A & P 2 - Ap Regulation

Front 1

What are the factors that affect BP?

Back 1

CO = SV x HR

Peripheral resistance (TPR): P / Q

Blood volume

MAP = CO x TPR

Front 2

What is the long term regulation of BP?

Back 2

increase blood volume --> increase BP, increase venous P and VR --> increase EDV and SV --> increase CO --> increase AP --> increase urinary excretion of sodium and water --> lower plasma volume

Front 3

What is the regulation of blood volume by ADH?

Back 3

decrease in blood volume sensed by atria causes release of vasopressin from posterior pituitary

vasopressin:
-potent vasoconstrictor --> increase TPR activating V1 receptors on arterioles
-reabsorption of water --> activates V2 receptors

stimuli for release:
-increase plasma omsolarity detected by central osmoreceptors

Front 4

What is the Renin-AT II-Aldosterone Axis?

Back 4

decrease in renal perfusion pressure causes release of renin from juxtaglomerular cells on afferent arteriole

-angiotensinogen --> angiotensin I in plasma by renin

-angiotensin I --> angiotensin II by ACE in lung

angiotensin II:
-stimulates release of aldosterone and causes vasoconstriction of arterioles (increase TPR)
-aldosterone increases reabsorption of salt, increase salt and water reabsorption increases BP and MAP

Front 5

What is the regulation of BP by ANP?

Back 5

in atria of heart

stimuli:
-response to an increase in atrial pressure

ANP causes dilation of arterioles to decrease TPR

inhibits renin release and causes excretion of water and salt by kidneys

Front 6

What are some circulatory changes during exercise?

Back 6

Vascular resistance:
-decrease in blood vessels that supply skeletal muscles but increase in blood vessels that supply GI tract and skin
-blood flow in brain stays SAME

-increase ejection fraction

-increase SV and CO

-increase HR

Front 7

What are the different types of circulatory shock?

Back 7

circulatory shock - inadequate tissue perfusion and/or inadequate oxygenation of tissues

Hypovolemic:
cause:
-loss of blood and loss of plasma (burns, severe vomiting, diarrhea)
effects:
-decrease circulating blood volume, decrease SV, CO, VR, arterial P
-cold shock - pale and cold skin, hypotension and tachycardia
compensation:
-baroreceptor reflex (activation of SNS)
-increase plasma and hemodilution (renin, ADH, capillary reabsorption)

Cardiogenic:
-insufficient CO despite adequate ventricular filling pressure
causes:
-MI
-cardiac tamponade (excessive pericardial fluid)
-arrythmia
compensation and symtoms:
-similar to hypovolemic

Septic:
-blood poisoning
-most often by gram negative infection
-LPSs released when cell wall degraded
-LPS contains toxic FA with coat
-after release of LPS, TNF and IL 1/6 are released
-high LPS causes systemic vasodilation, diminished cardiac contractility, and endothelial injury

Neurogenic:
causes:
-anasthesia
-brain damage
-fainting (syncope) due to cerebral ischemia
types:
organic:
-pathological
functional (vaso-vagal syncope):
-psychogenic
mechanisms:
-fainting --> decrease SNS
-vaso-vagal syncope ---> excitation of PSNS --> decrease HR --> decrease cerebral blood flow

Anaphylactic:
-Ag-AB mediated (histamine, serotonin)
-lowers BP
-increase capillary permeability

Front 8

What happens in Hypertension?

Back 8

systolic > 140; diastolic > 90

-90-95 % = primary or essential hypertension:
-idiopathic
-increase NaCl uptake, increase ECF volume and CO, increase in peripheral resistance

5-10 % = secondary hypertension:
-obstruction of renal blood flow
-hypersecretion of aldosterone and Adr and NAdr

Front 9

What is Essentail Hypertension and damaging effects?

Back 9

increase TPR always

most of the time - increase CO and HR

chronic stress (SNS) and high Na+ intake act synergistically in development of hypertenson

adaptive response is thickening of arterial wall --> atherosclerosis

kidney not able to properly excrete Na+ and H2O

Damaging effects:
Heart Failure
Kidney Disease
Stroke
Blood vessel damage (thickening of tunica media and acceleration of atherosclerosis and CAD)
silent killer