cRIT CARE Flashcards
What is pulse pressure?
Difference between systolic and diastolic
Represents force of the heart
Low - reduced stroke volume as preload decreased
Compartment syndrome
increased pressure within a closed osteofascial compartment, resulting in impaired local circulation and necrosis of muscle
Rhabdo tx
- Fluid resuscitation: Ensure good hydration to support urine output > 300 ml/h using IV
crystalloid until myoglobinuria has ceased. - Diuretics, e.g. mannitol, may also be used.
- Alkalinisation : Sodium bicarbonate infusion has been used to limit myoglobin- induced
tubular injury in the presence of acidic urine. It alkalinises the urine >
6.5 pH.
Preload
End diastolic volume of the ventricles
Regulation of BP
Short term - Baroreceptors (sensors located in the carotid sinus or aortic arch), sensing blood pressure via stretch .
Angiotensin II
Vasocontrictor
increases sodium reabsorption
Fasciotomy
Anterolateral - 15-20cm incision anterior to shaft of fibula. LM -TT - careful of SPN
Posteriomedial - 15-20cm incision, MM- TT
Pancreatitis station - management
I will resuscitate this patient by giving him a fluid bolus and providing analgesia!!
Nutrition
fluid
Cause of retroperitoneal bleeding
AAA, pancreatitis
Which factors stimulate pancreatic secreation
Vagal, secretin, CCK, gastrin
Pathogenesis of pancreatitis
Duct obstruction -> premature activation of pancreatic digestive enzymes -> autodigestion -> trypsin -> increase in vascular permeability
Why NJ tube feeding in pancreatitis
Passes duodenojejunal flexure - prevents CCK being released
Transmission of pain
1st order - Nociceptors -> alpha fast, delta slow
2nd order - spinal cord - spinotholamic tract
3rd order - primary somatosensory cortex - thalamus
ADH
released due to increase serum osmalirity and decreases in volume
Afterload
Pressure heart must work during systole
Signs of As
Ejection systolic murmur
Pardoxical splitting of S2
narrowed pulse pressure
CPP
Systemic diastolic arterial pressure - LVED Pressure
Hypocalcemia signs
Paraesthesia, tetany, larygospasm, seizure, confusion
QT prolongation, bradycardia, dilated cardiomyopathy
Hypercalcemia ECG
Short QT, Wide T, ST elevation, prominent U
How is CO2 carried in the blood
Bicarbonate
carboxyheamoglobin
dissolved
ABG - resp acidois compensation
- cellular bicarb - small amount
- renal - takes 3-5 days
Clinical markers of cardiac index
Pulse rate, systolic BP, CRT, Temp, urine output
what are the different types of pelvic fractures
Young Burgess
- Lateral compression
-Anteroposterior compression
- Vertical shear
What is inside a neutrophil
lysomal granuals
How do neutrophils bind
Margination - adhesion - transmigration - migration
What is cerebral perfusion pressure?
Net pressure gradient causing blood flow to the brain
CPP = MAP - ICPSV
Why does dilation occur in raised ICP?
Uncus of the temporal lobe of brain herniates through the tentorium cerebelli
occulomotor nerve compresed
parasympathetic paralysis
unopposed sympathetic - mydriasis
Burns:
How do you assess adequacy of fluid?
- Clinical measures of cardiac index
- Central venous pressure - reflection of right heart
- Hemotocrit
Types of burns
Superficial
- Dry, red, no blisters, pain , brisk CRT
Superficial partial thickness
- moist, red/pink, blisters, sluggish
Superfical deep
-moist, blotchy, pain, no CRT
Full thickness
- dry, black, no pain, no CRT,
Why no colloids in burns
Burns can lead to capillary leak
colloids leak into extravascular space, exerts oncotic pressure and triggers third space loss
What is cushings response?
physiological nervous system response (mixed vagal and sympathetic stimulation) to an elevated ICP that results in cushing’s triad.
Increased sytolic bP and widened PP
Bradycarida
irregular bretahing
Raised ICP clinical picture
Headache
N+V
Papiloedema
Dilated pupil - occulomotor
Lateral gaze - abducens
What are the effects of raised ICP?
Decreased CPP - ischemia
Midline shift - ventricular outflow obstruction
Herniation - occulomotor damage
compression of medulla - ventilation
Difference between neurogenic and spinal shock?
Neuorgenic is a form of distbutive shock - autonimic dysfucntion - lack of sympathetic
This leads to hypotension, bradycardia and vasodilation
spinal shock - transient
Loss of sensormotor
physiological repsonse - can improve
lack of reflexes and muscle
some featurres of neuor shock - bradyacraida and hypotension
Function of potassium
Fluid balance
nerve impulse function
muscles function
cardiac muscle function
Homeostasis of potassium
Potassium = intracellular
Na/k pump - insulin
Na/k - DCT- Aldosterone
Acid base stasis of blood
hyperkalemia on heart
Depolirasation of resting membrane -> BRADYCARDIA -> Cardiac arrest, decrease action potential
High urine output post AKI
Initially reduced GFR, then recovers, distal tubules do not recover - plasma filtered at glomerulus is not reabsorbed - extreme polyuria
Chronic renal failure and anaemia
Reduced production of EPO
Circulating bone marrow toxins -> bone marrow supression
ureamia increases cell wall fragidity
What leads to an increase in Aldosterone
Increased angiotensin ii
reduced sodium
Increased potassium
Counter current
Thick ascending limb imperable to water -
Stages of wound healing
- Heamostasis - vasoconstriction, platelets, activation of cascade
- inflammation - neutrophils
- inflammation - macrophages
- proliferative - fibroblasts , epitherlisation
- maturation, remnodelling
How does vascular surgery interfere with heamostasis?
Easier platelet activation, higher fibrinogen, shutdown of fibrinolysis
What is DIC
Pathological consumpative coagulopathy due to activation of the coagulation and fibrolynitc system. This leads to formation fo mico thrombi and consumption of clotting factors and fibronogen.
Signs of DIC
- Widespread heamorrhage
- Thombocytopenia , decreased fibrinogen and increased FDP
What is necrotising facsitis
Necrotising fasciitis is a life-threatening rapidly-progressing infection that spreads along the fascial planes and subcutaneous tissue.
fever
pyogenes -> IL1 and TNF alphas -> prostaglandin in hypothamus -> fever
Crystalloids
Water soulable moleulces
Colloids
Contain larger insoluable molecules
Why no colloids in trauma
in SIRS - Endothelial dysfunction - capillary leak.
colloids can seap through and pull out water
What is MAP?
Average arterial pressure mainatined throughout a cardiac cycle
Compents of TPN
Water, carbohydrates (50%), lipids (30%), proteins, vitamins, nitrogen, trace elements
Negatives of complete carbohydrate feed
glucose intolerance: as part of the stress response, critically unwell patients are often in a state of
hyperglycemia and glucose intolerance.
- Fatty liver: the excess glucose occurring as a consequence of the above is converted to lipid in the liver
- Respiratory failure: the extra CO2 released upon oxidation of the glucose may lead to respiratory failure and increased ventilatory requirements
- Relying solely on glucose may lead to a deficiency of the essential fatty acids.
How would you manage hypovalemic shock
- Fluids and bloods
- Control bleeding - pelvic binder, stabilising fractures, laparotomy
Pathophysiology of ARDS
- An acute phase, characterized by
1) Widespread destruction of the capillary endothelium, extravasation of protein-rich fluid and interstitial
edema
2) Migration of neutrophils and extensive release of cytokines
3) The alveolar basement membrane is also damaged, and fluid seeps into the airspaces, stiffening the
lungs and causing ventilation/perfusion mismatch. - A later reparative phase, characterized by
4) Fibroproliferation, and organization of lung tissue.
5) If resolution does not occur, disordered collagen deposition occurs leading to extensive lung scarring.
Portal HTN
Cirrhosis resulting from chronic liver disease and is characterized by liver cell damage, fibrosis and nodular
regeneration.
The fibrosis obstructs portal venous return and portal hypertension develops.
* Arteriovenous shunts within the liver also contribute to the hypertension
