hypotension Flashcards
PO 1.48
cardiovascular response to hypovoleamia and haemorrhage
hypotension definition
- <90systolic or <60 diastolic, a 20% fall in mean or systolic BP
- significance – decreased blood flow and O2/nutrient delivery to organs and removal of waste, unable to meet metabolic demands
PO 1.48
cardiovascular response to hypovoleamia and haemorrhage
Causes and classification of hypotension
SVR
MAP = CO x SVR CO = SV x HR
Decreased SVR:
• Reduced vascular tone
• Patient: SIRS, Septic shock – bacterial endotoxins (lipopolysaccharide) activates inflammatory cascade. Cytokines produced (TNF, interleukins) and XS NO – vasodilation
• Surgical - Spinal cord injury removes sympathetic tone
• Anaesthetic – residual agents, intrathecal opioids (sympathetcomy), histamine from morphine
Impaired vasoconstrictor response to baroreceptor
• Drop BP when stand or exercise
• Autonomic neuropathy in diabetes
PO 1.48
cardiovascular response to hypovoleamia and haemorrhage
Causes and classification of hypotension
CO
Decreased HR
- Patient – BB, Ca++ channel blockers, sick sinus, AV block, Sinus brady, vasovagal
- Surgical – sympathetic cervicalthoracic ganglionic injury
- Anaesthetic - Neostigmine
Decreased SV
• Decreased preload
- Patient – fasting, bowel prep, pregnant, standing
- Surgical – haemorrhage, dehydration in lights, evaporation (open > laparoscopic), 3rd spacing, pulmonary thrombus
- Anesthetic – inadequate replacement, venodilation, head up
• Decreased inotropy
- Patient – age, past MI, systolic failure, cardiomyopathy, autonomic dysfunction, hypcalceamia
- Surgical – cardiac surgery
- Anaesthetic – residual agent, high neuraxial block, sympathetic block from nerve block,
• Increased afterload
- Patient – aortic stenosis, age
- Surgical - ? pneumothorax
PO 1.48
cardiovascular response to hypovoleamia and haemorrhage
compensation - negative feedback cycle
• Involves – arterial and venous constriction, increased HR and inotropy and increased blood volume
Neurohormonal
• Baroreceptor (immediate) increase HR, inotropy, increase SVR (everywhere but heart and brain) and venous tone (mobilizes reservoir) to increase flow to heart and brain at expense of other organs
• Renin-angiotensin-aldosteron and vasopressin (slow)
- Increase blood volume and re-inforce vasoconstriction
• Ability to do each of these depends on cause
- MI – can’t increase HR or contractility as well
- Septic shock – difficult to vasoconstrict
Other
• Chemoreceptors
- increased lactic acid from switch to anaerobic glycolysis to produce ATP
- acidosis makes central and peripheral receptors stimulate sympathetic
- stagnant hypoxia in carotid body stimulates chemoreceptor firing
- brain ischeamia – sympathetic to systemic vasculature
• decreased capillary hydrostatic pressures from decreased post to pre-capillary resistance ratio
- increased capillary resorption – up to 1 L in few hours
- dilutes haematocrit and proteins so decreased O2 carrying capacity and decreased oncontic pressure limits amount u can resorb
- decreased flow to kidneys so goes elsewhere and decreased urine made
- restlessness – increased muscle pump
- delayed is increased plasma protein synthesis by liver
- erythropoietin levels increase (from bone marrow), reticulocyte levels peak at day 10 and red cells restored in 4-8 wks
PO 1.48
cardiovascular response to hypovoleamia and haemorrhage
decompensation - if hypotension severe and prolonged
- If can’t restore BP to adequate level timely or if >40% loss and BP drops again after initial resus
- Mechanisms – positive feedback cycle
Cardiac depression
o If MAP <60mmHg (autoregulation range), decreased perfusion and hypoxia, impairs inotropy so SV and CO drop so further MAP drop
Sympathetic escape
o Decreased MAP, decreased organ blood flow, tissue hypoxia, vasodilation to skeletal muscle and GI tract so big drop in SVR, further decreased MAP
Metabolic acidosis
o From hypotension causing anaerobic acidosis, acid impairs cardiac and smooth muscle contraction, decreases CO and SVR, MAP lower
Cerebral ischaemia
o Activates sympathetic but when cardiovascular centre hypoxic get autonomic depression, sympathetic withdrawal, further MAP drop, more cerebral hypoxia
Rheological factors?
Systemic inflammatory response
o Hypotension and sympathetic vasoconstriction causes increased blood viscosity, microvascular plugging with leukocytes and platelets, DIC, low flow makes RBC’s adhere and increases leukocytes endothelial adhesion, reduces organ perfusion, ischaemia, stimulation of inflammation
PO 1.48
cardiovascular response to hypovoleamia and haemorrhage
treatment
- If from blood loss – replace, may need pressor (adren, norad) to increase SVR via alpha activation, inotrope to stimulate cardiac function via beta (doubutamine)
- If from cardiogenic shock
- B agonists – dobutamine, dopamine
- cAMP dependent phosphodiesterase ihibitors like milronone inhibit cAMP degradation, stimulate heart and dilate arterial vessels to decrease afterload
• septic shock – pressors, fluid, antibiotics
central neuraxial blockade
what happens
compensation and level
prevention of hypotension
Get unopposed vagal tone - decrease BP, HR. Degree depends on level of sympathetcomy
- Venous and arterial tone determined by sympathetic fibres T2 – L1 innervating vasculature smooth muscle.
- T1 – T4 determine heart rate and contractility
If blocked get:
o venodilation, decreased VR
• worse if head up or uterus compresses IVC
• 75% of blood volume pools
o vaso dilation, decreased SVR
• less impact than vendilation
• decreased afterload means increased CO
o decreased HR and contractility if block T1-T4
Level
o Brainstem – inhibit vasomotor centre, nil sym response activated, profound decreased MAP, death
o T1-T4 – high block – can’t increase HR or contractility, compensate by:
- Low pressure baroreceptors – decreased ANP
o Mid thoracic – can get compensation by
- Increased HR and contractiltiy
- Vasoconstriction above level of block
- Venoconstriction to mobilize blood reservoirs in liver lung skin
- decreased GFR, renin, ANII, aldost activation
- ADH release from piuitary
o Sacral – no sympathetic blockade, min effect on TPR
Prevention
o Volume load 10-20ml/kg to compensate venous pooling
o Lie down and lateral tilt if pregnant
o SVR – phenylephrine, ephedrine, adrenaline
o HR contractility – atropine, ephedrine, adrenaline
