Cardiovascular and Respiratory Systems Study Guide

Cardiovascular System

Overview

The cardiovascular system comprises two main circuits:

• Pulmonary Circuit: The right side of the heart receives deoxygenated blood from tissues and pumps it to the lungs for gas exchange (CO_2 release and O_2 pickup).
• Systemic Circuit: The left side of the heart receives oxygenated blood from the lungs and pumps it to the body tissues.

Gross Anatomy of the Heart

Heart Wall Layers

• Epicardium: The outermost layer.
• Myocardium: The thickest layer, mainly composed of cardiac muscle, responsible for the heart's contractile function.
• Endocardium: The innermost layer lining the heart chambers.

Papillary Muscles and Chordae Tendineae

• These structures work together to prevent valve prolapse (inversion) during ventricular contraction.

Myocardial Wall Comparison

The myocardial wall thickness varies among the four chambers, reflecting their respective functions and pressure demands.

Autorhythmic vs. Contractile Myocardial Cells

• Autorhythmic Cells:
  • Make up 1% of cardiomyocytes.
  • Function as the heart's pacemaker cells.
  • Located in the SA node, AV node, bundle of His, and Purkinje fibers.
  • Generate pacemaker potentials that initiate heartbeats.
• Contractile Cells:
  • Make up 99% of cardiomyocytes.
  • Primary function is contraction.
  • Located throughout the atrial and ventricular muscle tissue.
  • Respond to electrical signals from autorhythmic cells to contract.

Cardiac Conduction System

Components and Pathway

1. Sinoatrial (SA) Node:
   • Located in the right atrium.
   • Primary pacemaker, generating 80 action potentials per minute.
2. Interatrial Bundle (Bachmann's Bundle):
   • Conducts electrical signals between the atria.
3. Atrioventricular (AV) Node:
   • Located between the atria and ventricles.
   • Slows conduction, generating 40-60 action potentials per minute.
4. Bundle of His:
   • Connects the AV node to the ventricles.
   • Generates 40 action potentials per minute.
5. Left and Right Bundle Branches:
   • Conduct impulses through the interventricular septum.
6. Purkinje Fibers:
   • Spread throughout the ventricles.
   • Generate 20 action potentials per minute.

Electrical Signal Pathway

SA node generates impulses → signal spreads through atria → AV node receives and delays signals → bundle branches carry the signal through the septum → Purkinje fibers depolarize ventricular cells.

Chronological Order of Excitation and Contraction

The coordinated sequence ensures proper mechanical contraction of the heart chambers.

ECG Waves and Cardiac Events

• P Wave: Represents depolarization of the SA node and atria, corresponding to atrial systole (contraction).
• QRS Complex: Represents ventricular depolarization; marks the beginning of ventricular systole and atrial repolarization.
• T Wave: Represents ventricular repolarization; occurs during ventricular diastole (relaxation).

Heart Sounds

• Lub: AV valves closing.
• Dub: Semilunar (SL) valves closing.

Systole and Diastole

• Systole: Contraction.
• Diastole: Relaxation.

SA Node Depolarization

Mechanism

• Pacemaker Potential: Slow depolarization due to both opening of Na+ channels and closing of K+ channels.
• Unstable Resting Membrane Potential: SA node cells have an unstable resting membrane potential, leading to slow depolarization.
• Threshold Reached: When the pacemaker potential reaches the threshold, it triggers an action potential.
• Action Potential Characteristics: Depolarization is caused by Ca^{2+} influx through Ca^{2+} channels; repolarization occurs due to Ca^{2+} channels inactivating and K+ channels opening.

Contractile Cell Depolarization, Plateau, and Repolarization

Mechanism

• Depolarization: Due to Na^+ influx through fast voltage-gated Na^+ channels. A positive feedback cycle rapidly
  opens many Na^+ channels, reversing the membrane potential. Channel inactivation ends this phase.
• Plateau Phase: Due to Ca^{2+} influx through slow Ca^{2+} channels. This keeps the cell depolarized because few K+ channels are open.
• Repolarization: Due to Ca^{2+} channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its resting voltage.

Fluid Volume, Pressure, Flow, and Resistance

Relationships

• Preload: Degree of stretch of cardiac muscles before contraction.
• Afterload: Pressure ventricles must overcome to eject blood.
• Contractility: Strength of ventricular contraction.
• Cardiac Output: Volume of blood pumped by each ventricle in one minute. CO increases if either SV or HR increases.

Cardiac Cycle Phases

Ventricular Filling (Diastole)

• AV valves are open; ventricles are relaxed, resulting in low pressure.
• Blood flows from high pressure (atria) to low pressure (ventricles).
• 80% of blood passively flows into ventricles; atrial systole occurs, delivering the remaining 20%.

Isovolumic Contraction

• Atrial diastole (repolarization), depolarization of ventricles.
• Ventricles begin to contract (systole); isovolumic contracting phase (valves closed).
• The volume of blood is maintained as valves are closed, causing pressure to increase.

Ventricular Ejection (Systole)

• P{ventricle} > P{artery}, SL valves open.
• Rapid ejection followed by reduced ejection.
• Remaining volume = end-systolic volume.
• Ejected blood volume = stroke volume (SV) = 70mL.

Isovolumic Relaxation

• Early ventricular diastole: ventricles relax & expand.
• Atria are relaxed and filling; blood in arteries closes SL valves.
• Atrial fills and pressure increases, AV valves will open, and the cycle begins again.

Key Parameters and Their Relationships

Definitions

• Cardiac Output (CO): Volume of blood pumped by each ventricle in one minute.
• Heart Rate (HR): Number of beats per minute.
• Stroke Volume (SV): Volume of blood ejected by each ventricle per beat.
• End-Diastolic Volume (EDV): Volume of blood in each ventricle at the end of ventricular diastole.
• End-Systolic Volume (ESV): Remaining volume of blood in the ventricle after ejection.
• Ejection Fraction (EF): Percentage of blood ejected from the ventricles with each contraction.

Formulas

• SV = EDV - ESV
• EF = (SV/EDV) \%
• CO increases if either SV or HR increases.
• Increased venous return stretches ventricles, leading to increased EDV and potentially increased SV (Frank-Starling Law).

Cardiac Reserve

• The difference between resting and maximal CO.
• The heart's ability to increase its pumping capacity above normal resting levels when needed.
• Maximal cardiac output can be 4-5 times the resting cardiac output.

Regulation of Cardiac Output

Autonomic Nervous System

• Sympathetic Nervous System: Increases HR and SV; activated by fear, releasing epinephrine, binds to B-receptors on the SA node, increasing Na^+ and Ca^{2+} influx; results in increased HR and contractility.
• Parasympathetic Nervous System: Decreases HR; activated by the vagus nerve, releasing acetylcholine; binds to M2 receptors on the SA node, opening K+ channels and closing Ca^{2+} channels; leads to hyperpolarization and decreased HR.

Hormonal Regulation

• Epinephrine: Increases HR and contractility.
• Thyroxine enhances the effects of norepinephrine and epinephrine.

Physiological Changes

• Exercise increases HR and CO.
• Body temperature: HR increases to regulate body temperature.

Pathological Conditions

• Tachycardia: Abnormally fast HR (> 100 beats/min) may lead to fibrillation.
• Bradycardia: HR slower than 60 beats/min may result in inadequate blood circulation.
• Hypertension: Increases afterload, reducing SV.

Other Factors

• Age, size, sex (females have faster HR than men).

Ion Effects on Cardiac Output

Calcium (Ca^{2+})

• Calcium influx through Ca^{2+} channels is crucial for depolarization, which initiates cardiac contraction.
• Increased Ca^{2+} influx leads to more cross-bridges forming, enhancing contractility; Ca^{2+} channel blockers decrease contractility.
• Hypocalcemia: (low calcium) depresses HR.
• Hypercalcemia: increased HR and contractility.

Potassium (K^+)

• K^+ efflux is responsible for repolarization, bringing the membrane potential back to its most negative voltage.
• Hypokalemia: K+ diffuses out of cardiomyocytes, prevents repolarization, results in a feeble heartbeat, arrhythmia, cardiac arrest in systole.
• Hyperkalemia: (high potassium): hyperpolarization, cardiac arrest in diastole.

Mean Arterial Pressure (MAP)

• MAP is the average blood pressure in arteries during one cardiac cycle.

Importance of Constant MAP

• Required for adequate perfusion (blood flow) to organs.
• Helps assess the risk of disorders like atherosclerosis, edema, and aneurysm.

Mechanisms to Maintain MAP

• Local Control:
  • Hyperemia: increased blood flow to tissues.
  • Myogenic response: contraction/dilation of arteriolar smooth muscle.
• Reflex Control:
  • Sympathetic nervous system: causes vasoconstriction via norepinephrine.
• Hormonal Control:
  • Epinephrine and vasopressin cause vasoconstriction.

Parameters Impacting MAP

The key parameters affecting MAP and their regulation.

Blood Vessels, Blood Flow, Blood Pressure, and Resistance

Physical Characteristics of Blood Vessels

Arteries

• Thick walls with three layers: tunica intima, tunica media, and tunica externa.
• Large lumen (central space); contains smooth muscle and elastic fibers for pressure regulation.
• Carry blood away from the heart.

Capillaries

• Very thin walls, consisting of only endothelium and basement membrane.
• Smallest blood vessels, forming networks between arteries and veins.
• Allow for the exchange of gases, nutrients, and waste.
• Three types: continuous, fenestrated, and sinusoid.

Veins

• Thinner walls compared to arteries, with less smooth muscle.
• Larger lumen than arteries.
• Contain valves to prevent the backflow of blood.
• Carry blood towards the heart.

Arterioles

Impact on Tissue Perfusion

• Arterioles have a greater impact on tissue perfusion than any other vessel.
• Control of blood flow: Arteries lead to capillary beds and control the flow of blood into these beds through vasodilation and vasoconstriction.
• They are active in vasoconstriction, allowing them to regulate blood flow to specific tissues.
• Pressure of regulation: Arterioles have thick tunica media with smooth muscle, allowing them to actively control blood pressure.
• They act as a pressure reservoir.
• Resistance vessels: Arterioles are considered resistance vessels due to their ability to constrict and dilate, significantly impacting overall peripheral resistance.
• Autonomic control: The autonomic nervous system can influence arterioles, leading to vasoconstriction or vasodilation as needed.

Capillary Exchange

Specific types of capillaries perform exchanges in the tissues according to their physical characteristics.

Venous Return

Mechanisms

• Skeletal Muscle Pump: Contraction of skeletal muscles, especially in the legs, compresses veins and pushes blood upward.
• Venous Valves: One-way valves in veins prevent the backflow of blood, ensuring it moves toward the heart.
• Respiratory Pump: Changes in intrathoracic pressure during breathing help draw blood back into the heart.
• Veins as a Volume Reservoir: With large lumens and thin walls that can expand to accommodate blood.

Blood Pressure Sensing and Regulation

Mechanisms

• Autonomic Nervous System: Involved in vasoconstriction and vasodilation; the sympathetic nervous system uses norepinephrine for vasoconstriction.
• Baroreceptors: Help regulate blood pressure.
• Renin-Angiotensin-Aldosterone System: Mentioned as part of blood pressure regulation.
• Other Methods: Local control mechanisms like myogenic response and hyperemia; hormonal control, including epinephrine and vasopressin for vasoconstriction.

Hypotension and Hypertension

Hypotension

• The pressure of blood circulating the body is lower than normal.
• Possible causes: Dehydration (drink more water), pregnancy, blood loss, medications, heart conditions (low HR, valve problems, heart attack).

Hypertension

• The pressure of blood in your vessels is too high.
• Possible causes: Stress, lifestyle, age.
• Treatment: Good diet, exercise, avoid smoking.

The Respiratory System

Functions of the Respiratory System

• Gas exchange.
• Regulation of body pH through ventilation.
• Conversion of molecules carried in the blood.
• Protection from inhaled particles.
• Sound production and vocalization.
• Sense of smell.
• Enhances venous return through the respiratory pump.

Capillary Types

• Continuous Capillaries:
  • Most common; complete endothelium with a basement membrane.
  • “Leaky” tight junctions.
  • Found in skeletal/smooth muscle, lungs, and brain; allows the exchange of small molecules and gases.
• Fenestrated Capillaries:
  • Have “windows” with a basement membrane.
  • Allow exchange of larger molecules; found in the small intestine, kidneys, and choroid plexus.
• Sinusoid Capillaries:
  • Extensive intercellular gaps and incomplete basement membrane.
  • Allow exchange of plasma proteins and even cells.
  • Rare: found in the liver, spleen, and bone marrow.

Conducting and Respiratory Zones

Conducting Zone

• Structures: Nose and nasal cavities, pharynx, larynx, trachea, bronchi, and bronchioles.
• Histological Characteristics: Lined with pseudostratified ciliated columnar epithelium; the presence of mucus-producing goblet cells; reinforcing cartilage in walls.

Respiratory Zone

• Structures: Respiratory bronchioles, alveolar ducts, alveoli.
• Histological Characteristics: Alveoli are lined with simple squamous epithelium (type 1 alveolar cells); Rich blood supply with capillaries forming a sheet over alveoli.
• Functions: Site of gas exchange between air and blood; approximately 300 million alveoli per lung for efficient gas exchange.

Pressure Gradient and Air Flow

Mechanism

• As blood flows through vessels, pressure decreases due to resistance.
• This creates a pressure gradient that drives airflow from areas of high pressure to low pressure.

Mechanisms Creating Pressure Gradient

• Respiratory Muscles: The diaphragm and other respiratory muscles promote ventilation; their contraction and relaxation create pressure changes in the thoracic cavity.
• Lung Elasticity: The elastic recoil of the lungs helps create pressure differences.
• Surface Tension: Surfactant, produced by type 2 alveolar cells, reduces the surface tension of alveolar fluid; prevents alveoli from collapsing during exhalation, maintaining proper pressure gradients.

Alveolar Cells

Type I Alveolar Cells

• Make up the wall of alveoli; a single layer of squamous epithelial cells.
• Function: Form the thin wall of alveoli, facilitating gas exchange.

Type II Alveolar Cells

• Secrete surfactant.
• Produce surfactant, which reduces surface tension and prevents alveolar collapse.

Alveolar Macrophages

• Present in the alveoli.

Muscles Involved in Breathing

• Intercostal Muscles: These are located between ribs and play a role in chest wall movement during breathing.
• Diaphragm: This is the primary muscle of respiration, separating the chest cavity from the abdominal cavity, contracts during respiration creating negative pressure in the pleural cavity and relaxes during expiration.

Respiratory Muscle Functions

• During inspiration, respiratory muscles contract, expanding the lungs.
• During expiration, the muscles relax, allowing the lungs to recoil.

Lung Volumes and Capacities

Definitions

• Functional Residual Capacity (FRC): Amount of air remaining in the lungs after normal breath out; FRC = ERV + RV
• Tidal Volume (TV): Amount of air inhaled or exhaled with each breath under resting conditions; approximately 500 mL for both adult males and females.
• Inspiratory Reserve Volume (IRV): Amount of air that can be forcefully inhaled after a normal tidal volume inhalation; approximately 3100 mL for adult males and 1900 mL for adult females.
• Expiratory Reserve Volume (ERV): Amount of air that can be forcefully exhaled after a normal tidal volume expiration; approximately 1200 mL for adult males and 700 mL for adult females.
• Total Lung Capacity (TLC): Maximum amount of air that can be forcefully exhaled after a normal tidal volume expiration; TLC = TV + IRV + ERV + RV; approximately 600 mL for an adult male.

Homeostasis of O2, CO2, H+, Through Ventilation

Ventilation Regulation

• The depth of breathing is more efficient than ventilation rate for gas exchange.
• During exercise, O2 demand increases, stimulating ventilation.
• Ventilation and pulmonary blood flow must match for efficient gas exchange.

Blood Chemistry Regulation

• Carbonic anhydrase catalyzes this reaction, playing a crucial role in blood pH homeostasis.
• In tissue CO2 production increases H^+ concentration, promoting O2 unloading from hemoglobin.
• In the lungs: the reverse reaction occurs, facilitating CO2 removal and O2 binding to hemoglobin.

Hemoglobin Role

• Acts as a buffer, binding to H^+ when it releases O2 in tissues.
• This helps transport CO2 removal and regulate blood pH.

Gas Exchange

Alveolus and Capillary Beds

• Oxygen diffuses from the alveolar air into the pulmonary capillaries.
• Carbon dioxide diffuses from the pulmonary capillaries into the alveolar air.
• This exchange occurs across the respiratory membrane.

Lung Capillary Beds

• Oxygen-poor blood enters the pulmonary capillaries.
• Oxygen diffuses into the blood binding into hemoglobin.
• Carbon dioxide diffuses out of the blood into the alveoli.
• The blood leaves the lungs oxygen-rich.

Tissue

• Oxygen-rich blood is released from hemoglobin and diffuses into the cells.
• Carbon dioxide produced by cellular respiration diffuses from the cells into the blood.
• This process is driven by concentration gradients and follows the principles of simple passive diffusion.