extra clinical stuff Flashcards
PO 1.48 cardiovascular response to pneumoperitoneum
MAP up or down depending on balance of factors
- vagal stimulation from peritoneal stretch
- gas insuflation can cause sympathetic response
- initial increase VR and CO, later decreased VR and CO
- high pressure causes increased SVR, afterload and catecholamine release
- tachycardia, decreased coronary blood flow, ischeamia
- haemorrhage
- hypercarbia and acidosis when gas absorbed
- venous gas embolism – elevate CVP, arrhythmia, MI, hypotension
PO 1.48 cardiovascular response to PPV and PEEP
o Inspiration increased ITP
• Initially LVEDV increase, so increase SV and CO
• As raised ITP mobilizes pulmonary reservoir
• Venous return decreases due to raised ITP
• RV outflow decrease due to increased resistence and decreased compliance of pulmonary circuit
• Afterload decreases
• LV outflow decreases due to decreased compliance aortic root so increased afterload
• But increased pressure gradient from thorax to abdo means less resistance
• And raised ITP decreases systolic wall tension (because radius decreases and wall thickness increased as its not stretched by blood) which decreases afterload
• ?? overall effect is decreased CO???
o Expiration, decreased ITP
• Initially LVEDV decrease, so decrease SV and CO
• As low ITP decreases pulmonary vascular resistance so increases pulmonary blood volume
• Then increased veous return, decreased RV afterload (due to decreased resistance), so increased LA return, increased LVEDV, SV and CO
o Baroreceptor reflex fights this:
• Low MAP means less firing barorecetpors of carotid sinus, so increased sympathetic activity to increase HR, contractility and vasovenoconstriction to maintain MAP
o PEEP and hypovoleamia exacerbate this effect
• Maintains low VR, adds to pulm vascualar resistance, loose your MAP
PO 1.48 cardiovascular response to surgery and trauma
PO 1.49 cardiovascular changes with aging
AGING- cellular level time dependant post maturity changes, lead to decline in physiological reserve
Heart
o Overall decreased max CO and therefore max O2 delivary due to decreased max SV and HR for following reasons
• Increased LV wall thickness and cardiac mass
• Reduced compliance due to collagen and fibrous tissue deposition
- less diastolic filling
- increased rate of filling and peak in passive filling then 2nd peak from atrial contraction, image 100
• increased preload to maintain SV
- function on flatter part of frank starling
- less cardiac output reserve
- less response to inotropes
- downregulation of B adrenoceptors
- increased basal sympathetic activity
- increased sensitivity to anaesthesia
- normal peak contractile force but prolonged contraction due to impaired calcium pump in SR
- calcific and fibrotic degeneration of conducting pathways
- more likely to get arrhythmia
- slower intrinsic sinus rate but HR preserved with increased sympathetic tone
• valves calficy thicken and dilate
PO 1.49 cardiovascular changes with aging
AGING- cellular level time dependant post maturity changes, lead to decline in physiological reserve
vessels and muscle
o calcification and intimal thickening
• worse if atherosclerosis
• reduced compliance and elastance
• MAP same but pulse pressure widens as systolic increases more than diastolic increases image 101
• Reduced max coronary flow
o Baroreceptors in carotid sinus and aortic arch less sensitive and slower sympathetic response
• Reduced adaptation to hypotension – especially on induction, with standing (may faint due to decreased cerebral perfusion due to slow autoregulation)
• decreased valsalver ratio (fastest:slowest HR)
o reduced endothelial production, smooth muscle response to metabolic vasodilators and bioavailability of NO
• means reduced exercise tolerance as decreased max muscle blood flow
Decreased skeletal muscle mass so decreased venous return via pump
PO 1.50 cardiovascular changes with morbid obesity
- increased total blood volume but decreased ml/kg – from 70ml/kg to 45ml/kg
- increased atherosclerosis so hypertension so increased LV work → LV hypertrophy, myocardial ischeamia, LV failure
- aortocaval compression so decreased VR and CO
- increased risk thromboembolic events
rapid transfusion 1L blood (20% increase blood volume)
Increased blood volume, preload, CO, BP and HR initially
o BP sensed by carotid sinus, venodilation and pooling of blood, decreased VR and CO and BP
- Pressure and metabolic autoregulation adjust resistance to maintain constant tissue blood flow – peripheral vasoconstriction
- Flow = change in pressure/resistance
o Increased capillary hydrostatic pressure means loose some fluid into tissues
o Osmolality and oncotic pressure unchanged so osmoreceptors in hypothalamus (need 1-2% change) and glomerulotubular imbalance do not contribute
o Increased O2 carrying removes stimulus to erythropoietin production, less new RBC’s
Excretion
o Increased BP causes pressure diuresis and natriuresis (even tho autoregulation maintains normal renal blood flow – the pressure is higher) via renal-body (pressure-volume) mechanism
o Low pressure volume receptors mean less ADH from posterior pituitary (happens at 8-10% increased volume)
Rapid transfusion 1L 5% dextrose (Intracellular: extracellular 2:1, interstitial: intravascular, 3:1)
- same increased in volume, CO, BP initially so get initial venous pooling
- BUT has oncotic pressure of zero, drops plasma oncotic pressure:
o Starlings forces means fluid lost to interstitial fluid and glucose taken up by cells
o Distributed in proportion to fluid compartments contribution to total body water (660ml ICF, 340ml ECF [ISF 255 and IVF 85ml]) – 2% (5000ml to 5085ml) increase blood volume
o No haemodynamic change - Volume doesn’t increase enough to activate volume receptors
- End plasma oncotic pressure unchanged
o But osmolality of body from 287mOsm/kg to 280 (2.5%) so osmoreceptors in hypothalamus activated, decreased ADH, half life 15mins so XS volume excreted in urine in 1 hour
rapid transfusion 1 L normal saline
- same increased volume, CO, BP initially
o [Na+] means only distributed in ECF – ¾ ISF and ¼ IVF, so increased IVF 250ml (4 L normal saline = 1 litre blood loss)
o volume increases by 5%, <10% so no activation of low pressure volume receptors and no ADH change
o no change in osmolality so no activation of hypothalamus so no ADH change - excretion – quickest due to immediate glomerulotubular imbalance-
o increased volume drops oncotic pressure (cos no proteins in normal saline) causes glomerulotubular imbalance of kidneys so GFR increases so less H2O and Na reabsorbed in proximal tubule, increased urine immediately
o renal-body (pressure-volume) fluid mechanism slower as body initially minimizes increase in BP but it does increase due to vasoconstriction to keep flow the same – excrete water and Na
rapid transfusion 5% albumin
- same as blood except O2 carrying capacity reduced so tissues must increase flow to meet O2 requirements
o autoregulation – vasodilation
o decreased blood viscosity
anaemia - ho body compensates
- O2 flux equation,Oxygen delivary = CO x [hb] x saturation x 1.34
- how the body compensates
o increase CO and so delivary - from autoregulation causing vasodilation
- from low bp causing Na and H2O retention
- Also get increased myocardial consumption so no good if hb too low
- Limited if also hypovoleamic
o increased oxygen extraction (from increased gradient as low tissue pO2 and increase red cell 23DPG shift ODC to right)
- more unloading at tissues
- o redistribute blood flow to cells where O2 supply more critical
- less to kidneys
o erythropoietin levels increase so get new RC’s
hyperventilation and chest compression
weighlifter syncope
CBF = CPP/CVR
hyperventilation - decreased pCO2, cerebral vasoconstrction, so decreased flow (each 1mmHg decreased pCO2 decreases CBF by 4%)
compression - like phase 2 valsalver, increased ITP, decreased carotid arterial pressure and increased JVP mean further decrease in cerebral blood flow
weightlifter - hyperventilation and valsalver - BP maintained until phase 3 cos muscular activity keeps it up in phase 2
