G4 peripheral and coronary circulation Flashcards
What is the Starling model of fluid equation
Jv = Lp S [ (Pc - Pi) - σ (Πc - Πi) ]; where
What does LpS stand for in the Starling model of fluid equation
- Lp S is the permeability coefficient/filtration coefficient of the capillary surface, and is affected by shear stress and endothelial dysfunction.
◦ It is a product of the hydrolic permability coefficient (Lp) and surface area of the capillaries (S)
◦ High Kf indicates high water permeability
What is the hydrostatic pressure gradient in normal capillary blood vessels
◦ Pc, capillary hydrostatic pressure is usually:
‣ 32 mmHg at the arteriolar end of the cpaillary
‣ 15 mm Hg at the venular end
What affects capillary blood pressure
Systemic blood pressure
Precapillary vasoconstriction - shock states
Veinous obstruction
Posture
What is the normal intersititial hydrostatic pressure>
‣ negative (-5-0 mmHg) in most tissues (except for encapsulated organs, where it is slightly positive, +3 to +6 mmHg)
What modifies capillary hydrostatic pressure?
‣ Affected by anything that modifies lymphatic drainage, eg.:
* Tourniquet
* Immobility, decreased muscle pump activity
* Lymph node removal
* Inflammation, eg burns (where it becomes extremely negative, eg. -20 to -30 mmHg)
Capillary oncotic pressure and its influencing factors? What is the intersitial osmotic pressure?
- Πc - Πi is the capillary-interstitial oncotic pressure gradient
◦ Πc, capillary oncotic pressure = 25mmHg
◦ Affected by the protein content of blood, eg.:
‣ hypoalbuminaemia (eg. liver disease)
‣ Hypoproteinaemia (eg. malnutrition, nephrotic syndrome)
◦ Πi, interstitial oncotic pressure = 5 mmHg
‣ Affected by the protein content of interstitial fluid, which is usually low but which can increase in local inflammation
What is teh reflection ocoefficent
- σ is the reflection coefficient for protein permeability and is a dimensionless number which is specific for each membrane and protein - it modifies the oncotic pressure to reflect the effect leakage of protein across the membrane will have on forces and correct the magnitude of the measured gradient to account for he in effectiveness of some of the oncotic pressure gradient
◦ σ = 0 means the membrane is maximally permeable
◦ σ = 1 means the membrane is totally impermeable
◦ In the muscles, σ for total body protein is high (0.9)
◦ In the intestine and lung, σ is low (0.5-0.7)
What is the balance of the Starling forces?
The balance of these forces is for filtration (20ml/min out; 18ml/min back in) with bulk flow out of the capillary - usually 2-4L of net filtration fluid per day (2mL/min_. This is mobilised back into venous circulation via lymphatics.
How is blood flow regulated?
Explain the main mechanisms by which peripheral circulations autoregulate
- Myogenic
- Metabolic
- Flow related - Proximal vasodialtion, paracrine signalling
- Non metabolic humeral mediators
- Organ specific buffer responses - kidneys, liver, maternoplacental
Explain the myogenic mechanisms of peripheral autoregulation
◦ This is an intrinsic property of all vascular smooth muscle - peripheral circulation control may occur via end organ arteries (muscular arteries) or resistance arterioles
‣ Seen in the brain, heart and kidney in particular, notably not in the skin
‣ E.g. flow maintained constant in cerebral circulation over range of 50-150 mean carotid artery pressure
◦ Vessel wall stretch produces smooth muscle cell depolarisation —>opening mechanical gated calcium channels in response to stretch —> calcium influx —> vasoconstriction by myosin light chain phosphorylation
How is metabolic autoregulation performed? What are potential mediators>
◦ Blood flow increases in response to increased tissue demand, eg. in exercising skeletal muscle; whereby metabolic byproducts which reflect tissue activity have local vasoconstriction/dilation properties
◦ Vasodilation in response to increased demand allows for increased oxygen tissue delivery module to reduced resistance and increased flow
◦ Potential mediators include potassium, hydrogen peroxide, lactate, hydrogen ions (pH), adenosine, ATP and carbon dioxide, endothelin, prostacyclin, nitric oxide
What is non metabolic mediators
Histamine, bradykinin release
◦ Bradykinin - vasodilation in salivary glands, gut and skin ◦ Histamine - released from basophils as a part o the inflammatory response causing vasodilation and increasing flow - can be regional regulation ◦ In contrast locally released serotonin and TXA2 in response to local tissue injury from platelet activation causes vasoconstriction reducing regional flow to a specific area
What is flow related autoregulation
- Flow or shear-associated regulation
◦ This is the phenomenon of proximal vasodilation in response to distal vasodilation.
◦ This shear stress promotes the release of various vasodilatory mediators from the affected endothelium and produces vasodilation of the larger proximal arteriole. - Conducted vasomotor responses
◦ Regional control of one region by the vasomotor events of another neighbouring region.
◦ Mediated by conduction of cell-to-cell signals from a small arteriole upstream to a larger arteriole
Organ specific regulatory mechanisms
- Renal
- Hepatic
- Organ-specific regulatory mechanisms:
◦ Hepatic arterial buffer response:
‣ hepatic arterial flow increases if portal venous flow decreases, and vice versa.
◦ Renal tubuloglomerular feedback
‣ This is a negative feedback loop which decreases renal blood in response to increased sodium delivery to the tubule
‣ The mechanism is mediated by ATP and adenosine secreted by macula densa cells, which cause afferent arterolar vasoconstriction
◦ Maternoplacental blood flow
‣ Blood flow is gradually increased over the course of pregnancy by the actions of the trophoblast asit invades the spiral arteries of the uterus however the vascular bed of the pregnant uterus is generally fully dilated and autoregulation capacity is absent and flow is pressure dependent
Where do the coronary vessels arise from
Sinuses of valsalva above the aortic cusps in the aortic root
Where does the left main arise from
- Left main - from the left posterior coronary sinus above the L cusp of the aortic valve
What are the cusps of the aortic valve
Left, right, anteiror
What are the cusps of the tricuspid valve
anterior, septal and posterior
What are the cusps of the mitral valve
Anterior and posterior
What are the cusps of the pulmonary valve
anterior cusp (AC), the left cusp (LC), and the right cusp (RC).
Describe the apth of the left coronary artery and its branches
◦ Divides into left anterior descending (from which the diagonal and septal branches arise) and left circumflex (runs in AV groove posteriorly) from which obtuse marginal branches arise +/- RCA anastomoses for posterior descending
◦ Supplies most of the septum and LV; 40% SA node by circumflex
What % of people have a dominant SA node supply from left
◦ Divides into left anterior descending (from which the diagonal and septal branches arise) and left circumflex (runs in AV groove posteriorly) from which obtuse marginal branches arise +/- RCA anastomoses for posterior descending
◦ Supplies most of the septum and LV; 40% SA node by circumflex