2. • “ ACUTE CIRCULATORY FAILURE “
with inadequate or inappropriately
distributed tissue perfusion
resulting in generalized cellular
hypoxia
3. • Body’s inability to deliver adequate oxygen to
meet the metabolic demands of the tissues.
• Initially compensated
• Continued presence of an inciting trigger +
body’s exaggerated response
lead to progression of shock
if untreated,irreversible tissue injury
irreversible shock
6. HYPOVOLEMIC SHOCK
• Characterized by fluid loss ( internal / external )
• Decreased preload
Water/electrolyte
loss
plasma
loss
blood
loss
7. CARDIOGENIC SHOCK
• Poor myocardial contractility leading to cardiac
pump failure
• Due to :
CHD
Myocarditis
Cardiomyopathies
Arrhythmias
8. OBSTRUCTIVE SHOCK
• Decreased cardiac output secondary to restriction
of all cardiac chambers
• Due to :
Tension pneumothorax
Pericardial tamponade
Pulmonary embolism
Anterior mediastinal masses
Coarctation of aorta
9. DISTRIBUTIVE SHOCK
• Caused by inadequate vasomotor tone
Capillary leak
Maldistribution of fluid into interstitium
• Post-spinal cord or brainstem injury
Anaphylaxis
Poisonings
10. SEPTIC SHOCK
• Complex interaction of
distributive,cardiogenic and hypovolemic
shock
• Bacterial/Viral/Fungal
11. Hypovolemic shock – blood VOLUME
problem
Cardiogenic shock - blood PUMP
problem
Distributive shock – blood VESSEL
problem
13. COMPENSATORY MECHANISMS
• >> Heart rate
• >> Stroke volume
• >> Vascular smooth muscle tone
• >> O2 extraction from the blood
• Redistributing blood flow to
brain,kidneys,adrenals and heart at the
expense of skin and GIT
14. To compensate for the metabolic acidosis,
- >> RR with >>CO2 elimination
- Renal excretion of hydrogen ions
- Retention of bicarbonate ions
To maintain intravascular volume,
- Sodium regulation through RAAS
- ADH secretion
- Cortisol and catecholamine synthesis and release
23. TREATMENT
GOAL – RESTORE CIRCULATING VOLUME AND TISSUE
PERFUSION , CORRECT THE CAUSE
1.Assess airway
2.Administer oxygen
3.Establish IV access
4.Fluid bolus of 20ml/kg isotonic fluid given
5.Continue fluid boluses (maximum of 3) until
perfusion improves or hepatomegaly develops
6.In case of shock refractory to fluids,start
inotrope (dopamine)
24. CARDIOGENIC SHOCK
PATHOPHYSIOLOGY
Impaired pumping ability of LV
Inadequate systolic emptying of LV
>>LV filling pressure
>>Left atrial pressure
<< Stroke volume
<< CO
>>Pulmonary capillary pressure
Pulmonary interstitial and intralveolar edema
26. TREATMENT
GOAL - >> CO, treat reversible causes, <<
myocardial workload
1.Assess airway , administer
oxygen/mechanical ventilation
2.IV access
3.Inotropic agents,vasoactive drugs to >>
cardiac contractility and to decrease
systemic vascular resistance
27. 4.Cautious administration of fluids
(5-10ml/kg boluses over longer time)
5.Morphine to decrease preload and
anxiety
6.Vasodilators for afterload reduction
7.Short acting beta blockers for refractory
tachycardia
29. CLINICAL PRESENTATION
• Muffled heart sounds
• Distended neck veins
•Pulsus paradoxus ( << in SBP by
more than 10mmHg on inspiration )
• Signs of right heart failure plus
cyanosis,tachycardia,hypotension
PERICARDIAL
EFFUSION
PULMONARY
EMBOLISM
30. TREATMENT
• Pericardial drainage in case of
pericardial effusion
• Immediate needle decompression then
thoracostomy for chest tube in case of
tension pneumothorax
• Anticoagulants or embolectomy for
pulmonary embolism
31. DISTRIBUTIVE SHOCK
Some tissues inadequately
perfused
(splanchnic circulation)
Some tissues
over perfused
(skeletal muscle,
skin)
PATHOPHYSIOLOGY
Maldistribution of blood flow
37. DEFINITIONS
SIRS
• Requires 2 of the following 4 features to be
present:
o Temperature >38.5° or <36.0° C
o Tachypnea >2SD ABOVE NORMAL FOR AGE
o Tachycardia >2SD ABOVE NORMAL FOR AGE
o WBC ELEVATED OR DEPRESSED FOR AGE/>10%
IMMATURE NEUTROPHILS
38. INFECTION
• Suspected or proven infection or a clinical
syndrome associated with high probability
of infection
SEPSIS
• SIRS plus a suspected or proven infection
39. SEVERE SEPSIS
• Sepsis plus organ dysfunction,hypoperfusion
or hypotension
(including but not limited to lactic
acidosis,oliguria,acute mental status changes)
40. Identifying Acute Organ Dysfunction as a
Marker of Severe Sepsis
Tachycardia
Hypotension
CVP
PAOP
Jaundice
Enzymes
Albumin
PT
Altered
Consciousness
Confusion
Psychosis
Tachypnea
PaO2 <70 mm Hg
SaO2 <90%
PaO2/FiO2 300
Oliguria
Anuria
Creatinine
Platelets
PT/APTT
Protein C
D-dimer
41.
42. MODS
• Presence of altered organ function such that
homeostasis cannot be maintained without
medical intervention
43. WORK UP
• Laboratory studies
o CBP
o Comprehensive chemistry panel (serum elec,abg,BUN,serum
creat,GRBS,LFT,serum lactate)
o Coagulation studies
o Blood & urine cultures
• Imaging studies
o Chest radiography
o Abdominal radiography
o Others according to the suspected cause.
45. •Antibiotics should be administered within the first hour of
recognition of septic shock
• Selection of antibiotic agents is empirically based on
an assessment of patient's immunity
the potential source of infection
the most likely responsible organisms.
•Antibiotic choice must be broad spectrum, covering gram-positive,
gram-negative, and anaerobic bacteria when the source is unknown
•Regimen for septic shock of unknown cause is
oGentamicin
o3rd generation cephalosporin
o if pseudomonas is suspected,ceftazidime
46. • Vancomycin must be added if resistant
staphylococci or enterococci are suspected.
• If there is an abdominal source, a drug effective
against anaerobes should be included
“metronidazole”
• Antibiotics are continued for at least 5 days after
shock resolves and evidence of infection subsides
• Abscesses must be drained and necrotic tissues
(eg, infarcted bowel) surgically excised.