Outline of Lecture
Clinical Case
A 22 years old young man met road traffice accident resulting in profuse bleeding from deep cut in left thigh, fracture neck of left femur resulting in haematoma formation. O/E pulse 110/min, Weak, Skin is cold, BP 80/50 mm Hg
Q-1: What is your diagnosis?
Q-2: What is pathophysiology of this condition?
DEFINITION
Profound hemodyamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate perfusion of vital organs
Shock
“Transition between life and death”
Failure to oxygenate & nourish the body adequately
Mortality > 20%
Pathophysiology
Shock affects mitochondria first
Without oxygen mitochondria convert fuels to lactate → lactic acid
Failure of the krebs cycle
Oxygen is the final electron accepter to form water
Lactic Acid
Early shock
Skeletal muscle and splanchnic organs 1st affected
Lactic acid production
Resuscitation
Pyruvate delivery from glycolysis can overwhelm krebs cycle
Systemic Response
Decreased vascular wall tension increases sympathetic stimulation (blocked in sepsis)
Increased epi, norepi, corticosteroids, renin, and glucagon
Increased glycogenolysis and lipolysis
Increased glucose and FFA’s to TCA can overwhelm it
Immune Response
Neutrophil and macrophage activation due to hypoxia
Enzymatic organ damage
Capillary plugs causing microischemia
TNF and Interleukins released
Types of Shock
Cardiogenic (intracardiac vs extracardiac)
Hypovolemic
Distributive
sepsis****
neurogenic (spinal shock)
adrenal insufficiency
anaphylaxis
Cardiogenic Shock, intracardiac
Myocardial Injury or Obstruction to Flow
Arrythymias
valvular lesions
AMI
Severe CHF
VSD
Hypertrophic Cardiomyopathy
Presentation of Cardiogenic Shock
Pulmonary Edema
JVD
hypotensive
weak pulses
oliguria
Cardiogenic Shock, extracardiac
(Obstructive)
Pulmonary Embolism
Cardiac Tamponade
Tension Pneumothorax
Presentation will be according to underlying disease process.
Hypovolemic Shock
Reduced circulating blood volume with secondary decreased cardiac output
Acute hemorrhage
Vomiting/Diarrhea
Dehydration
Burns
Peritonitis/Pancreatitis
Presentation of Hypovolemic Shock
Hypotensive
flat neck veins
clear lungs
cool, cyanotic extremities
evidence of bleeding?
Anticoagulant use
trauma, bruising
oliguria
Distributive Shock
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.
Distributive Shock: Presentation
Febrile
Tachycardic
clear lungs, evidence of pneumonia
warm extremities
flat neck veins
oliguria
Diagnosing Shock
Response to fluids
Echo/EKG
CXR
Evidence of infection
Swan-Ganz Catheter?
Swan-Ganz Catheter
Utilized to differentiate types of shock and assist in treatment response.
Probably overused by physicians. Studies documenting increased mortality in patients with catheters versus no catheters, although somewhat swayed by selection bias.
Swan-Ganz Interpretation
Management
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 60 (1/3 systolic + 2/3 diastolic)
Keep O2 sats >92%, intubate if neccesary
Correction of hypotension
Normal Saline should be administered anytime a patient is hypotensive. If hypotension exists give more NS. ***
If possible give blood as it replaces colloid.
Vasopressors
Inotropic agents for cardiogenic shock
Intra-aortic Balloon Pump for cardiogenic
Autonomic Drugs in Shock
Management of Cardiogenic Shock
Attempt to correct problem and increase cardiac output by diuresing and providing inotropic support. IABP is utilized if medical therapy is ineffective. Catheterization if ongoing ischemia
Cardiogenic shock is the exception to the rule that NS is always given for hypotension NS will exacerbate cardiac shock.
Management of Septic 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
Management of Hypovolemic Shock
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.
Addison’s Disease
Deficiency of cortisol and aldosterone production in the adrenal glands
This is suspected when patient is non-responsive to fluids and antibiotics.
Electrolytes may reveal hyponatremia and hyperkalemia
Hydrocortisone 100 mg IV immediately then taper appropriately
Epidemiology
Mortality
Septic shock – 35-40% (1 month mortality)
Cardiogenic shock – 60-90%
Hypovolemic shock – variable/mechanism
