how do we measure heart performance? cardiac output = blood volume per minute! cardiac output =...
Post on 19-Dec-2015
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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/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