Physiology By Ak Jain.pdfl
Diann Wald
Pulmonary circulation includes a vast network of arteries, veins, and lymphatics that function to exchange blood and other tissue fluids between the heart, the lungs, and back. They are designed to perform certain specific functions that are unique to the pulmonary circulation, such as ventilation and gas exchange. The pulmonary circulation receives the entirety of the cardiac output from the right heart and is a low pressure, low resistance system due to its parallel capillary circulation. The system can be divided into the following components:
It is appropriate to mention that a similar system of lymphatics and vessels exists between the parietal and visceral pleurae, draining the pleural fluid which plays an important role in providing a viscous medium for expansion of lungs during their respiratory excursion. The large negative pleural pressure (approximately -4 to -7 mmHg) exists because of an efficient efferent venous and lymphatic system that keeps the alveoli closely tethered to the visceral pleura and prevents them from collapsing inwards.
Pulmonary edema: Any disturbance in the starling forces (see below, pathophysiology) operating in the pulmonary circulation can lead to an accumulation of fluid in the alveoli, impairing gas exchange, and causing respiratory distress. Pulmonary edema can either be cardiogenic or non-cardiogenic. Causes include elevated hydrostatic pressure (i.e heart failure), decreased serum oncotic pressure (i.e. low albumin), decreased lymphatic clearance (i.e. lymphedema), increased vessel permeability (i.e. inflammation), and decreased surfactant (i.e. prematurity).[2]
Pulmonary embolism: A dislodged clot from a distant source (most commonly a deep venous thrombus) can embolize to the pulmonary circuit and lead to ischemia and, if prolonged, infarction of the lung parenchyma as well as severely impaired gaseous exchange. It is important to note that the peripheral parenchyma is more prone to infarcation as it is purely reliant on the pulmonary circulation for oxygenation (see below, function).[3]
Pulmonary hypertension: An increase in the mean pulmonary artery pressure beyond 25 mmHg is known as pulmonary arterial hypertension. It leads to impaired gas exchange and commonly manifests as exertional dyspnea. If prolonged, it can lead to right ventricular stain and right heart failure, a phenomenon known as cor-pulmonale.[4]
Pleural effusion: A disturbance in the starling forces (see below, pathophysiology) of the pleural circulation can lead to accumulation of fluid in the pleural space, a phenomenon known as pleural effusion. This manifests as pleuritic chest pain and respiratory distress.[5]
The fetal circulation begins to form as early as 15 days after conception in the form of immature placental vessels and slowly grows to form a fully functional four-chambered heart, beating independently from the maternal circulation by the fourth week of gestation.[6]
The growing fetus receives its nutrients and excretes metabolic waste products via the placental vessels that connect the umbilical veins, which in turn drain into the inferior vena cava and then into the right atrium. The fetal circulation is designed to shunt blood across the liver and lungs during fetal life via the ductus venosus, foramen ovale, and the ductus arteriosus. The blood from the right atrium makes its way to the systemic circulation without actually reaching the lungs. The pulmonary vessels remain closed under high pressure, and it is only after birth as the newborn takes its first breaths that the pulmonary artery pressures fall, shunts existing in the fetal life close, and blood begins to enter the lungs for exchange of gases for the fetus is no longer dependent on the placental circulation. A failure in this process sometimes leads to persistent pulmonary hypertension, causing respiratory distress in the newborn. The condition requires multi-disciplinary management using supplemental breathing, artificial surfactant, and vasodilators to lower the pulmonary artery pressure.[7][8]
The pulmonary circulation has many essential functions. Its primary function involves the exchange of gases across the alveolar membrane which ultimately supplies oxygenated blood to the rest of the body and eliminates carbon dioxide from the circulation. The bronchial circulation provides oxygenated blood to the lung parenchyma. There is an overlap between the bronchial and pulmonary circulations in terms of oxygenating the lungs, especially near central regions. The peripheral aspects of the lungs becoming increasingly dependent on the pulmonary circulation and is more prone to infarction as a result. The low-pressure venous system and an intricate system of lymphatics ensure that there is no build-up of edema fluid in healthy lungs.
An understanding of the pressure gradients across the pulmonary circuit is important in realizing that minor derangements in these pressures can lead to adverse outcomes such as pulmonary edema and respiratory shunts.
It is important to note that low pressures in the pulmonary capillaries allow for easy exchange of gases in the lung alveoli. The pressure in the left atrium is difficult to measure directly, and a surrogate pressure, known as the pulmonary capillary wedge pressure (PWP), is often used. PWP can differentiate between primary and secondary pulmonary hypertension. A high PWP suggests a cardiac origin, whereas a low PWP suggests a pulmonary origin.
A hydrostatic pressure gradient exists, by virtue of gravity, from the apex of the lung to the base: 23 mmHg (distributed as -15 mmHg from the level of the heart to the apex of the lung and +8 mmHg from the level of the heart to the base of the lung). This results in a 5-fold greater blood flow at the base of the lung as compared to the apex of the lung. Three zones of pulmonary blood flow can be delineated based on the pulmonary capillary pressure (Pcp)and the pulmonary alveolar air pressure (Ppac).
Zone 1: The Pcp is always less than the Ppac here, and there is no blood flow in the pulmonary capillary bed during any phase of the cardiac cycle. Zone 1 circuits are not seen in the normal lung and are only seen in certain conditions, such as after massive blood loss or if a person is breathing against a positive airway pressure (PEEP). PEEP, in basic terms, overventilates the lung and increases alveolar pressures in order to improve alveolar ventilation in an unhealthy lung.
Zone 2: Here the Pcp rises above the Ppac only during systolic blood flow, and so gas exchange occurs only during systole and not in diastole. Zone 2 blood flow is seen at the apices of the normal lung.
Zone 3: Here the Pcp remains greater than the Ppac in all phases of the cardiac cycle, allowing for an efficient exchange of gases. At the time of exercise, the pulmonary blood flow increases and all Zone 3 lung converts to Zone 2.[10]
This is a peptide released by the left ventricular myocardium in response to elevated filling pressures and blood volumes. It is a very sensitive and specific marker of cardiogenic edema. High levels of Pro-BNP strongly suggest a cardiogenic cause while low levels can effectively rule out a cardiogenic cause; however intermediate values have little significance and require further investigation.[11][12][13]
This is an invasive tool used to evaluate the pulmonary capillary wedge pressure (PWP). It entails the insertion a catheter from a peripheral access site to the pulmonary artery. A value greater than 18 mmHg is highly suggestive of a cardiogenic cause of pulmonary edema as it corresponds to an elevated left atrial pressure.[14]
Pulmonary edema is the accumulation of free fluid in the alveoli resulting in a decrease in the capacitance of the parenchyma and impairing gas exchange across the alveolar membrane. Acute onset pulmonary edema can lead to severe respiratory distress and death in 20 to 30 minutes.
An imbalance in these forces in the form of raised pulmonary hydrostatic pressure (for diastolic: left ventricular failure), decreased plasma osmotic pressure (e.g., protein-losing enteropathy) or increased capillary membrane permeability (e.g., infections like pneumonia, inhalation of toxic gases like carbon monoxide) leads to pulmonary edema.[2]
Since the baseline left atrial pressure (and hence the pulmonary capillary wedge pressure) is 7 mmHg, this gives a protective factor of 21 mmHg, i.e., the left atrial pressure can rise by an additional 21 mmHg before pulmonary edema develops. However, beyond this value, the rate of accumulation of fluid is rapid, and pressures beyond 30 mmHg can lead to death due to pulmonary edema in 20 to 30 minutes (i.e. acute cardiogenic shock). However, in long-standing cases (i.e. chronic mitral stenosis), the pulmonary capillary wedge pressure may be as high as 40 mmHg before edema develops as both the heart and lungs have had time to compensate.[15]
Starling forces can be used to determine the direction of net water movement, thus evaluating filtration out of or absorption into the capillary. The starling equation for fluid flux (volume per time) can be found below.
In the lungs there are additional forces to be considered, alveolar air pressure and surface tension, with air pressure driving fluid into the vasculature, and surface tension pulling water into the lungs.
Acute pulmonary edema can have a cardiogenic or non-cardiogenic origin. The differentiation can be made clinically. Cardiogenic edema is commonly preceded by an acute coronary event and is usually associated with elevated left ventricular filling pressures. Non-cardiogenic causes are commonly included in the umbrella term of acute respiratory distress syndrome (ARDS) which is associated with wide-spread systemic inflammation and release of cytokines causing increased permeability of the pulmonary alveolar capillaries and causing an exudative edema as compared to a transudative edema as seen in acute heart failure. ARDS is commonly seen in settings of systemic sepsis, burns, or massive blood transfusions.
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