Laplace's Law defines the relationship between the wall tension (T) and the pressure (P) and the radius (r) for a thin-walled cylindrical shell (Fig. 15).
The tension is directly related to the pressure and the radius.
If the wall has a thickness, then the circumferential wall stress is given by Lame's equation (Fig. 15), where the wall tension (T) is related to the pressure (P) and the radius (r) and inversely related to the wall thickness (h).
In other words, hypertrophy of the wall is a compensatory mechanism, which tends to bring back the wall tension to near-normal levels. Dilatation or enlargement, on the other hand, significantly increases the wall tension. This relationship needs to be kept in mind for it operates in many disorders, both physiological and pathological. One of the important determinants of myocardial oxygen consumption is the wall tension developed in the left ventricle. The other factors include heart rate and contractility or inotropic state (Table 13).
High left atrial pressure, however produced, will lead to elevated pulmonary venous and capillary bed pressure. This in turn will cause symptoms of dyspnea. When the pressure is significantly elevated it can produce symptoms of orthopnea, which is dyspnea on assuming supine position relieved by raising the head or sitting up, as well as paroxysmal nocturnal dyspnea. The latter requires the sleep mechanism, and it usually occurs at night. The patient will give a history of waking up short of breath from sleep after having gone to sleep a few hours prior to the episode. Sitting up and dangling the feet or getting up and standing for a while relieves the dyspnea. The extravascular fluid shifts gradually into the vascular compartment during sleep. This expands the blood volume and raises the left atrial pressure. In normal subjects, the left ventricle accom-
Clinical Features of Left Atrial and Pulmonary Hypertension
Symptoms of high left atrial pressure
• Paroxysmal nocturnal dyspnea
• Palpitation if in atrial fibrillation
Symptoms of pulmonary hypertension
• Low-output symptoms
• Exertional presyncope/syncope (from fixed output)
Signs of pulmonary hypertension
• Wide split S2 if RV failure
• Sustained subxiphoid impulse
& x = y (RV diastolic dysfunction with raised RV filling pressure) & x < y (early RV systolic failure)
& y descent with large v wave (tricuspid regurgitation with RV dilatation) JVP, jugular venous pulse; LICS, left intercostal space; RV, right ventricular.
modates the extra volume by increasing the output, and the consequent increase in renal blood flow increases the urine output. However, when the left atrial pressure is somewhat elevated already, this shift from the extravascular to the intravascular compartment is not tolerated and results in symptoms of pulmonary congestion. The classical paroxysmal nocturnal dyspnea occurs in patients with decompensated left ventricles. In mitral stenosis, where the left ventricle is underfilled and normal, one may get the history of paroxysmal nocturnal dyspnea. However, it is often atypical. The patient never gets comfortable completely after being up or tends to wake up more than once in the night because the left atrial pressure is significantly elevated because of the mitral obstruction (Table 14). Occasionally the patient with elevated left atrial pressure may complain of a nocturnal cough instead of dyspnea.
In the absence of mitral stenosis, high left atrial pressure secondary to heart failure will often be associated with the presence of a pathological S3.
The pulmonary congestion may result in basal rales or crepitations (crackles) when the lungs are auscultated. These crepitations result from the congestion of the smaller airways with swelling, resulting in the closure of the airways during expiration as the lungs collapse. With expansion of the lungs on inspiration, the closed airways snap open, causing these snapping sounds. These crackles, heard when the patient is supine, may sometimes clear up on patients assuming an erect posture because of a decrease in the venous return resulting in lowered left atrial pressure. When the pulmonary congestion is significant, it would require active therapy for improvement. When untreated or ineffectively treated, it may end in a vicious cycle of hypoxemia, worsening left ventricular function, further rise in left atrial pressure, and worse pulmonary congestion. Acute pulmonary edema may follow with marked shortness of breath associated with labored breathing with the use of the accessory muscles. Cyanosis may occur and the patient may start coughing up pink froth. Because of pulmonary venous congestion, the fluid is blood tinged, making it pink. The surfactant in the lung causes the fluid to bubble, hence the froth. Hypoxemia and low cardiac output will be associated with sinus tachycardia. Untreated, this may deteriorate. There could be gradual slowing of the heart rate, with the patient losing consciousness resulting in hypoxemic cardiorespiratory arrest.
The pulmonary signs of crackles, however, are not specific for high left atrial pressure and more often present in other causes of pulmonary disease, including pneumonia, chronic obstructive pulmonary disease, and pulmonary fibrosis. Furthermore, pulmonary edema can also occur in the absence of elevated left trial pressure.
When pulmonary hypertension is severe, the vascular changes that develop in the pulmonary arterial bed not only raise the pulmonary vascular resistance but also act as severe obstructive lesion peripherally reducing flow and output. This is further aggravated when the right ventricle becomes decompensated. The main symptoms of pulmonary hypertension are therefore one of low output. The output may become relatively fixed and fail to increase with exertion and may actually paradoxically fall, causing symptoms of presyncope and/or syncope with exertion. The oxygen saturation may also fall with exertion. The hypoxemia may also predispose to the development of arrhythmias. Often patients may also complain of vague atypical chest pain. The cause of this is not easily explainable (Table 14).
Pulmonary hypertension would cause the pulmonary component of the second heart sound (P2) to become more sharp and loud. The P2 may become palpable in the second left interspace, where it is often best heard. A palpable S2 (when confirmed to be a result of the loud P2 by auscultation) in the second left interspace usually is a good sign of pulmonary hypertension, and the pulmonary systolic pressure may be 75 mmHg or higher when this sign is present. The S2 split is usually narrow when the right ventricle is still compensated because the effect of the higher pulmonary impedance will be to bring the P2 earlier, making the split narrower. When the right ventricle is decompen-sated, however, the S2 split may become wide because of a delayed P2 component as a result of poor and delayed right ventricular relaxation. The split may not vary well with respiration when this happens; it may be confused with a fixed splitting of S2. However, following exercise or in the post-Valsalva strain phase, the S2 split can be shown to vary making this a useful maneuver during auscultation.
The increased right ventricular pressure and the consequent increase in its wall tension may give rise to a sustained right ventricular impulse on subxiphoid palpation. One may also feel along with it an atral kick because of a strong right atrial contraction. This is usually present only in the early compensated state of significant pulmonary hypertension.
Signs of Wide Pulse Pressure with Decreased Peripheral Resistance
• Corrigan pulse (visible carotid pulse)
• Quincke's sign (increased capillary pulsation)
• Pistol shot sounds
• Duroziez's bruit (systolic and diasystolic bruit over femorals, brought out by compression)
• Collapsing pulse
• de Musset's sign (rocking head movement)
• Positive Hill's sign (blood pressure in the leg higher than in the arm >15 mm)
The decreased right ventricular compliance because of diastolic dysfunction and right ventricular hypertrophy will lead to increased right ventricular diastolic pressure. This is reflected in the right atrial and the jugular venous pressures. Thus, pulmonary hypertension will often lead to elevated jugular venous pressure and abnormal jugular venous pulse contour. This has been discussed in detail in Chapter 4. Here it suffices to summarize the sequence ofjugular contour changes in pulmonary hypertension. In the presence of pulmonary hypertension, the jugular venous pulse contour of x' > y indicates compensated right ventricular function, x' = y indicates right ventricular diastolic dysfunction with raised filling pressures, xX < y indicates early right ventricular systolic failure, and y descent with large v wave denotes tricuspid regurgitation and right ventricular dilatation (Table 14).
Signs of Wide Pulse Pressure With Decreased Peripheral Resistance
These are listed in Table 15.
The respiratory variations in the timing of both the A2 and the P2 components of the S2 and their effects on the splitting of the S2 are shown in Fig. 16.
In the normals, the sequence of the components is A2 followed by P2 because the left ventricle is a more powerful chamber. Its contraction and relaxation are much faster than that of the right ventricle. On inspiration, there is decreased intrathoracic pressure with increased venous return to the right side. The lungs expand and the pulmonary impedance falls. Thus, the increased right ventricular volume and the decreased pulmonary impedance make the P2 come later on inspiration. The expansion of the lungs on inspiration diminishes the pulmonary venous return to the left heart. This may make the A2 come slightly earlier on inspiration. The effect ofthese changes on inspiration is to make the A2 and the P2 move away from each other, resulting in a split. The reverse changes occur on expiration. The A2 comes later, and the P2 comes earlier. The components come together with the splitting narrowing.
Right Bundle Branch Block (RBBB)
In RBBB the right ventricular electrical depolarization is delayed; therefore, the right ventricular mechanical events are also delayed by the same amount. Otherwise the variations are the same as in the normal. The right ventricular delay causes a wider
splitting of S2 because of delayed P2 on inspiration. The P2 does not come close to A2 during expiration. Thus, the split remains on expiration (audible expiratory splitting), although there is significant movement in A2- P2 intervals with respiration.
Left Bundle Branch Block (LBBB)
In LBBB, the left ventricular depolarization and mechanical events are delayed. Therefore, both the mitral component of the S1 (M1) and the A2 are delayed. This delay causes the A2 to occur after P2, resulting in an abnormal sequence. This leads to a reversal of the splitting on inspiration called "paradoxical splitting." The P2 moves as in the normal, but because of the delay in A2, the two components come together during inspiration and move away from each other during expiration.
In aortic stenosis, a paradoxical splitting of the S2 can occur as a result of delayed A2 (closure of aortic valve). This is not because of an electromechanical delay as in LBBB, but rather because of increased ejection time as a result of the stenotic valve causing outflow obstruction. Unlike the case in LBBB, the Ml in this case is not delayed. Ischemia can also cause similar change.
In atrial septal defect, there is a left-to-right shunt across the atrial septum. The respiratory variations in the venous return and the consequent right-sided filling are compensated by the variations in the shunt with the result that the right ventricle receives more or less the same amount of blood on both inspiration and expiration. In addition, the overfilled pulmonary arterial bed from the left-to-right shunt does not allow any significant changes in the pulmonary impedance on inspiration. The left-sided filling also remains relatively the same for similar reasons. This results in a relatively fixed splitting of A2 and P2.
In chronic pulmonary hypertension, the P2 becomes louder because of significant increase in the pulmonary arterial pressure and the high pulmonary arterial resistance. The high pulmonary impedance does not drop much with inspiration. This will result in a P2 that occurs somewhat early and does not change much with respiration. This will result in a narrow split of the S2 or a single S2.
In acute pulmonary hypertension as seen in large acute pulmonary embolism, the P2 is not only loud but in fact may be delayed, resulting in a wide-split S2. It may remain wide until full compensatory mechanisms come into play. The wide split may become normal eventually unless recurrent embolism leads to the development of chronic pulmonary hypertension.
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