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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.
The Bernoulli equation is valid for a discrete or focal narrowing, but not for a multi-level obstruction or a gradually progressive narrowing. As such, although often used for a PDA or a hypoplastic arch to calculate gradients, one must be aware that the values are unlikely reflective of true gradients and may be over or under-estimated in certian cases.
This is based on the law of conservation of energy by unit of volume.
P = static pressure inside the liquid; g = acceleration due to gravity 9.8 m/s2 and rho (p) is the volumic mass of the liquid (kg/m3).
Bernoulli's equation is widely used in echocardiography to estimate pressure gradients across stenotic lesions or shunts. The simplified formula, ΔP = 4V², where V is the maximum velocity of blood flow, is a significant simplification of the law of conservation of energy. It assumes a brutal and rapid acceleration of flow (V2 >> V1) and a patient lying flat (eliminating gravity components). Limitations: This simplified formula cannot be applied to progressive accelerations, such as flow through a long tube (e.g., a conduit between RV and pulmonary artery) or a patent ductus arteriosus (technically). It is a "great approximation" that needs correlation with clinical findings and sometimes cardiac catheterization.
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
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).
Comparing the right and left ventricles in an adult heart, significant differences in their mechanical properties are observed. The right ventricle's compliance curve is considerably flatter than the left ventricle's. This implies that for the same pressure, the right ventricle can accommodate a larger volume. The right ventricle's contractility, or end-systolic elastance, is lower than that of the left ventricle, indicated by a less vertical slope. Overall, in an adult, the left ventricle is less compliant but more contractile than the right ventricle. The compliance curve of the left ventricle exhibits an exponential morphology. The end-systolic elastance curve is represented as a straight line.
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.
Fick's Principle:
Oxygen Consumption and Flow (VO2 = Q x A-V O2 difference)
Fick's principle relates oxygen consumption (VO2) to blood flow (Q) and the arterio-venous oxygen difference.
In practice, this is often simplified to calculate the pulmonary-to-systemic flow ratio (QP/QS) based on oxygen saturations.
QP/QS = (Systemic Arterial Saturation - Mixed Venous Saturation) / (Pulmonary Venous Saturation - Pulmonary Artery Saturation).
In a normal heart without any communication between the red (systemic) and blue (pulmonary) circulations, pulmonary flow (Qp) equals systemic flow (Qs), making Qp/Qs = 1. When a shunt exists, Qp will differ from Qs:
Qp > Qs: Occurs when excess blood flows into the lungs (e.g., left-to-right shunts).
Qp < Qs: Indicates low pulmonary blood flow (e.g., right-to-left shunts).
Typically, systemic arterial saturation is ~98-100%, pulmonary venous saturation is ~100%, and mixed venous saturation at rest is 70-75%. In many stable congenital heart disease patients without respiratory issues, the difference between arterial and mixed venous saturation (Ao-MV) is around 30%.
For example, if Aortic saturation (SatAo) is 98%, Mixed Venous saturation (SatMV) is 70%, and Pulmonary Artery saturation (SatPA) is 98%, then QP/QS = (98-70) / (100-98) = 28/2 = 14
In situations with mixed blood (e.g., single ventricle, truncus arteriosus), the aortic saturation equals the pulmonary artery saturation. In these cases, the finger pulse oximetry saturation can directly provide an estimate of the QP/QS ratio using a simplified Fick formula.
Fick applied to hemodynamics
VO₂ (ml/min) = Q (L/min) × (A–V)O₂ (ml O₂/L)
Oxygen Consumption (VO2): Defined as Cardiac Output (Q) multiplied by the Arteriovenous (A-V) Oxygen Difference. If cardiac output decreases, the body compensates by extracting more oxygen from the blood, leading to a larger A-V oxygen difference and a decrease in mixed venous oxygen saturation (SvO2).
(A–V)O₂ = Arteriovenous difference in O₂ content = CaO₂ – CvO₂
CaO₂ = 1.34 × Hb × SVO₂ + (0.0031 × PaO₂)
CvO₂ = 1.34 × Hb × SVO₂ + (0.0031 × PvO₂)
At rest: Pulmonary artery O₂ saturation (Sat O₂ PA) = 75% (25% of O₂ extracted from Hb)
During exercise: Sat O₂ PA decreases due to increased O₂ extraction, cardiac output (Qc) increases → VO₂ increases
In circulatory failure: Sat O₂ PA decreases at rest to compensate for the drop in cardiac output (Qc)
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.
Dicrotic Notch
Dicrotic Notch
The dicrotic notch is a small, brief upward deflection observed on the descending limb of an arterial pressure waveform, most prominently in the aortic pressure trace, but also present in the pulmonary arterial pressure waveform. It marks the closure of the semilunar valves—the aortic valve in systemic circulation and the pulmonary valve in pulmonary circulation—signifying the end of ventricular systole and the onset of diastole. This notch results from a brief increase in pressure from the rebounds off the closed valve due to inertia and downstream vascular resistance, combined with the elastic recoil of the arterial walls. This rebound causes a transient rise in pressure, visible as the dicrotic notch. It is typically seen in invasive arterial pressure waveforms, such as those obtained from aortic, femoral, or pulmonary artery catheters. The dicrotic notch corresponds to the beginning of isovolumetric relaxation, just before the atrioventricular (AV) valves open and ventricular filling begins.
Clinical and Hemodynamic Significance
Systemic Circulation (Aortic Pressure Waveform)
Aortic Regurgitation: The dicrotic notch may be blunted or absent due to the backflow of blood into the left ventricle during diastole. With significant AR, there is no IVRT because the LV continues to fill during diastole from the onset of diastole.
Aortic Stenosis: The upstroke is delayed, and an anacrotic notch may be seen instead. The dicrotic notch may be less prominent due to prolonged ejection time and reduced stroke volume.
Low Systemic Vascular Resistance (SVR): Seen in vasoplegia, sepsis, or with vasodilator therapy, the dicrotic notch may be diminished or shifted downward due to reduced arterial recoil. Vasopressin, norepinephrine and phenylephrine, or other agents increasing SVR, may re-establish or re-increase the dicrotic notch - when effective in increasing SVR.
Increased Arterial Compliance: In conditions like aging or arteriosclerosis, the notch may be less distinct due to dampened wave reflection.
Pulmonary Circulation (Pulmonary Artery Pressure Waveform)
Pulmonary Valve Regurgitation: Similar to aortic regurgitation, the dicrotic notch may be absent or blunted.
Pulmonary Arterial Hypertension (high PVR): The notch may be accentuated due to increased pulmonary vascular resistance and stiffness.
Pulmonary Stenosis: Causes a delayed systolic upstroke and may obscure the dicrotic notch.
Right Ventricular Dysfunction: May alter the timing and appearance of the dicrotic notch due to impaired ejection dynamics.
Summary:
Prominent dicrotic notch: Often seen with increased afterload or vasoconstriction.
Low or absent notch: May indicate semilunar or truncal valvular insufficiency, low vascular tone, or high diastolic runoff (e.g., AV fistulas, aortopulmonary shunts, left to right PDA, MAPCAs).
Therapeutic Implications: The appearance of the dicrotic notch can guide vasoactive therapy—for instance, vasoconstrictors may restore a diminished notch in vasodilatory states.
Fetal Circulation and the Transitional Period
Fetal Circulation and the Transitional Period
The fetal circulation is a specialized system that operates in parallel rather than in series, as seen after birth. This unique setup is essential for fetal development and allows the fetus to be perfused even if one ventricle is compromised.
Key Characteristics and Shunts
Fetal circulation operates as a parallel system rather than the series system observed postnatally. Oxygenated blood from the placenta returns via the umbilical vein, bypasses hepatic circulation through the ductus venosus, and enters the inferior vena cava. This relatively well-oxygenated blood is directed across the right atrium through the foramen ovale into the left atrium, left ventricle, and aorta—perfusing the brain and myocardium. Poorly oxygenated systemic venous return from the upper body enters the right atrium via the superior vena cava and is ejected by the right ventricle predominantly into the pulmonary artery, then diverted through the ductus arteriosus into the descending aorta due to high pulmonary vascular resistance. Three fetal shunts are essential: the ductus venosus, the foramen ovale, and the ductus arteriosus. These structures enable the fetus to maintain preferential streaming of oxygenated blood and support vital organ perfusion. Pulmonary blood flow remains low due to active vasoconstriction and gradually increases in the third trimester.
Pulmonary Vasoconstriction: A fundamental aspect of fetal physiology is that the lungs are powerfully vasoconstricted, meaning very little blood flows into the intrapulmonary arteries. This vasoconstriction is primarily due to hypoxia in the fetus (and pulmonary parenchymal compression) and persists until the fetus breathes. The primary site of oxygenation for the fetus is the placenta. Blood returns from the placenta via the umbilical vein, carrying highly oxygenated blood, for example, at 85% saturation. This umbilical venous blood largely bypasses the liver through the ductus venosus (also known as the canal of Arantius) and enters the inferior vena cava (IVC). Pulmonary vascular resistances are approximately ten times higher in the fetus than systemic resistances. The placenta primarily handles gas exchange, limiting the need for high pulmonary blood flow.
Fetal Shunts: To bypass the non-functional lungs and the liver, the fetal circulation utilizes three main shunts:
Ductus Arteriosus: This allows blood ejected from the right ventricle into the pulmonary artery to directly enter the descending thoracic aorta, bypassing the lungs.
Ductus Venosus (or Canal of Arantius): This bypasses hepatic (liver) resistances, allowing oxygenated blood from the umbilical vein to directly enter the inferior vena cava.
Foramen Ovale: This opening between the right and left atria directs preferentially oxygenated blood from the inferior vena cava (IVC) into the left atrium, bypassing the right ventricle and pulmonary circulation. Once this highly oxygenated blood from the IVC enters the right atrium, it is preferentially directed across the foramen ovale into the left atrium. This preferential flow is facilitated by a "channel" within the right atrium, formed by structures like the valve of Eustachius and the network of Chiari, which guides the blood towards the foramen ovale. During fetal life, the foramen ovale is wide open, allowing for equalization of pressures between the right and left atria. This ensures that the blood from the IVC can easily move from the right to the left side of the heart. Approximately 27% of the combined fetal cardiac output (CFCO) traverses the foramen ovale from the right atrium to the left atrium. This contrasts with the circulation in conditions like hypoplastic left heart syndrome, where the foramen ovale may be restrictive or the flow direction is reversed (left-to-right) due to different physiological demands or anatomical constraints.
Blood Flow and Outputs
The fetal cardiac output is referred to as Combined Fetal Cardiac Output (CFCO), as both ventricles work conjointly to ensure blood flow. Unlike postnatal life where right and left hearts function in series, fetal ventricles operate in parallel and contribute unequally to total cardiac output—termed combined ventricular output (CVO). The right ventricle accounts for approximately two-thirds (~66%), while the left ventricle contributes one-third (~34%). This disproportion is driven not by loading conditions but by intrinsic properties of the ventricles: Compliance (diastolic function) determines the ventricular filling volumes under similar atrial pressures. Contractility (systolic function) determines the ejection volumes under equivalent afterload conditions.
Ventricular Contributions: The participation of each ventricle to the CFCO is disproportionate:
The right ventricle (RV) contributes approximately 66% of the CFCO.
The left ventricle (LV) contributes approximately 34% of the CFCO.
Flow Distribution from Ventricles:
From the pulmonary artery (connected to RV): 66% of CFCO. Only a small portionreaches the lungs, while the majority (59%) travels through the ductus arteriosus to the descending aorta.
From the aorta (connected to LV): 34% of CFCO.
3% goes to the coronary arteries to supply the heart with the higher oxygenated blood coming via the FO.
21% goes to the cephalic vessels (brain) and upper body, also with higher oxygenated blood coming via FO.
Only 10% passes through the aortic isthmus (the narrowest part of the aorta, between the left subclavian artery and the ductus arteriosus insertion).
Descending Aorta Flow: The 10% from the aortic isthmus combines with the 59% from the ductus arteriosus, resulting in 69% of CFCO flowing into the descending thoracic aorta, which then goes to the umbilical arteries for oxygenation at the placenta.
Venous Return:
Superior Vena Cava (SVC): 21% from the brain and arms returns to the right atrium.
Coronary Sinus: 3% returns to the right atrium.
Inferior Vena Cava (IVC): 69% (including placental return via ductus venosus) returns to the right atrium.
Pulmonary Veins: Only 7% returns from the lungs to the left atrium.
Atrial Flow: The right atrium receives 93% of the venous return. 66% of this goes to the RV, and 27% crosses the foramen ovale to the left atrium. The left atrium receives the 7% from the pulmonary veins plus the 27% through the foramen ovale, filling the LV with its 34% share.
Oxygenation (Saturations) and Oxygen Distribution
The fetal circulation ensures that the most oxygenated blood is preferentially directed to the vital organs: the heart and the brain.
Placental Oxygenation: Blood arriving at the placenta is highly desaturated (e.g., 55% saturation). After oxygenation in the placenta, blood returns via the umbilical vein at a high saturation (e.g., 85%).
Path of Oxygenated Blood: This highly oxygenated blood from the umbilical vein primarily bypasses the liver via the ductus venosus and enters the inferior vena cava. It then flows into the right atrium and is preferentially shunted across the foramen ovale into the left atrium, then to the left ventricle, and into the ascending aorta.
Distribution to Heart and Brain: The ascending aorta supplies the coronary arteries (for the heart) and the brachiocephalic vessels (for the brain and upper limbs) with blood that has a higher oxygen saturation (e.g., 65% aortic saturation). This preferential flow is crucial for their growth and anabolism.
Path of Less Oxygenated Blood: Blood from the SVC (e.g., 35% saturation) and the less oxygenated portion of the IVC mainly enters the right ventricle and pulmonary artery (e.g., 50% pulmonary artery saturation). Due to pulmonary vasoconstriction, most of this blood (59%) bypasses the lungs via the ductus arteriosus, joining the descending aorta. The descending thoracic aorta has a slightly lower saturation (e.g., 55%) as it's a mixture of blood from the ascending aorta and the ductus arteriosus, before returning to the placenta via umbilical arteries.
Source: Rudolph, Abraham. Congenital diseases of the heart: clinical-physiological considerations. John Wiley & Sons, 2011.
Determinants of Ventricular Contribution and Morphology
The disproportionate contribution of the RV and LV to the CFCO, and consequently the size of the cardiac structures, is primarily due to the intrinsic properties of the ventricular myocardium. The amount of blood flowing through any cardiac structure dictates its development. Structures subjected to high flow develop larger diameters and volumes. For instance, the pulmonary artery, receiving the majority of right ventricular output, is anatomically larger than the aorta in fetal life. Similarly, regions like the aortic isthmus, which carry relatively little flow (~10%), develop as narrow segments. Any deviation from this physiological balance—such as a left-sided inflow or outflow tract obstruction—can alter downstream structures: Reduced left heart filling (e.g., mitral atresia) leads to hypoplasia of the left ventricle and ascending aorta. Reduced aortic outflow (e.g., aortic stenosis) impairs isthmic growth, predisposing to coarctation.
Similar Preload and Postload: Both ventricles fill at the same preload (diastolic pressure) because the foramen ovale widely open allows pressure equalization between the atria. They also empty against similar postload (arterial pressure) because the widely open ductus arteriosus connects the pulmonary artery and aorta, exposing both ventricles to the same fetal, pulmonary, and placental resistances.
Intrinsic Properties:
Compliance: The right ventricle is slightly more compliant (easier to fill for a given pressure), leading to a larger end-diastolic volume in the RV compared to the LV.
Contractility (Elastance): The left ventricle is slightly more contractile (generates greater tension for a given length). However, the overall effect on volumes is such that the RV's end-systolic volume is also somewhat larger than the LV's.
Resulting Volumes: These intrinsic properties lead to the RV having a larger stroke volume than the LV, explaining its 66% contribution versus the LV's 34%.
Morphological Consequences: The quantity of blood traversing a cardiac structure determines its size or volume.
This explains why in a normal fetus, the right ventricular cavity is larger than the left ventricular cavity.
Similarly, the pulmonary artery is typically larger than the aorta, and the aortic isthmus is the smallest part of the aorta because it carries the least amount of blood (10%).
The Transitional Period
While the sources do not provide an exhaustive step-by-step description of the transitional period at birth, they highlight the critical changes that occur:
Changes at Birth: Once the baby is born and begins to breathe, a cascade of events alters the circulation:
Increased Oxygenation: Breathing leads to higher oxygen partial pressure in the blood.
Decreased Pulmonary Vascular Resistance: Oxygen acts as a powerful pulmonary vasodilator, causing the pulmonary arterioles to dilate and dramatically reduce resistance in the lungs. This allows blood to flow freely into the pulmonary circulation.
Closure of Shunts:
The ductus arteriosus constricts and closes in response to increased oxygen levels, redirecting all right ventricular output to the lungs. The drop in PVR and increase in SVR will favour a progressive reversal of the ductus arteriosus shunt towards left to right, this increases the oxygen levels travelling through the ductus and triggers vasoconstriction mechanism. The ductus arteriosus constricts and closes, becoming the ligamentum arteriosum.
The foramen ovale typically closes due to increased pressure in the left atrium (from increased pulmonary venous return) and decreased pressure in the right atrium (from cessation of umbilical blood flow), reversing the normal fetal shunt. Because the pulmonary blood flow increases, there is increasing filling towards the left atrium. When the ductus arteriosus is left to right, the Qp>Qs which increases pulmonary blood flow and left atrial venous return, this contributes to the increase in LA filling which favours the closure of the flap from the foramen ovale. There is also a progressive increase in compliance of the RV (facing lower PVR) and decrease compliance of the LV (facing higher SVR). Inter-atrial shunting is dependent on underlying ventricular compliance. This phenomenon promotes the progressive transition from a right to left, then bidirectional and eventually left to right shunting at the inter-atrial level.
Shift to Series Circulation: These changes transform the parallel fetal circulation into a series circulation characteristic of postnatal life, where blood flows from the right heart to the lungs, then to the left heart and systemic circulation. Lung aeration leads to a significant increase in partial pressure of oxygen (PaO2) and a sharp decrease in pulmonary vascular resistances. These resistances eventually stabilize to about one-third of systemic resistances. The LV is genetically designed to be contractile with a thick wall, while the RV has a thinner wall and is more compliant.
The left ventricle's workload increases dramatically at birth as it takes on the full systemic circulation. It undergoes significant hypertrophy, becoming more muscular and specialized for contractility and maintaining systemic cardiac output. The right ventricle, no longer facing systemic pressures (and now facing low PVR), de-muscles, its compliance significantly increases compared to fetal life, and its contractile performance decreases, adapting to its adult low-pressure, high-volume role.
Clinical Implications: Any abnormalities in the fetal circulation's structure or the shunts' function (e.g., a restrictive foramen ovale in hypoplastic left heart syndrome, or an early closing ductus in transposition of the great arteries) can lead to severe neonatal emergencies. For instance, a small aortic isthmus, normal in fetal life, can become a coarctation of the aorta after birth if its flow was too low during development.
Hemodynamic Impact on Morphogenesis
Coarctation of the Aorta: When left ventricular output is reduced (e.g., mitral stenosis), aortic isthmus flow diminishes, resulting in a narrow segment prone to postnatal coarctation.
Tricuspid Atresia: Absence of a functional right AV valve means all systemic venous return passes through the foramen ovale into the left heart. The foramen must be large, and the left ventricle enlarges. If no VSD is present, the right ventricle is nearly absent.
Hypoplastic Left Heart Syndrome (HLHS): In cases of mitral and aortic atresia, the left heart structures are absent or extremely small. Systemic perfusion depends entirely on ductal patency and right-to-left shunting. The foramen ovale is small, and the ductus arteriosus becomes a critical structure.
Pulmonary Atresia with VSD: The right ventricle is disconnected from the pulmonary artery, and flow is redirected through a large VSD to the aorta. The morphology of the ductus arteriosus changes, often originating more proximally on the aortic arch and taking a tortuous path.
D-Transposition of the Great Arteries (D-TGA): While gross circulatory patterns remain, oxygen saturation profiles reverse. The aorta carries desaturated blood, reducing cerebral and coronary oxygenation. Fetal arterial oxygen saturation is higher in the pulmonary artery, promoting vasodilation and closure of the ductus arteriosus and foramen ovale—key risks for postnatal adaptation.
Transitional period
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.
Reference:
Rudolph, Abraham. Congenital diseases of the heart: clinical-physiological considerations. John Wiley & Sons, 2011.
CPC M3C Necker Physiologie Partie 1 Morphogenèse et Physiologie
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.
Recap: The Frank-Starling law describes the relationship between ventricular filling (preload) and the force of contraction (stroke volume). Contractility is represented by the slope of the pressure-volume curve during systole. The LV has a steeper slope (more contractile) than the RV. For the same change in volume, the LV generates a greater pressure increase. Relaxation (Diastole) and Compliance are represented by exponential curves. The LV is less compliant (its compliance curve is above the RV's curve) and relaxes less rapidly than the RV. This means for a given volume, the LV will have a higher diastolic pressure than the RV. The area enclosed by the pressure-volume loop represents cardiac work.
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.
Recap of Poiseuille's Law: The link betewee Pressure, Resistance, and Flow (Delta P = R x Q). It is the correlate of the Ohm's law in electricity. This law, typically applied to fluid flow in tubes, states that pressure difference (ΔP) equals resistance (R) multiplied by flow (Q). In the pulmonary circulation, this translates to:
(Mean Pulmonary Artery Pressure - Left Atrial Pressure) = Pulmonary Flow (Qp) x Pulmonary Vascular Resistance (PVR). In the systemic circulation: (Mean Aortic Pressure - Right Atrial Pressure) = Systemic Flow (Qs) x Systemic Vascular Resistance (SVR). These formulas are fundamental to hemodynamic analysis.
In pulmonary hypertension: (mPAP - Pulmonary venous pressure) = (mPAP - Left Atrial pressure). mPAP = Qp x PVR + LA pressure.
Increased of Qp: (high pulmonary flow, left to right shunt). Seen in hyper-flow lesions, especially left-to-right shunts. This type of PH is often reversible with shunt closure.
Increased PVR (respiratory disorders, hypoxia, connective tissue disorders, embolis, HIV, medications that are vasoconstrictors, PPHN, idiopathic, etc.);
Increased in LA pressure (LV dysfunction, LV cardiomyopathy, mitral stenosis, mitral regurgitation, pulmonary venous stenosis, pulmonary occlusive venous disease, diastolic LV dysfunction, hypoplastic LV, hypertrophied LV).
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
Combining Poiseuille's Law and Fick's Principle:
Resistance Ratio: By combining Poiseuille's law and Fick's principle, the pulmonary-to-systemic resistance ratio (PVR/SVR) can be derived:
PVR/SVR = (QS/QP) x (Mean PAP - PaOG) / (Mean AoP - PaOD).
This ratio is crucial in hemodynamics, with a target value of less than one-third indicating a good balance.
Thermodilution for flow measurement is generally unreliable in the presence of intracardiac shunts, as the injected cold saline will be contaminated by the shunt, leading to inaccurate results. Therefore, the Fick principle using oxygen saturations (derived from blood gases and hemoglobin levels) is the preferred method for measuring QP/QS and subsequently calculating resistances in these cases.
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.
Wall Tension and Ventricular Adaptation: Laplace's law states that wall tension (parietal stress) in a cardiac chamber is proportional to its intracavitary pressure and radius, and inversely proportional to its wall thickness. This explains how ventricles adapt to increased pressure by increasing wall thickness (hypertrophy) to maintain stable wall tension. The LV naturally has a thicker wall due to higher systemic pressures. While less used for reasoning in congenital heart disease, it's fundamental in general cardiac physiology.
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.
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.pdfKey mechanical events within the cycle include:
Diastole (Filling): The atrioventricular valve opens, allowing the ventricle to fill until the end-diastolic volume is reached. The end-diastolic pressure is determined by the ventricle's compliance.
Isovolumic Contraction: The atrio-ventricular valve closes, and the ventricle contracts without changing volume until its pressure surpasses great vessel pressure.
Systole (Ejection): The semilunar valve opens, and blood is ejected, causing ventricular volume to decrease. This phase concludes when the ventricle reaches its end-systolic elastance curve.
Isovolumic Relaxation: The aortic or pulmonary valve closes, and the ventricle relaxes without changing volume until the atrio-ventricular valve reopens.
These phases define the characteristic loop: diastole, isovolumic contraction, systole, and isovolumic relaxation.
biology-13-00055.pdf
Decrease PVR: oxygen, low CO2, alkalosis, low hematocrit, pulmonary vasodilator, anesthesia
Increase PVR: hopoxia, hypercapnia, acidosis, high hematocrit, hypervolemia, agitation, increased mean airway pressure, hypothermia
Wiggers Diagram of cardiac physiology - Pressure curves in ventricle, atrium and great vessel
Wiggers Diagram of cardiac physiology - Pressure curves in ventricle, atrium and great vessel
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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