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Thread: The Diagnostic Role of Central Venous Pressure

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    Post The Diagnostic Role of Central Venous Pressure

    Technological advances have resulted in many state-of-the-art diagnostic modalities such as ultrasound, computed tomography, nuclear imaging, and genetic typing. Nonetheless, certain tried-and-true elements of the physical examination remain unsurpassed in guiding the emergency physician to an accurate and rapid evaluation of patients. This article will focus on the importance of one such element—bedside assessment of central venous pressure (CVP) in the diagnosis of emergent diseases involving various organ systems.


    CASE 1: ACUTE ABDOMINAL PAIN
    A 42-year-old woman in excellent general health presents to the emergency department with a chief complaint of right upper quadrant abdominal pain of one hour's duration. There is no significant medical history. Her vital signs are: pulse, 102 and regular; blood pressure, 110/70 mm Hg; respiratory rate, 22; axillary temperature, 99.8F. Physical examination finds an alert, moderately obese, noncyanotic, and nonicteric woman in acute distress. Auscultation of the lungs and heart is normal. The abdomen is flat and soft, without voluntary or involuntary guarding; however, right upper quadrant tenderness without a palpable mass is noted. Bowel sounds are normal. Leg examination is normal, as is the test for Homan's sign.

    The initial clinical impression is acute cholecystitis. However, this patient's complete blood count is normal, and there is no significant elevation in her serum aminotransferase levels. Also, her serum alkaline phosphatase, lipase, and amylase values are normal, and so are her chest x-ray, electrocardiogram, and abdominal ultrasound. Specifically, the gallbladder is normal in size on ultrasound; its wall is not thickened and there is no wall edema. No gallstones are present.

    In light of these clinical findings, acute cholecystitis is highly unlikely. Pneumonia and acute myocardial infarction (MI) can also be safely ruled out. While a normal gallbladder ultrasound study is highly unlikely in a patient with acute cholecystitis, it does not totally rule out this diagnosis.

    On further examination, the emergency physician notes that the patient's CVP is elevated, suggesting acute right heart failure. The most likely etiology is pulmonary embolism; a ventilation-perfusion scan demonstrates multiple perfusion defects.

    The patient's right upper quadrant pain is due to passive congestion of the liver, with stretching of the hepatic capsule. This case demonstrates the importance of always keeping in mind that acute abdominal pain may be intrathoracic in origin.


    HOW TO ASSESS CVP

    Central venous pressure is the pressure within the jugular veins that directly enter the superior vena cava, which is equivalent to right atrial pressure. Thus, CVP provides important information about hemodynamics in the right side of the heart. Elevated CVP occurs in patients who have right heart failure of any etiology, restrictive cardiomyopathy, pericardial disease, tricuspid valvular stenosis, and superior vena cava syndrome.

    To assess CVP, the head of the patient's bed should be elevated to 45. The patient's head is usually in midline, though some examiners prefer to turn the head slightly to the left, away from the side to be examined. It is preferred to assess CVP via the right internal jugular, which is in a direct line with the superior vena cava. However, it may be difficult to inspect this vein because of its anatomic course. Fortunately, in most patients, the right external jugular vein provides an accurate assessment of CVP. Rarely, this vein may be kinked, giving a false impression of high venous pressure. In such cases, stripping the vein will not result in it filling from below.

    The height of the distended venous column in the proximal jugular veins reflects right atrial pressure. Therefore, the examiner locates the highest point of venous filling in the jugular vein and measures the vertical distance between this point and the sternal angle (angle of Louis). If the distance is more than 4 cm, the CVP is abnormally elevated. This is all that needs to be determined, whether the CVP is elevated or normal; it is not necessary to measure CVP more precisely in cm H2O or mm Hg.

    There are patients who, even in the sitting position, exhibit jugular venous filling above the level of the clavicle. In these patients, CVP is considerably elevated and there is no need to place the patient in the 45 position.


    CASE 2: PERIPHERAL EDEMA

    A 64-year-old man has a long history of alcohol abuse. For two years, he has had the cutaneous stigmata of liver disease. Seven months earlier, he was diagnosed with bronchogenic carcinoma, for which he underwent pulmonary resection followed by mediastinal irradiation. He now has a two-week history of progressive leg swelling and worsening abdominal distension.

    Physical examination shows a thin man with mild scleral icterus, spider angiomata, and red palms. His lung fields are clear; heart tones are soft, without murmurs or gallops. Shifting dullness is elicited; no abdominal mass is felt. There is 2+/4 bilateral pitting edema of the legs.

    Chronic liver disease, with its attendant portal hypertension and hypoalbuminemia, can cause ascites and peripheral edema. However, because this patient's CVP is elevated, the suspected cause of his fluid retention shifts from hepatic disease to a cardiac etiology. Given his history of mediastinal irradiation, constrictive pericarditis is suspected and, in fact, is proved to be present.

    Peripheral edema may result from several different pathophysiologic mechanisms, including increased capillary hydrostatic pressure, low plasma oncotic pressure, increased capillary permeability, and lymphatic obstruction. When assessing a patient who has peripheral edema, the emergency physician should consider three questions: Is the edema unilateral or bilateral? Is CVP normal or elevated? Is the face involved?

    Unilateral edema is usually due to local venous obstruction, as in deep vein thrombosis or postphlebitic syndrome (which can be bilateral), or to lymphatic obstruction from prior surgical lymph node resection or lymph node irradiation. Further, lymphatic obstruction may result from malignancy in lymph nodes or from infection, such as filariasis in tropical regions.

    Bilateral edema with a normal CVP is found in patients with portal hypertension and in those with hypoalbuminemia. Portal hypertension is most commonly related to hepatic disease, but it also occurs in patients with splenic vein thrombosis. Hypoalbuminemia causes a low oncotic pressure that enables serum to seep out of capillaries into the interstitial space. Low albumin is, of course, common in the cirrhotic patient. However, the clinician should remember that nephrotic syndrome is also characterized by hypoalbuminemia with peripheral edema, ascites, and even anasarca. When ascites causes abdominal tension, upward pressure on the diaphragm may cause an elevation in CVP. Paracentesis of a small volume of ascitic fluid will reduce CVP to a normal level.

    Bilateral edema with a normal CVP may also be found in the hypothyroid patient. In addition, many medications—notably corticosteroids, nonsteroidal anti-inflammatory drugs, interleukin-2, minoxidil, and calcium channel blockers—may cause this condition. In the presence of underlying myocardial dysfunction, it is important to remember that salt-retaining medications may provoke biventricular heart failure resulting in elevated CVP.


    BILATERAL EDEMA WITH ELEVATED CVP

    Bilateral edema with elevated CVP is found in several cardiopulmonary diseases, including right heart failure, constrictive pericarditis, high-cardiac-output heart failure, restrictive cardiomyopathy, and superior vena cava syndrome. Other physical signs commonly found in patients with right heart failure include hepatomegaly due to passive congestion of the liver, ascites, an S4 gallop at the lower left sternal border (right ventricular gallop), and a murmur of tricuspid valve regurgitation.

    The most common cause of right heart failure is chronic left ventricular heart failure secondary to coronary artery disease, hypertension, or valvular disease. Pulmonary parenchymal and vascular diseases characterized by pulmonary hypertension—namely, chronic bronchitis, pulmonary fibrosis, and chronic pulmonary embolic disease—are also well-recognized causes of right heart failure. Less commonly, collagen vascular disease (especially scleroderma) may be complicated by right heart failure.

    Tricuspid valvular stenosis is most commonly of rheumatic origin and generally occurs in association with other valve pathology. Rarely, carcinoid syndrome may cause tricuspid stenosis; more commonly, it results in tricuspid regurgitation. Signs of tricuspid valvular stenosis are similar to those of right heart failure.

    The most common causes of constrictive pericarditis in the United States are previous mediastinal irradiation and prior cardiac surgery. Constriction after radiotherapy typically becomes clinically evident an average of seven years after treatment. However, it may occur as early as one month following irradiation. Therefore, in the patient who has had mediastinal radiotherapy, CVP should be assessed at every visit. If CVP is elevated, the patient should promptly undergo cardiac evaluation. Kussmaul’s sign, which is the absence of a decrease or an increase in jugular venous pressure during inspiration, is a classic sign of constrictive pericarditis. However, it is not specific for this condition; it also occurs in right ventricular infarction (RVI) and restrictive cardiomyopathy.

    Ascites is typically present in the patient with constrictive pericarditis. In contrast to the cirrhotic patient who has tense ascites, however, paracentesis in the pericarditis patient will not reduce CVP to a normal level.

    A number of disparate conditions may cause high-cardiac-output heart failure with resultant increased CVP. These include systemic arteriovenous (AV) fistulas due to a congenital anomaly or, more commonly, following penetrating trauma such as a bullet or stab wound. Additionally, a synthetic AV dialysis fistula or the intraosseous AV shunting seen in Paget's disease may cause high-output heart failure. Other causative disorders include hyperthyroidism and the thiamine-deficiency disease beriberi.

    High-output heart failure patients will develop dysp-nea and peripheral edema. Other clinical signs include tachycardia, widened pulse pressure, pulmonary crackles, an S3 gallop, and bounding pulses. Myocardial impairment secondary to the high-output state will cause right atrial pressure and CVP to be elevated.

    Hypervolemia due to excessive intravenous (IV) administration of sodium and water or retention of dietary sodium by the kidneys in both acute and chronic renal failure may result in biventricular heart failure with peripheral edema and elevated CVP. Superior vena cava syndrome causes elevated CVP and bilateral edema, but the edema involves the arms, not the legs. Malignancy, especially non-Hodgkin's lymphoma and small-cell lung carcinoma, are the most common etiologies. (Hodgkin’s disease rarely causes superior vena cava syndrome.) A rare nonmalignant cause is fibrosing mediastinitis due to Histoplasma infection. An increasingly frequent etiology is thrombosis of the superior vena cava related to indwelling central venous lines, including catheters placed for chemotherapy, chronic hemodialysis, or parenteral nutrition and even cardiac pacemakers. In addition to elevated CVP and bilateral arm edema, patients with superior vena cava syndrome usually have dilated chest veins and facial and neck swelling.

    Restrictive cardiomyopathy patients have the same clinical presentation as those with constrictive pericarditis—namely, elevated CVP, congestive hepatomegaly, ascites, and bilateral peripheral edema. Causes of this rare disorder include amyloid or iron infiltration (hemochromatosis) of the myocardium, sarcoidosis, and endomyocardial fibrosis. These patients require cardiac catheterization and, in many cases, myocardial biopsy to establish the diagnosis.

    The presence of facial edema should alert the emergency physician to one of the following: superior vena cava syndrome, nephritic syndrome, nephrotic syndrome, or hypothyroidism. Nephritic syndrome, characteristic of acute glomerulonephritis, is manifested by hypertension, azotemia, and hypervolemia. The patient will have peripheral edema in addition to facial swelling.


    CASE 3: EPIGASTRIC DISCOMFORT

    There are three mechanical complications of myocardial infarction (MI) that are acute and life-threatening and produce elevated CVP. Right ventricular infarction and rupture of the ventricular septum produce a clinical picture of acute right heart failure and hypotension. In the latter case, the patient will have a loud holosystolic murmur along the lower left and, often, right lower sternal border. Acute MI complicated by rupture of the free ventricular wall, the third complication, will produce pericardial tamponade with its classic signs of hypotension, tachycardia, elevated CVP, and paradoxical pulse. Echocardiographic demonstration of right atrial and right ventricular diastolic collapse enables the physician to make a prompt diagnosis of tamponade. Unrelated to infarction, tamponade may be caused by cardiac trauma (penetrating or blunt), pericarditis (related to uremia and collagen vascular disease), or, rarely, idiopathic pericarditis.

    Consider this final patient presentation. A 56-year-old man has persistent lower sternal and epigastric discomfort with nausea, but he does not seek medical attention for six hours. Evaluation in the emergency department reveals an acute inferior MI. Initial examination shows normal vital signs and a soft apical S4 gallop, but no clinical signs of heart failure. The patient is treated with aspirin and an IV beta blocker and thrombolytic agent.

    Six hours later, the patient’s blood pressure is 70/40 mm Hg, his pulse is 126 and regular, and his respiratory rate is 36. Sinus rhythm is noted on the cardiac monitor. His lung fields are clear. An apical S4 gallop is again heard, but there is no murmur or friction rub.

    Key questions in this case include: What is the cause of this patient’s hypotension? Is he in cardiogenic shock? Is he hypovolemic?

    A chest x-ray shows this patient has no pulmonary congestion, but his CVP is markedly elevated. The diagnosis of RVI is considered and confirmed on a repeat ECG using right chest leads V4R, V5R, and V6R. The hypotension and tachycardia seen in RVI result from an acute decrease in right ventricular stroke volume that in turn leads to a reduction in pulmonary blood flow, left ventricular filling, and ultimately systemic cardiac output.

    In contrast, cardiogenic shock after acute MI usually accompanies a loss of more than 40% of the left ventricular myocardium. The shock is due to an acute decrease in left ventricular stroke volume, causing the patient to exhibit cool extremities, mental obtundation, oliguria and, in two thirds of cases, pulmonary congestion. In these patients, CVP will be normal unless there is profound elevation of the mean left atrial pressure with secondary right heart failure.

    Hypovolemia (specifically, reduced total body fluid volume) would not be considered in this patient because of his high CVP and absence of diuretic therapy. More commonly and unrelated to acute MI, tamponade is caused by aortic dissection that ruptures into the pericardial cavity. Major risk factors for dissection are Marfan’s syndrome and chronic hypertension. However, acute hypertension associated with cocaine abuse is now more frequently recognized as a cause of acute dissection.

    Acute tamponade is not characterized by peripheral edema. However, a few patients may exhibit subacute tamponade before the hemodynamic features of an acute manifestation. In these patients, peripheral edema may develop.

    Finally, the emergency physician must be aware that tension pneumothorax causes an abrupt elevation in CVP, together with absent breath sounds on the ipsilateral side, tachypnea, agitation, hypoxemia and, later, hypotension. Deviation of the trachea in tension pneumothorax is often a late sign and its absence should not deflect the physician from the diagnosis.

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