Cardiovascular Anatomy and Physiology REVIEW Reading: Brubaker 2:37-56

Normal Heart Myocardial Infarct (LAD) Photos: Klatt, Edward C. MD, WebPath.edu

Primary Cardiac Function = Tissue Perfusion Morbidity and Mortality of Cardiovascular Disease: Inadequate Cardiac Output Reduced Perfusion (O 2 ) to the “BIG THREE” vital organs: Brain, Heart, Lungs Other Organ Failure: Kidneys, Liver, GI, Skeletal Muscle

Cardiac Anatomy Cardiac Anatomy: Pericardium: Visceral / Parietal connective tissue “wrapping” Epicardium: next to the heart Pericardial space: fluid filled Fibrous/serous pericardium: Prevents overdistension of the heart and produces fluid Cardiac Tamponade: Life threatening Accumulation of fluid in p. space

Layers of Heart Tissue Layers 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: Myocardium: Cardiac muscle layer Endocardium: Connective + Epithelial Tissue Structural “Scaffolding Valves Chordae Tendinae

Endothelial “Scaffolding ”  Endocardium The fibrous network forms chambers of the Ventricles

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

Coronary Arteries: Left Coronary Artery: Origin: Left side of AORTA Supplies: Anterior/Left Heart Right Coronary Artery: Origin: Rt. Side of AORTA Supplies: Right Heart

Rt. Marginal Branch

Coronary Artery Bloodflow Regulation: Aortic Pressure is primary regulator Sympathetic: Net Increase in Bloodflow Parasympathetic: Maintain Bloodflow Metabolic: Bloodflow = VO 2

Cardiac Cycle and Coronary Artery Flow: Systole: The aortic valve opens, and “covers” the Coronary arteries Blood flow is prevented Diastole: The aortic valve closes, “opens” the coronaries Blood Flow is restored What would be the effect of increased HR on Coronary blood flow (perfusion)?

Coronary Artery Disease: CAD 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 Coronary Artery Atherosclerotic Artery Photos: Klatt, Edward C., WebPath.com

Cardiovascular Function: PUMP: Heart contractions propel Blood throughout the circulation!

Cardiac Cycle Cardiac Cycle: Ventricular Systole: Ventricles Contract – eject blood Tri/Bicuspid valves close First Heart Sound: “Lubb” Ventricular Diastole: Ventricles relax, fill Pulmonary/Aortic Valves close Second Heart Sound: “Dupp”

The Atria: “Collection” of blood from either: Right: The systemic circulation (low PO 2 ) Left: The pulmonary circulation (high PO 2 ) Atrial Contraction: Empties the final 30% of the End Diastolic Volume (EDV) What is the impact of Atrial Fibrillation On Cardiac Output?

Right Ventricle pumps blood to the lungs u Right Ventricle contracts u Increased pressure causes tricuspid valve closure u Blood leaves heart via Pulmonary Artery u Only artery with O 2

Left Ventricle Pumps Blood to the Body u The Left Ventricle contracts u Mitral Valve: Closes u Aortic Valve: Opens u Blood is pumped out via the Aorta Aorta

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 Blood Pressure Systolic: Systole causes increased pressure in the arterial vessels: Systolic pressures indicate the strength of cardiac contraction Diastolic: During diastole, arterial pressure is at it’s lowest Diastolic Pressures indicate the total resistance to blood flow

Cardiac Output: HR X SV CO = HR X SV “Emergencies” SNS Autonomic NS Increase HR/SV = Increase CO “Relaxing” – Status Quo: PSNS Autonomic NS Decrease HR = Decrease CO

Electrophysiology of the Heart: ECG P: Atrial Depolarization/contraction QRS: Ventricular Depol/Contraction T: Ventricular Repolarization

Cardiac Muscle Cells Cardiac Muscle Cells: Striated, Branched, Intercalated Discs Slower Action Potential than nerve or skeletal muscle cells Voltage Gated Ca++ Channels!

Electrical Activity: Excitation - Contraction To 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 Potential mV ECG AP

Why the Plateau Phase 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… Contractions of the ventricles and atria must alternate The excitation of the heart muscle follows a predictable path

Conduction System: SA Node: bpm AV Node: Slows the message down AV Bundles: (also His): L./R. Bundle Branches: Purkinje Fibers:

Heart Conduction System The Sino-Atrial node (SA) serves as the pacemaker for the heart. When the SA node fires, it causes both atria to contract The excitation- contraction signal is then “conducted” to the ventricles via the AV Node SA

Heart 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 Heart Rate  The SA node has an Intrinsic Rate of 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 System  “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 System  “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 System  The adrenal medulla (above kidney) secretes Catecholamines:  Epinephrine  Norepinephrine  Stimulated by and mimics the Sympathetic Nervous System  Slower/Longer acting

Regulation of Cardiac Output: Cardiac Output: Changes in CO are responses to “Homeostatic Emergencies”: Pressure Emergencies Chemical Emergencies

Baroreceptors: Sensing Pressure Emergencies Increase CO = Increase Systolic BP Emergency 1: Decreased Pressure Increase SNS: Increased HR X SV = Increased CO Problem 2: Increased Pressure Decrease SNS: Decrease HR = Decreased CO

Chemoreceptors: Sensing Metabolism Emergencies Emergency 1: Increased Metabolic Rate: Increased CO 2, 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 Law Increased Venous Return Increased cardiac muscle stretch Increase contraction force Increased 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 Heart Remember that though the nerves are no longer signaling, there is another (though slower and longer acting) source of control…

Blood Vessels And Circulation

Peripheral Circulation: Systemic Circulation: Blood vessels directing blood to the body tissues Left Heart to Right Heart Pulmonary Circulation: Blood vessels directing blood to the lungs for gas exchange Right Heart to Left Heart What do we call the circulation to The heart?

Perfusion Homeostasis Perfusion 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”: 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 O 2 and nutrient rich…”Supply” to tissues

Arteries: Structure/Function High 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 O 2 – carrying wastes for removal

Veins: Structure/Function Low 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 Pressure Cardiac Output: Reflected by Systolic blood pressure Vascular Resistance: Reflected by Diastolic Pressure Vessel Diameter Blood Viscosity Vessel Length

Pressure and Resistance Increased Resistance = Increased Pressure Increased Resistance = Increased Work of the Heart Measurement: 120/80 mm Hg

Vasoconstriction: Decreases Vessel Diameter Increases Resistance Increases Diastolic BP Increases Work of Heart Increases SBP later SNS, Cold, Hemorrhage etc cause vasoconstriction to “rescue” vital organs

Vasodilation: Increases Vessel Diameter Decreases Resistance Decreases Diastolic Pressure PSNS, Heat, Local Exercise Demand cause vasodilation to perfuse skin, muscles for special situations

Arteriosclerosis Limits Vasodilation Increases Resistance Increases Pressure Risk Factors: Obesity, Cholesterol, Inactivity, Smoking, Aging, Heredity

Systolic and Diastolic BP: Systolic: Ventricular Systole Greatest Arterial Pressure Reflects CO and heart’s contribution to BP Diastolic: Ventricular Diastole Lowest Arterial Pressure Reflects the resistance of the vessels to CO

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?