SHOCK Objectives: at the end of this lecture you would be able to : 1- define shock 2- recognize types of shock and their causes 3- correlate pathophysiologic changes with clinical features . 4- know the broad lines of monitoring and treatment of shock

1
SHOCK Objectives at the
end of this lecture you would be able to 1-
define shock2- recognize types of shock and
their causes3- correlate pathophysiologic
changes with clinical features .4- know the
broad lines of monitoring and treatment of shock
patients .
2
Shock A physiological state characterized by a
significant, systemic reduction in tissue
perfusion, resulting in decreased tissue oxygen
delivery and insufficient removal of cellular
metabolic products, resulting in tissue injury.
3

SHOCK
Definition SHOCK is an acute circulatory
failure, characterized by dysfunction of the
microcirculation , inadequate blood flow to
vital organs and inability of the body cell mass
to metabolize the nutrients normally.

• Shock is not a synonym to hypotension!

4
What are the functions of the cardio-vascular
system?
5
Definition of Shock

• Cellular level
• Reduction of mitochondrial oxygen
• Anaerobic glycolysis of ATP
• Accumulation of pyruvate Lactatic
  Acidosis

6
SHOCK
Classification of Shock

• A- Classification of Shock by Causes
• (1) Hypovolemic shock
  
• (2) Cardiogenic shock
• (3) Neurogenic shock
• (4) Anaphylactic shock
• (5) Septic shock

7
B. Classification of Shock according to
hemodynamic changes ?Hypodynamic Shock
Cardiac Output ?,
Vascular Resistace?,
Cold Skin ? Hyperdynamic
Shock Cardiac Output ?,
Vascular Resistace ?,
Warm Skin
8
Different kind of Reason
Inadequate Blood Flow
Metabolic Disturbances
Circulatory Failure

Special Clinical Syndrome
9
Systemic pathophysiologic responces of Shock

Low blood flow
Skin,fat,skeletal
muscls,kidney,intestines
Heart,brain normal or
Redistribution of blood flow
10
Etiology Hemodynamic Changes in Shock
VO2 sat SVR CO CVP example Etiology of shock
low high low low hypovolemic preload
low high low high cardiogenic contractility
distributive afterload
11
Etiology Hemodynamic Changes in Shock
(Afterload)
VO2 SAT SVR CO CVP EXAMPLE ETIOLOGY OF SHOCK
DISTRIBUTIVE AFTERLOAD
High Low High Low/High Hyperdynamic Septic
Low/High High Low Low/High Hypodynamic Septic
Low Low Low Low Neurogenic
Low Low Low Low Anaphylactic
12

• Hypovolemic Shock
• Decreased preload?small ventricular end-diastolic
  volumes ?inadequate cardiac generation of
  pressure and flow
• Causes
• -- bleeding trauma, GI bleeding, ruptured
  aneurysms, hemorrhagic pancreatitis
• -- protracted vomiting or diarrhea
• -- adrenal insufficiency diabetes insipidus
• -- dehydration
• -- third spacing intestinal obstruction,
  pancreatitis, cirrhosis

13
Classes of acute hemorrhage
Class I Class II Class III Class IV
Blood loss lt 750 cc 0-15 750-1500 15-30 1500-2000 30-40 gt2000cc gt40
HR Normal
PP Normal
BP Normal Normal
UOP Normal Normal Decreased Negligible
Mental Normal Anxious Confused Lethargic
Fluid Crystalloid Crystalloid Crysblood Crysblood
ATLS 2004. 70kg male
14

• Signs Symptoms Hypotension, Tachycardia,
  change, Oliguria, Deminished Pulses.
• Markers monitor urine output UOP, central venous
  pressure CVP, blood pressure BP, heart rate HR,
  hemaocrit Hct, mental state MS, cardiac outputCO,
  lactic acid and pulmonary capillary wedge
  pressurePCWP
• Treatment IVF (crystalloid), Trasfusion ,
• Stem ongoing Blood Loss

15
TRUE OR FALSE ?The earliest sign of hypovolemic
shock is hypotension .
16
TRUE OR FALSEIn early stage of hypovolemic shock
the skin would be warm due to vaso-dilation .
17
Septic/Inflammatory ShockThis type is due to
infection/sepsis G(-/ ) speticemia, pneumonia,
peritonitis, meningitis, cholangitis,
pyelonephritis, necrotic tissue, pancreatitis,
wet gangrene, toxic shock syndrome, etc.
Mechanism It is due to release of
inflammatory mediators which leads to
1-Disruption of the microvascular endothelium
2-Cutaneous arteriolar dilation and sequestration
of blood in cutaneous venules and small veins
18
Signs Early warm with vasodilation
(hyper dynamic circulation), often adequate
urine output, fever and tachypnea. Late--
vasoconstriction, hypotension, oliguria, altered
mental status (hypodynamic circulation).Findings
Early hyperglycemia, respiratory
alkalosis, hemoconcentration, WBC typically
normal or low. Late Leukocytosis, lactic
acidosis VeryLate Disseminated Intravascular
Coagulation Multi-Organ System Failure.
19
Treatment Intravenous fluid IVF, Blood
transfusion, antibiotics, Drainage (ie abscess)
vasopressor agents .
20
TRUE OR FALSE In hyperdynamic state of septic
shock there is rapid washout of metabolites
because of increased blood supply to the tissues
21

• Cardiogenic Shock
• Mechanism Intrinsic abnormality of heart ?
  inability to deliver blood into the vascular tree
  with adequate power
• Causes
• 1. Cardiomyopathies myocardial ischemia,
  myocardial infarction, cardiomyopathy,
  myocardiditis, myocardial contusion
• 2- Mechanical cardiac valvular insufficiency,
  papillary muscle rupture, septal defects, aortic
  stenosis

22
3- Arrythmias bradyarrythmias (heart block),
tachyarrythmias (atrial fibrillation, atrial
flutter, ventricular fibrillation) 4-
Obstructive disorders pulmonary embolism PE,
tension peneumothorax, pericardial tamponade,
constrictive pericaditis, severe pulmonary
hypertension
23

• Signs and symptoms Dyspnea, rales, gallop, low
  BP, oliguria
• Monitor/findings CXR pulmonary venous
  congestion, elevated CVP, Low CO.
• Treatment this will be according to cause eg
• Congestive heart failure CHF diuretics
  vasodilators /- pressors.
• Left ventricular LV failure pressors
  , decrease afterload, intraaortic ballon pump
  ventricular assist device.

24
Neurogenic Shock Mechanism Loss of autonomic
innervation of the cardiovascular system
(arterioles, venules, small veins, including the
heart) Causes Spinal cord injury Regional
anesthesia Drugs Neurological disorders
25
Characterized by loss of vascular tone
reflexes.Signs Hypotension, Bradycardia,
Accompanying Neurological deficits. Treatment
IVF, vasoactive medications if refractory
26

• Anaphylactic shock
• This type occurs due to binding of a foreign
  antigen to immunogloin E (IGE) on the mast cells
  and basophils , releasing large amounts of
  histamine and SRS-A ( slow-release
  substance-anaphylaxis) which will produce
  bronchospasm , laryngeal edema and respiratory
  distress with hypoxia , massive vasodilatation
  hypotension and shock.This type occurs on
  exposure to penicillin , anesthetic drugs , serum
  injections and stings .

27
Monitoring of shock
1-General monitoring Heart rate Breathing
28
Monitoring of shock
2.Colour and temprature of skin
29
Monitoring of shock
3.BP
Systolic Pressure was lower than 12kPa(90mmHg)
4. Urina
Oliguria
30
Monitoring of shock
Special monitoring 1.CVP
5-10cmH2O
CVPlt5cmH2O Inadequecy of blood volume
CVPgt12cmH2O Cardiac dysfunction
2.Lung arterial pressure 3.Cardiac
output 4.Blood gas PO2
75-100mmHg
Pco2 40mmHg
PH 7.357.45 5.Coagulation
test
31
(No Transcript)
32
Treatment of the shock
Position of Body 30?
33
TRUE OR FALSE shock in intestinal obstruction
is multifactorial .