Physiology Flashcards
(35 cards)
What factors influence cerebral blood flow?
Defined as the volume of blood per 100g of brain tissue/min
Normal = 50ml/100g/min
—Autoregulation —Cerebral perfusion pressure —CMRO2 —PaO2 —PaCO2 —Drugs used in anaesthesia —Temperature
What are the functions of the stomach?
Range of functions:
—Storage of large meals
—Mixing
—Secretory function: HCl, Gastrin, pepsinogen, Intrinsic Factor
—Hormonal/endocrine: secretion of hormones for GI tract function
—Immune: barrier to infective pathogens
What is myasthenia gravis?
Autoimmune disease with IgG auto-antibodies produced against the nicotinic ACh receptors in the neuromuscular junction.
Symptoms range from ocular, bulbar, respiratory or widespread.
How would you anaesthetise for a mediastinal mass?
Considerations:
—Change from negative pressure to positive pressure ventilation may cause tracheobronchial obstruction
Maintain SPONTANEOUS VENTILATION
—Changes in patient position may compress everything
—Compression of SVC - SVC obstruction
—Indications for anaesthetic (e.g. thymoma = Myasthenia Gravis and considerations for that)
Pre:
—CT/MRI to establish where mass is in relation to airways/vessels
—ECHO
—high dose steroids pre-op (e.g. lymphoma)
Peri:
—Anti-sialogogue
—Gas induction in head up position
—Maintain spontaneous ventilation
—Awake extubation
—If compresses - lateral or prone positioning, use of rigid bronchoscopy may be required
What is aldosterone?
Aldosterone is a mineralocorticoid steroid hormone synthesised in the zona glomerulosa of the adrenal gland to act on the distal tubules/collecting ducts of the nephron to conserve Na/H2O and increase BP
What is insulin?
Insulin is a polypeptide hormone formed in beta cells of islets of Langerhans
Bind to tyrosine kinase receptors to cause increased uptake of glucose into cells
Formed from breakdown of pro-insulin by cleaving C peptide
Released in 2 phases - rapid release from vesicles followed by release as it is synthesised
Released in response to:
—rise in plasma glucose concentration (facilitated diffusion into beta-islet cells)
—adrenaline/beta-2adrenergic activation
Effects are:
—facilitate glucose uptake
—encourage storage of glycogen/fatty acids
—inhibit breakdown of stored glucose
What do we mean by the ‘stress response to surgery’?
Refers to a series of hormonal, inflammatory, metabolic and psychological changes occurring in response to surgery/trauma
—Hypothalamic stimulation causes ACTH, GH, ADH, adrenaline, RAAS
—Immune response: inflammation/cytokines, suppressed T cells
What is glucagon?
A peptide hormone produced in alpha cells in islets of Langerhans
Stimulated by hypoglycaemia and adrenaline
Inhibited by: insulin, somatostatin, ketones/fatty acids
What factors affect cerebral blood flow?
Cerebral blood flow is proportional to CPP and inversely proportional to cerebral vascular resistance
PO2 PCO2 CMRO2 Temperature CPP CVR - anaesthetic drugs
What is the oxygen cascade?
The sequential reduction in PO2 from the atmosphere to cellular mitochondria
How is CO2 transported in the blood?
Bound to bicarbonate
Bound to carbamino compounds (Hb; Bohr shift and Haldane shift)
Dissolved
Describe the control of ventilation
Mainly done by central chemoreceptors
Controlled to maintain homeostasis of pH, PaO2 and PaCO2
Respiratory centre in the brainstem: —Dorsal respiratory group (inspiration) —Pneumotaxic centre —Ventral respiratory group (expiration) —Apneustic centre
Peripheral chemoreceptors (aortic arch/carotid bodies) Central chemoreceptors (ventral medulla)
How is coronary blood flow autoregulated?
Metabolic: H+, K+, CO2 release
Myogenic: stretch
Endothelial: NO, prostaglandin (PGI2)
Autonomic: ANS (minor role)
Hormonal: ANP, Angiotensin II
What factors affect myocardial oxygen supply?
Coronary perfusion pressure (=aortic pressure - intraventricular pressure or LVEDP) Perfusion time/HR Coronary vessel patency Coronary vessel diameter Blood viscosity (haematocrit)
What factors determine myocardial oxygen consumption?
HR Contractility Afterload Tissue mass Temperature
What happens in pericardial tamponade?
Increase in pericardial space causing compression of chambers and haemodynamic instability
Starling’s forces unable to work - decreased output
Due to decreased cardiac filling. Pericardial pressure normally = to intrapleural pressure
When pericardial pressure raised it reduces filling in all 4 chambers
What is the definition of sepsis?
How do we score it?
Dysregulated host response to infection SOFA score (RS, CNS, CVS, Liver, Coagulation, Renal) qSOFA score >1
|Severe sepsis = above, plus organ dysfunction
|Septic shock = hypotension despite fluid resus (25% mortality)
What is cardiac output?
CO = SV x HR
SV = the amount of blood ejected from the ventricle per contraction
Comprises:
—Preload (blood volume, intrathoracic pressure, body posture)
—Contractility (sympathetic stimulation, catecholamines, inotropes, calcium)
—Afterload (SVR, inotropes, intrapericardial pressure)
What are the respiratory differences in a neonate?
—Immature respiratory centre so control not well developed
—Periodic breathing - rate varies; occ apnoeas
—Reduced response to hypercarbia
—Horizontal ribs; flatter diaphragm
—Fewer Type 1 fibres
—Compliant rib cage
—Small diameter airways
Describe the autonomic regulation of cardiac function
Regulated by SNS and PNS
—PNS more rapid control of HR
SNS:
-from T1-T5
-R ganglia influence chronotropy (closer to SAN)
-L ganglia control inotropy (L ventricle and inotropy)
Increases membrane permeability to Ca/Na ->effect on resting membrane potential etc
PNS:
-R Vagus - SAN
-L Vagus - AVnode
Increase membrane permeability to K ->hyperpolarised membrane potential
What is cerebral perfusion pressure?
Determines CBF at extremes of MAP (i.e. outside of autoregulation)
CPP = MAP - ICP
Normal = ~80 - 100mmHg
What is preload?
How can we increase it or decrease it?
The initial length of cardiac muscle fibres before contraction begins
The intraluminal pressure that stretches the ventricle to its end-diastolic dimensions
-related to the diastolic length of the cardiac myocyte
Starling’s law: the force of cardiac contraction depends on the preceding diastolic length of the ventricular fibres - so an increased preload increases SV
Difficult to measure, so LVEDV/P used as a surrogate (depends on compliance)
Affected by: blood volume, intrathoracic pressure, body posture
What is afterload?
How can you increase it/decrease it?
- The stress developed in the LV wall during ejection; reflects the force opposing the shortening of cardiac myocytes
- Resistance the LV must overcome to eject blood
- MAP & SVR reflect LV afterload; can be increased or decreased with vascular tone alteration, intrapericardial pressure or inotropes
- As afterload increases, both the rate and extent of sarcomere shortening decrease, resulting in a reduction in SV
- Governed by SVR; an increase in afterload results in a reduction in SV (as less blood is ejected from the heart per beat, there is a greater volume of blood remaining in the ventricle at end-systole causing greater LVEDV
What is contractility?
The intrinsic ability of the cardiac myocyte to do work for a given preload and afterload
Factors that affect contractility = inotropic
Sympathetics, catecholamines, inotropes
Drugs: inotropes, Ca; milrinone, dobutamine (inodilator - increases inotropy and vasodilates)
