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Afterload
Afterload
The tension that the heart must overcome to eject blood. It is largely determined by arterial pressure. In other words, the tension or stress that builds up in the ventricular wall during ejection is referred to as afterload. While afterload is closely associated with systemic vascular resistance for the left ventricle (or pulmonary vascular resistance for the right ventricle), it is also influenced by alterations in ventricular size and thickness.
When examining the graph of contractility versus afterload, it becomes evident that as afterload increases, contractility decreases. This relationship is particularly pronounced in the neonatal myocardium due to its immaturity, resulting in a steeper decline. The effect is also more pronounced for the right ventricle (RV) compared to the left ventricle (LV), with the RV being more "intolerant" of increased afterload unless it has adapted to a chronic elevation. Consequently, the RV is more prone to acute failure in response to a sudden rise in afterload, such as during a pulmonary vasoconstriction crisis.
Atrial pressure wave curve
Atrial pressure wave curve
In an atrial pressure waveform, the "a" wave represents atrial contraction, the "c" wave corresponds to the onset of systole with bulging of the tricuspid valve into the right atrium during ventricular contraction, and the "v" wave reflects the filling of the atrium against a closed tricuspid valve during ventricular systole; essentially, the "a" wave is the active filling of the atrium, the "c" wave is a passive pressure change due to the tricuspid valve movement, and the "v" wave is the passive filling of the atrium against a closed valve.
Right atrium
The a wave is higher than the v wave in the right atrium typically, while the v wave is higher than the a wave in the left atrium. The difference in the prominence of the a wave and v wave between the right atrium (RA) and left atrium (LA) is primarily due to differences in compliance, resistance, and pressure gradients in the right and left heart circuits. In infants, the mean right atrial pressure typically ranges from 0 to 4 mmHg, with lower a and v waves observed. In premature neonates, RA pressures tend to be even lower.
The right ventricle (RV) is highly compliant, meaning it accommodates incoming blood more easily. This results in a relatively low right atrial afterload, allowing for a stronger atrial contraction and a higher a wave. The v wave, which represents right atrial filling, is usually smaller because venous return from the systemic circulation occurs at a relatively low pressure.
a wave becomes more pronounced in conditions such as RV hypertrophy, tricuspid valvular stenosis or atresia, and any pathology reducing RV compliance, including constrictive pericarditis.
Arrhythmias contribute to elevated a waves. Classic example is "cannon" a wave seen in complete atrioventricular dissociation, where atrial contraction occurs against a closed tricuspid valve (also be present in other arrhythmias).
c wave in RA can become more pronounced and may occur later in the cardiac cycle in cases of tricuspid regurgitation, where it merges with the v wave, forming a prominent cv wave. v wave can also be amplified in scenarios where right ventricular compliance is reduced, as well as in cardiac failure, where right atrial pressures are generally elevated.
If large atrial septal defects, the a and v waves are often similar in height, accompanied by deep x and y descents in the pressure waveform.
Left atrium
Characterized by a prominent v wave. v wave dominance is not directly linked to the LV or systemic circulation but reflects pulmonary blood flow and is transmitted from the pulmonary arteries.
The v wave represents atrial filling during ventricular systole, and in the left atrium, it is larger than the a wave due to pulmonary venous return occuring under higher pressure than systemic venous return, leading to greater LA distension and a more prominent v wave. Also, the mitral valve remains closed longer due to higher LV early diastolic pressure, causing a larger pressure buildup in the LA.
The a wave is relatively smaller because: the LV is stiffer and less compliant than the RV, increasing left atrial afterload and limiting the effectiveness of atrial contraction. Also, the left atrium contributes less to left ventricular filling compared to the right atrium's contribution to the RV.
If a pulmonary vein drains into the RA, the v wave remains dominant within the vein until it nears its entry point into RA, where the a wave becomes more pronounced, mirroring the right atrial pressure waveform.
In total anomalous pulmonary venous return, a prominent v wave is observed in pulmonary veins.
When pulmonary blood flow is elevated, v wave may extend to the junction of the common pulmonary venous trunk and systemic veins. In such cases, if the RA exhibits a dominant a wave, a similar pattern is often noted in the left atrium, since all of its blood supply comes from the right atrium.
With a large left-to-right shunt, the v wave is typically more prominent than the a wave. Additionally, in infants and young children with significant left-to-right shunting, a pressure gradient may exist between the pulmonary veins and left atrium.
In conditions with reduced pulmonary blood flow, such as pulmonary atresia, the pulmonary venous and left atrial pressure waveforms do not exhibit a marked v wave.
In infants, the mean left atrial pressure is generally lower, ranging from 3–6 mmHg, with both a and v waves proportionally reduced.
Autoregulation
Autoregulation
Autoregulation refers to the ability of an organ or tissue to maintain a consistent level of blood flow despite changes in perfusion pressure. It is a physiological mechanism essential for ensuring that critical tissues, such as the brain, heart, and kidneys, receive adequate oxygen and nutrients under varying conditions, such as changes in blood pressure.
Maintains Homeostasis: Autoregulation ensures a stable internal environment by regulating blood flow according to the metabolic demands of the tissue.
Pressure Independence: Within a certain range of arterial pressures (the "autoregulation range"), blood flow remains relatively constant. Outside this range, autoregulatory mechanisms may fail, leading to hypo- or hyperperfusion.
Autoregulation is achieved through two primary mechanisms:
Myogenic Mechanism: Description: Vascular smooth muscle responds to changes in pressure. Example: If blood pressure increases, arterioles constrict (vasoconstriction) to reduce blood flow and prevent excessive perfusion. Conversely, if pressure drops, arterioles dilate (vasodilation) to maintain flow. Purpose: Protects tissues from damage due to pressure extremes.
Metabolic Mechanism: Description: Blood flow adjusts based on the metabolic needs of the tissue. Example: When a tissue becomes metabolically active (e.g., during exercise), it consumes more oxygen and produces metabolic byproducts like carbon dioxide, hydrogen ions, and adenosine. These byproducts promote vasodilation, increasing blood flow to meet the tissue's needs.
Cerebral Autoregulation: Maintains consistent blood flow to the brain, critical for neuronal function. Sensitive to changes in carbon dioxide (CO₂) and oxygen (O₂) levels.
Renal Autoregulation: Protects kidney function by stabilizing glomerular filtration rate (GFR) despite fluctuations in systemic blood pressure. Mechanisms include the myogenic response and tubuloglomerular feedback.
Coronary Autoregulation: Adjusts blood flow to the heart muscle based on myocardial oxygen demand.
Bernoulli Principle
Bernoulli Principle
States that an increase in the speed of a fluid occurs simultaneously with a decrease in pressure or potential energy. The Bernoulli Principle is a fundamental concept in fluid dynamics that describes the behavior of a fluid moving along a streamline. It states that in a steady, incompressible flow with negligible viscosity, the total mechanical energy of the fluid remains constant. This principle implies that an increase in the fluid's speed leads to a decrease in its pressure or potential energy, and vice versa. The Bernoulli Principle states that for an incompressible, non-viscous fluid flowing in a streamline, the sum of the pressure energy, kinetic energy, and potential energy per unit volume remains constant.
Assumptions and Limitations:
Incompressibility: Assumes the fluid density remains constant.
Non-viscous Fluid: Assumes negligible viscosity, meaning there is no internal friction.
Steady Flow: Assumes the flow parameters (velocity, pressure, etc.) do not change with time.
Streamline Flow: Assumes the flow is along streamlines, which are paths followed by fluid particles.
Boyle's Law
Boyle's Law
Boyle's Law states that the pressure of a given mass of gas is inversely proportional to its volume, provided the temperature remains constant. This means that if the volume of the gas increases, the pressure decreases, and vice versa. This relationship implies that the product of the initial pressure and volume is equal to the product of the final pressure and volume.
Cardiac pressures and saturations
Cardiac pressures and saturations
Dalton's Law
Dalton's Law
States that the total pressure exerted by a mixture of gases is equal to the sum of the partial pressures of the individual gases.
Fick's Law
Fick's Law
Describes the rate at which a substance (e.g., a gas) diffuses across a membrane. It is dependent on the surface area, the concentration gradient, and the membrane's permeability. It quantifies how the concentration of a substance changes over time due to diffusion.
Flow-pressure interaction
Flow-pressure interaction
Flow-Pressure Interaction refers to the relationship between fluid (liquid or gas) flow and the pressure driving that flow. Pressure Gradient: The difference in pressure between two points in a fluid system that drives the flow. Fluids move from areas of high pressure to areas of low pressure. Flow Rate: The volume of fluid passing through a cross-sectional area per unit time, typically measured in liters per minute (L/min) for liquids or liters per second (L/s) for gases.
Factors Affecting Flow-Pressure Interaction:
Radius of the Vessel: The flow rate is highly sensitive to the radius of the vessel. Small changes in radius can lead to significant changes in flow rate (proportional to the fourth power of the radius).
Viscosity of the Fluid: Higher viscosity fluids encounter more resistance and flow more slowly for a given pressure gradient.
Length of the Vessel: Longer vessels create more resistance to flow.
Pressure Gradient: A larger pressure gradient increases the flow rate.
Dynamic changes:
Autoregulation: In organs like the brain and kidneys, blood vessels can change their diameter to maintain a constant flow despite changes in pressure.
Compliance and Elastance: Vessel or airway walls can stretch (compliance) or recoil (elastance), affecting how pressure changes influence flow.
Force-frequency relationship
Force-frequency relationship
The Force-Frequency Relationship (FFR) describes how the contractile force of cardiac muscle changes with varying frequencies of stimulation. This relationship is crucial in understanding how the heart responds to different rates of electrical stimulation and adapts its force of contraction accordingly. Generally, within physiological limits, an increase in the frequency of stimulation leads to an increase in the force of contraction. However, this follows a "U" shape, and at high frequency this may lead to decrease in cardiac function. One key important concept is that coronary perfusion is dependent on the diastolic aortic blood pressure relative to the right atrial pressure, since the coronary sinus drains into the right atrium in the majority of cardiac configurations. The force-frequency relationship thus refers to the connection between heart rate and contractility. To a certain extent, the myocardium adapts to maintain contractility at higher heart rates, compensating for inadequate filling time. However, this adaptation does not apply in the context of heart failure. Reduced filling time also impacts coronary perfusion. Medications that optimize heart function may increase heart rate, but they do not result in a synergistic increase in contractility, leading to a blunted force-frequency relationship.
Mechanism:
Myocardium
Calcium Handling: The primary mechanism underlying the FFR involves intracellular calcium dynamics. With increased frequency of stimulation, there is an enhanced influx of calcium ions during each action potential and improved calcium release from the sarcoplasmic reticulum (SR). This leads to a greater availability of calcium for binding to troponin, resulting in stronger contractions.
Sarcoplasmic Reticulum (SR) Calcium Load: At higher frequencies, the SR calcium load increases, augmenting the amount of calcium released with each beat.
Calcium Sensitivity: At higher stimulation rates, the sensitivity of the contractile proteins to calcium may also increase, contributing to stronger contractions.
Within the normal physiological range of heart rates (e.g., 60-180 beats per minute in humans), the force of contraction increases with increasing heart rate due to the mechanisms described above.
Negative FFR at Extremely High Rates: At very high stimulation frequencies, the force of contraction can decrease, a phenomenon known as negative FFR. This is due to incomplete calcium reuptake, decreased calcium release, and potential depletion of ATP reserves.
Heart Failure: In heart failure, the FFR is often blunted or reversed, meaning that increases in heart rate do not produce the expected increase in contractile force. This is due to impaired calcium handling and reduced SR calcium content. Understanding the FFR is essential for optimizing pacemaker settings to ensure that heart rate increases lead to appropriate increases in cardiac output. This is the basis of resynchronization therapy. Cardiac Resynchronization Therapy (CRT): CRT devices use principles of the FFR to improve the synchronization of ventricular contractions in patients with heart failure.
The FFR is typically assessed in isolated cardiac muscle preparations or in intact hearts by varying the frequency of electrical stimulation and measuring the resultant contractile force.
Factors Influencing FFR:
Temperature: Changes in temperature can affect calcium handling and thus the FFR.
Ion Concentrations: Variations in extracellular calcium and sodium concentrations can influence the FFR by affecting calcium influx and efflux.
Drugs: Certain drugs, such as beta-adrenergic agonists, can enhance the FFR by increasing calcium influx and SR calcium uptake.
Frank-Starling Law
Frank-Starling Law
The Frank-Starling Law (also known as the Frank-Starling mechanism or Starling's law of the heart) is a fundamental principle in cardiac physiology. It describes the relationship between the volume of blood filling the heart (the end-diastolic volume) and the force of cardiac contraction (stroke volume). This law explains how the heart is able to adjust its pumping capacity to accommodate varying volumes of incoming blood. The Frank-Starling Law states that the force of the heart's contraction is directly proportional to the initial length of the cardiac muscle fibers (preload). In other words, an increase in the volume of blood filling the heart (end-diastolic volume) leads to a stronger contraction and greater stroke volume. The Frank-Starling mechanism ensures that the volume of blood the heart pumps out matches the volume of blood returning to it. This balance is crucial for maintaining consistent blood flow and pressure. In heart failure, the Frank-Starling mechanism may be impaired. The heart may not be able to increase its force of contraction in response to increased preload, leading to inadequate cardiac output. Conditions that lead to fluid overload can excessively stretch the heart muscle fibers, moving them beyond the optimal point on the Frank-Starling curve and resulting in reduced contractility. Cardiomyopathies: Diseases that affect the structure or function of the heart muscle can alter the Frank-Starling relationship.
Neonatal vs adult curve is flatter unless you are at lower filling pressures. As such, administration of significant amount of volumes in the context of normal preload is unlikely to improve neonatal myocardial contractilty, expect in infants with hypertrophic cardiomyopathy or other etiologies with restrictive non-compliant hearts in which higher preload may be necessary to improve contractility by the Frank Starling Law.
Mechanism:
Preload: Refers to the degree of stretch of the cardiac muscle fibers at the end of diastole, just before contraction. This is influenced by the volume of blood returning to the heart.
Myocyte Stretch: As the volume of blood filling the heart increases, the cardiac muscle fibers are stretched to a greater length. This optimal stretching increases the sensitivity of the myofilaments to calcium, enhancing the force of contraction.
Calcium Sensitivity: The increased stretch leads to better overlap of actin and myosin filaments in the sarcomeres of the heart muscle cells, enhancing cross-bridge formation and, thus, increasing the force of contraction.
Source: Wikipedia
Gas Diffusion
Gas Diffusion
The process by which gas molecules spread from an area of high concentration to an area of lower concentration.
Gas Solubility
Gas Solubility
The ability of a gas to dissolve in a liquid, influenced by temperature, pressure, and the nature of the gas and liquid.
Hagen-Poiseuille Equations
Hagen-Poiseuille Equations
The Hagen-Poiseuille Equation describes the flow of an incompressible, Newtonian fluid in a long, straight cylindrical pipe with a constant circular cross-section. This equation is fundamental in fluid dynamics and helps to understand the factors affecting laminar flow through vessels and tubes. The Hagen-Poiseuille equation quantifies the volumetric flow rate of a fluid through a cylindrical pipe, considering factors such as fluid viscosity, pipe length, radius, and pressure difference. The equation assumes laminar flow. It does not apply to turbulent flow, which occurs at higher flow rates or in larger pipes. It is valid only for Newtonian fluids, where the viscosity remains constant regardless of the flow conditions. The equation does not account for factors like pipe roughness or bends in the pipe, which can significantly affect flow in practical situations.
Assumptions:
The fluid is incompressible and Newtonian.
The flow is steady and laminar.
The pipe is straight, rigid, and cylindrical with a constant circular cross-section.
There are no significant external forces acting on the fluid other than pressure.
Assumptions regarding flow within a vessel are based on the following principles: the fluid must be Newtonian, the flow should be laminar, the fluid must be non-compressible, and the flow should be non-accelerating. Key factors that influence this flow include pressure, resistance, blood viscosity, and the diameter of the vessel.
Effect on Pulmonary vasculature (theoretical concepts and unproven)
A rise in carbon dioxide will vasoconstrict
Oxygen vasodilates
Mean airway pressure increase will lead to pulmonary vasoconstriction by external constriction
Viscosity may decrease flow
Effect of Systemic vasculature (theoretical concepts and unproven)
A rise in carbon dioxide will vasodilate
Oxygen vasoconstricts
Mean airway pressure may decrease left ventricular transmural pressure
Viscosity may decrease flow
Henry's Law
Henry's Law
Henry's Law describes the relationship between the partial pressure of a gas above a liquid and the concentration of that gas dissolved in the liquid. Henry's Law states that at a constant temperature, the amount of a gas that dissolves in a liquid is directly proportional to the partial pressure of that gas in equilibrium with the liquid. It explains how oxygen and carbon dioxide dissolve in blood. For example, the amount of oxygen that dissolves in the blood is proportional to the partial pressure of oxygen in the alveoli.
Hooke's Law
Hooke's Law
Hooke's Law describes the behavior of elastic materials when they are deformed by an external force. This law states that the force needed to extend or compress a spring by some distance is proportional to that distance. It describes the relationship between the force applied to an elastic object and the resulting deformation. The restoring force is the force exerted by the material to return to its original shape. The negative sign in the equation indicates that this force is in the opposite direction of the applied force (restorative). Hooke’s Law is valid only within the elastic limit of the material. Beyond this limit, the material may deform plastically (permanently) or fracture.
Relevant in the hypertrophic ventricles who are stiffer (poor compliance) - small changes in volume will lead to much higher degree increase in pressure. The compliant heart tends to have smaller increase in pressure with the same degree of increased volume.
Laplace's Law
Laplace's Law
Relates the pressure within a spherical or cylindrical object to the tension in the wall and the radius of the object.
Preload
Preload
Preload is a critical concept in cardiovascular physiology that refers to the initial stretching of the cardiac myocytes (heart muscle cells) prior to contraction. It is closely related to the volume of blood returning to the heart and filling the ventricles at the end of diastole (the relaxation phase of the cardiac cycle). Preload is a key determinant of stroke volume and cardiac output. Preload is often reflected by the end-diastolic volume (EDV) or end-diastolic pressure (EDP) that stretches the ventricles of the heart to their greatest geometric dimensions under variable physiologic demand. It reflects the volume of blood in the ventricles at the end of diastole before the heart contracts. Determinants of preload:
Venous Return: The amount of blood returning to the heart from the systemic circulation (RV) or the pulmonary circulation (LV). Increased venous return enhances preload. Inter-atrial shunting in newborns may influence ventricular preload depending on the volume and directionality of the shunt.
Blood Volume: Total blood volume in the body. Higher blood volume can increase preload.
Atrial Contraction: Contributes to ventricular filling during the late phase of diastole, particularly important during high heart rates.
Ventricular Compliance: The ability of the ventricles to stretch and accommodate the incoming blood. More compliant ventricles can handle a higher volume without a significant increase in pressure.
Intrathoracic Pressure: Changes in pressure within the thoracic cavity during respiration can influence venous return and hence preload. For example, deep inspiration decreases intrathoracic pressure and increases venous return.
See other resources: here and here
RV Preload
Reduction in Venous Return: Positive pressure ventilation increases intrathoracic pressure, which decreases the pressure gradient between the systemic veins and the right atrium. This reduction in the pressure gradient leads to decreased venous return to the heart. This results in reduced RV preload, which means less filling of the right ventricle during diastole. Hypovolemic Patients**: Patients with low blood volume are more susceptible to significant decreases in RV preload, potentially leading to reduced cardiac output and hypotension.
RV Afterload
Increase in Pulmonary Vascular Resistance (PVR): Positive pressure ventilation can increase alveolar pressure, leading to compression of pulmonary capillaries and an increase in PVR.
However, under-insufluation and alveolar collapse may also contribute negatively to PVR. As such, there is a inverse U-shape relationship where there is a tight zone where alveolar recruitment may optimize PVR.
In patients with preexisting right heart failure or pulmonary hypertension, increased RV afterload can exacerbate right ventricular dysfunction and lead to worsening of heart failure symptoms.
LV Preload
Reduction in Pulmonary Venous Return: The reduction in RV preload due to decreased venous return results in less blood being pumped into the pulmonary circulation and subsequently to the left atrium. This results in decreased LV preload, which means less filling of the left ventricle during diastole. Reduced LV preload can lead to decreased stroke volume and cardiac output. This effect is more pronounced in patients with compromised LV function.
LV Afterload
Reduction in LV Afterload: Positive pressure ventilation increases intrathoracic pressure, which is transmitted to the aorta and other large arteries. This results in a reduction of transmural pressure (the difference between intrathoracic pressure and blood pressure within the aorta), effectively reducing LV afterload. This results in decreased resistance against which the left ventricle must pump blood, potentially improving LV ejection. For patients with LV dysfunction or heart failure, reduced afterload can enhance stroke volume and cardiac output.
Pressure Gradient
Pressure Gradient
The difference in pressure between two points in a fluid system, which drives the flow of the fluid.
Stress-Velocity Relationship
Stress-Velocity Relationship
The relationship between the stress on the heart muscle and the velocity of muscle shortening during contraction. The Stress-Velocity Relationship describes how the velocity of muscle shortening during contraction is related to the applied stress (force per unit area) on the muscle. This relationship is crucial in understanding the mechanical properties and performance of muscle tissues, including cardiac muscle. It describes how the speed (velocity) at which a muscle fiber shortens is inversely related to the load (stress) it is under. This principle is particularly important for understanding how muscles generate force and movement. Stress-Velocity Relationship is typically represented by a hyperbolic curve when force (stress) is plotted against velocity. As the load on the muscle increases, the velocity of shortening decreases, approaching zero as the muscle generates its maximum isometric force. In the heart, the stress-velocity relationship helps to explain how the heart muscle adapts to different loading conditions. Under higher afterload (increased stress), the velocity of contraction decreases, affecting the rate of blood ejection from the ventricles. Consider a scenario where a muscle is lifting a weight. As the weight (load) increases, the speed at which the muscle can lift the weight decreases. Conversely, when the muscle lifts a lighter weight, it can do so more quickly. This inverse relationship illustrates the basic principle of the stress-velocity relationship.
Compliance/Elastance:
Compliance/Elastance:
Compliance is the ability of a hollow organ to stretch and expand. Elastance is the ability to return to its original shape after deformation.
Compliance: A measure of the ability of a hollow organ (like the lungs, blood vessels, or heart chambers) to expand and increase volume with increasing pressure. High compliance means the organ can expand easily.
Elastance: The inverse of compliance, indicating the ability of the tissue to return to its original shape after being distended. High elastance means the tissue is stiff and resists deformation.
Ventricular compliance affects diastolic filling. High compliance allows for adequate filling at lower pressures, while low compliance (high elastance) can impair filling and increase diastolic pressures. Arterial compliance affects blood pressure and pulse pressure. Lower arterial compliance (higher elastance) leads to higher systolic pressures and increased workload on the heart.
Pressure-Volume Curve: A graphical representation showing the relationship between pressure and volume. In the cardiovascular system, it shows how the volume of a ventricle changes with pressure. A steeper slope indicates lower compliance (higher elastance).
Transitional Physiology
Transitional Physiology
In the prenatal setting, pulmonary vascular resistance (PVR) is high and systemic vascular resistance (SVR) is low, due to the low-resistance placental circulation. After birth, there is an acute and progressive drop in PVR, accompanied by an abrupt rise in SVR—driven by catecholamine release and the removal of the low-resistance placenta. The foramen ovale and ductus arteriosus initially become bidirectional, then shift to a left-to-right shunt before ultimately closing.
From: Changes in systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) during gestation. (Lakshminrusimha and Saugstad, 2016).
The transitional bidirectionality at the atrial level occurs because left and right atrial pressures are transiently similar. As the right ventricle (RV) adapts to the now low-resistance pulmonary circulation, it undergoes remodeling—becoming thinner-walled, less muscular, and developing a lower end-diastolic pressure. In contrast, the left ventricle (LV), which now supports the systemic circulation, develops a slightly higher end-diastolic pressure. This pressure is transmitted to the left atrium, which is now well-filled by pulmonary venous return, further promoting a left-to-right shunting pattern. The foramen ovale (FO) closes through a combination of functional and anatomical processes that occur after birth. The reversal of the pressure gradient causes the septum primum (a flap-like structure) to be pushed against the septum secundum, effectively sealing the foramen ovale—this is referred to as functional closure. Over time, fibrous tissue fuses the septum primum and septum secundum, resulting in anatomical closure and the formation of the fossa ovalis. In approximately 75–80% of individuals, this process is complete within the first year of life. In up to 25% of the population, the FO remains patent (PFO), though it is usually asymptomatic unless associated with conditions such as cryptogenic stroke or paradoxical embolism.
Similarly, the ductus arteriosus (DA) remains patent in fetal life due to circulating prostaglandins from the placenta, as well as local prostaglandin production by specialized ductal endothelial cells—particularly active at lower gestational ages. The ductus is also highly sensitive to oxygen, which promotes constriction. With advancing gestational maturity, there is progressive thickening and increased sensitivity of the smooth muscle tissue surrounding the ductus. After birth, the closure of the DA occurs in two phases: functional and anatomical. As the newborn begins to breathe, oxygen tension (PaO₂) rises, triggering smooth muscle constriction of the ductus. Concurrently, the low-resistance placental circulation is removed, increasing systemic vascular resistance (SVR), while pulmonary vascular resistance (PVR) decreases as the lungs expand. These changes reverse the pressure and resistance gradients across the ductus—initially from right-to-left, then bidirectional as PVR approximates SVR, and eventually left-to-right as PVR falls well below SVR. Ductal flow diminishes significantly when PVR and SVR become comparable. Increased oxygen levels and decreased circulating prostaglandin E2 (PGE2), no longer maintained by the placenta, further promote ductal constriction, leading to functional closure. In term infants, this typically occurs within 12 to 24 hours after birth. Following functional closure, the DA undergoes intimal proliferation, smooth muscle migration, and fibrosis, resulting in permanent anatomical closure and formation of the ligamentum arteriosum, usually within 2–3 weeks in healthy term infants.
Ventriculo-arterial coupling
Ventriculo-arterial coupling
The relationship between the ventricle and the arterial system, influencing cardiac performance and efficiency. Ventriculo-arterial (VA) coupling describes the relationship between the mechanical properties of the heart (ventricle) and the arterial system. It is an important concept in cardiovascular physiology as it reflects the efficiency of the heart in pumping blood and the arterial system in accommodating and distributing that blood. Ventricular Elastance (Ees): Represents the contractility or the stiffness of the ventricle during systole. It is the slope of the end-systolic pressure-volume relationship (ESPVR). Arterial Elastance (Ea): Represents the arterial load or afterload. It is a measure of the arterial system’s opposition to the blood ejected by the ventricle. Ea can be approximated by the ratio of end-systolic pressure (ESP) to stroke volume (SV): Ea=ESP/SV. VA coupling is assessed using pressure-volume loops obtained through invasive hemodynamic monitoring. These loops provide detailed information about the relationship between pressure and volume throughout the cardiac cycle. Optimal VA coupling minimizes the cardiac energy expenditure for a given cardiac output, reducing myocardial oxygen demand and enhancing overall cardiovascular efficiency.
Viscosity
Viscosity
A measure of a fluid's resistance to flow.
Wall tension (Law of Laplace)
Wall tension (Law of Laplace)
The force exerted in the wall of a blood vessel or cardiac chamber. Wall tension refers to the force per unit length exerted circumferentially in the wall of a cylindrical structure, such as a blood vessel or the heart's ventricle, due to the pressure of the fluid inside it. The Wall tension is often described by the Law of Laplace. In blood vessels, wall tension helps to maintain structural stability and regulate blood flow. In the heart, wall tension affects myocardial oxygen demand and is related to conditions such as hypertrophy and heart failure. Increased wall tension in the ventricles can lead to cardiac hypertrophy (thickening of the heart muscle) as an adaptive response to reduce tension. It may also compromise coronary blood flow. The Law of Laplace provides a simplified model and assumes uniform pressure and wall thickness, which may not be the case in all physiological or pathological conditions. Real biological tissues have complex, anisotropic properties, meaning their mechanical behavior can vary in different directions.
Work (Cardiac)
Work (Cardiac)
Cardiac work refers to the amount of energy the heart expends to pump blood throughout the circulatory system. Cardiac work is the energy the heart uses to eject blood against arterial pressure during each cardiac cycle. It is typically expressed as the work done per minute, known as the cardiac power output.
External Work (EW): The work done by the heart to eject blood into the aorta and pulmonary artery. It is primarily the product of stroke volume and the pressure against which the heart pumps.
Internal Work (IW): The energy used for processes within the heart, such as muscle contraction and maintaining ion gradients. This is not directly involved in blood ejection.
Stroke Work (SW): The work done by the heart in one beat to pump blood.
Determinants of Cardiac Work:
Preload: The initial stretching of the cardiac myocytes prior to contraction. Increased preload leads to increased stroke volume and thus increased cardiac work.
Afterload: The resistance the heart must overcome to eject blood. Higher afterload increases the pressure work and cardiac workload.
Heart Rate: An increase in heart rate raises the number of contractions per minute, thereby increasing cardiac work.
Contractility: The intrinsic strength of the cardiac muscle contraction. Enhanced contractility increases stroke volume and cardiac work.
Windkessel Effect
Windkessel Effect
The Windkessel Effect refers to the ability of large elastic arteries (such as the aorta) to dampen the pulsatile nature of blood flow generated by the intermittent ejection of blood from the heart, thus ensuring a more steady flow through the smaller arteries, arterioles, and capillaries. This effect is crucial for maintaining continuous blood flow during both systole (when the heart contracts) and diastole (when the heart relaxes). "Windkessel" is a German word that translates to "air chamber" or "reservoir." The concept was originally used to describe air-filled chambers in early firefighting water pumps that helped to smooth out the flow of water. Systole: During the contraction phase of the cardiac cycle, blood is ejected into the large elastic arteries (e.g., the aorta). The walls of these arteries stretch to accommodate the increased volume of blood. Diastole: During the relaxation phase, the elastic recoil of the artery walls helps to maintain pressure and drive blood forward into the smaller arteries and capillaries, even though the heart is not actively pumping at this time. The Windkessel effect helps to ensure continuous blood flow through the capillaries, even when the heart is between beats. By damping the pulsatile output of the heart, the Windkessel effect helps to reduce the workload on the heart and prevent damage to the microcirculation.
Arterial Stiffness: With aging or conditions such as hypertension (or prematurity, IUGR), the compliance of large arteries can decrease, leading to increased arterial stiffness and a reduced Windkessel effect. This can result in higher systolic blood pressure and increased cardiac workload.
Heart Failure: The reduced ability of the heart to generate strong pulsatile outputs can be partially compensated by the Windkessel effect, helping to maintain peripheral blood flow.
Hemodynamics is Physiology
Hemodynamics is Physiology
Presentation given in the context of the NHRC by Dr Patrick McNamara
July 10th, 2024: Amazing presentation by Dr Patrick McNamara on Physiology. The Youtube recording is now available. This talk was given in the context of the NHRC Foundation Curriculum. I invite you all to listen to this great review of cardiovascular physiology and cardio-pulmonary interactions.
10 juillet 2024 : Présentation du Dr Patrick McNamara sur la physiologie. L'enregistrement Youtube est maintenant disponible. Cette conférence a été donnée dans le contexte du programme de la Fondation NHRC. Je vous invite tous à écouter cette grande revue de la physiologie cardiovasculaire et des interactions cardio-pulmonaires.
Neonatal Hemodynamics: From Developmental Physiology to Comprehensive Monitoring
Neonatal Hemodynamics: From Developmental Physiology to Comprehensive Monitoring
fped-06-00087.pdf
biology-13-00055.pdf
Wiggers Diagram of cardiac physiology
Wiggers Diagram of cardiac physiology
Obtained from Wikipedia - adh30 revised work by DanielChangMD who revised original work of DestinyQx; Redrawn as SVG by xavax, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons
https://upload.wikimedia.org/wikipedia/commons/9/91/Wiggers_Diagram_2.svg
Mullaly R, El-Khuffash AF. Haemodynamic assessment and management of hypotension in the preterm. Arch Dis Child Fetal Neonatal Ed. 2024 Feb 19;109(2):120-127. doi: 10.1136/archdischild-2022-324935. PMID: 37173119.
120.full.pdfEPIQ_Blood pressure guidelines_ver June 29_2022.pdfA Physiologic Approach to Hemodynamic Monitoring and Optimizing Oxygen Delivery in Shock Resuscitation
A Physiologic Approach to Hemodynamic Monitoring and Optimizing Oxygen Delivery in Shock Resuscitation
A_Physiologic_Approach_to_Hemodynamic_Monitoring_a.pdfHassan R, Verma RP. Neonatal Hypertension. [Updated 2022 Oct 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK563223/
A huge thank you to Karger for making the graph below on normative blood pressure values available to benefit the NeoCardioLab community. Following my request, I received the following message: "Our Editorial Office has forwarded your request. After consulting with the publication manager, I'm happy to inform you that we have granted free access to the article. The article titled 'Oscillatory Blood Pressure Values in Newborn Infants: Observational Data Over Gestational Ages' will now be freely accessible to all readers." (Added May 12, 2025)
Un immense merci à Karger d’avoir rendu le graphique ci-dessous sur les valeurs normales de la pression artérielle accessible, au bénéfice de la communauté NeoCardioLab. À la suite de ma demande, j’ai reçu le message suivant : « Notre bureau de rédaction a transmis votre demande. Après consultation avec le responsable des publications, j’ai le plaisir de vous informer que nous avons accordé un accès libre à l’article. L’article intitulé “Oscillatory Blood Pressure Values in Newborn Infants: Observational Data Over Gestational Ages” sera désormais accessible gratuitement à tous les lecteurs. » (Rajouté le 12 mai 2025)
Presentation by Dr Carolina Michel Macias on Hypotension in prematurity given for the NH-TNE fellowship training program at McGill on September 30, 2024
Presentation by Dr Carolina Michel Macias on Hypotension in prematurity given for the NH-TNE fellowship training program at McGill on September 30, 2024
HypotensionPrem.pdf
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