Cardiovascular Anatomy and Physiology

REVIEW

Reading:

Brubaker 2:37-56

Normal HeartNormal Heart Myocardial Myocardial Infarct (LAD)Infarct (LAD)

Photos: Klatt, Edward C. MD, WebPath.edu

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

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

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

Heart Layers: Heart Layers:

Myocardium: Cardiac muscle layer

Endocardium: Connective + Epithelial TissueStructural “ScaffoldingValvesChordae Tendinae

Endothelial “ScaffoldingEndothelial “Scaffolding””

Endocardium The fibrous network forms chambers of the Ventricles

Myocardium:Myocardium:

You end up with a very strong muscle in the shape of a multi-chambered pump

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

Rt.MarginalBranch

Coronary Artery Bloodflow Coronary Artery Bloodflow Regulation:Regulation:Aortic Pressure is primary

regulatorSympathetic: Net Increase in

BloodflowParasympathetic: Maintain

BloodflowMetabolic: Bloodflow = VO2

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)?

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!

Fatty Arteries:

Normal CoronaryArtery

AtheroscleroticArtery

Photos: Klatt, Edward C., WebPath.com

Cardiovascular Cardiovascular Function:Function:

PUMP: Heart contractions propel Blood throughout the circulation!

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”

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?

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

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

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

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

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

Electrophysiology of Electrophysiology of the Heart: ECGthe Heart: ECG

P: Atrial Depolarization/contractionQRS: Ventricular Depol/ContractionT: Ventricular Repolarization

Cardiac Muscle CellsCardiac Muscle Cells:Striated, Branched, Intercalated

DiscsSlower Action Potential than

nerve or skeletal muscle cellsVoltage Gated Ca++

Channels!

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.

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

Myocardial Action PotentialMyocardial Action Potential

mV

-100

+40

0

4

0

1 2

3

4

ECG

AP

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

Coordinating the Beats…Coordinating the Beats…

Contractions of the ventricles and atria must alternate

The excitation of the heart muscle follows a predictable path

Conduction System:Conduction System:SA Node: 90-100 bpmAV Node: Slows the message

downAV Bundles: (also His):L./R. Bundle Branches:Purkinje Fibers:

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

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”

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

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

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

Endocrine SystemEndocrine System

The adrenal medulla (above kidney) secretes Catecholamines: Epinephrine Norepinephrine

Stimulated by and mimics the Sympathetic Nervous System Slower/Longer acting

Regulation of Cardiac Regulation of Cardiac Output:Output:Cardiac Output: Changes in

CO are responses to “Homeostatic Emergencies”:

Pressure EmergenciesChemical Emergencies

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

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

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….

Final Question: In a Heart

Transplant, the heart is “denervated”

How does someone with a heart transplant respond to exercise?

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…

Blood Vessels And Blood Vessels And CirculationCirculation

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?

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

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)

Arteries: Vessels taking

blood Away From The Heart

Usually O2 and nutrient rich…”Supply” to tissues

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

Veins: Vessels returning

blood Back To The Heart

Usually low in O2 – carrying wastes for removal

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

Arterial Blood PressureCardiac Output: Reflected by

Systolic blood pressureVascular Resistance:

Reflected by Diastolic PressureVessel DiameterBlood ViscosityVessel Length

Pressure and Resistance

Increased Resistance = Increased Pressure

Increased Resistance = Increased Work of the Heart

Measurement: 120/80 mm Hg

Vasoconstriction:Decreases Vessel DiameterIncreases ResistanceIncreases Diastolic BP

Increases Work of HeartIncreases SBP later

SNS, Cold, Hemorrhage etc cause vasoconstriction to “rescue” vital organs

Vasodilation:Increases Vessel DiameterDecreases ResistanceDecreases Diastolic PressurePSNS, Heat, Local Exercise

Demand cause vasodilation to perfuse skin, muscles for special situations

Arteriosclerosis

Limits VasodilationIncreases ResistanceIncreases PressureRisk Factors:

Obesity, Cholesterol, Inactivity, Smoking, Aging, Heredity

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

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?