Spontaneous Circulation focuses on advanced ECG interpretation, cardiac pharmacology, hemodynamic assessment and resuscitation, and managing acute coronary syndrome. It is devoted to translating the best evidence-based treatments from critical care, resuscitation, and trauma for bedside use in the emergency department.
Tuesday, August 05, 2014
When a patient arrives to your ED fresh from karate class still in her uniform, you get a feeling about where the case is heading. This patient was 49, and reported that she always had some aches after karate. This evening, though, her pain was very different — and much more concerning. The pain had started about an hour into her class and worsened over the next 30 minutes. It was a severe achy pain over her left chest that radiated to her neck and was associated with pronounced diaphoresis. This prompted an expedited cardiac workup.
The ECG showed a sinus tachycardia with ST-elevation in V2-V3, I, aVR, aVL, with depression in II, III, aVF, and V5-V6. The ST-elevation in V2-V3 with inferior reciprocal depression (II, III, aVF) was concerning for myocardial injury in the anteroseptal region caused by left anterior descending artery (LAD) occlusion. EPs should have a high suspicion for very proximal LAD, left main, or Circumflex occlusion when seen in conjunction with ST-elevation in I, aVL, and aVR.
She was taken immediately for coronary angiography, and was found to have an extensive thrombosis originating in the left main and extending into the proximal LAD and Circumflex arteries. The clot was removed by aspiration thrombectomy, and further angiography and intravascular ultrasound revealed dissection of the coronary arteries originating in the left main and propagating down the LAD. A small perforation of the LAD was seen just proximal to the first diagonal takeoff.
Spontaneous coronary artery dissection (SCAD) is an uncommon event, and occurs when the layers of the artery separate, creating a false lumen. Hemorrhage into the false lumen propagates the dissection distally. The true lumen of the vessel can become blocked by thrombus or the dissection flap. Obstruction of the lumen reduces perfusion and causes myocardial ischemia and necrosis. Patients present with symptoms of ischemic cardiac chest pain and with associated ECG and enzyme changes typical of NSTEMI or STEMI. ACS is often the initial concern, but the diagnosis of SCAD is made during coronary angiography.
The dissected medial flap shows up as a thin radiolucent line. Overlying thrombus is seen as haziness in the true lumen. SCAD is often treated with percutaneous intervention. Using IVUS, the dissection flap can be identified, and a guide wire can be placed carefully in the true lumen. Stenting open the flap seals the dissection, preventing further propagation, restoring flow in the true lumen, and relieving ischemia. Coronary artery bypass surgery is often difficult. Grafting to the true lumen is difficult with long dissections, and the vascular tissue is often too fragile to support suturing.
Atherosclerotic plaque rupture can cause complex intramural hematoma formation in the vascular wall dissecting the layers, but the dissection rarely propagates much further than the extent of the atheroma. More commonly, though, dissection associated with atherosclerotic plaque rupture can occur during balloon angioplasty or PCI. As the vessel is dilated, the fibrous cap and intimal layer can be torn, leading to dissection. Dissection in these scenarios is not usually labeled SCAD.
SCAD, in contrast, is not associated with coronary artery disease. Women make up the majority of cases, and they tend to be younger. A significant percentage occurs in the peripartum period, and the LAD is the most affected coronary artery. SCAD has also been associated with Marfan syndrome, fibromuscular dysplasia, and peripheral eosinophilia disease.
Unfortunately for our patient, she had profound cardiogenic shock and was emergently placed on VA ECMO (which I will cover in the future) despite thrombectomy and stenting of the dissection flap. She had little recovery of her cardiac function over the next two weeks, and was transitioned to a left ventricular assist device (LVAD) as destination therapy.
LVADs provide mechanical pump support for patients with severe heart failure as permanent treatment or a bridge to therapy. The most common device used today is the HeartMate II (Thoratec). It uses a continuous flow axial pump that is implanted in the abdominal wall. The inflow cannula (relative to the pump) draws blood from the apex of the left ventricle, and the blood is pumped through the outflow cannula into the proximal ascending aorta.
(New Engl J Med 2007;357:885.)
The pump is powered and controlled by an external controller and batteries that are connected to the implanted pump by a driveline. Important parameters reported by the LVAD are pump speed (RPM), power, pulsatility index, and flow estimate.
Patients with LVADs can present to the emergency department for any condition. The most important rule for evaluating a patient with an LVAD is to assess the patient as you would normally, completely independent of the device. Specific assessment of the LVAD itself is shown in Table 1, and common LVAD complications are listed in Table 2.
The patient did well, and she was discharged home after several more weeks in the hospital. She maintains close follow-up in the LVAD clinic and close contact with her LVAD coordinator. She is being evaluated for an underlying connective disorder.
Monday, July 07, 2014
Our patient was having an uneventful and ordinary day. He got his children off to school, and spent the morning at the office completing paperwork. By noon he had eaten lunch, and went to the company workout center. It was Wednesday, so it was arms day. He started as he always did with 20 minutes of cardio on the elliptical machine, then shoulders, biceps, triceps, forearms — big muscle to small muscle. It was at the end of his first rep of triceps that things changed.
He felt some dizziness, and the nausea began within 30 seconds or so. He couldn't hold himself upright, and slouched sideways off the bench onto the ground, losing consciousness. Others had seen him slide to the floor, and tended to him immediately. He did not have a pulse, and chest compressions were started. Another person ran to get an AED, which advised a shock. A jolt of electricity and remarkably he had a pulse and regained consciousness.
He was brought by ambulance to the ED, and said he felt fairly well besides minor chest wall pain from the CPR. The patient didn't have exercise-related chest pain or chest tightness, and denied a sense of racing heart or palpitation prior to the event. He had not had any previous known cardiac history or previous exertional syncope. He had no family history of premature coronary artery disease, cardiomyopathy, or sudden cardiac death.
Vital signs and physical exam were unremarkable. A 12-lead ECG was obtained. (Figure 1.) The ECG shows sinus rhythm with some right axis deviation and nonspecific ST-T changes; otherwise no current of injury, infarction pattern, or ischemic changes were seen. QTc is not prolonged, and no Brugada pattern or evidence of Wolf-Parkinson-White are present.
Figure 1. 12-lead ECG on presentation to the emergency department.
An emergent transthoracic echocardiogram was performed, and a parasternal long axis view is shown in Figure 2. Left ventricular hypertrophy was present, systolic function was at the lower limits of normal, and he had a mild asynchronous kinesis of the septum. Most notably, he had an inferolateral wall motion abnormality, with a suggestion of thinned myocardium over the segment.
Figure 2a and 2b.
Watch videos of an emergent transthoracic echocardiogram in the parasternal long axis view here and here. Left ventricular hypertrophy was present, systolic function was at the lower limits of normal, and he had a mild asynchronous kinesis of the septum.
Myocardial segments with abnormal enhancement or wall motion disturbances are named and localized according to the 17 segments-model of the American Heart Association. In cross-section, the left ventricle can be divided into apex, mid, and basal sections, and then subdivided circumferentially. (Figure 3.) Individual myocardial segments can be assigned to the three major coronary arteries with the recognition that anatomic variability exists.
Figure 3. Left ventricle segment definitions.
Given the concern for coronary artery disease, coronary angiography was performed and showed no significant coronary artery disease. LVEDP was 20, and no evidence of gradient across aortic valve was seen. The initial working diagnosis was possible catecholaminergic polymorphic ventricular tachycardia (CPVT) because it followed intense exercise. Given the echocardiographic finding, this is likely to be scar-mediated, probably from previous silent myocardial infarction with possible recanalization. This can best be evaluated with a cardiac MRI. (Figure 4.)
Figure 4. Cardiac MRI.
One of the benefits of cardiac MRI is the ability to evaluate the myocardium’s response to Gadolinium contrast. The contrast is taken up in normal and injured myocardium, but it is washed out easily of normal tissue. There is a delay in eliminated the contrast in certain conditions (approximately 10-15 minutes), and is termed delayed enhancement.
The pattern of the delayed enhancement provides insight to the etiology causing the damaged myocardium. Ischemic cardiomyopathy is seen as ventricular dysfunction in a coronary artery distribution. Tissue involvement always progresses from the subendocardium through to full transmural thickness, depending on the extent of injury. Both acute and chronic myocardial infarctions demonstrated delayed enhancement. The contrast in acute infarctions enters the damaged myocardial cells through the leaky myocyte membrane, but in chronic infarctions the late enhancement is a result of retention of contrast in the fibrous interstitium. On the other hand, nonischemic myocardial disease usually does not occur in patterns consistent with a coronary artery distribution and often can be limited to midwall or epicardial regions. (Figure 5.)
Figure 5. Patterns of delayed enhancement on cardiac MRI.
Delayed enhancement can also identify two important features of ischemic myocardium: stunning and hibernation. Myocardial stunning can occur following an acute myocardial infarction despite restoration of coronary artery flow. The myocytes are dysfunctional, but can regain contractile function over time. The myocardial function is likely to improve if the delayed enhancement is less than 50 percent of the transmural thickness. Hibernating myocardium, however, occurs in chronic ischemic heart disease. Myocytes that are chronically deprived of oxygen can enter a low-energy sleep state; this is potentially reversible by revascularization. Hibernating myocardium can be identified on MRI as areas that do not enhance with contrast. The function is likely to improve after revascularization if the nonenhancing thickness is greater than 50 percent of the transmural thickness.
The cardiac MRI delayed images for our patient show an akinetic segment of marked myocardial thinning in the inferolateral wall of the mid left ventricle with near transmural delayed enhancement. (Figure 6.) This is consistent with sequelae of previous myocardial infarction, and indicates nonviable myocardium in this territory. There was no evidence for an acute or recent myocardial infarction.
Figure 6. Delayed image from patient’s cardiac MRI.
The patient later reported treating himself for heartburn several months before his cardiac arrest, which could have been an unrecognized acute coronary event that resulted in scarring. The cardiac arrest appears to be a primary arrhythmic event probably mediated by a myocardial scar. He was treated with aspirin, beta-blockade, ACE inhibitor, and high-intensity statin even in the absence of underlying obvious coronary disease based on the presence of myocardial scar and suspicious previous symptoms. An ICD was placed for secondary prevention of sudden cardiac death.
Wednesday, June 04, 2014
She watched the Camry coming straight at her, obeying the laws that Newton laid out: a body in motion stays in motion until an external force intercedes.
Her husband, daughter, and the TV weatherman had told her not to go out. Ice had descended on the city earlier in the day, making even the walk to the garage precarious. But she needed milk to make a cake for the next day’s party, and the store was only three blocks away. Her plan was simple: store, milk, home. That might have worked if not for the Camry that became a hockey puck on the ice.
The next couple of hours were a blur but proceeded as readers would expect: 911, paramedics, backboard, cervical collar, ambulance, IV, medicine, stabilization bay, ultrasound, x-rays, more medicine, scanner, hospital bed. All she remembered from that first day through her fentanyl fog was someone saying, “Only a fractured hip. With surgery, this should all be a bad memory in a year.”
She had suffered an acetabular fracture and femoral head fracture. (Figures 1 and 2.)
Figure 1. Pelvic AP x-ray.
Figure 2. Still image from CT scan showing details of acetabular fracture and femoral head fracture.
The next morning she developed atrial fibrillation with a rapid ventricular rate. (Figure 3.) Surgery was postponed, and cardiology was consulted. She was asymptomatic and maintained normal blood pressure despite the rhythm change. The ECG showed diffuse ST-segment depression concerning for subendocardial ischemia, which could be attributed to her known coronary artery disease. She had suffered an NSTEMI about four years earlier, and had two stents placed in the proximal- and mid-RCA. She also had diffuse LAD and circumflex disease. The atrial fibrillation and rapid rate were felt to be secondary to adrenergic stimulation. This improved with additional pain control and beta-blockade, and she spontaneously converted to normal sinus rhythm.
Figure 3. ECG on hospital day 2 when the patient developed atrial fibrillation with rapid ventricular rate.
On hospital day 5, her physicians thought she was safe for surgery, and she underwent a successful ORIF of the posterior acetabulum and total hip arthroplasty. But then she developed chest pain, diaphoresis, and nausea on post-op day 1. Her heart rate slowed to 30 bpm, and she was hypotensive: 90 mm Hg systolic. She responded to a 1000 mL bolus of 0.9% saline and atropine. A 12-lead ECG was obtained.
She awoke the day after surgery hopeful, looking forward to beginning recovery. Breakfast done and waiting for physical therapy, it started. She felt hot and sweaty for several minutes before the chest pain began, followed by nausea. She knew something was wrong, and the seriousness was reinforced by the number of people in her room scurrying about. Her rate slowed to 30 bpm. Blood pressure was below 90 mm Hg systolic. The rapid response team gave her a 1000 mL bolus of 0.9% saline and atropine with good response. A 12-lead ECG was obtained. (Figure 4.)
Figure 4. ECG on the morning of hospital day 6 showing inferior STEMI.
The ECG shows Q-waves in the inferior leads with ST-segment elevation. The R:S ratio is >1 in the right precordial leads suggestive of a true posterior injury. Reciprocal changes are noted in leads I and aVL. A first-degree atrioventricular block was also present. These changes were diagnostic of an inferior ST-elevation myocardial infarction. The bradycardia and hypotension that the patient experienced is suggestive of Bezold-Jarisch reflex, a common epiphenomenon with inferior infarctions.
A STEMI is a clear indication for emergent revascularization, but factors here complicated the medical decision-making. She was at a very high risk of bleeding given her recent orthopedic surgery. Dual antiplatelet therapy and anticoagulation would exacerbate the bleeding risk, which would persist not only during the angiography but afterward if any intervention were performed. Nevertheless, she was treated with aspirin, and taken to the cardiac catheterization lab with the intention of defining the coronary anatomy and identifying the culprit lesion.
She was found to have diffuse disease in the LAD and circumflex coronary arteries but without high-grade obstructive disease. Patent left-to-right collaterals were also seen, as was a 100% occlusion of the ostium of the RCA. (Figure 5.)
Using balloon angioplasty, this was reduced to 30%, which reestablished flow. (Figure 6.) Unfortunately, a thrombectomy catheter could not cross the lesion. No stenting was performed. Any stent placed, whether bare metal or drug-eluting, would have required dual antiplatelet therapy that would have placed her at high risk of bleeding. The distal RCA was small in caliber, indicating chronic disease. Placing a stent would also have required additional contrast dye, which would have placed the patient at risk for contrast-induced nephropathy. A temporary pacemaker was placed given her episode of bradycardia.
She remained hemodynamically stable, and developed no decrease of her renal function. Troponin I peaked at 17 ng/mL. No other episodes of chest pain occurred. She recovered completely from her hip surgery over the following weeks. A month after her STEMI, she underwent PCI to the RCA ostia and mid LAD without any bleeding complications. She was discharged from the hospital on the first day of spring with snow still covering the ground.
Monday, May 12, 2014
He had been through this before. The patient, a 57-year-old man, had come through the doors of this emergency department many times. He had a favorite seat in triage. He knew what questions the nurse would ask him once he was in a room, and that the doctor would repeat those same questions. Then tests and labs, then moved upstairs for a couple of days before going home, hopefully feeling better. He knew all of this. Today, though, everything he thought he knew was wrong.
He had once considered himself lucky. He even survived a gunshot to the chest as a young man. But that notion had faded long ago. His health had been getting worse for years. He suffered with diastolic heart failure, COPD, and stage 3 chronic kidney disease brought on by years of poorly treated hypertension and diabetes. He had been told during one of his stays in the hospital that he had depression. He didn't doubt it. He had resigned himself to never getting completely well, but the past couple of days had been even worse.
He had not slept in days, and was extremely fatigued. He was unable to catch his breath, and was in mild distress. Oxygen saturations were 70%, which improved with supplemental oxygen by Oxymizer. He was not having any chest pain, and his blood pressure was in the 100s mm Hg systolic, way below his baseline and surprising given that he had not taken his medications for weeks. Exam was remarkable for generalized edema, diffuse crackles, and JVD elevation. Creatinine was nearly twice his baseline, and BNP was extremely elevated. Serial troponin measurements were normal. An ECG and x-ray were obtained and are shown in Figures 1 and 2.
Figure 1. Electrocardiogram on presentation.
Figure 2. AP Chest radiograph on presentation.
The ECG shows a normal sinus rhythm with short PR interval. A Q-wave is present in lead III, and nonspecific T-wave changes show in the precordial leads. It is unchanged in comparison with previous tracings. The chest x-ray shows pronounced cardiomegaly, vascular congestion, and diffuse interstitial opacities consistent with pulmonary edema.
The diagnosis seemed clear. It was the same diagnosis the patient knew, the same diagnosis he had had every other time he had come to the hospital: exacerbation of his diastolic heart failure, with cardiorenal syndrome. He was treated with nitroglycerin and bumetanide/metolazone to promote diuresis. Which worked. Sort of. Despite a large volume of urine output, his shortness of breath was not improving, and his creatinine continued to worsen. A transthoracic echocardiogram was obtained to assess cardiac function and volume status. Watch this video to see the patient’s echocardiogram showing the parasternal long axis view, and this one to see the patient’s echocardiogram showing the parasternal short axis view.)
Given the patient’s body habitus, the transthoracic echocardiogram was a technically difficult study. Echocardiographic contrast agents in this situation can be useful to help with interpretation. Contrast, usually some form of gas bubble that scatters ultrasound waves, is used for two principle reasons: to detect left to right shunts and to opacify the left ventricle to define the endocardial border, which allows better determination of ventricular dimensions, wall motion, and ejection fraction. Contrast is given intravenously, and it needs to transverse the pulmonary circuit to opacify the left ventricle. Larger bubbles are more stable, but the bubbles need to be less than 10 micrometers to pass through the pulmonary capillaries. The bubbles can be stabilized by surrounding them with a durable structure and using inert gases rather than air. Table 1 lists commonly used echo contrast agents.
The echocardiogram with the help of contrast showed normal left ventricular size and performance (ejection fraction of 65%) without any wall motion abnormality. The right atrium and ventricle were markedly enlarged, however, and there was decreased right ventricular systolic contractility. The right-sided dilation was causing significant tricuspid insufficiency. The estimated pulmonary artery systolic pressure was 27 mm Hg above the right atrial pressure. A notable finding was a D-shaped septum, implying a relative increase in right ventricular end-diastolic pressure. These findings were concerning for increased pulmonary arteriolar vascular resistance versus worsening volume overload. The patient underwent a right heart catheterization to assess this.
Pressure tracing from right heart catheterization.
The right heart catheterization showed that the pulmonary artery pressure was 72/31 (mean 46) mm Hg with an occlusion pressure is 18 mm Hg. This indicates essentially high-normal left-sided pressures and severe pulmonary hypertension. Much to everybody’s surprise, the patient, rather than suffering from left ventricular diastolic failure (heart failure with preserved ejection fraction) that would require elevated left ventricular end diastolic pressures, was actually underfilling his left ventricle. The patient had severe pulmonary hypertension with right-sided heart failure (cor pulmonale).
Multiple possible etiologies for the patient’s pulmonary hypertension included COPD, chronic cocaine use causing pulmonary fibrosis/ILD, and chronic hypoxia from untreated obstructive sleep apnea. He had a prescription for CPAP, but had refused to wear it. The right ventricle was hypertrophied and dilated, which gives an indication that this was chronic rather than acute. (Table 2.)
Unfortunately for the patient, his right heart failure continued to decompensate. Despite aggressive attempts at reducing the pulmonary hypertension with inhaled prostacyclins and nitrous oxide, he required escalating vasopressor support. He developed refractory shock and multiorgan failure, and his family elected to pursue comfort care measures.
Monday, April 07, 2014
The patient first felt winded one night after doing the dishes. She was breathing so hard by morning that she was barely able to get out of bed. And a cough had started. “The flu” went through her mind. She stayed home from work to rest, but all day she just couldn’t catch her breath. The cough got worse and was making her chest hurt, and she felt her heart racing. She was exhausted by evening, but knew she wasn’t going to be able to sleep. The temperature was below 0°F outside, but she bundled up and drove herself the three miles to the emergency department. Barely able to speak by the time she stepped up to the triage desk, she was only able to get out “You need to slow my heart down.” The nurse knew that look.
The patient sat down hard in the wheelchair rescuing her from the burden of standing. “Medical Resus” was paged overhead, and the nurse rushed the patient back.
A (airway) was clearly intact as the patient was placed on the cart. Everyone knew that B was going to be problem. The monitoring cables were on before most people noticed, and there was an uncomfortable pause for several seconds while everyone in the Resus Bay waited for the first SpO2. 68%. Heart rate 146 bpm. That’s all it took. An IV was placed, and the patient was intubated in the next few minutes. Attention turned to the cause of respiratory failure. An ECG and chest radiograph was obtained, and are shown in Figures 1 and 2.
Figure 1. Presenting ECG.
Figure 2. Chest radiograph.
The ECG demonstrated atrial fibrillation with rapid ventricular response with ST-segment depression in the lateral leads concerning for myocardial ischemia. Bilateral pulmonary infiltrates show on the chest xray, which also shows a double density along the left heart border representing the bulging of the left atrial appendage. Key items on the differential at this point would include decompensated heart failure, acute coronary syndrome, infectious pneumonia, sepsis, and ARDS. A few minutes with the ultrasound revealed this key image. (Click here to see the video.)
A remarkable hypertrophied and calcified mass is on the ventricular side of the mitral valve, with severely impaired opening of the mitral valve during diastole. The anterior leaflet billows while remaining fixed at the commissure, visually described as a “hockey stick.” The patient’s presentation and this ultrasound are diagnostic of severe mitral stenosis. It was once much more common, but the incidence of mitral stenosis has been gradually declining in the United States. The patient has decades of being asymptomatic after the stenosis is initiated. Patients have several more decades once symptoms do occur before they become debilitating. Ten-year survival once this happens, however, approaches 10 percent. (Table 1.)
Most cases of mitral stenosis by far can be attributed to rheumatic disease. The immune response against Group A streptococcal antigens cross-react with structural glycoproteins of heart valves, especially the mitral valve, with leads to an ongoing auto-inflammatory response and destruction of the native valve. The hallmark of rheumatic mitral stenosis is commissural fusion, scarring and thickening of the valve, and shortening and thickening of the tendinous cords. Radiation therapy has quickly become a significant secondary cause of mitral stenosis.
Distinguishing between rheumatic heart and radiation stenosis can be difficult, even after a careful history. Commissural fusion does not seem to exist in radiation-associated mitral stenosis. Radiation also tends not to damage the papillary muscles and chordae tendineae. Radiation, however, tends to cause significantly more valvular calcification. Dyspnea is the most common feature of clinically significant mitral valve stenosis. Exacerbation of symptoms can be precipitated with increased cardiac demand (exercise, stress, critical illness) and atrial fibrillation with rapid ventricular rate. Restriction of the cardiac output causes fatigue, and cough and hemoptysis can be present. Evidence of elevated right and left heart pressures such as pulmonary and lower extremity edema are also often present. The physical exam, however, is not specific for mitral stenosis, and even the classic lowpitched rumbling middiastolic murmur is lost as the mitral stenosis progresses. (Table 2.)
A stenotic mitral valve significantly changes cardiac hemodynamics once the valve area falls to less than 2 cm2 (normal 46 cm2). High velocities and a large transmitral pressure gradient are needed because the entire cardiac output must pass through the stenosis. These higher gradients are generated by increased left atrial pressure in systole and diastole, and are transmitted upstream to the pulmonary vasculature and right side of the heart, causing pulmonary edema, pulmonary hypertension, and elevated central venous pressures. The left ventricular end diastolic pressure remains low from the reduced preload, and cardiac output is therefore depressed despite these higher pressures. The systemic vasculature compensates with higher resistance. The transmitral pressure gradient is a useful indicator of severity:
● Mild: <5 mm Hg
● Moderate: 5-10 mm Hg
● Severe: >10 mm Hg
Ultrasound is the primary means of evaluating mitral stenosis, and several techniques can determine the valve area and transmitral pressure gradient:
● 2D planimetry. The opening area of the valve can be measured in the parasternal short axis view at the level of the mitral. The gain and view must be carefully optimized to avoid underestimating the valve area.
● Pressure half-time (PHT). The prolonged emptying time between the left atrium and left ventricle can be exploited because the time that pressure takes to half of its initial maximum value has been shown to be empirically related to the valve area (MVA=220/PHT). The continuous wave Doppler velocity is measured at the level of the mitral valve in an apical four-chamber view. The pressure gradient is related to the maximum velocity by a simplification of Bernoulli’s equation (p=4V2). The time it takes for the A pressure half-time of 220 msec corresponds to a valve area of 1 sq cm.
● Continuity equation. Uses mitral and aortic flow in addition to the cross-section area of the left ventricular outflow tract to derive the mitral valve area. The area is measured by planimetry and flow measured by Doppler assessment of velocity time integral (VTI). This method is less commonly used because of the accumulation in measurement errors.
● Proximal isovelocity surface area (PISA) method. Utilizes a fluid dynamic feature where accelerating flow forms hemispheres of isovelocities. This utilizes the flow convergence region proximal to the high velocity trans mitral jet in diastole. It is highly accurate but difficult to perform in transthoracic views and best utilized during transesophageal echocardiography.
The transmitral gradients are highly heart rate-dependent, and patients who develop rapid atrial fibrillation can quickly deteriorate. There is reduced filling time, which demands much higher filling pressures, which in turn causes significant pulmonary edema and occasional hemoptysis from pulmonary venous rupture. Treating mitral stenosis is directed at controlling the heart rate and maintaining sinus rhythm (e.g., digoxin, diltiazem, beta-blockade). Left ventricle contractility is generally preserved in mitral stenosis. β-blockade does result in decreased right ventricular contractility, which in pulmonary hypertension can further compromise the cardiac output and systemic blood pressure.
The loss in right ventricle contractility, however, is more than offset by the beneficial effects of reducing the heart rate. Loop diuretics should be used for diuresis and their venodilation effects (mediated by angiotensin II and prostaglandins) to reduce pulmonary vascular congestion. Left atrial dilation and stasis substantially increases the risk of thromboembolism, especially in atrial fibrillation, and therefore anticoagulation is critical. Surgical intervention is ultimately required, and involves carefully choosing balloon mitral valvuloplasty, mitral valve commissurotomy, or mitral valve replacement.