4 Factors Contibuting to Cardiac Output

• HR
• SV
• TPR
• VR

As HR increases, Filling Time Decreases!

DIGITALIS

• Decrease HR with no direct action on contractility or SV
• But as filling time increases,
• EDV increases
• so SV increases
• according to…...

Venous Return

• Abdomino-Thorasic Pump
• Skeletal Muscle Pump
• Ventricular Diastole
• Ventricular Systole

Total Peripheral Resistance

• Increased TPR ---> Increased Arterial Pressure
• Increases work of heart and length of systole ( esp. isovolumetric phase)
• Decrease SV initially
• Also increases Arterial - Venous DP
• increases amount of blood on venous side
• Increase VR and CO?

How do we resolve this apparent conflict/problem?

• Depends upon ability of ventricles to increase SV
• Consider exercise......

Blood Pressure

BP expressed in mm Hg

BP = CO x TPR

PRESSURE MEASURED BY BARORECEPTORS

• AORTIC ARCH
• CAROTID SINUS

VAGUS NERVE

• PARASYMPATHETIC FIBERS
• BARORECEPTORS FROM AORTIC ARCH
• STRETCH RECEPTORS FROM LUNGS

BARORECEPTORS

• AORTIC ARCH
• CAROTID BODIES

SAMPLE PROBLEMS

HR SV TPR VR CODPPP

ACh

Epi

NE

 

 

CHEMORECEPTORS

• P_O2 RECEPTORS
• CAROTID AND AORTIC BODIES
• BRAIN STEM - MEDULLA
• SENSITIVE TO DISSOLVED O₂
• ONLY IMPORTANT AT LOW P_O2

Carbonic Anhydrase

CO₂ + H₂O <--> H₂CO₃ <--> H⁺ + HCO₃

Lungs Kidneys

CHEMORECEPTORS

• CO₂ & pH
• AORTIC & CAROTID BODIES
• MEDULLA
• CO₂ + H₂O <--> H₂CO₃ <--> H⁺ + HCO₃^-

(AS CO₂ INCREASES, PLASMA & CSF pH DECREASES)

CO₂ DISSOLVES FROM PLASMA INTO CSF ACROSS BLOOD - BRAIN BARRIER

CO₂ + H₂O <--> H₂CO₃ <---> H⁺ + HCO3^-

AS PLASMA CO₂ INCREASES, PLASMA pH DECREASES

CO₂ DISSOLVES INTO CSF, AND CSF pH DECREASES, STIMULATING MEDULLARY RECEPTORS

• INPUTS:
• BARORECEPTORS (PNS)
• CHEMORECEPTORS (CNS & PNS)
• ATRIAL VOLUME RECEPTORS
• CEREBRAL CORTEX
• VASOVAGAL SYNCOPE (FAINTING)
• CORTICOHYPOTHALAMIC RESPONSE
• FLIGHT OR FIGHT RESPONSE

MEDULLARY CARDIOVASCULAR CENTER

• VASOMOTOR CENTER
• PRESSOR AREA

• CARDIOINHIBITORY CENTER
• DEPRESSOR AREA

PRESSOR OR VASOMOTOR CENTER IS SPONTANEOUSLY ACTIVE AND ALWAYS SLOWED BY DEPRESSOR WHICH IS ACTIVATED BY BARORECEPTORS

REFLEX RESPONSES

• VASOVAGAL SYNCOPE
• FAINTING
• CORTICOHYPOTHALAMIC DEFENSE REACTION
• FIGHT OR FLIGHT

Questions of the Day:

• Define cardiac contractility.
• How do ACh and epinephrine change cardiac contractility?

RENAL CONTROL OF BLOOD VOLUME

Mammalian kidneys are designed to reabsorb Na⁺ and retain it in body fluids

increase Na⁺ reabsorption -->increase water reabsorption -->increase blood volume --->

RAISE BP

ANTIDIURETIC HORMONE
(VASOPRESSIN)

• 9 amino acid peptide
• released from posterior pituitary
• released in response to:

- elevated plasma p

- lowered BP or lowered blood volume

-(decreased atrial EDV and/ or decreased baroreceptor distention)

ADH

• Normally ADH causes Na+ and water reabsorption by kidneys to increase blood volume and decrease plasma p
• ADH released in response to low BP and not released when BP is high

ATRIAL NATRIURETIC PEPTIDE (ANP)

• 28 amino acid peptide hormone
• released from atrial myocytes (muscle cells)
• released in response to distention (high atrial EDV) due to high BP

ATRIAL NATRIURETIC PEPTIDE

INHIBITS Na⁺ - K⁺ ATPase in kidney

THUS Na⁺ AND WATER ARE LOST IN URINE lowering blood volume

VOLUME RECEPTORS

ATRIAL STRETCH RECEPTORS:

DECREASE ADH

and

INCREASE ANP

(increase urine output and decrease blood volume)

ARTIAL STRETCH RECEPTORS RESPOND TO INCREASED BV BY:

RENIN -ANGIOTENSIN - ALDOSTERONE

LOW RENAL BLOOD FLOW

(< 20% OF CO) --->

ACTIVATION OF POTENT VASOCONSTRICTOR:

ANGIOTENSIN