Cardio 10 Flashcards
Describe intrinsic factors.
- Frank-starlin
-length tension relationship - Preload (SV)
-EDV - Contractility (SV)
- Afterload (SV)
-arterial resistance - HR (contractility)
CO = SV X HR
Describe extrinsic factors.
- Neural control
-ANS - Humoral control
-substances secreted or absorbed into the body fluids
-hormones & locally produced factors that interfere w cardiac function & blood flow
What are the different types of vasoconstrictor agents of humoral control?
- NE & EPI
- Angiotensin II
- Vasopressin or ADH
- Endothelin-1 (ET1)
- Thromboxane A2 (TXA2)
What are the different types of vasodilator agents of humoral control?
- NO
- Histamine
- Bradykinin
Describe NE & EPI as a vasoconstrictor in humoral control.
-released from nerve terminals
-cathecolamines secreted from adrenal medulla
-direct effects on the heart & indirect effects on circulation
>positive chronotropic & ionotropic effect
-vasodilation in some tissues
Describe angiotensin II as a vasoconstrictor in humoral control.
-increase TPR
-decrease Na & H2O excretion by kidneys
>increase arterial pressure
Describe vasopressin or ADH as a vasoconstrictor in humoral control.
-produced by magnocellular neurons that have cell bodies in the hypothalamus & axons in the neuro-hypophysis
-increase BP = imp in hemorrhage
-increase H2O reabsorption from kidneys
>increase blood volume
Describe endothelin-1 (ET1) as a vasoconstrictor in humoral control.
-local chemical signal made by vascular endothelial cells
-increases BP
-vascular homeostasis with other local chemicals like NO
-overproduction = disease -> ‘hypertension’
Describe thromboxane A2 (TXA2) as a vasoconstrictor in humoral control.
-local chemical signal made by platelets
-controls vascular smooth muscle & platelet aggregation
>works antagonistically with prostacyclin
-minimizes blood loss
Describe NO as a vasodilator in humoral control.
-local chemical signal (lipophilic gas) made my endothelial cells & some parasympathetic nerve endings
>relaxes vascular smooth muscle = cause vasodilation in small arteries esp
-stimulus: increase in blood flow velocity
>release of NO = increases diameter of large upstream blood vessels when blood flow increases downstream
increased flow & stress stimulates release of NO
Describe the acute control of local blood flow.
-endothelial derived NO synthase (eNOS or NOS3) = enzymes synthesize NO from arg
>NO diffuses to smooth muscle cell
>activates & increases cGMP
>cGMP activates PKG = vasodilation
>cGMP is degraded by PDE-5
EX: viagra blocks PDE-5 & prolongs vasodilation
Describe histamine as a vasodilator in humoral control.
-local chemical signal made by mast cells in damaged tissue & by basophils in the blood
-released when body is damaged (allergic reaction)
-increases blood flow
-increases capillary porosity
>allows leakage of both fluid & plasma proteins into issue (EDEMA)
Describe bradykinin as a vasodilator in humoral control.
-local chemical signal made by the action of an enzyme (kallikrein) from globulin proteins that are in plasma/tissue fluids
-formed in sweat glands (activated by sympathetic system)
-increased capillary permeability (edema)
-regulates blood flow in inflamed tissues, skin, salivary & GI glands
How do tissues control their own local blood flow according to their needs?
-deliver O2 & nutrients (glucose, amino acids, fatty acids)
-remove CO2 & H+ ions from tissues
-maintain conc of ions in tissues
-transport hormones & others to tissue
How is blood flow to tissues regulated at the min level that will supply the tissue requirements?
-kidneys: large blood flow
-inactive muscles: low blood flow
-tissues dont need lg blood flow all the time (more blood flow than the heart can pump)
-by controlling blood flow = tissues never experience O2 nutrition deficiency
>workload of heart is at min
Describe the rate of the metabolism & oxygen relationship.
-greater the rate of metabolism or less the availability of oxygen = greater formation of vasodilator substances in tissue cells
Describe active hyperemia.
-increase in blood flow in response to an increase in metabolic rate
EX:
>skeletal muscle during exercise
>GI tract during digestion of food
>coronary flow during increase in HR
Metabolic control of blood flow (active hyperemia).
Describe reactive hyperemia.
-if blood supply to a tissue is blocked for a short period of time & then unblocked = blood flow increases
-metabolic blood flow regulation
Reactive hyperemia mechanism.
Active hyperemia X Reactive hyperemia.
Describe blood flow auto regulation. ACUTE
-metabolic control mechanism
-intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure
-increase in arterial pressure= rise in blood flow (less than a min = blood flow returns to normal even though arterial pressure is elevated)
[flow = perfusion pressure/resistance]
-if perfusion pressure decreases to an organ = blood flow initially falls = then returns to normal in the next few mins
independent response from neural & hormonal influences
