CH18 PowerPoint

Cardiovascular System

Circulatory System: the heart, blood vessels, and blood.

Cardiovascular System: Heart, arteries, veins, and capillaries.

Arteries vs. Veins →

Capillaries: The site of exchange between blood & tissues.

  • pulmonary circuit refers to the pathway from the heart to the lungs and back

  • systemic circuit involves the pathway from the heart to the rest of the body and back

Blood Vessels & Cardiac Muscle Structure

Blood Vessels →

Heart: Central organ of the circulatory system.

Blood Vessels:

  • Arteries: Carry blood away from the heart.

  • Veins: Return blood to the heart.

  • Capillaries: Facilitate exchange with air sacs & cells.

Cardiac Muscle

Cardiomyocytes (Cardiac Myocytes):

  • No terminal cisternae (lacking triads)

  • Possess large T-tubules (permit extracellular calcium influx)

  • These cells cannot undergo mitosis.

Intercalated Discs:

  • Interdigitating Folds: Enhance surface area for cell connections.

  • Mechanical Junctions: Desmosomes provide structural unity.

  • Electrical Junctions: Gap junctions allow functional unity by permitting electrical impulses to pass.

Cardiac Muscle is Autorhythmic

Origin of Heartbeat: Signal for heartbeat = from heart muscle itself

  • The nervous system only modifies the heart rate.

  • Independent/coordinated heart activity depends on gap junctions & the intrinsic cardiac conduction system.

Comparison between Skeletal & Cardiac Muscle

Neural Stimulation

Skeletal Muscle → Requires neural stimulation for each fiber.

Cardiac Muscle →

  • Pacemaker Cells: Spontaneously depolarize, no neural input.

    • Skeletal muscle strength increases w/ more motor units activated.

    • Cardiac muscle acts as a functional syncytium, meaning the entire heart functions together w/o recruitment.

Stimulus for Calcium Release →

  • Skeletal muscle, AP open calcium channels on terminal cisternae.

  • In cardiac muscle, action potentials open both slow Ca²⁺ release channels & extracellular Ca²⁺ channels.

ATP Production

  • Both types of muscles utilize anaerobic & aerobic respiration, but cardiac muscle mainly uses aerobic respiration.

Pacemaker Cells

*Approx. 1% of cardiac cells are specialized noncontractile pacemaker cells.

  • unstable resting membrane potential (RMP).

  • Continuously depolarize, drifting toward threshold.

Pacemaker & Action Potentials

Cardiac Conduction System → Composed of noncontractile cardiac cells specialized for initiating & conducting impulses thru the heart:

  1. Sinoatrial (SA) node: Primary pacemaker.

  2. Atrioventricular (AV) node: Relays impulses between atria & ventricles.

  3. Atrioventricular (AV) bundle (Bundle of His): Conducts impulses into the ventricles.

  4. Right and Left Bundle Branches: Branch off from the AV bundle.

  5. Purkinje Fibers: Deliver impulses to ventricular myocardium.

Physiology of the SA Node

Cells of SA Node: Exhibit unstable resting membrane potential (RMP).

  1. Pacemaker Potential:

    • changing membrane potential triggers an AP.

    • Begins at -60 mV, w/ continuous drift towards the threshold (-40 mV) facilitated by Na⁺ influx thru “slow” voltage-gated ion channels.

    • no outflow of K⁺ to counterbalance the + ion influx.

    • interior of the cell becomes increasingly +, drifting towards the threshold.

  2. Reaching threshold (-40 mV) triggers voltage-gated fast calcium channels to open, allowing Ca²⁺ to diffuse in from extracellular fluid (ECF).

*This rapid influxgenerates the depolarization phase of the AP.

*pacemaker cell depolarization is due primarily to Ca²⁺ influx.

Depolarization Peak: just above 0 mV.

  • Fast voltage-gated Ca²⁺ channels close.

  • Voltage-gated K⁺ channels open, prompting K⁺ to exit the cell, which leads to repolarization (falling phase).

  • Once repolarization is complete, K⁺ channels close, & Na⁺ channels reopen, initiating a new pacemaker potential.

*each depolarization of the SA node triggers a heartbeat

Auto-Rhythmicity of Pacemaker Cells

Locations of Pacemaker Activity:

  • SA Node: 75 APs per min.

  • AV Node: 50 APs per min.

  • Bundle Branches & Purkinje Fibers: 30 APs per minute each.

Ectopic Focus: slower pacemaker activity when faster structures become nonfunctional.

Impulse Conduction

When SA node fires, an AP travels across the atria via gap junctions reaching the AV node

Impulse Delay at AV Node: the smaller diameter of muscle fibers & fewer gap junctions result in slowed conduction

*allows time for the atria to contract & push blood into the ventricles b4 the signal is passed on

Atrial and Ventricular Connectivity

Atria & ventricles are not directly linked by gap junctions- the AV node/AV bundle serves as the only electrical connection, maintained by the fibrous skeleton, which acts as an electrical insulator.

*AV node bifurcates into right & left bundle branches within ventricular septum.

Purkinje Fibers: complete the conduction pathway to the apex, rapidly transmitting the impulse to the ventricular walls.

Importance of Purkinje Fibers:

  • ventricular myocardium cannot rely on gap junctions due to mass; hence Purkinje fibers assist in quick depolarization.

  • The left ventricle contains elaborate Purkinje network than the right.

  • Papillary muscles are connected to Purkinje fibers to tense AV valves

Contraction Timing

*ventricular myocardium depolarizes in 200 – 220 ms following SA node firing, facilitating synchronized contraction.

Ventricular Systole: initiated @ apex, pushes blood upwards toward semilunar valves, w/ muscle cells oriented in a spiral pattern (like wringing a towel)

Contractile Cell Depolarization

Contractile Cardiac Myocytes: have a stable resting potential around -90 mV.

*action potential arrives by conduction system or thru gap junctions (into contractile myocyte)

Action Potential Mechanism:

  • voltage-gated Na⁺ channels open, Na⁺ diffuses in, leads depolarization to threshold.

  • Once threshold is reached, Na⁺ channels open due to positive feedback, peaking +30 mV before closing.

Electrical Behavior of Myocardium

Myocardial Action Potential Phases:

  • Rapid depolarization due to influx of Na⁺.

  • Following depolarization, Na⁺ channels close, & K⁺ channels open for repolarization.

  • Slow Ca²⁺ channels open, causing Ca²⁺ influx from ECF to prolong depolarization, creating a plateau phase.

  • Ca²⁺ channels close while K⁺ channels stay open for rapid repolarization.

Role of Ions in Myocyte Function

*influx of Na⁺ depolarizes cardiac contractile cells.

Slow Ca²⁺ entering from ECF extends the depolarization, allowing for a plateau phase:

  • cardiac muscle exhibits prolonged depolarization of approx. 200-250 ms w/ resting 80 HR.

Ca²⁺ released from the sarcoplasmic reticulum binds to troponin, triggering actual contractions.

Repolarization Phase

End of Plateau Phase: Ca²⁺ channels close, while K⁺ channels remain open allowing K⁺ to diffuse out of the cell & Ca²⁺ is pumped back into extracellular fluid & sarcoplasmic reticulum, leading to myocardial relaxation.

Cardiac Rhythm and Cycle

Systole: contraction phase.

Diastole: relaxation phase.

Sinus Rhythm: Normal heartbeat regulated by SA node, 70-80 beats per min.

Arrhythmia: irregularities in heart rate/rhythm.

The Cardiac Cycle

One complete contraction & relaxation of all 4 heart chambers includes:

  • Ventricular Filling: Blood fills the ventricles.

  • Isovolumetric Contraction: Ventricles contract w/o volume change.

  • Ventricular Ejection: Blood is ejected from the ventricles.

  • Isovolumetric Relaxation: Ventricles relax w/o volume change.

Phases of Ventricular Filling

Occurs during ventricular diastole →

  • As ventricles expand, volume increases as pressure decreases.

  • When pressure in ventricles falls below atrial pressure, AV valves open allowing blood flow into ventricles. (Semilunar valves remain closed during this phase)

Three Phases of Ventricular Filling

  1. Rapid Ventricular Filling: blood flows passively from atria to ventricles through open AV valves with closed semilunar valves.

  2. Diastasis: slower filling phase where AV valves drift toward closure, completing approximately 70% of ventricular filling.( Atrial depolarization marked by P wave occurs @ end of this phase)

  3. Atrial Systole: atrial contraction completes the filling process by adding the final 30% of ventricular filling, raising internal pressure.

    • End-Diastolic Volume (EDV): total volume of blood in the ventricles at the end of filling (~130 ml), with 40 ml contributed by atrial systole.

Isovolumetric Contraction Phase

Atrial Repolarization: Following atrial contraction, atria relax and remain in diastole.

Ventricular Depolarization: Generates the QRS complex on the ECG, subsequent contraction begins.

Ventricular Pressure Increase: A sharp rise in pressure reverses the pressure gradient, closing AV valves as blood surges against valve cusps.

Isovolumetric Contraction: All 4 valves are closed during this phase as ventricles contract w/o changing volume.

*Heart Sound S1 (Lub): Generated as AV valves close.

Isometric vs. Isotonic Contraction

Isovolumetric → ventricles contract w/o a change in volume since arterial pressures prevent semilunar valve opening.

  • Myocytes exert force but cannot shorten due to the incompressibility of blood.

Ventricular Ejection Phase

Threshold Pressure: When ventricular pressure surpasses arterial pressure, semilunar valves open:

*Peak pressures: 120 mmHg in left ventricle, 25 mmHg in right ventricle.

Ejection Dynamics: Initial rapid ejection followed by reduced pressure yields decreased ejection volume.

Blood Volume Ejected During Ejection Phase

*ventricles do not expel all blood during this phase:

Stroke Volume (SV): Amount of blood ejected per beat (~70 ml).

End-Diastolic Volume (EDV): Total volume pre-ejection (~130 ml).

Ejection Fraction (EF): Percent of EDV ejected (cardiac health) (e.g., 54% from 70/130).

End-Systolic Volume (ESV): Volume left in ventricles after ejection (EDV - SV = ESV).

Isovolumetric Relaxation Phase

*Begins early ventricular diastole marked by the T wave on ECG as ventricles repolarize.

Ventricular Recoil: Involves pressure drops due to elastic recoil of the fibrous skeleton.

*ventricular pressure declines, backflow from arteries causes semilunar valves to close:

  • Resulting in Dicrotic Notch: A slight pressure increase in the aorta upon closure of the semilunar valves, generating heart sound S2.

Isovolumetric Phase

Isovolumetric expansion: All valves remain closed w/ no volume changes until AV valves reopen, & filling resumes.

Quiescent Period: total relaxation state of the heart where no chambers contract, allowing blood to flow into the atria with AV valves open. (70% ventricular filling)

Control of Blood Flow & Volume Changes

  1. Blood flow thru the heart is managed by pressure gradients

  2. Pressure gradients emerge from synchronized contraction & relaxation cycles of different chambers.

  3. Blood flows following the gradient from high-low pressure via available openings (valves) w/o muscular/nerve involvement.

  4. Same Volume Ejection: Each ventricle pumps equivalent blood amounts during each cycle (~70 ml) despite differing pressures (e.g., right ventricle at 1/5 left pressure). (*Imbalance can lead to complications (e.g., RV pumping more pressure than LV can handle causes fluid accumulation in lungs))

Left-Sided Heart Failure

(Most common type) of heart failure, arises when R ventricular output exceeds the L.

Over time, more blood enters pulmonary circulation than returns, resulting in →

  • Increased ESV in left ventricle, it cannot accommodate all incoming blood from pulmonary veins.

  • Fluid accumulation in the lungs presents as pulmonary congestion.

Right-Sided Heart Failure

*Occurs when output from the left ventricle exceeds the right ventricle.

Leads to fluid buildup in systemic tissues as blood pools due to inadequate right ventricular output.

Jugular Vein Distention: A secondary sign indicating heart failure.

Biventricular Heart Failure

Congestive heart failure when fluid builds up in either lungs/peripheral tissues

  • begins as left-sided heart failure, may progress to right-sided failure over time.

*Decreased cardiac output, systemic congestion, & poor prognostic outcomes

Cardiac Output Definition and Calculations

Cardiac output = volume of blood ejected by each ventricle per minute.{ ml/min}$$

Cardiac Reserve: Difference between maximum cardiac output & resting cardiac output.

Heart Rate Variability

Pulse Frequencies:

  • Newborns: 120 bpm

  • Young adult females: 72-80 bpm

  • Young adult males: 64-72 bpm (Ageing leads to an increased heart rate)

Tachycardia: resting adult HR >100 bpm, often compensatory for decreased stroke volume.

Bradycardia: persistent resting heart rate <60 bpm; common in endurance-trained athletes, reflecting larger hearts & increased stroke volume w/ fewer beats.

Chronotropic (modifications) Effects on Heart Rate

Positive Chronotropic Effects: Factors that elevate heart rate.

Negative Chronotropic Effects: Factors that decrease heart rate.

Cardiac Centers in Medulla

Cardio-Acceleratory Center (CAC): sympathetic control via cardiac accelerator nerves targeting SA & AV nodes.

*Norepinephrine binding to beta-adrenergic receptors induces a + chronotropic response

Cardioinhibitory Center (CIC):

Via vagus nerve to the SA node & AV node, employing parasympathetic activity.

*Acetylcholine binding to muscarinic receptors decreases heart rate.

Chemical Influences on Heart Rate

Catecholamines (Epinephrine, Norepinephrine): powerful cardiac stimulants by binding to beta-1 receptors, triggering 2nd messenger systems (cAMP) leading to Ca²⁺ influx, quicker depolarization.

Caffeine: enhances heart rate thru inhibition of cAMP breakdown.

Nicotine: stimulates catecholamine release, impacting HR positively.

Thyroid Hormone: upregulates adrenergic receptors, increasing sensitivity to sympathetic influences.

Potassium Levels →

  • Hyperkalemia: High K⁺ levels cause increased diffusion into myocytes, leading to depolarization and reduced excitability.

  • Hypokalemia: Low K⁺ levels cause hyperpolarization, requiring greater stimuli for action potential initiation.

Calcium Levels →

  • Hypercalcemia: Increases heart rate & contractility, overly much can induce complications.

  • Hypocalcemia: Decreases heart rate.

Additional Influences on Heart Rate

Age: Heart rate is fastest during gestation, decreasing w/ age.

Gender: Women exhibit generally faster HRs than men, linked to variations in RBC compositions

Exercise → Bainbridge Effect: Increased venous return stretches atrial walls triggering sympathetic activation.

Body Temperature: higher temperatures accelerate cardiac metabolism, increasing heart rates; cold conditions reduce heart rate as seen during hypothermia.

Proprioceptors: cells in muscles inform the cardiac center of physical activity status, facilitating proactive HR adjustments before demand increases.

Baroreflexes: activated in response to blood pressure changes (e.g., decreased BP raises heart rate, and vice versa).

Stroke Volume Contributions

Stroke volume signifies the volume of blood discharged from one ventricle per heartbeat

  1. Preload: Tension in ventricular myocardium before contraction.

  2. Contractility: Strength of contraction at a given preload.

  3. Afterload: Arterial blood pressure resisting semilunar valve opening.

Preload Dynamics

Preload reflects the tension or stretch in the heart wall prior to contraction, associated with volume returned to the heart.

  • Increased myocardial stretch enhances contractile force due to formation of additional crossbridges in sarcomeres.

Frank-Starling Law of the Heart: EDV rises, stroke volume increases due to enhanced myocardial stretch.

Venous Return and Contractility

Venous Return Impacts: higher venous return, due to increased pressure or lower heart rates, leads to enhanced stroke volume.

*As more cardiomyocytes stretch, contraction force increases considerably.

Contractility Variants:

  • Positive Inotropic Agents: E.g., glucagon & epinephrine; increase contraction force.

  • Negative Inotropic Agents: E.g., acidosis or hyperkalemia; decrease contractility.

Factors Affecting Afterload & Exercise Impacts

Afterload → Resistance faced by the heart during contraction due to arterial blood pressure just outside the semilunar valves.

*Increased afterload adversely affects stroke volume, notably under conditions obstructing arterial flow (e.g., restrictive lung diseases or pulmonary hypertension).

Exercise:

cardiac output increases via → Early proprioceptor signals indicating activity increase HR & enhanced venous return through muscular contractions.

*Sustained exercise fosters ventricular hypertrophy, improving stroke volume capabilities, allowing for lower resting heart rates while maintaining output capability.