W.4: Shock syndrome Flashcards
Definition of shock
A physiological state characterized by a significant, systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery and insufficient removal of cellular metabolic products, resulting in tissue injury.
Perfusion: Oxygen, nutrient delivery and CO2 elimination requires 4 things..
- A properly beating heart
- Adequate transport medium, blood and Hb
- An intact functioning vessel system
- A functioning respiratory system
Short term perfusion problems will lead to?
- Syncope
- Orthostatic collapse
- Carotis hyperesthesia
- Electric shock
- Spinal cord injury
Long term perfusion issues leads to?
Shock syndrome
Vessel tone is controlled by
The sympathetic and parasympathetic nervous system
Function of pre-capillary sphincters
They control blood flow through the capillaries in response to oxygen demand of the tissue
Compensated shock
Body is able to compensate and maintain tissue perfusion
Progressive shock
Body begins to loose its ability to compensate - inadequate perfusion begins
Irreversible shock
Cell and tissue damage result in multisystem organ failure leading to death
Shock stage I (potentially reversible)
Low cardiac output or vasodilation (-> compensated hypotension)
Shock stage II (potentially reversible)
Decreased perfusion, major end-organ dysfunction (-> decompensated hypotension) -> microcirculatory failure, endothelial damage
Shock stage III (irreversible)
Cellular membrane injury (-> Cellular death)
Cell death, steps
- Hypoxia -> anerobic met. -> lactic acid accumulation -> Na/K-pump fails
- Ion shift: Na into cell -> brings water with it
- Cell swelling
- Mitochondrial swelling -> no prod. of ATP
- Lysosomes released, cell membrane breaks
- Cell destruction -> tissue death
Some clinical markers of shock (5)
- Brachial sys. BP: <110mmHg
- Sinus tachycardia: >90bpm
- Shock index: RRsys/pulse <= 1 (norm=2)
- Resp. rate: <7 or >29 breaths/min
- Urine ouput: <0.5ml/kg/hr
What is hypovolemic shock?
Classic shock, which is the most common. It is the standard used to compare other forms of shock in differential diagnosis. (Hemorrhagic->blood loss, dehydration->fluid loss)
What is obstructive shock?
- Pulmonary embolism/blocked pulmonary circulation
- Tension pneumothorax/increased intrathoracic pressure
- Cardiac tamponade/pressure on myocardium. Decreased preload.
What is cardiogenic shock?
Heart (pump) failure (40% of myocardium damaged by AMI)
Types of distributive shock (3)
- Neurogenic
- Anaphylactic
- Septic
Neurogenic shock
Spinal cord injury, drug overdose or poisoning which affects nervous systems ability to maintain vascular tone leading to vasodilation.
Anaphylactic shock
Vasodilation and fluid shifting from capillary to cell. Leads to micro clotting and smooth muscle contraction (bronchospasm)
Septic shock
Vasodilation and fluid shifting due to overwhelming infection.
Causes of hypovolemic shock
- Hemorrhage: eg. trauma, surgery, hemothorax, hematoma..
- Fluid loss from GI: Diarrhea, vomiting
- Fluid loss from urinary tract: Diabetes, salt-wasting disorders, adrenocortical insufficiency, diuretics
- Fluid loss from the skin: Excessive burn, skin inflammation
- Internal sequestration of fluid: Loss of volume into the interstitial space or body cavities
E/NE stimulate alpha receptors to cause..
Vasoconstriction
E/NE stimulate beta receptors to cause..
Bronchodilation and cardiac stimulation
Causes of cardiogenic shock
- Impaired pump function
- Myocardial infarction
- Asthma
- Severe acidosis
- Barbiturate intoxication
- Toxins of septic shock
- Valvular stenosis, septal rupture
- Pericardial tamponade
- Pneumothorax
- Embolism
Characteristics of distributive shock
- Normovolemia
- Normotension
- Decreased TPR (generalized vasodilation)
- Increased CO
- Redness, fever
- Increased HR
What happens when we have long lasting hypoperfusion of tissues?
- Accumulation of metabolites
- Decreased peripheral resistance: cerebral ischemia, cardiac ischemia
- Positive feedback mechanisms
Mediators in shock
- Amins (histamine, serotonine)
- Lipids (eicosanoids, PAF)
- Proteolytic cascade (kinin-kallikrein, complement system, clotting factors, plasminogen)
- Cytokines (interleukins, TNF, GCSF, GFs, IFs)
- Free radicals (O2-, NO, lipid and protein peroxides)
Reaction of muscle tissue in shock
Glucose uptake increases, glucose ox. dec. -> pyruvate and lactate release inc., inc. protein degradation -> keton acids
Pathological changes of kidney in shock
Part of MOF (multiple organ failure) because of:
- Vasoconstriction
- Decrease of concentrating ability
- Decrease of the urin quantity
- Degradation of tubular epithel, anuria (failure of the kidney to produce ruin), uraemia (increased urea in the blood)
- Dialysis
Pathological changes of lungs in shock
Part of MOF (mortality 70%), overactivation of immune responses, liquid sequestration in alveola, adult respiratory distress syndrome (ARDS)
Role of adipose tissue in shock
Shock is fatal in obese people, centralization of circulation -> stop flow in adipose tissue -> anaerob metabolism, cell death, reperfusion injury, danger of ARDS
Changes of lipid metabolism in shock
Increased lactic acid, pyruvate, alanin, ketonic acid, fatty acid synthesis
Anaphylactic shock is caused by
- Person exposed to antigen that triggers IgE activated mast cells
- Decreased sympathetic innervation of vasculature caused by drugs (eg. Penicillin) or foods (eggs, nuts, seafood)
