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3rd Year Students´ Lecture
Pathophysiology
Shock is a cardiovascular derangement.
Definition:
A 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.
Changes:
1. Delivery oxygen and metabolic substrates
2. Removing products of cellular metabolism
3. Thermoregulation
Cellular physiology
•Cell membrane ion pump dysfunction
•Leakage of intracellular contents into the extracellular space
•Intracellular pH dysregulation
Resultant systemic physiology
•Cell death and end organ dysfunction
•MSOF and death
Etiology of
shock
example
CVP
CO
SVR
VO2 sat
preload
hypovolemic
low
low
high
low
contractility
cardiogenic
high
low
high
low
afterload
distributive:
Hyperdynamic Septic
Low/High
High
Low
High
Hypodynamic Septic
Low/High
Low
High
Low/High
Neurogenic
Low
Low
Low
Low
Anaphylactic
Low
Low
Low
Low
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Primarily cardiac origin
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Sudden cardiac death (SCD)  arrhytmias
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ischaemic (with or without MI)
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cardiomyopathy (DCM)
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drugs and toxins (cocaine  first cause in youngs!)
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electrophysiological (Long QT sy.)
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cardiac pump failure
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diminished preload (haemorrhage, tamponade, etc)
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excessive afterload (pulmonary embolism)
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decreased contractility (AMI, electrolyte / acid base, etc)
Secondary cardiac arrest events
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hypoxia
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drawning ( vagal reflex  asystolia AND/OR hypoxia)
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severe asthma ( right heart failure AND/OR hypoxia)
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suffocation (foreign body, blood, vomitus, etc)
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multiple organ failure (MOF)
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anaphylaxia ( diminished preload)
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hypothermia ( asystolia OR VF)
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
State of unconsciousness from which patient cannot be aroused
Unconsciousness = Immediate Life Threat
 Loss of breathing
 Aspiration
 Asystolia
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Possible causes
Not enough oxygen
Not enough energy
Not enough blood flow to deliver O2, glucose, FFA…
Direct brain injury
 Structural (trauma)
 Metabolic (toxins, infections, temperature)
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Glasgow Coma Scale: GCS
Verbal
Max 15
Min 3
Motor
Oriented
5
Confused
4
Inappropriate
3
Incomprehensible
2
None
1
Obeys Commands
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Localizes
5
Eye Opening
Withdraws
4
Spontaneous
4
Abnormal Flexion
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To Speech
3
To Pain
2
None
1
Abnormal Extension
None
2
1
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Damage of portion of brain due to interruption of blood supply
Mechanisms
Thrombosis - Blockage of vessel by thrombus

Usually forms at area narrowed by atherosclerosis

Typically in older persons
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Frequently occurs during sleep
Hemorrhage - Vessel ruptures

Associated with hypertension, aneurysms of cerebral blood vessels
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Usually characterized by
H
Sudden onset
H
Severe signs, symptoms
Embolism - Blood clots, plaque fragments travel through vessel; lodge, block flow
Often associated with:
H Atherosclerosis of carotids
H Chronic atrial fibrillation
Alterations in consciousness
H Altered behavior
H Confusion
H Dizziness
H Coma
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Major cause of morbidity and mortality in children
Leading cause of death in children > 1 yr is trauma
Head injuries responsible for most trauma deaths
Adverse outcomes result from
 Primary injury
 Result of mechanical forces producing tissue deformation at the
moment of injury
 Secondary ischemic injury
Associated with post injury hypotension, hypoxemia, and intracranial
hypertension
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

•
first recorded in bombing of London during WWII: 5 people who were
crushed presented in shock with swollen extremities, dark urine.
Later died from renal failure.
5-35% of patients with rhabdomyolysis develop ARF
• mortality is 3-50%
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Acute renal failure (ARF) is a rapid deterioration in renal function
characterized by progressive azotemia.
Azotemia - high blood conc. of nitrogen waste products
ARF is differentiated into 3 major categories
 Prerenal, Intrarenal, Postrenal
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
Failure in one or both gas exchange functions: oxygenation and carbon
dioxide elimination
In practice:
PaO2<60mmHg or PaCO2>46mmHg
Derangements in ABGs and acid-base status

Hypercapnic v Hypoxemic respiratory failure
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ARDS and Acute Lung Infection
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Hyperglycemia
 Increased hepatic production of glucose.
 Diminished glucose uptake by peripheral tissues
 Insulinopenia/hyperglucagonemia
Ketoacidemia
 The ketoacid is acetoacetic acid. Byproduct is acetone. The non-keto acid is
beta-hydroxybutyric acid
 Increased lipolysis and hepatic ketogenesis
 Reduced ketolysis by insulin-deficient peripheral tissues
Fluid and Electrolyte Depletion
 Osmotic diuresis and dehydration due to hyperglycemia
 On average, water deficit is about 5L, sodium 500mmol, potassium 400mmol,
chloride 400mmol.
Initial presentation of Type 1 Diabetes (Can also occur in type 2 diabetics)
Increased insulin requirements in Type 1 diabetics (Infection, trauma, myocaridial
infarction, surgery)
Mortality 5% in patients under 40. Up to 20% in elderly.
Estimates of 5-8 episodes per 1000 at risk diabetics annually.
One of the more common serious complications of insulin pump users – occurring
1 per 80 months of treatment. Typically due to unrecognized pump failure.
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Extreme form of thyrotoxicosis.
Occurs with stressful illness, thyroid surgery.
Manifested by marked delirium, severe tachycardia, vomiting, diarrhea,
dehydration, and very high fever.
Mortality rate is high.
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Following stress (trauma, surgery, infection, or prolonged fasting) in
patient with latent insufficiency.
Following sudden withdrawal of adrenocortical hormone in a patient
with chronic insufficiency
Following bilateral adrenalectomy or a functioning adrenal tumor that
had suppressed the other adrenal
Following sudden destruction of the pituitary gland (pituitary necrosis)
or when thyroid hormone is given to a pt with hypoadrenalism
Following injury to both adrenals by trauma, hemorrhage, anticoagulant
therapy, thrombosis, infection, or metastatic carcinoma.
Diagnosis

Weakness, abdominal pain, fever, confusion, nausea, vomiting, diarrhea
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Hypotension, dehydration, hyperpigmentation

Hyperkalemia, Hyponatremia, Azotemia
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ACTH test

Note: More than 90% of serum cortisol is protein bound. Pts with serum
albumin <25g/L have low serum total cortisol levels but normal serum
free cortisol levels and normal adrenal function. Serum FREE cortisol
levels should be used in critically ill patients.
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Definition - Altered mental status with coagulopathy in setting of acute liver
disease. Hepatic encephalopathy occurring within 8 weeks of onset of illness
defines Fulminant Hepatic Failure.
Etiology

Viral, toxic

Cardiac
Metabolic Considerations

Hypoglycemia -- decreased hepatic glycogen stores, impaired
gluconeogenesis results in hyperinsulin state and insulin resistance. There is
impaired glucose homeostasis and hypoglycemia.

glucagon, insulin secondary to decreased hepatic clearance, leads to
decreased insulin/glucagon ratio, which favors catabolism.
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Aromatic amino acids are increased, probably because of decreased hepatic
clearance.

Branch chain amino acids are cleared into skeletal muscle and are not
elevated, so AAA > BCAA

AAA and BCAA compete for entry to CNS. AAA, particularly tryptophan is
converted to serotonin and other possible false neurotransmitters.
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Etiology

excessive alcohol intake over many years
- 70%

biliary disease

idiopathic
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miscellaneous: metabolic (diabetic ketoacidosis, pregnancy, end-stage
renal failure, hyperipidaemia)

mechanical (posttraumatic, postERCP, penetrating DU)
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infectious (mumps, EBV, HIV, HBV)

vascular (SLE, TTP, shock)
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drugs ( thiazides, oestrogens, salicylates, paracetamol etc.)

toxic
Protective mechanisms:
containtment within storage garnules
potent enzyme inhibitors
production of enzymes in an inactive form
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