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SHOCK OVERVIEW

ALFIANTO MARTIN
Shock : inadequate tissue perfusion resulting in cellular injury.
Impaired cardiac pump, circulatory system, and/or volume can lead to inadequate tissue perfusion à cellular
injury à tissue damage à organ failure à death

Shock recognize by :
• Hypotension : systolic BP < 90 mmHg / MAP < 60 mmHg
• Altered consciousness and or fainting : ↓ cerebral perfusion
• Poor peripheral perfusion : cool peripheries, pallor, early septic shock there may be vasodilation with warm
peripheries, CRT ↑
• Oliguria
• Tachypnea
• Tachycardia à BP = CO (HRxSV) X SVR
STAGES OF SHOCK

1. Initial stage – tissue are under perfused, decrease CO, increased anaerobic
metabolism, lactic acid is building
2. Compensatory stage – reversible. Sympathetic nervous system (SNS) activated
to compensate the decrease tissue perfusion.
3. Progressive stage – failing compensatory mechanism : profound
vasoconstriction from SNS à ischemia à lactic acid production is high à
metabolic acidosis.
4. Irreversible stage – cellular necrosis and MODS occur
• Hypovolemic shock :
blood volume problem
• Cardiogenic shock : blood
pump problem
• Distributive shock : Blood
vessel problem
CLINICAL APPROACH TO SHOCK

• HISTORY : trauma, risk factor for infection, blood loss, MI or pulmonary


embolism, past medical history, medication, allergic history
• Physical :Vital sign, cardiac and respiratory function, extremities, JVP
• Blood test : CBC, creatinine, ureum, INR, PTT, AST, ALT, lactate, troponin,
urinalysis, TSH, glucose
• Microbiology : sputum culture, blood culture, urine culture
• Imaging : CXR, CT-scan, echocardiogram, USG
• ECG
• ABG
MANAGEMENT OF SHOCK

• Address the priority – ABC/CAB


• Monitor vital sign
• Monitor ECG
• Check ABG
• IV fluid & blood transfusion
• Inotropic and vasoactive agent, assisted ventilation, and invasive monitoring.
• Treat for causes : Laparotomy, thrombolysis, pericardiocentensis/ cardiac surgery,
antidotes for certain poison, antibiotic.
HYPOVOLEMIC SHOCK

% Blood Pulse BP LoC Therapy


(volume loss)

0-15% • Causes : blood


< 100 loss & fluid loss120/80
(internal and external)
Normal/ agitated none
(0-750 ml)
15-30% > 100 110/70 agitated I.V fluids
(750-1500 ml)

30-40% > 120 90/75 agitated Fluids + blood


(1500-2000 ml)

> 40% (> 2000 ml) > 140 palpable obtunded Surgery + fluid +
blood
CARDIOGENIC SHOCK

Defined with systolic blood pressure below 90 mmHg or decrease of 30 mmHg mean arterial
pressure, ultimately develop and propagates tissue hypo perfusion which is not responsive with fluid
replacement and secondary due to cardiac dysfunction.

Causes : CAD, systolic and diastolic dysfunction, valvular dysfunction, cardiac arrhythmia.

Management :
• Optimizing cardiac function
Fluids, diuretic, inotropes, vasopressor, and vasodilators.
• Revascularization
fibrinolysis and thrombolytic, PCI, CABG
DISTRIBUTIVE SHOCK

Most common distributive/ vasogenic shock :


• Anaphylaxis à results from widespread systemic allergic reaction to
antigen.
• Sepsis à complex interaction between the pathogen or toxin with host’s
immune system.
• Neurogenic shock à loss or suppression sympathetic tone, most common
ec spinal cord injury.
ANAPHYLACTIC SHOCK

Acute, potentially fatal, multi organ systemic reaction caused by release of chemical mediators from mast
cell and basophil mediated by IgE.

Anaphylactic response
• Circulatory response : vasodilatation, hypotension, tachycardia
• Respiratory compromise : stridor, wheezing, bronchospasm
• Cutaneous manifestation : urticarial, erythema, pruritus, angioedema

Management :
• Airway!!
• Epinephrine
• IV fluid
• Antihistamine
• Corticosteroid
• Inotropes
• Patient education
SEPTIC SHOCK

• SEPSIS à life- threatening organ dysfunction caused by a dysregulated host


response to infection
• Organ dysfunction can be identified as an acute change in SOFA (Sequential Organ
Failure Assessment) score à respiratory, cardiovascular, neurology, liver,
coagulation, kidney function
• Septic shock à a clinical construct of sepsis with persisting hypotension requiring
vasopressor to maintain MAP > 65mmHg, and having serum lactate > 2 mmol/L
(18mg/dL) despite adequate volume resuscitation.
• Most common cause gram negative bacteria à complex interaction between the
pathogen and host’s immune system
NEUROGENIC SHOCK

• Transection of the spinal cord → disruption of sympathetic pathways →


loss of vascular sympathetic tone → vasodilation (typically cervical or
high thoracic lesions
• Evaluation à CT spine (esp cervical, thoracic)
• Treatment
Ø C-spine immobilization
Ø IV fluids: Prior to starting pressors
Ø Vasopressors: Dopamine, norepinephrine.