Physio. Ch.13 Part 3 Cardiac Output and its Control

Cardiac Output (CO)

• The volume of blood that is pumped out of the heart from each ventricle

• Measured in L or mL per minute

• Varies greatly depending on heart rate (HR) and stroke volume (SV)

- Stroke volume times heart rate

• Average is 72000 L per day

Heart rate (HR)

• How many times the heart beats in a minute

• Average 72bpm

- Sympathetic: Increase in heart rate

- Parasympathetic: Decrease in heart rate

- Epinephrine: Increased heart rate by binding B1 receptors

• Controlled by the medulla oblongata

Extrinsic control of cardiac output

• Control of cardiac output by factors other than the heart

- ANS innervation and hormone secretion

Intrinsic control of cardiac output

• Control of cardiac output by the heart

ANS impute on the heart

• Both devisions effect heart rate and stroke volume

- Sympathetic: Increase in heart rate

- Parasympathetic: Decrease in heart rate

• Both devisions effect the SA and AV node

Neural Control of HR

• Sympathetic effects expanded, increases AP frequency of pacemaker cells

- Process: NE release → binds to β1 adrenergic receptors on SA nodal cells → activates cAMP second messenger system →cAMP increases opening of funny channels and T-type calcium channels

- Effect: Enhanced movement of sodium and calcium into pacemaker cell, Faster spontaneous depolarization

• Parasympathetic effects expanded, neural input from vagus nerve decreases AP frequency of pacemaker cells

- Process: ACh release → binds M-2 cholinergic receptors on SA nodal cells → G protein increases opening of potassium channels and suppresses opening of funny channels & T-type calcium channels →Hyperpolarization → Decreased rate of spontaneous depolarization

• Parasympathetic dominates at rest

Hormonal Control of HR

• Done primarily by epinephrine (E)

- Binds B1 receptors to increase AP production in SA node and the speed at which the AP moves through cardiac fibers

• Thyroid hormones

- Unknown effects

• Insulin

- Unknown effects

• Glucagon

- Increased heart rate

Changes in Stroke Volume

• Ventricular contractility

• End-diastolic volume (EDV)

• Afterload

Ventricular contractility

• Factor used to control stroke volume

• A change in the force of ventricular contraction at any given end-diastolic volume

- Stroke volume increases when ventricular contractility increases

• Regulated by sympathetic and circulating epinephrin

- Sympathetic: Neurons project to myocardium of

atria and ventricles

- Epinephrin: Binds to B1 receptors, increasing cAMP levels, increase Ca flow into cell and Cl release from SR, contractions become more common

End-diastolic volume (EDV)

• Factor used to control stroke volume

• Stroke volume increases when EDV increases

• Higher EDV cause muscle fibers to lengthen

- Come near to but never reach their optimal length

- Higher affinity of troponin to Ca, causing more cross bridges

Afterload

• Arterial pressure the ventral muscle has to work against after contraction starts

- Determined by pressure of the aorta or inferior vena cava at time of contraction

• Factor used to control stroke volume

• Inverse relationship to stroke volume

• As MAP increases after load increases to

Starling’s Law of the heart

• Rate of Venus return increase → more strain to be put on the ventricular myocardium → ventricles contract harder to match

• Application

- Regulates heart size

- EDV increase = force of ventricle contraction raises → increase in stroke volume

Ventricular end-diastolic pressure “Preload”

• Tension on the myocardium before contraction

• Primarily determined by EDV

• When increases SR increases to

• Determined by time heart has to fill

- Slower heart rate means larger EDV and therefore larger preload

Central venous pressure

• The pressure of the blood contained in the large veins that lead into the heart

Congestive Heart Failure (CHF)

• Cardiac output can not sustain blood flow to the body

• Results from

- Myocardial infarction, congenital defects, hypertension, aortic valve stenosis, or disturbances in electrolyte levels (K+ and Ca2+)

• Subdivided

- Left-side failure: Increases left atrial pressure; pulmonary congestion and edema; shortness of breath

- Right-side failure: raises right atrial pressure; systemic congestion and edema

Ischemic Heart Disease

• Heart muscles don’t have enough oxygen to support their function

• Ischemia: inadequate oxygen due to reduced blood flow

• Common cause: Atherosclerosis

• Causes lactic acid build-up

- Pain results

• Enzyme levels increase

- Creatine phosphokinase: 3 to 6 hours, return to normal in 3 days

- Lactate dehydrogenase: 48 to 72 hours, elevated about 11 days