cardiovascular anatomy and physiology review reading: brubaker 2:37-56
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Cardiovascular Anatomy and Physiology
REVIEW
Reading:
Brubaker 2:37-56
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Normal HeartNormal Heart Myocardial Myocardial Infarct (LAD)Infarct (LAD)
Photos: Klatt, Edward C. MD, WebPath.edu
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Primary Cardiac Function = Primary Cardiac Function = Tissue PerfusionTissue PerfusionMorbidity and Mortality of
Cardiovascular Disease:Inadequate Cardiac OutputReduced Perfusion (O2) to the
“BIG THREE” vital organs:Brain, Heart, Lungs
Other Organ Failure: Kidneys, Liver, GI, Skeletal Muscle
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Cardiac AnatomyCardiac Anatomy: Pericardium: Visceral / Parietal
connective tissue “wrapping”Epicardium: next to the heartPericardial space: fluid filledFibrous/serous pericardium:
Prevents overdistension of the heart and produces fluid
Cardiac Tamponade: Life threateningAccumulation of fluid in p. space
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Layers of Heart TissueLayers of Heart Tissue:Pericardium: Double Layered
Outer, Fibrous: Tough connective fibrous tissue - Parietal
Inner, Serous: Epithelial and thin connective tissue layer -Visceral, epicardium
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Heart Layers: Heart Layers:
Myocardium: Cardiac muscle layer
Endocardium: Connective + Epithelial TissueStructural “ScaffoldingValvesChordae Tendinae
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Endothelial “ScaffoldingEndothelial “Scaffolding””
Endocardium The fibrous network forms chambers of the Ventricles
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Myocardium:Myocardium:
You end up with a very strong muscle in the shape of a multi-chambered pump
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Coronary Arteries:Coronary Arteries:
Left Coronary Artery: Origin: Left side of AORTASupplies: Anterior/Left Heart
Right Coronary Artery:Origin: Rt. Side of AORTASupplies: Right Heart
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Rt.MarginalBranch
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Coronary Artery Bloodflow Coronary Artery Bloodflow Regulation:Regulation:Aortic Pressure is primary
regulatorSympathetic: Net Increase in
BloodflowParasympathetic: Maintain
BloodflowMetabolic: Bloodflow = VO2
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Cardiac Cycle and Cardiac Cycle and Coronary Artery Flow:Coronary Artery Flow:Systole: The aortic valve opens,
and “covers” the Coronary arteries Blood flow is prevented
Diastole: The aortic valve closes, “opens” the coronariesBlood Flow is restored
What would be the effect of increased HR on Coronary blood flow (perfusion)?
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Coronary Artery Disease: Coronary Artery Disease: CADCAD When critical bloodflow to the heart
muscle is compromised, The Heart Cannot “Rest” from its work! DEMAND > SUPPLY (Ouch!)
Arteriosclerosis: “Hardening of the arteries” (could be just aging) ATHEROsclerosis: The hardening and
progressive narrowing is caused by lipid deposits provoking fibrosis and calcification
Progressively PATHOLOGICAL!
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Fatty Arteries:
Normal CoronaryArtery
AtheroscleroticArtery
Photos: Klatt, Edward C., WebPath.com
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Cardiovascular Cardiovascular Function:Function:
PUMP: Heart contractions propel Blood throughout the circulation!
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Cardiac CycleCardiac Cycle:Ventricular Systole:
Ventricles Contract – eject bloodTri/Bicuspid valves closeFirst Heart Sound: “Lubb”
Ventricular Diastole: Ventricles relax, fillPulmonary/Aortic Valves closeSecond Heart Sound: “Dupp”
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The Atria: The Atria: “Collection” of blood from either:
Right: The systemic circulation (low PO2)
Left: The pulmonary circulation (high PO2)
Atrial Contraction: Empties the final 30% of the End
Diastolic Volume (EDV)What is the impact of Atrial FibrillationOn Cardiac Output?
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Right Ventricle pumps blood to the lungs
Right Ventricle contracts
Increased pressure causes tricuspid valve closure
Blood leaves heart via Pulmonary Artery Only artery with O2
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Left Ventricle Pumps Blood to the Body
The Left Ventricle contracts
Mitral Valve: Closes Aortic Valve: Opens Blood is pumped out
via the Aorta
Aorta
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Terms: Terms: Preload: The pressure in the left
ventricle immediately before contraction: Mostly related to volume EDV
Afterload: The pressure in the left ventricle immediately after contraction:Mostly related to Vascular resistance
Ejection Fraction: The amount of blood ejected by the LV – expressed as a % of the EDV
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Systemic Arterial Systemic Arterial Blood PressureBlood PressureSystolic: Systole causes increased
pressure in the arterial vessels: Systolic pressures indicate the
strength of cardiac contractionDiastolic: During diastole, arterial
pressure is at it’s lowestDiastolic Pressures indicate the
total resistance to blood flow
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Cardiac Output: HR X SVCardiac Output: HR X SVCO = HR X SV“Emergencies”
SNS Autonomic NSIncrease HR/SV = Increase CO
“Relaxing” – Status Quo:PSNS Autonomic NSDecrease HR = Decrease CO
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Electrophysiology of Electrophysiology of the Heart: ECGthe Heart: ECG
P: Atrial Depolarization/contractionQRS: Ventricular Depol/ContractionT: Ventricular Repolarization
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Cardiac Muscle CellsCardiac Muscle Cells:Striated, Branched, Intercalated
DiscsSlower Action Potential than
nerve or skeletal muscle cellsVoltage Gated Ca++
Channels!
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Electrical Activity: Electrical Activity: Excitation - ContractionExcitation - ContractionTo contract, cardiac muscle
cells must depolarize and propagate an Action Potential
The Conduction of Action Potentials and Contractions must be well coordinated to efficiently pump blood.
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Action Potentials:Cardiac vs. Skeletal Depolarization
Na+ and Ca++ Channels open
Plateau: All but Ca++ channels close
Repolarization K+ open and Ca+
+channels close
Depolarization: Na+ channels open
Repolarization: Voltage Gated K+ channels open / Na+ channels close
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Myocardial Action PotentialMyocardial Action Potential
mV
-100
+40
0
4
0
1 2
3
4
ECG
AP
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Why the Plateau Phase Why the Plateau Phase and Calcium?and Calcium? Plateau Phase: Longer Relative
Refractory period: Cannot be re-stimulated – permitting
coordinated contraction of entire heart muscle.
Calcium: Important in the automaticity of cardiac myocytes Links excitation to contraction Increases contraction force
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Coordinating the Beats…Coordinating the Beats…
Contractions of the ventricles and atria must alternate
The excitation of the heart muscle follows a predictable path
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Conduction System:Conduction System:SA Node: 90-100 bpmAV Node: Slows the message
downAV Bundles: (also His):L./R. Bundle Branches:Purkinje Fibers:
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Heart Conduction SystemHeart Conduction SystemThe Sino-Atrial node (SA) serves as the pacemaker for the heart.When the SA node fires, it causes both atria to contractThe excitation-contraction signal is then “conducted” to the ventricles via the AV Node
SA
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Heart Rate ControlHeart Rate Control Each heart cell can contract
independently and automatically The entire heart must not contract at
the same time. Excitation-Contraction of the heart is
coordinated from “top to bottom” The excitation-contraction pathway
is called “The Conduction System”
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Extrinsic Control of Extrinsic Control of Heart RateHeart Rate
The SA node has an Intrinsic Rate of 90-100 bpm – “Default Rate”
External controls modify the heart rate: both at rest and during exercise
Controls: Parasympathic Nervous System, Sympathetic Nervous System, Endocrine System
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Parasympathetic Nervous Parasympathetic Nervous SystemSystem “Maintenance” control Vagus nerve innervates heart at the SA
Node with some control of the AV Node Causes reduced HR Neurotransmitter: Acetylcholine
(“cholinergic”) Atropine blocks blocks PSNS and
increases HR
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Sympathetic Nervous Sympathetic Nervous SystemSystem “Rescues” in homeostatic emergencies (like
exercise) Increases HR Increases Systolic contractility (Increased BP) Increases Mental acuity (you are prepared for
battle!) Neurotransmitter: Norepinepherine
(Adrenaline = “adrenergic”) Propranolol (SNS Beta-receptor blocker)
reduces HR
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Endocrine SystemEndocrine System
The adrenal medulla (above kidney) secretes Catecholamines: Epinephrine Norepinephrine
Stimulated by and mimics the Sympathetic Nervous System Slower/Longer acting
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Regulation of Cardiac Regulation of Cardiac Output:Output:Cardiac Output: Changes in
CO are responses to “Homeostatic Emergencies”:
Pressure EmergenciesChemical Emergencies
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Baroreceptors: Sensing Baroreceptors: Sensing Pressure EmergenciesPressure Emergencies Increase CO = Increase Systolic BP Emergency 1: Decreased Pressure
Increase SNS: Increased HR X SV = Increased CO
Problem 2: Increased PressureDecrease SNS: Decrease HR =
Decreased CO
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Chemoreceptors: Sensing Chemoreceptors: Sensing Metabolism EmergenciesMetabolism Emergencies Emergency 1: Increased Metabolic
Rate: Increased CO2, H+ (decreased pH) Increased SNS …CO
Problem 2: Decreased Metabolic Rate: What’s the Problem? Decreased CO2/ H+ (increased pH) Decreased SNS …CO Conserver the rescue efforts
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Intrinsic Regulation of Cardiac Output: Starling’s LawIncreased Venous Return
Increased cardiac muscle stretchIncrease contraction forceIncreased SV = Increased CO
Occurs without SNS/PSNS involvement
Exercise….
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Final Question: In a Heart
Transplant, the heart is “denervated”
How does someone with a heart transplant respond to exercise?
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Hints: Remember – Starling’s Law of
the HeartRemember that though the
nerves are no longer signaling, there is another (though slower and longer acting) source of control…
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Blood Vessels And Blood Vessels And CirculationCirculation
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Peripheral Circulation:Systemic Circulation:
Blood vessels directing blood to the body tissuesLeft Heart to Right Heart
Pulmonary Circulation: Blood vessels directing blood to the
lungs for gas exchangeRight Heart to Left Heart
What do we call the circulation to The heart?
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Perfusion HomeostasisPerfusion Homeostasis: Internal Environment: Depends
on appropriate perfusion (Blood flow)
Homeostasis: A constant balance of choices in maintaining central blood pressure (to maintain the “Big 3”) and distribution to demanding tissues
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Three Vessel “Tunics”:Three Vessel “Tunics”:
Tunica Adventitia (Externa): Fibrous connective tissue
Tunica Media: Smooth Muscle and elastic connective tissue
Tunica Intima: Endothelium (forms the valves in veins)
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Arteries: Vessels taking
blood Away From The Heart
Usually O2 and nutrient rich…”Supply” to tissues
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Arteries: Structure/FunctionHigh Pressure Conduits:
Elastic Connective Tissue: Expands with systole, and recoils with diastole
Smooth Muscle: Assist in “pumping” and “directing” blood flow
Endothelium: Smooth inner surface
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Veins: Vessels returning
blood Back To The Heart
Usually low in O2 – carrying wastes for removal
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Veins: Structure/FunctionLow Pressure “Pools”:
Sometimes called “capacitance vessels” because they have a large reservoir (capacity) for blood
Less connective tissue and smooth muscle than arteries
Endothelium: Specialized valves assist blood flow toward heart
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Arterial Blood PressureCardiac Output: Reflected by
Systolic blood pressureVascular Resistance:
Reflected by Diastolic PressureVessel DiameterBlood ViscosityVessel Length
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Pressure and Resistance
Increased Resistance = Increased Pressure
Increased Resistance = Increased Work of the Heart
Measurement: 120/80 mm Hg
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Vasoconstriction:Decreases Vessel DiameterIncreases ResistanceIncreases Diastolic BP
Increases Work of HeartIncreases SBP later
SNS, Cold, Hemorrhage etc cause vasoconstriction to “rescue” vital organs
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Vasodilation:Increases Vessel DiameterDecreases ResistanceDecreases Diastolic PressurePSNS, Heat, Local Exercise
Demand cause vasodilation to perfuse skin, muscles for special situations
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Arteriosclerosis
Limits VasodilationIncreases ResistanceIncreases PressureRisk Factors:
Obesity, Cholesterol, Inactivity, Smoking, Aging, Heredity
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Systolic and Diastolic BP:Systolic: Ventricular Systole
Greatest Arterial PressureReflects CO and heart’s contribution to
BPDiastolic: Ventricular Diastole
Lowest Arterial PressureReflects the resistance of the vessels to
CO
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Assignment:Assignment:We have focused on Short-Term
regulation of blood pressure…What causes chronic
hypertension?Answer: What is the role of the
kidneys and other hormones in the long term control of blood pressure?