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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
Normal Cardiac Output
Total Blood Volume = ~ 5 liters
CO @ Rest: 5 L/min
All 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. Autonomic
Somatic 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)
2)
3)
4)
5)
Origin of neural signal
Preganglionic neuron
Autonomic ganglion
Postganglionic neuron
Target organ
Main Differences:
Postganglionic neuron
Cholinergic
vs
Adrenergic
Target tissue receptor
Muscarinic
vs
α-adrenergic
β-adrenergic
Adrenal Medulla releases Epinephrine
Epi = Adrenaline
Epi Produces a Sympathetic-like Effect
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!
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
Cardiac Output = heart rate x stroke volume
Mechanisms of Altered Stroke Volume
Stroke Volume (EDV – ESV)
Stroke Volume is directly related to contraction force
What effects the FORCE of Myocardial Contraction?
Force of Ventricular Contraction
Mechanisms of Altered Stroke Volume
Stroke Volume is directly related to contraction force
1)
Myocardium Muscle Fiber Length
More STRETCH = longer fibers = greater contraction force = more blood expelled
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 Pump
Lower Pressure is created in Inf. Vena Cava & Right Atrium during inspiration
Bulk 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)
Acetylcholine (Neuro)
Mechanism: Altered Calcium Concentrations in Myocardium
Acetylcholine
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 Gland
Epinephrine (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
Systemic Circuit
Pulmonary
Circuit
Heart
Artery
SYSTOLE
Heart
Artery
DIASTOLE
MEAN ARTERIAL PRESSURE (MAP) :is responsible for bulk flow of blood
:is measured on ARTERIES
Cardiac Output = generates MAP
Arteriole Resistance Controls Flow
& Impacts MAP
HIGH R = narrow arteriole = low flow
LOW R = wide arteriole = high flow
MAP = CO x R
R = Arteriole Resistance to Flow
More Cardiac Output = larger MAP
Less Cardiac Output = smaller MAP
More Resistance = smaller arteriole = greater MAP but slower flow
Less Resistance = larger arteriole = lower MAP but greater flow
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 & Flow
via 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:
Resting tissue
Results in:
Low levels in O2, Glucose
INCREASE in O2, Glucose
High Levels in CO2, Lactic Acid, ADP
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!
MAP = CO x R
Alpha receptors are located on most of the vasculature
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
Epi
MAP = CO x R
β2-receptors are not innervated by ANS!!!!!
Not located elsewhere!
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 REFLEX
1) 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!
Pathological MAP: Hypertension
180
Systolic > 130
Blood Pressure (mm Hg)
160
Diastolic > 100
Hypertensive, MAP > 130 mm Hg
140
120
Normal, MAP = 100 mm Hg
Normal = 120/80
100
80
60
Time
Increase Length
Main Causes
Hardening
Increase in R
Decrease Diameter
(clogging, thrombi,
Atheroscelrosis)
LOSS of Elasticity
Main Consequences: Heart Failure/Attack, Emboli (broken off blood clots)
Poor Vision, Cerebral Hemorrhage
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
Injury: Cut, Wound, etc.
Activation of Clotting Cascade,
Tissue Factors, Platelets
+ feedback loop
Blood Clot
Dissolves
Atherosclerosis
Damage to Endothelium = initiation of disease process
Chemically: LDL, toxins
Mechanically: 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 = Embolus
Emboli 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
Anti-Coagulants: Clot Inhibitors
Aspirin: blocks thromboxane synthesis
Platelet Factors = ADP & Thromboxane
W/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