How do we measure heart performance?

Cardiac Output = Blood Volume per Minute!

Cardiac Output = heart rate x stroke volume

Heart rate = # of beats per minute; can measure by taking pulse; normally ~ 75 b/min

Stroke Volume = volume of blood ejected by L. Ventricle in one cardiac cycle

Stroke volume = end DIASTOLIC volume – end SYSTOLIC volume

Stroke Volume = 135 mL – 65 mL = 70 mL per beat

Cardiac Output = 75 beat/min x 70 mL/beat = 5250 mL/min = 5.2 L/min

Normal Cardiac Output

Total Blood Volume = ~ 5 liters

CO @ Rest: 5 L/minAll blood in body is completely circulated every minute at rest!

CO @ Exercise: 30-35 L/Min

How does your body alter Cardiac Output to meet metabolic demands?

How does your body Alter Cardiac Output?

Cardiac Output = heart rate x stroke volume

1) Autonomic Nervous System

2) Endocrine (Hormonal) Control

3) Mechanically (Stroke Volume only)

Somatic vs. AutonomicSomatic motor output is consciously controlled

Autonomic motor output is NOT consciously controlled

Functional subdivisions of ANS:Parasympathetic vs. Sympathetic

Parasympathetic = Cranio-Sacral Division

SLOWING, RELAXING effect

Sympathetic = Thoraco-Lumbar Division

SPEED-UP, EXCITE, FIGHT

Autonomics are everywhere

Autonomics are Reflex Arcs

Autonomic Nervous System: General Anatomy

5 Parts:

1) Origin of neural signal2) Preganglionic neuron3) Autonomic ganglion4) Postganglionic neuron5) Target organ

Main Differences:

Postganglionic neuronCholinergic vs Adrenergic

Target tissue receptorMuscarinic vsα-adrenergicβ-adrenergic

Adrenal Medulla releases Epinephrine

Epi Produces a Sympathetic-like Effect

Epi = Adrenaline

How does your body Alter Cardiac Output?

Cardiac Output = heart rate x stroke volume

Altering Cardiac Output: Heart Rate

Heart rate is controlled by AUTONOMIC NERVOUS SYSTEM & Hormones!

Remember: Heart electrical signals are initiated by Pacemaker cells (Autorhymicity) Their rate of depolarization is altered by ANS & Hormones

2) Parasympathetic ANS decreases HR

3) Symapthetic ANS increases HR

4) Sympathetic stimulates Adrenal GlandEpinephrine (hormone) released to blood

increases HR

Cardiac Output = heart rate x stroke volume

Mechanisms of Altered Stroke Volume

Stroke Volume is directly related to contraction force

Force of Ventricular Contraction

Str

oke

Vo

lum

e (E

DV

– E

SV

)

What effects the FORCE of Myocardial Contraction?

Mechanisms of Altered Stroke Volume

1) Myocardium Muscle Fiber Length More STRETCH = longer fibers = greater contraction force = more blood expelled

Stroke Volume is directly related to contraction force

Frank-Starling Law of the Heart

EDV determines STRETCH

What determines EDV?

Venous Return: amount of blood entering R. Atrium

Increase Venous Return by:

1) Skeletal Muscle Pump Return MORE Blood from Muscle Veins

2) Constriction of Veins via Sympathetic ANS Forces Blood in Veins Back to RA

Compression Tights

What determines EDV?

Venous Return: amount of blood entering R. Atrium

Increase Venous Return by:

3) Respiratory PumpLower Pressure is created in Inf. Vena Cava & Right Atrium during inspirationBulk Flow pushes more blood towards RA

Cardiac Output = heart rate x stroke volume

1) Venous Return > EDV > Fiber Length > Contractile Force

Mechanisms of Altered Stroke Volume

Stroke Volume is directly related to contraction force

1) Myocardium Muscle Fiber Length

2) Contractility Controlled by Autonomics (Neurotransmitters) & Endocrine (Hormones)

Norepinephrine (Neuro)Epinephrine (Hormone)

AcetylcholineAcetylcholine (Neuro)

Mechanism: Altered Calcium Concentrations in Myocardium

Summary: Altering Heart Performance

Homeostasis and Heart Function

Cardiac Output is altered in response to: Blood Pressure, pH, and/or

CO2

1) O2, CO2 and pressure receptors carry sensory info to Brain Stem

2) Parasympathetic ANS decreases HR

venous return contractility

3) Symapthetic ANS increases HR

venous return contractility

4) Sympathetic stimulates Adrenal GlandEpinephrine (hormone) released to blood

increases HR contractility

Cardiovascular Physiology

1) Blood

2) Heart

3) Peripheral Circulation - tubes

The primary function of the Cardiovascular system is to

1) deliver nutrients/oxygen and

2)remove wastes/CO2

from the cells in your body

Basic Anatomy of Circulation

Pulmonary Circuit

Systemic CircuitSystemic Circuit

SYSTOLE

DIASTOLE

Heart

Heart

Artery

Artery

MEAN ARTERIAL PRESSURE (MAP) :is responsible for bulk flow of blood :is measured on ARTERIES

Arteriole Resistance Controls Flow & Impacts MAP

HIGH R = narrow arteriole = low flowLOW R = wide arteriole = high flow

Cardiac Output = generates MAP

MAP = CO x R R = Arteriole Resistance to Flow

More Resistance = smaller arteriole = greater MAP but slower flow

Less Resistance = larger arteriole = lower MAP but greater flow

More Cardiac Output = larger MAP

Less Cardiac Output = smaller MAP

Vascular Anatomy effects Resistance

Arteries have more smooth muscle & elastic material than veins!

Smooth Muscle

Contraction varies with chemical input and varies widely!

Neurotransmitters from ANS

Hormones from Endocrine Glands

Vasoactive Chemicals from Blood Vessels & Tissues

Control of Vascular Resistance & Flowvia smooth muscle

1) Chemical Control

2) Neural Control

3) Endocrine Control

Local Control SHUNTS blood to different parts of body

Note: Cardiac output = the total flow to all organs

Shunting just redistributes the flow!

Local Control of Blood Flow: Meta-Arterioles feeding into capillaries

Metabolically ACTIVE tissue Results in:

Low levels in O2, Glucose

High Levels in CO2, Lactic Acid, ADP

Resting tissueResults in:

INCREASE in O2, Glucose

DECREASE in CO2, Lactic Acid, ADP

Leading to VASODILATION Leads to VASOCONSTRICTION

2) Neural control of Blood Flow: Widespread

Blood Vessels ONLY have SYMPATHETIC INNERVATION!Blood Vessels ONLY have SYMPATHETIC INNERVATION!

Alpha receptors are located on most of the vasculature

MAP = CO x R

Endocrine Control of Blood Flow:Epinephrine, Widespread

Epinephrine enters circulation and binds β2-receptors

β2-receptors are ONLY located Heart, Liver, Skeletal Muscles

Epi on β2-receptors lead to VASODILATION

β2-receptors are not innervated by ANS!!!!! Not located elsewhere!

Epi

MAP = CO x R

Local Control = Precapillary sphincters

- local, chemical control

Widespread = vascular Smooth Muscle – sympathetic, adrenal

MAP drives blood flow…..So the body carefully monitors and maintains MAP

1) Short Term maintenance of MAP – Cardiovascular Regulation

2) Long Term maintenance of MAP – Kidney & Hormonal Regulation

MAP = CO x R

Short & long term mechanisms will alter cardiac output & vascular resistance

Short-Term Mechanisms for MAP homeostasis:ANS/ADRENAL via

BARORECEPTOR REFLEX1) Baroreceptors in Carotid Body & Aorta

2) Signal processed in Brainstem

3) IF High MAP Stimulates Parasym.

Decrease in HR, Stroke Vol.

MAP = CO x R

4&5) IF Low MAP Stimulates Sympathetics &

Adrenal Gland Increase in HR, Stroke Volume Peripheral Vasoconstriction Vasodilatation at Heart, Skel. Musc.

Liver MAP = CO x R

Long-Term Mechanisms for MAP homeostasis

1) Renin-Angiotensin-Aldosterone

2) Vasopressin (Anti-diuretic Hormone)

3) Atrial-Natriuretic Hormone

We will discuss these AFTER kidney physiology……because they all involve the kidney!

60

80

100

120

140

160

180

Time

Blo

od P

ress

ure

(mm

Hg)

Pathological MAP: Hypertension

Normal, MAP = 100 mm Hg

Hypertensive, MAP > 130 mm Hg

Systolic > 130

Diastolic > 100

Normal = 120/80

Main Consequences: Heart Failure/Attack, Emboli (broken off blood clots)Poor Vision, Cerebral Hemorrhage

Main Causes

LOSS of Elasticity

Increase in R

Decrease Diameter(clogging, thrombi, Atheroscelrosis)

Hardening

Increase Length

Fluid Volume

Blood: Functions

1) Transport of nutrients, gases, wastes

2) Transport of processed molecules (Vitamin precursors, recycled

products)

3) Transport of hormones & enzymes

4) Buffer for pH and Fluid/Ion Balance

5) Body Temperature Homeostatis

6) Immune Response

Blood: Composition

We will talk RBC, Gases, Globulins with Respiratory physiology!

Clotting: dealing with extensive damage

Blood ClotDissolves

Injury: Cut, Wound, etc.

Activation of Clotting Cascade, Tissue Factors, Platelets

+ feedback loop

Atherosclerosis

Damage to Endothelium = initiation of disease process

Chemically: LDL, toxinsMechanically: Hypertension

Normal

Moderate Atherosclerosis Severe Atherosclerosis

Inflammatory-Immune-Clotting

Ruptured Atheroscelortic Plaque

Initiates Clot (Thrombus) Formation

Too much clotting results in Thrombus and/or Embolus!

Thrombus breaks free = EmbolusEmboli are a major cause of

heart attack & stroke!

Can originate from anywhere….e.g. varicose veins!

Emboli can get lodged in any small artery

Results in ISCHEMIA >>> Infarct >>>> Cell Necrosis

Aspirin: blocks thromboxane synthesis

Anti-Coagulants: Clot Inhibitors

Platelet Factors = ADP & ThromboxaneW/out Thromboxane fewer

platelets are attracted to injury

Fewer clots form; existing clots shrink

Clot Intiation

tPA- Tissue Plasminogen Activator

Thrombolytic: Clot BUSTER

Cardiovascular Physiology: Summary

1) Blood – carries nutrients

2) Heart – creates pressure gradient – blood flow

3) Peripheral Circulation – carries blood to tissues

The primary function of the Cardiovascular system is to

1) deliver nutrients/oxygen and

2)remove wastes/CO2

from the cells in your body