How do we measure heart performance Cardiac Output Blood Volume per Minute

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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
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Normal Cardiac Output

• Total Blood Volume 5 liters
• CO _at_ Rest 5 L/min
• All blood in body is completely circulated every
  minute at rest!
• CO _at_ Exercise 30-35 L/Min

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

• Cardiac Output heart rate x stroke volume

• Autonomic Nervous System
• Endocrine (Hormonal) Control
• Mechanically (Stroke Volume only)

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Somatic vs. Autonomic

• Somatic motor output is consciously controlled
• Autonomic motor output is NOT consciously
  controlled

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Functional subdivisions of ANSParasympathetic
vs. Sympathetic
Parasympathetic Cranio-Sacral Division
SLOWING, RELAXING effect
Sympathetic Thoraco-Lumbar Division
SPEED-UP, EXCITE, FIGHT
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Autonomics are everywhere
Autonomics are Reflex Arcs
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Autonomic Nervous System General Anatomy

• 5 Parts
• Origin of neural signal
• Preganglionic neuron
• Autonomic ganglion
• Postganglionic neuron
• Target organ

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Neurotransmitters Receptors in the ANSA
complicated system!
Neurons are Cholinergic release
neurotransmitter Acetylcholine
Adrenergic release neurotransmitter
Norepinephrine
Dendrites Nicotinic - respond to
acetylcholine or target organ Muscarinic -
respond to acetylcholine
a-Adrenergic respond to Norepinephrine
ß-Adrenergic - respond to Norepinephrine
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• Sympathetic Cholinergic Preganglionic Neuron
• Nicotinic Receptor on Postgang.
• Adrenergic Postganglionic Neuron
• Adrenergic Receptor on
  Effector

2) Para-Sympathetic Cholinergic Preganglionic
Neuron Nicotinic Receptor on
Postgang. Cholinergic
Postganglionic Neuron Muscarinic
Receptor on Effector
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Adrenal Medulla releases Epinephrine
Epi Adrenaline
Epi Produces a Sympathetic-like Effect
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How does your body Alter Cardiac Output?

• Cardiac Output heart rate x stroke volume

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• Altering Cardiac Output Heart Rate

Heart rate is controlled by AUTONOMIC NERVOUS
SYSTEM Hormones!
2) Parasympathetic ANS
decreases HR 3) Symapthetic ANS
increases HR 4) Sympathetic stimulates
Adrenal Gland Epinephrine (hormone) released to
blood increases HR
Remember Heart electrical signals are initiated
by Pacemaker cells (Autorhymicity) Their
rate of depolarization is altered by ANS
Hormones
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Mechanisms of altered Heart Rate
Adrenal Gland (Epi)
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Cardiac Output heart rate x stroke volume
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Mechanisms of Altered Stroke Volume
Stroke Volume is directly related to contraction
force
Stroke Volume (EDV ESV)
What effects the FORCE of Myocardial Contraction?
Force of Ventricular Contraction
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Mechanisms of Altered Stroke Volume
Stroke Volume is directly related to contraction
force

• Myocardium Muscle Fiber Length
• More STRETCH longer fibers greater
  contraction force more blood expelled

Frank-Starling Law of the Heart
EDV determines STRETCH
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What determines EDV?

• Venous Return amount of blood entering R. Atrium

• Increase Venous Return by
• Skeletal Muscle Pump
• Return MORE Blood from Muscle Veins
• Respiratory Pump
• Low Pressure is created in Inf. Vena Cava RA
• Bulk Flow pushes more blood towards RA
• Constriction of Veins via Sympathetic ANS
• Forces Blood in Veins Back to RA

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Cardiac Output heart rate x stroke volume
1) Venous Return gt EDV gt Fiber Length gt
Contractile Force
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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)
Acetylcholine (Neuro)
Acetylcholine
Mechanism Altered Calcium Concentrations in
Myocardium
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Ca2
Ca2
Ca2 Spark
Acetylcholine
Ca2 Signal
Contraction
NE
Force of Myocardium
Ach
Amount of Calcium INFLUX
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Summary Altering Heart Performance
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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
Gland Epinephrine (hormone) released to blood
increases HR contractility
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Cardiovascular Physiology

• Blood
• Heart
• 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
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Mean Arterial Blood Pressure
Your body monitors MAP to maintain a pressure
gradient to drive blood flow! BULK FLOW!
MAP CO x R R Arteriole Resistance to Flow
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MAP CO x R R Arterial Resistance to Flow
More Resistance smaller artery less
flow Less Resistance larger artery
more flow
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Monitoring of MAP

• Short Term maintenance of MAP Cardiovascular
  Regulation
• Long Term maintenance of MAP Kidney Hormonal
  Regulation

MAP CO x R
Short long term mechanisms will alter cardiac
output vascular resistance
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Vascular Anatomy effects Resistance
Arteries have more smooth muscle elastic
material than veins!
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Smooth Muscle

• Contraction varies with chemical input!
• Neurotransmitters from ANS
• Hormones from Endocrine Glands
• Vasoactive Chemicals from Blood Vessels
  Tissues

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MAP is measured on ARTERIES!
MAP is measured at ARTERIES
Resistance is measured at arterioles
metaarterioles
MAP CO x R R Arteriole Resistance to Flow
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Control of Blood Flow

• Local Control
• Neural Control
• Endocrine Control

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Heart
Artery
SYSTOLE
Heart
Artery
DIASTOLE
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Arterioles
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Arterioles
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Local Control SHUNTS blood to different parts of
body
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Local Control of Blood Flow Meta-Arterioles
feeding into capillaries
Metabolically ACTIVE tissue
Resting tissue
VASOCONSTRICTION INCREASE in O2,
Glucose DECREASE in CO2, Lactic Acid, ADP
VASODILAITION Decrease in O2, Glucose INCREASE
in CO2, Lactic Acid, ADP
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Can Local Control AFFECT MAP?
Arterioles
Which artery has larger pressure?
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MAP is measured on ARTERIES!
MAP is measured at ARTERIES
Resistance is measured at arterioles
metaarterioles
MAP CO x R R Arteriole Resistance to Flow
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Control of Blood Flow

• Local Control
• Neural Control
• Endocrine Control

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Neural control of Blood Flow Widespread
Blood Vessels ONLY have SYMPATHETIC INNERVATION!
MAP CO x R
Alpha receptors are located on most of the
vasculature
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Endocrine Control of Blood FlowEpinephrine,
Widespread
Epinephrine enters circulation and binds
ß2-receptors ß2-receptors are ONLY located
Heart, Liver, Skeletal Muscles Epi on
ß2-receptors lead to VASODILATION
ß2-receptors are not innervated by
ANS!!!!! Not located
elsewhere!
Epi
MAP CO x R
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Local Control Precapillary sphincters- local,
chemical controlWidespread vascular
Smooth Muscle sympathetic, adrenal
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Short-Term Mechanisms for MAP homeostasis

• Baroreceptors in Carotid Body Aorta
• Signal processed in Brainstem
• High MAP
• Stimulates Parasym.
• Decrease in HR, Stroke Vol.
• MAP CO x R
• 45) Low MAP
• Stimulates Sympathetics Adrenal Gland
• Increase in HR, Stroke Volume
• Peripheral Vasoconstriction
• Vasodilation at Heart, Skel. Musc. Liver
• MAP CO x R

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Long-Term Mechanisms for MAP homeostasis

• Renin-Angiotensin-Aldosterone
• Vasopressin (Anti-diuretic Hormone)
• Atrial-Natriuretic Hormone

We will discuss these AFTER kidney
physiologybecause they all involve the kidney!
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Pathological MAP Hypertension
Systolic gt 130
Diastolic gt 100
Hypertensive, MAP gt 130 mm Hg
Normal, MAP 100 mm Hg
Normal 120/80
Hypertension can result with Heart Failure,
Emboli, Heart Attack, Poor Vision, Cerebral
Hemorrhage
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Cardiovascular Physiology Summary

• Blood carries nutrients
• Heart creates pressure gradient blood flow
• 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