage protocol
TAKE HOME
• Make sure you do not lose the gold hour opportunity
• Opportunity to gain IV access
• Opportunity to correct reversible cell injury
Mulewa shock
Mulewa shock
Mulewa shock
Mulewa shock

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Mulewa shock

  • 1. SHOCK 7TH YEAR MEDICAL STUDENTS PRESENTED BY DR MULENGA MULEWA
  • 2. Definition 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.” Hypovolemic shock- inadequate fluid for vascular system Distributive shock- increased size of vascular system Cardiogenic shock- inadequate pumping action Ghana Emergency Medicine Collaborative Advanced Emergency Trauma Course
  • 3. • Obstructive- obstruction of blood flow in lungs or heart
  • 4. Basic Physiology • BP = CO x PR • CO = SV x HR 4900ml =70ml x 70bpm • Stroke Volume is a function • Preload • Afterload • Myocardial Contractility Ghana Emergency Medicine Collaborative Advanced Emergency Trauma Course
  • 5. COMPENSATORY MECHANISMS • Baroreceptors • Renin Angiotensin Aldosterone System • ANP • ADH • Activation of thirst centres • Chemoreceptors and respiratory centres
  • 6. What is Unique about Children • Poor ability to concentrate urine • Neonates & infants urine output 1 – 2ml/Kg/hr • Compare elderly urine outuput <0.5ml/Kg/hr • Blood vol 8 – 9% of ideal body weight • Children have more insensible losses compared to adults
  • 7. CLASSIFICATION OF CIRCULATORY SHOCK • 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
  • 8. CONT’N OF CARDIOGENIC SHOCK CARDIOGENIC 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
  • 9. OBSTRUCTIVE SHOCK • Extra-cardiac obstructive shock - due to obstruction to flow in the cardiovascular circuit and characterized by either impairment of diastolic filling or excessive afterload
  • 10. EXTRACARDIAC OBSTRUCTIVE 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
  • 11. • Distributive shock - caused by loss of vasomotor control resulting in arteriolar/venular dilatation and characterized (after fluid resuscitation) by increased cardiac output and decreased VR
  • 12. DISTRIBUTIVE Septic (bacterial, fungal, viral, rickettsial) Toxic shock syndrome Anaphylactic, anaphylactoid Neurogenic (spinal shock) Endocrinologic • Adrenal crisis • Thyroid storm Toxic (e.g., nitroprusside, bretylium)
  • 13. • Hypovolemic shock - due to decreased circulating blood volume in relation to the total vascular capacity and characterized by a reduction of diastolic filling pressures
  • 14. HYPOVOLEMIC Hemorrhagic • Trauma • Gastrointestinal • Retroperitoneal Fluid depletion (non haemorrhagic) • External fluid loss - Dehydration - Vomiting - Diarrhea - Polyuria • Interstitial fluid redistribution - Trauma - Anaphylaxis
  • 15. CLINICAL CORRELATES OF HAEMORRHAGE CLASS I CLASS II CLASS III CLASS IV BLOOD LOSS (ml) = 750 750-1500 1500-2000 >2000 BLOOD LOSS % =15 15-30 30-40 >40 PULSE RATE <100 >100 >120 >140 BP NORMAL NORMAL DECREASED DECREASED PULSE PRESSURE NORMAL/ INCREASED DECREASED DECREASED DECREASED ORTHOSTASIS ABSENT MINIMAL MARKED MARKED CAP REFILL NORMAL DELAYED DELAYED DELAYED RR 14-20 20-30 30-40 >34 UO (ml/hr) >30 20-30 5-15 <5 CNS MSE SLIGHT ANXIETY MILD ANXIETY ANXIOUS/ CONFUSED CONFUSED/ LETHARGY
  • 16. PHASES OF SHOCK • Discrete phases based on physiological changes • PHASES: (1) compensated phase (2) decompensated phase (3) terminal shock • Clinical signs vary with phases • Prognosis depend on phase
  • 17. Initial Patient Assessment • Recognition of Shock • Clinical signs and symptoms depends on the severity of the shock • Early manifestations include tachycardia and cutaneous vasoconstriction Ghana Emergency Medicine Collaborative Advanced Emergency Trauma Course
  • 18. CLINICAL FEATURES • Hypotension • Rapid Pulse • Cold skin and extremities • Pale skin • Intense thirst • Rapid respirations • Restlessness and coma • History related to the cause
  • 19. TREATMENT • According to available protocols • Pt prep is important • Need to plan our surgery • Need good pre op, intra op and post op care • Anticipate haemorrhage in certain cases
  • 20. • WHAT IF PATIENT COMES BLEEDING • WHAT IF PATIENT COMES WITH BURNS • WHAT IF PATIENT COMES WITH IO
  • 21. Treating Hypovolemic Shock • In SGY we have what we call the golden hour ABCDEs + call for help • Airway and Breathing • Would prefer O2 sat greater than 95% • Placing O2 on the patient • Circulation • Hemorrhage Control • Vascular Access, Large bore IV x 2 • Xmatch • IVF Ghana Emergency Medicine Collaborative Advanced Emergency Trauma Course
  • 22. Monitoring Continuous monitoring • Oxygen Saturation • Urine output LR Hopson, 2005 Source Undetermined Ghana Emergency Medicine Collaborative Advanced Emergency Trauma Course
  • 23. Treating Hemorrhagic Shock •Identify & reverse the cause •Restore tissue perfusion •Restore organ function Ghana Emergency Medicine Collaborative Advanced Emergency Trauma Course
  • 24. Initial Fluid Therapy • Adult with normal Cardiac Function • 1 to 2 Liters of LR or NS rapidly • Pediatric • 20ml/kg of LR or NS rapidly • Evaluate patients response to fluid Ghana Emergency Medicine Collaborative Advanced Emergency Trauma Course
  • 25. THE CRYSTAL RANDOMISED TRIAL • JAMA: effects of fluid resuscitation with colloids Vs crystalloids on mortality in critically ill patients with hypovolaemic shock • 359 (25.4%) deaths Colloids Vs 390 (27.0%) deaths in crystalloids. This outcome was 28 day period mortality • 434 (30.7%) colloid mortality over 90 days period Vs 493 (34.2%) crystalloid mortality
  • 26. Evaluation of Treatment •Assess organ perfusion •Urinary output •Mental Status •Skin exam •Vitals Ghana Emergency Medicine Collaborative Advanced Emergency Trauma Course
  • 27. MECHANISMS OF CELLULAR INJURY IN SHOCK 1) Cellular ischemia 2) Free radical reperfusion injury 3) Inflammatory mediators (local and circulating)
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  • 30. NOTE • Children have their own major haemorrhage protocol
  • 31. TAKE HOME • Make sure you do not lose the gold hour opportunity • Opportunity to gain IV access • Opportunity to correct reversible cell injury