Cardiopulm_Physiology

Front 1

Increased Sypmthetic Stim from Vasomotor Center to the Heart has what direct result

Back 1

Inc. Symp Tone on Heart increases Phase 4 Depolarization on Heart.
Increased Contractility
---Both of these increase CO

Front 2

How else does Inc. Symp Tone affect Heart--indirectly via vasculature

Back 2

Inc. Symp Tone on Veins causes VasoConst--sends pool to R. Atria=Inc. Preload in Ventricles. =Inc. CO
-Arterioles VasoConst= increases TPR
With BP= COxTPR, BP is Inc extrinsically here (along with Inc in CO seen in last card)

Front 3

What effect does and increase in Arterial Sympathetic Tone have on BP? Describe effect

Back 3

Inc. in Arterial Symp Tone causes VasoCons, thus inc. TPR. Increasing TPR inc. Afterload Since, BP=COxTPR, BP increases

Front 4

How does constriction of Veins affect Contractility? BP?

Back 4

VasoCon milks reserved blood in veins to R. Atria-->Ventricles increasing Preload and SV. Since SV is proportional to Contractility, it too is inc.
CO=SVxHR, so inc SV = inc. CO = inc. BP (BP=COxTPR)
--note, though VasoCon of veins does inc TPR, the volume change is much more important.

Front 5

What is Major effect--via Symp Stim--of Vasoconstriction in Veins? In Arteries?

Back 5

Venous VasoCon = Increases Preload

Arterioles VasoCon= Increase TPR

Both act to inc BP since inc. Preload inc. CO (CO=SVxHR, inc Preload=inSV) and inc. TPR, given BP=COxTPR

Front 6

Sympathetic Stim. of Contractile Tissue causes release of ?? onto which Receptors?

Back 6

Norepinephrine
on Beta 1 receptors

Front 7

Sympathetic Stim. of Vascular Tissue causes release of ?? onto which Receptors?

Back 7

Norepinephrine on
Alpha Receptors

Front 8

Describe Affects of Arteriole constriction in terms of Volume and TPR

Back 8

Large shift in TPR (Afterload)
insignificant shift in volume

Front 9

Epinephrine and Norepinephrine secreted from Adrenal Glands act as Hormones (as opposed to ANS Neurotransmitters) and excite which Receptors?
Effect of these receptors on vasculature?

Back 9

Beta 2 receptors (heart has beta 1)
Cause constriction or dilation
--landing on Alpha receptors on vasc WILL cause Vasoconstriction though, thus, net is likely to be inc BP

Front 10

Above 75 bpm, further increasing HR have what effect on CO?
note: CO=SVxHR usually

Back 10

Marginal to Decreasing
(leading up to 75bpm, inc. HR inc. CO)
Above 75bpm, you compromise preload by infringing on rapid refill phase of ventricles

Front 11

These guys act as brakes when other reflexes are trying to elevate BP to disadv. levels for other organs

Back 11

Low Pressure Baroreceptors
-found in atria and pulmonary Vasc.
-have several diff reflexes

Front 12

How is Flow Calculated?

Back 12

Flow (Q) = delta P / R
= pressure drop across organ/tissue divided by resistance
--usually assume central control maintains BP constant

Front 13

Describe the Myogenic Reflex, with regard to Mechanical Forces on Vessel Wall Tone Locally

Back 13

Increased Pressure--like a bolus--causes vasoconstriction--
--this is counerintuitive, but Local Tiss Organ reads inc. press as unecessary inc. in perfusion to area. To reduce this it constricts.

Front 14

Describe what Shear Stress causes with regard to Mechanical Forces on Vessel Wall Tone Locally

Back 14

Increased Shear Stress causes vasodilation.
ie, drag downstream causes dilation upstream. Accommadation to shear.

Front 15

Increase of: CO2, H+, K+, PO4,
& Dec. of O2 has what metabolic regulatory effect on Smooth Muscle/Wall Tone

Back 15

Causes Vascular Relaxation
Vasodilation. Indicates need to perfuse organ/tissue with fresh blood.
Opp levels cause Vasoconstriction (except in lungs--exact opp for both)

Front 16

When does Reactive Hyperemia occur

Back 16

When an organ/tissue is reperfused after obstruction removed, and accumulation of vasodillator metabolites causes extreme vasodilation

Front 17

Normal Local Response to Inc Metabolites/Dec O2, to perfuse areas with high metabolic demand describes what?

Back 17

Describe Active Hyperemia

Front 18

If you stand up quickly, you may get a dec. in BP, and your vasculature may vasodilate, seeming to further exacerbate dec BP. Describe why this is appropriate

Back 18

This is a Myogenic Reflex, NOT meant to control/alter BP, rather to dec. vascular Resistance so that important organs, such as BRain receive blood flow. NEt effect is to ensure that with BP change, a subsequent inc/dec of tissue Flow does NOT occur due to BP.

Front 19

A sudden Inc in BP stretching Arteriole Walls results in a Local Reflex that Contracts the Smooth Muscle (Vasoconstriction), seemingly inc. TPR. What is going on

Back 19

The Stretched Arteriole recogs unnecessary perfussion to surrounding tissue, so it constricts to maintain Normal Q/Flow. NOT to alter BP via TPR or alter BP at all.

Front 20

What is the clinically negative effect of Myogenic Reflex in a chronically hypertensive patient with regard to smooth muscle.

Back 20

Since this local response is habitually triggered to reduce Flow due to Inc BP, the SM will continually constrict and hypertrophy.

Front 21

If vasodilatic metabolites buildup cause inc. perfusion downstream, causing an upstream inc. in shear stress. WHat effect will this stress have on Wall Tone

Back 21

Will vasodilate to compliment required flow elsewhere. (contrast to Inc. P. causes constriction to maintain current flow in current region)