2. SHOCK
- Shock is a acute process characterised by
body’s inability to deliver adequate oxygen
to meet the metabolic demands of vitals
organs and tissues.
3. TYPES OF SHOCK
- Hypovolemic shock
- Cardiogenic shock
- Obstructive shock
- Distributive shock
- Septic shock ——— it is often used synonymously with
distributive shock
6. OBSTRUCTIVE SHOCK
● Tension pneumothorax
● Pericardial tamponade
● Pulmonary embolism
● Anterior mediastinal
mass
● Critical coarctation of
aorta
Decreased cardiac output
secondary to direct
impediment to right or left
heart outflow or restriction
of all cardiac chambers
7. DISTRIBUTIVE SHOCK
● Anaphylaxis
● Neurogenic: loss of
sympathetic vascular
tone secondary to
spinal cord or brain
stem injury
● Drugs
Abnormalities of
vasomotor tone from loss
of venous and arterial
capacitance
8. SEPTIC SHOCK
● Bacterial
● Viral
● Fungal
( immunocompromised
patients are at high risk)
Septic shock compasses
multiple form of shock
- Hypovolemic: third spacing
of fluids into extracellular ,
interstitial space
- Distributive: shock with
decreased afterload
- Cardiogenic: depression of
myocardial function by
endotoxins
12. Viral sepsis Influenza virus, entero virus, hemorrhagic virus
group, RSV, HSV, CMV, EBV, VZV, human
Immunodeficiency virus etc.
Fungal Candida, aspergillosis, zygomycetes, etc.
13. COMPENSATED AND DECOMPENSATED SHOCK
● shock,leading to inadequate oxygen delivery to organs and tissues.
Compensatory mechanisms attempt to maintain blood pressure by increasing
cardiac output and systemic vascular resistance (SVR).
● The body also attempts to optimize oxygen delivery to the tissues by
increasing oxygen extraction and redistributing blood flow to the brain, heart,
and kidneys at the expense of the skin and gastrointestinal tract. These
responses lead to an initial state of compensated shock, in which blood
pressure is maintained.
● If treatment is not initiated or is inadequate during this period, decompensated
shock develops, with hypotension and tissue damage that may lead to
multisystem organ dysfunction and ultimately death
14. COMPENSATORY MECHANISMS
● In the early phases of shock, multiple compensatory physiologic mechanisms act
to maintain blood pressure and preserve tissue perfusion and oxygen delivery.
● Cardiovascular compensation - include increases in heart rate, stroke volume,
and vascular smooth muscle tone, which are regulated through sympathetic
nervous system activation and neurohormonal responses
● Respiratory compensation- involves greater CO2 elimination in response to the
metabolic acidosis and increased CO2 production from poor tissue perfusion.
● Renal compensation- excretion of hydrogen ions and retention of bicarbonate
also increase in an effort to maintain normal body pH
15. ● Maintenance of intravascular volume is facilitated via sodium regulation
through the renin– angiotensin–aldosterone and atrial natriuretic factor ,
cortisol and catecholamine synthesis and release, and antidiuretic hormone
secretion
● Despite these compensatory mechanisms, the underlying shock and host
response lead to vascular endothelial cell injury and significant leakage of
intravascular fluids into the interstitial extracellular space
18. Insufficient oxygen at the tissue level
resulting in a shift to less-efficient anaerobic metabolism.
Lactic acidosis
19.
20. PATHOPHYSIOLOGY OF SEPTIC SHOCK
● Septic shock is often a unique combination of distributive, hypovolemic, and
cardiogenic shock.
● Hypovolemia from intravascular fluid losses occurs through capillary leak.
Cardiogenic shock results from the myocardial depressant effects of sepsis,
and distributive shock is the result of decreased SVR.
● The degree to which a patient exhibits each of these responses varies, but
there are frequently alterations in preload, afterload, and myocardial
contractility
21. ● In septic shock, it is important to distinguish between the inciting infection
and the host inflammatory response. Normally, host immunity prevents the
development of sepsis via activation of the reticuloendothelial system along
with the cellular and humoral immune systems.
● The inflammatory cascade initiated by shock can lead to hypovolemia,
cardiac and vascular failure, acute respiratory distress syndrome (ARDS),
insulin resistance, decreased cytochrome P450 activity (decreased steroid
synthesis), coagulopathy, and unresolved or secondary infection.
22. ● Tumor necrosis factor (TNF) and other inflammatory mediators increase
vascular permeability, causing diffuse capillary leak, decreased vascular tone,
and an imbalance between perfusion and metabolic demands of the tissues.
● TNF and interleukin (IL)-1 stimulate the release of proinflammatory and
antiinflammatory mediators, causing fever and vasodilation .
● Proinflammatory mediators include IL-6, IL-12, interferon-γ, and macrophage
migration inhibitory factor; anti inflammatory cytokines include IL-10,
transforming growth factor-β, and IL-4.
23. ● Arachidonic acid metabolites lead to the development of fever, tachypnea,
ventilation–perfusion abnormalities, and lactic acidosis. Nitric oxide, released
from the endothelium or inflammatory cells, is a major contributor to
hypotension.
● Myocardial depression is caused directly by myocardial-depressant factors,
TNF, and some interleukins, and further depressed via depleted
catecholamines, increased β-endorphin, and production of myocardial nitric
oxide.
● This host immune response produces an inflammatory cascade of toxic
mediators, including hormones, cytokines, and enzymes. If this inflammatory
cascade is uncontrolled, derangement of the microcirculatory system leads to
subsequent organ and cellular dysfunction
