Shock Flashcards
Define shock
A potentially life threatening condition characterized by inadequate tissue perfusion, resulting in impaired cellular metabolism and functioning
Discuss the pathophysiology relating to the stages of shock
Impaired o2 delivery to cells --> anaerobic metabolism --> lactic acid production / less ATM produced -- > increasing acidosis/loss of cell membrane permeability --> Na/K+ channel pump lost --> fluid shifts --> lysosomal enzymes released --> cell death and organ failure
*also decreased systemic blood flow = intravascular clotting
Identify the classifications of shock
Hypovolaemia
Cardiogenic (pump failure)
Obstructive - (physical obstruction of blood circulation) eg PE, tamponade
Distributive - (systemic vasodilation) septic, anaphylactic, neurogenic
Identify the three types of distributive shock
- Septic shock
- Anaphylactic shock
- Neurogenic shock
What pathophysiology occurs during impaired cellular metabolism
causes impaired oxygen use
- -> anaerobic metabolism
- -> lactate
- -> metabolic acidosis
- -> decreased affinity for haemoglobin
anaerobic metabolism
- -> decreased ATP
- -> Na/K+ pump
- -> increased intracellular Na+ and water
- -> decreased circulatory volume (increases clotting cascade) and cellular oedema causing inflammatory response and release of lysosomal enzymes
The three stages of shock
Compensatory stage:
- Decreased CO stimulates baroreceptors and chemoreceptors –> adrenaline and noradrenaline released
- Blood flow to the heart, lungs and brain maintained –> decreased blood flow to the kidneys –> RAAS activated –> ADH released
- If corrected, pt can recover
Progressive stage:
Compensatory mechanisms fail
Decreased ATP production
Hypoxia of vital organs –> decreased cellular perfusion and tissue ischemia –> failure of NA/K pump, altered membrane permeability –> metabolic acidosis –> decreased CO, myocardial ischemia
Acute renal failure, increased risk of disseminated intravascular dissemination (DIC).
Aggressive management required to prevent MODS
Irreversible/Refractory stage:
- Compensatory mechanisms overwhelmed
- Severe tissue hypoxia - ischemia, necrosis and death of cell
- Build up of toxins
- MODS
- Recovery unlikely
Definition and pathophys of hypovolaemic shock
Caused by a loss of IV volume.
- Decreased preload –> decreased CO
causes. . - SNS activation and catecholamine release increasing SVR and decreasing CO
- stimulates RAAS and interstitial shift which increases volume and increased CO –> stimulates RAAS causing..
decreased CO
decreased tissue perfusion
impaired cellular metabolism
Symptoms of hypovolaemic shock
Tachypnoea Decreased UO Hypotension Weak, thready pulse cool, pale acidosis agitated
Definition and pathophys of cardiogenic shock
Pump failure - cardiac pathology causing inadequate CO and tissue hypoxia
Ineffective forward motion of blood causes
- ineffective vent emptying –> increased pulmonary pressures –> APO –> decreased oxygenation
- decreased SV, decreased CO, decreased cellular O2 supply
Ineffective tissue perfusion –> impaired cellular metabolism
Decreased CO causes
- catecholemine release
- RAAS activation
Clinical manifestations of cardiogenic shock
- possible APO/crackles
- increased WOB/tacypnoea
- tachycardia
- arrhythmia’s
- hypotension
- weak pulse
- cool, clammy skin
- Increased CVP, distended neck veins
- peripheral oedema
- decreased urine output
- elevated lactate
- agitation
Definition and pathophysiology of obstructive shock
A blockage of a major vessel interferes with cardiac output and decreases stroke volume.
Structural compression
- -> decreased venous return
- -> decreased stroke volume
- -> decreased CO
- -> decreased cellular O2 supply
- -> deceased tissue perfusion
- -> impaired cellular function
Definition and pathophysiology of distributive shock
Excessive vasodilation and impaired distribution of blood flow (problem with systemic vascular resistance)
warm and in shock + wide pulse pressures = distributive due to vasodilation
Definition and pathophysiology of anaphylactic shock
Systemic hypersensitivity reaction - IgE mediated gross immune/inflammatory response
allergen molecules enter blood stream –> bind to mast cells –> allergen binds to mast cell –> mast cells degranulate and release histamine, prostaglandin, leukotrines, chemokines
histamine binds to h1 receptor site in endothelium, causing increased vasodilation and increasing cap membrane permeability causing fluid shifts to interstitial space and widespread oedema
adrenaline binds to adrenergic receptors in the epithelium stopping the effect of histamine
Clinical manifestations of anaphylactic shock
Angioedema Stridor Hypotension Abdo cramps Diarrhoea Flushing Urticaria
Definition and pathophys of neurogenic shock
occurs from lesion (C5 or above) on the spinal cord disrupting the CNS or drugs - increased parasympathetic tone
- results in massive vasodilation without compensation
Disruption of SNS –> loss of sympathetic tone –> bradycardia and vasodialation –> decreased BP and venous return –> decreased SV and CO –> decreaesd O2 supply –> decreased tissue perfusion –> impaired cellular metabolism
