Cardiovascular System III - L08 - 10/07

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Capillary Fluid Exchange - Bulk Flow Definition
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Terms in this set (28)
Capillary Fluid Exchange - Bulk Flow Definition
Filtration/ Reabsorption of fluids and their solutes
Hydrostatic Pressure (P)
Pushing pressure (exerted by water in the blood), due to volume from fluid

Pc = hydrostatic capillary pressure = push fluid out of capillary and into tissue

Pi = hydrostatic pressure in interstitium = push fluid out of tissue and into capillary
Image: Hydrostatic Pressure (P)
Oncotic/ Osmotic Pressure (Ļ€)
Pulling pressure due to solutes

Ļ€c = Capillary oncotic pressure = pulls fluid into capillary out of tissue

Ļ€i = interstitial oncotic pressure = pulls fluid into tissue and out of capillary
Image: Oncotic/ Osmotic Pressure (Ļ€)
Starling forces - Net Filtration Pressure
Relates capillary and interstitial oncotic and hydrostatic pressures to net filtration.

NFP = (Pc + Ļ€i) - (Pi +Ļ€c)

Filtration: (Pc + Ļ€i) > (Pi +Ļ€c); fluid out of capillary

Reabsorption: (Pc + Ļ€i) < (Pi +Ļ€c); fluid into capillary
Describe the difference in starling forces along the capillary
Arteriolar end has greater filtration because it needs to drop of nutrients. The filtration slowly decreases and becomes reabsorption as the capillary progress toward the venous end, where waste products need to be picked up.
Image: Describe the difference in starling forces along the capillary
Mean Arterial Pressure
MAP = CO x TPR

CO = SV x HR
TPR = Total Peripheral Resistance

Use image to test yourself after thorough review
Image: Mean Arterial Pressure
Autonomic Innervation of the CV system
- SNS and PNS both innervate the SA node/AV node but the ventricles are mostly innervated by the SNS

- Only the SNS innervates blood vessels, adrenal medulla, and kidney
Image: Autonomic Innervation of the CV system
ANS Regulation of the Heart

Chronotropy, Inotropy, Lusitropy
Chronotropy: Change in HR Pacemaker potential (SA nodE)

Inotropy: Change in contractility; alterations of intracellular Ca levels

Lusitropy: Rate of relaxation
Image: ANS Regulation of the Heart Chronotropy, Inotropy, Lusitropy
ANS Regulation of the Heart > Chronotropy (SNS & PNS Regulation) > Heart Rate
SNS Regulation: Increases rate of depolarization (slope) at SA node

NEpi binds Ī²1 adrenergic receptors > Gs > cAMP > PKA > ā†‘ Na+ (funny) and Ca2+ (T- and L-type) permeability

PNS Regulation: Decrease rate of depolarization (slope) > hyperpolarization at SA node

Vagal Nerve > ACh binds M2 muscarinic receptors > G inhibitory > ā†‘ K+ permeability & ā†“ T-type Ca + Na (funny) permeability
Image: ANS Regulation of the Heart > Chronotropy (SNS & PNS Regulation) > Heart Rate
ANS Regulation of the Heart > Inotropy & Lusitropy (SNS Regulation) > Heart Contractility
SNS regulation: ā†‘ inotropy (contractility) and ā†‘ lusitropy (speed of relaxation)

Inotropy
Catecholamines binds Ī²1 adrenergic receptors > Gs > cAMP > PKA > Phosphorylates LTCC & RyR (Ca induced Ca from SR) > ā†‘ā†‘ Ca > ā†‘ Contractility ()

Lusitropy
Catecholamines binds Ī²1 adrenergic receptors > Gs > cAMP > PKA > Phosphorylates Phospholamban PLN > Removes inhibition of PLN on SERCA2a > SERCA pumps Ca back into SR > ā†‘ ventricular relaxation speed
SNS (Ī±-AR) Vascular RegulationVasoconstriction - Increase vascular resistance - Increase arterial pressure Venoconstriction - Decrease venous compliance - Increase CBV/ VRSummary of ANS Innervation of CV SystemTest ya selfNeural Reflex Mechanisms in BP Control > Arterial Baroreceptor Reflex (high-pressure receptors) 1. What are they? 2. Location? 3. What do they sense? 4. What is their response?What are they? High-pressure receptors Location? Carotid sinus and aortic arch What do they sense? Arterial stretch (pressure) What is their response? Modulate ANS to maintain blood pressure ā†‘ BP = ā†‘ Firing Frequency ā†“ BP = ā†“ Firing FrequencyDescribe the transmission of the Arterial Baroreceptor signal through ANS regulatory pathwaysNow reverse everything and figure it outNeural Reflex Mechanisms in BP Control > Atrial Baroreceptor Reflex (low-pressure [volume] receptors)Locations 1. Vena Cava 2. Right Atrium 3. Pulmonary Artery Mechano/ Stretch Receptors - Respond to changes in blood volume ADH ā†‘ resorption Renin ā†‘ BPList the components of the Renin-angiotensin system (RAS) and explain how they are formed.Angiotensinogen (Renin)> Angiotensin I (Angiotensin-converting enzyme [ACE])> Angiotensin II > Angiotensin II Type 1 Receptor (AT1R)Describe the stimuli for RAS activation and the multiple roles that the RAS playsGOAL IS TO RAISE BLOOD PRESSURE Activation of RAS 1. Loss of blood volume 2. Drop in blood pressure 3. Decreased filtrate flow rate in glomerulus Ang II Roles 1. Vasoconstriction 2. Retention of Na/ H2O 3. Secretion of Aldosterone 4. Release of ADH 5. Stimulation of SNS 6. Stimulation of thirstExplain the effects and mechanisms of action of antidiuretic hormone (ADH) on blood pressure1. Hypothalamic Stimulation - Hyperosmolarity - ā†“ Atrial Receptor Firing - Ang II - SNS stimulation 2. Signal sent to posterior pituitary to release vasopressin > ā†‘ blood volume and systemic vascular resistance > ā†‘ Arterial PressureAcute Local Control of Blood Flow to OrgansBlood flow through capillary bed when the precapillary sphincters are relaxed Blood flow bypasses the capillary bed when the precapillary sphincters are constricted MAP = CO * TPR Resistance to low is locally regulated by adjusting the radius of arteriolesAcute Metabolic Blood Flow ControlIncreased metabolism = Vasodilation Decreased metabolism = Vasoconstriction - Increased metabolism increases tissue blood flow - Reduced O2 increases tissue blood flowExamples of Acute Metabolic Blood Flow Control > Active HyperemiaIncreased blood flow due to increased tissue metabolismExamples of Acute Metabolic Blood Flow Control > Reactive Hyperemia- Build up of metabolic waste following ischemia - Buildup of metabolic waste leading to vasodilation/ increased flowAcute Autoregulation of Blood Flow & Net EffectAutoregulation: intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure Perfusion pressure is the pressure flowing through an organ Net Effect: Maintenance of near constant blood flow for a particular metabolic levelMetabolic Theory of Autoregulationā†‘ Arterial Pressure > ā†‘ Blood Flow > ā†‘ O2 & Washout of tissue vasodilators > Vasoconstriction > Blood flow returns to normalMyogenic Theory of Autoregulation- Inherent to vascular smooth muscle - Vessel constricts in response to an increase in pressure (ā†‘P = Q x ā†‘R) - Vessel dilates in response to a decrease in pressure (ā†“P = Q x ā†“R)Acute Metabolic Blood Flow Control > Endothelial InfluencesVasodilators 1. Nitric Oxide (NO): Relaxation ā†‘ Flow > activates NO receptors > ā†‘ Ca > activation of cNOS > ā†‘ NO > ā†‘ cGMP > relaxation 2. Prostacyclin (PGI2) - Prevents vasoconstriction - Prevents platelet Arachidonic Acid (COX)> PGI2 > ā†‘ AC > ā†‘ cAMP > vasodilation Vasoconstrictor 1. Endothelin-1 (ET-1) Big-ET-1 (Endothelin-Converting Enzyme)> ET-1 > activates Gq > inc. IP3 > ā†‘ Ca > Vascular smooth muscle contraction Involved in pathogenesis of heart failure, coronary spasm, hypertension, pulmonary hypertensionSummary of Factors Affecting TPRIntegrated Control of Blood Pressure