Anatomy of the Heart
Right Chamber: Provides oxygen-poor blood through the Lungs |
Left Chamber: Provides oxygen-rich blood through the Body |
Right Atrium: Oxygen-poor blood (from body) travels to the right AV (Tricuspid) Valve |
Right Ventricle: Oxygen-poor blood (right atrium) travels to the Pulmonary Artery via the Pulmonary (Semilunar) Valve |
Left Atrium: Oxygen-rich blood (from lungs) travels to the left ventricle through the left AV (Bicuspid/Mitral) Valve |
Left Ventricle: Oxygen-rich blood (left atrium) travels to the Aorta via the Aortic (Semilunar) Valve |
Heart Valves: Allows blood to flow in one direction |
High Pressure Behind Valve: Valve opens |
High Pressure In Front of Valve: Valve closed; does NOT open, ONLY opens in one direction |
Chordae Tendineae: Tendinous fibers that connect AV valves to Papillary Muscles, preventing Everting of the AV valves during ventricular contraction |
Connective Tissue: Dense fibrous ring that surrounds each heart valve and separates the atria from the ventricles, providing an anchor for the heart valves/cardiac muscle |
Endocardium: Thin layer of endothelial tissue surrounding the inside of the heart chamber |
Myocardium: Middle layer linked by Intercalated Disks, forming 2 contacts: Desmosomes and Gap-Junctions |
Desmosomes: Responsible for clustering cells |
Gap-Junctions: Allow low-resistant electrical flow between muscle cells, forming a Functional Syncytium |
Epicardium: Thin outer membrane containing a small volume of Pericardial Fluid |
Pericardial Fluid: Fluid that prevents heart from getting friction |
Mechanical Events of the Cardiac Cycle
Systole: Contraction and Emptying |
Diastole: Relaxation and Filling |
End-Diastolic Volume: Blood volume left at the end of Diastole (Maximum amount of blood held in chamber during the cycle) |
Isovolumetric Ventricular Contraction: Chamber is closed (no blood can enter/leave); pressure Increases |
End-Systolic Volume: Blood volume left after Systole (Complete ejection) |
Stroke Volume: Amount of blood pumped out (End Diastolic Volume - End Systolic Volume) |
Isovolumetric Ventricular Relaxation: Chamber is closed (no blood can enter/leave); Pressure Decreases |
Regulation of Cardiac Output
Cardiac Output (C.O.): Blood volume pumped (per minute) depending on the heart rate and stroke volume |
Heart Rate: Regulated by Parasympathetic and Sympathetic Nervous Systems |
Stroke Volume: Volume of venous blood return (Intrinsically) and the Sympathetic Nervous System (Extrinsically) |
C.O. Equation: C.O. = H.R. x S.V. |
Heart Rate Regulation: Mainly controlled by autonomic input, affecting the hypersensitivity of SA node |
Parasympathetic: Vagus Nerve contributes to the SA/AV nodes and the contractile cells |
Parasympathetic Input: Mediated by Acetylcholine (ACh), a neurotransmitter |
Acetylcholine: Causes heart rate to decrease |
Parasympathetic and Sympathetic Inputs
Blood
Blood Flow: Calculated by Pressure Gradient and Resistance and Viscosity |
Equation: F = (Delta) P/R |
Flow Rate (F): Blood volume going through a vessel **(Proportional to r4) |
Pressure Gradient (P): Difference of pressure from the beginning compared to the end of a vessel |
Resistance (R): Resistant of flow (Proportional to 1/r4) (3 Factors): |
(1) Blood Viscosity: Blood friction due to plasma protein (conc.) and red blood cell count |
(2) Vessel Length: Blood friction along vessel walls (Proportional to length) |
(3) Vessel Radius: Blood friction along vessel walls (Inversely Proportional to 1/r4) |
Baroreceptors
Baroreceptor Reflex: Regulates cardiac output and total peripheral resistance |
Baroreceptors: Mechanoreceptors detect blood pressure through force of the pressure |
Baroreceptor Reflex (High BP): Decrease heart rate, stroke volume, arteriolar, and venous vasodilation |
Baroreceptor Reflex (Low BP): Increase heart rate, stroke volume, arteriolar, and venous vasodilation |
Local Physical Control
Temperature: Inversely proportionate to Arteriolar Smooth Muscle Tone |
Myogenic Response: Arteriolar smooth muscle contract when stretched |
Intrinsic (Local) Metabolic Changes (Control)
Local Metabolic Changes: Cause dilation in smooth muscle tone via Mediators (Nitric Oxide) |
O2 Concentration: Decreases as metabolism increases (Inverse) |
CO2 Concentration: Increases as metabolism increases (Proportional) |
pH: CO2 increases and blood pH lowered by Lactic Acid |
Extracellular K+ Concentration: Increased neuronal activity exceeding Na+/K+ ATPase |
Osmolarity: Increase solute concentration |
Adenosine: Released when metabolism is increased |
Prostaglandins: Derived from fatty acid metabolism |
Histamine Release: From damaged tissues, causing vasodilation and inflammation |
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Electrical Activity of the Heart
Autorhythmicity: Self-generated rhythmic activity from cardiac muscle cells that produce Pacemaker Activity |
Pacemaker Cells: Clustered into Nodes, regulating rate and coordination of contractions |
Pacemaker Activity: 1% of cardiac muscle (Autorhythmic and Intrinsically) that self-generate AP at a regular frequency via Pacemaker Potentials |
Contractile Cells: 99% of the cardiac muscles that are responsible for pumping but DO NOT self-generate AP |
Autorhythmic Cells: Cyclically generate AP (through heart) to trigger rhythmic contractions |
Nodes: Clusters of cells that produce pacemaker activity |
Sinoatrial (SA) Node: Cluster of pacemaker cells (right atrium), firing 70 AP per minute (Fastest) |
Atrioventricular (AV) Node: Cluster of pacemaker cells (right atrium), firing 50 AP per minute (Slower) |
Bundle of His: Pacemaker cells (AV node) that branches to the left/right ventricles |
Purkinje Fiber: Small pacemaker cells (Bundle of His), spreading through ventricular myocardium, firing 30 AP per minute (Slowest) |
Interatrial Pathway: Cardiac cells that carry pacemaker activity (Right atrium -> Left atrium) |
Internodal Pathway: Cardiac cells that transmit pacemaker activity from the SA node to the AV node |
AV Nodal Delay: 100ms delay in AV Node conduction, ensuring that the ventricles contract after atrial contraction |
Mechanical Events of the Cardiac Cycle Diagram
Parasympathetic Release of Acetylcholine
SA Node: Higher permeability to K+, delaying inactivation of K+ channels, causing Greater Hyperpolarization and Slow K+ of pacemaker potential |
AV Node: Higher permeability to K+, reducing excitability and delay response to input from SA Node |
Atrial Contractile Cells: Reduces Ca2+ permeability and strength of contraction |
Sympathetic Release of Norepinephrine
Sympathetic Nerves: Increase heart rate by supplying the SA/AV Nodes and ventricles via Norepinephrine through Beta-Adrenergic receptors |
SA Node: Lower K+ permeability speeds up inactivation K+ channels leading to Less Hyperpolarization and faster K+ |
AV Node: Increase conduction velocity, reduce AV nodal delay, and slightly increase Ca2+ permeability |
Bundle of His & Purkinje Fibers: Similar actions as the AV Node |
Atrial/Ventricular Contractile Cells: Increase contractile strength via increasing Ca2+ permeability |
Basic Organization
Arteries: Large vessels that carry blood away from the heart |
Arterioles: Small (Diameter) vessel branches from arteries that lead to the organs |
Capillaries: Smallest (Diameter) vessels formed when arterioles branch |
Venules: Vessels that form when capillaries join together |
Veins: Large (Diameter) vessels formed by merging venules |
Microcirculation: Collection of arterioles, capillaries, and venules |
Functions
Arteries: Channel for low resistance blood flow due to Pressure Reservoir |
Pressure Reservoir: Driving force during Ventricular Diastole due to elasticity of artery walls (Elastin), which can expand and store pressure |
Arterioles: Vascular resistance in circulatory system regulates cardiac output and arterial pressure, both Intrinsically and Extrinsically |
Capillary Exchange: Exchanges materials between blood and interstitial space |
Interstitial Fluid: Same composition as arterial blood |
Exchange: Through (1) Diffusion and (2) Bulk Flow |
Diffusion: Blood moving down its concentration gradient |
Bulk Flow: Maintains fluid balance between blood and extracellular space; permits flow of plasma (NOT proteins/blood cells) |
Ultrafiltration: Bulk flow in tissues |
Reabsorption: Bulk Flow in capillaries |
Veins: Reservoir for blood and channel for blood flow to heart |
Venous Capacity: Volume of blood veins can withstand |
Venous Return: Volume of blood entering each atrium per minute |
Factors That Influence Bulk Flow
(1) Capillary Blood Pressure (Pc): Pushes fluid from capillaries to the interstitial fluid |
(2) Plasma-Colloid Osmotic Pressure (πp): Draws water into capillaries from interstitial fluid via protein concentration |
(3) Interstitial Fluid Hydrostatic Pressure (PIF): Pushes fluid into capillaries from the interstitial fluid |
(4) Interstitial Fluid-Colloid Osmotic Pressure (πIF): Draws water out of capillaries to the interstitial fluid |
Ultrafiltration: Positive net pressure |
Reabsorption: Negative net pressure |
Net Pressure: (Pc + πIF) - (PIF + πp) |
Blood Pressure Abnormalities
Hypertension : High BP above 140/90 mmHg |
Primary Hypertension: 90% of cases, unknown |
Secondary Hypertension: 10% of cases, occurs 2nd to 1st |
Hypotension: Low BP below 100/60 mmHg |
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Pacemaker Activity of Cardiac Cells
Pacemaker Activity of Cardiac Autorhythmic Cells
Electrical Activity of the Heart (Cont.)
Excitation-Contraction Coupling: Ca2+ entry into the cytosol differs from that in skeletal muscle cells |
Dyhydropyridine Receptors: Voltage-gated Ca2+ channels in cardiac T-Tubules |
AP Invades T-Tubule Membranes: Dyhydropyridine Receptors open, letting Ca2+ enter the cytosol |
Ca2+ Entry: Triggers more Ca2+ release from the SR; both sources of cytosolic Ca2+ drive contraction strength based on Ca2+ concentration (Proportional to # of cross-bridges) |
Electrocardiogram (ECG): Records heart's electrical activity (AP) via surface voltage differences to detect abnormalities |
ECG Waveforms (P-Wave): Depolarization of the Atria |
ECG Waveforms (QRS-Complex): Depolarization of the Ventricles |
ECG Waveforms (T-Wave): Repolarization of the Ventricles |
ECG Waveforms (PR-Segment): AV Node Delay |
Electrocardiogram Waveforms
Heart Sounds
Lub: Low-pitched, soft and relative long (AV Valves closes) |
Dup: High-pitched, sharp and short sound (Semilunar Valves closes) |
Murmurs: Uncommon heart sounds (cardiac disease) from turbulent blood flow through broken valves |
Stenotic Valve: Does NOT OPEN Completely; Producing Whistling sounds |
Insufficient Valve: Does NOT CLOSE Properly; Producing Swishing sounds |
Stroke Volume Regulation
Extrinsically: Sympathetic Nervous System controls neural activity |
Intrinsically: Venous Blood Return (Volume) |
Function of Both Factors: Increase SV by raising contraction strength |
Intrinsic Control: The Frank-Starling Law of the Heart (End-diastolic volume and SV) |
Frank-Starling Curve
Sympathetic Stimulation: Shifts the Frank-Starling curve to the left |
At End-Diastolic Volume: Increase Ca2+, which increases contractile force and SV |
Heart Failure: Decrease cardiac contractility and shifts curve downward and to the right |
Frank-Starling Curve (Graph)
Sphygmomanometer
Sphygmomanometer: Used to measure Systolic and Diastolic pressure by listening to sound of blood |
Pressure >120 mmHg: No blood flow and no sound |
Pressure between 120-180 mmHg: Turbulent blood flow and intermittent sounds |
Pressure <80 mmHg: Smooth blood flow and no sound |
Pressure Throughout the Systemic Circulation
Left Ventricular Pressure: Between 0 mmHg (During Diastole) to 120 mmHg (During Systole) |
Arterial Pressure: Fluctuates between 120 mmHg (Systolic) to 80 mmHg (Diastolic) |
Arteriolar Pressure: Large pressure drop (Systolic to Diastolic convert to Non-Pulsatile Pressure) |
Pressure: Decline at slower rate (When blood flows through capillaries and venous system) |
Arterial Pressure
Pulse Pressure: Difference between Systolic and Diastolic pressure |
Mean Arterial Pressure: Regulated by blood pressure reflexes |
Mean Arterial Pressure Diastolic Pressure + 1/3 Pulse Pressure |
Arterial Pressure (Graph)
Factors Influencing Venous Return
Sympathetic Activity: Causes vasoconstriction, increasing venous pressure/return |
Skeletal Muscle Activity: Skeletal muscles contract, squeezing veins and increases venous pressure |
Venous Valves: Prevent backflow (In lumen of large veins) |
Respiratory Activity: Chest pressure decreases during respiration, increasing pressure between veins and lower body/chest |
Cardiac Suction: Below 0 mmHg during ventricular contraction, increasing venous pressure and pulling venous blood into atria |
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