Paradoxical pulse is a drop in blood pressure > 10 mmHg during inspiration; it represents an exaggeration of the physiological phenomenon consisting of inspiratory lowering of BP (normal up to 10 mmHg). In cardiac tamponade, inspiration, which causes an increase in blood flow to the right chambers, increasing their volume, secondarily causes a displacement of the interventricular septum to the left, so that the left heart lodges and expels less blood during systole and the pulse, therefore, decreases. In a normal heart this exaggerated displacement, caused by the pressure exerted by the tamponade on the RV free wall, does not occur. Sinus X represents the systolic collapse of the venous pulse, i.e., the pressure drop due to atrial relaxation (also partly due to a downward displacement of the RV base during systole). Sinus Y represents the diastolic collapse of the venous pulse, i.e., the pressure drop that occurs from the moment blood enters the tricuspid valve into the ventricle. In cardiac tamponade, the deep sinus X is characteristic. In constrictive pericarditis, the deep Y sinus. For all these reasons, the correct answer is 5.

Paradoxical pulse is a drop in blood pressure > 10 mmHg during inspiration; it represents an exaggeration of the physiological phenomenon consisting of inspiratory lowering of BP (normal up to 10 mmHg). In cardiac tamponade, inspiration, which causes an increase in blood flow to the right chambers, increasing their volume, secondarily causes a displacement of the interventricular septum to the left, so that the left heart lodges and expels less blood during systole and the pulse, therefore, decreases. In a normal heart this exaggerated displacement, caused by the pressure exerted by the tamponade on the RV free wall, does not occur. Sinus X represents the systolic collapse of the venous pulse, i.e., the pressure drop due to atrial relaxation (also partly due to a downward displacement of the RV base during systole). Sinus Y represents the diastolic collapse of the venous pulse, i.e., the pressure drop that occurs from the moment blood enters the tricuspid valve into the ventricle. In cardiac tamponade, the deep sinus X is characteristic. In constrictive pericarditis, the deep Y sinus. For all these reasons, the correct answer is [HIDDEN].

A patient with a history of febrile illness and chest pain comes to the hospital with dyspnea and tachypnea. On physical examination his blood pressure is low, jugular venous pressure is elevated with a deep descending sinus "X" and he has a paradoxical pulse. What pathology should you suspect?

Pericardial effusion with cardiac tamponade.

Cases from the Osler Medical Service at Johns Hopkins University.

PRESENTING FEATURES: A 70-year-old African American man was admitted with a history of fever, chills, and malaise of several days' duration. His past medical history was notable for end-stage renal disease requiring hemodialysis, coronary artery disease, and aortic stenosis requiring a bioprosthetic aortic valve replacement. On the day of admission, the patient was noted to have a shaking chill while undergoing dialysis through his catheter and was admitted to the hospital. He complained of pain at the catheter insertion site, shortness of breath, and dyspnea on exertion, but denied chest pain. On physical examination, the patient had a temperature of 100.4 degrees F, with a heart rate of 64 beats per minute, blood pressure of 127/72 mm Hg, and an oxygen saturation of 97% on room air. He was a mildly obese man in no apparent distress. He had shotty cervical lymphadenopathy and a right subclavian dialysis catheter in place, with erythema and pus at the entry site. His jugular venous pressure was 10 cm H(2)O. Lung examination showed bibasilar rales. Heart sounds were normal, with no rub or gallop. He had a 2/6 systolic ejection murmur best heart at the left sternal border as well as a 3/6 holosystolic murmur at the apex that radiated to his left axilla. Examination of the abdomen and extremities was unremarkable. The patient's neurological examination was unremarkable, and he was alert and oriented to person, place, and time. Laboratory studies showed an elevated white blood cell count of 16,700 cells/microL. His blood urea nitrogen level was 43 mg/dL and his serum creatinine level was 4.9 mg/dL. Multiple blood cultures grew methicillin-resistant Staphylococcus aureus. An admission, chest radiograph showed no infiltrate. An admission electrocardiogram showed normal sinus rhythm with first degree atrioventricular block, left anterior fascicular block, and left ventricular hypertrophy. shows rhythm strips from lead II electrocardiograms 5 months before admission (top), on admission (middle) and 5 days after admission (bottom). What is the diagnosis?

[Recurrent autoreactive pericardial effusion. Impact of an aetiological classification of pericarditis].

A 36 year-old man suffered from fever, fatigue, pleurodynia and precordial discomfort. His family physician suspected febrile tracheobronchitis and treated it with ampicillin for 5 days. Because symptoms persisted an ECG was done which suggested acute myocardial infarction. The patient underwent an emergency coronary angiography which excluded coronary artery disease and aortic dissection. Pericarditis was suspected and the patient put on aspirin, 500 mg/d. Because of persisting cardiac symptoms an echocardiography was performed which revealed systolic separation between epi- and pericardium, characteristic of a small pericardial effusion after acute pericarditis. The symptoms improved after one week of treatment with diclofenac and the ECG had become normal. Two months later the patient was seen at our cardiac outpatient clinic. He had night sweats, sporadic precordial pain and severe dyspnoe. Further investigations revealed tachycardia (120/min), hypotension (95/70 mm Hg), pulsus paradoxus and jugular vein sustension. Echocardiography revealed a large pericardial effusion ("swinging heart"), which explained the low voltage and the electrical alternans in the ECG. Pericardiocentesis was carried out the same day to relieve the tamponade. It was followed by pericardioscopy and epi- as well as pericardial biopsy. 485 ml of a serous effusion were drained. Cytology and histology demonstrated a lymphocytic fibrinous pericarditis. Polymerase chain reaction (PCR) on viral and bacterial RNA and DNA of potentially cardiotropic agents remained negative. The pigtail catheter was left in place and 80 mg of gentamycin were given intrapericardially on day 1 and 2, followed by 500 mg of crystalloid triamcinolone acetate after the PCR was found to be negative. Oral treatment with 0.5 mg colchicine three times a day (off-label use) was started and maintained for 6 months. After 9 months no effusion was detected and the patient was free of symptoms. After exclusion of bacterial and viral pericardial infection, a high single dose of intrapericardial triamcinolone combined with long-term oral colchicine has proven to be a highly efficacious treatment of autoreactive pericarditis which will avoid relapses in most cases.

Aortic Valve Disease -- History and Physical

Aortic regurgitation when acute and/or severe can be suspected when the patient has a wide pulse pressure, and a low pitched early diastolic murmur is auscultated again over the right sternal border at the second intercostal space. Accentuated P2 may also be noticed due to elevated pressures in the pulmonary vasculature. Chronic aortic regurgitation may illicit a blowing diastolic decrescendo murmur with a positive correlation between the duration of murmur and the severity of the disease. Often auscultation of a laterally and inferiorly displaced apical impulse is present and sustained. Often there is the phenomenon of Corrigan pulse (water hammer), a bounding and forceful pulse that rapidly increases and collapses. Other less common physical exam findings include the de Musset sign, which is subtle head bobbing with a pulse, as well as the Quincke sign and Muller sign (pulsations on the fingernails and uvula, respectively). Similar physical exam findings to aortic stenosis can also be seen late in disease progression. Acute aortic regurgitation will present differently depending on the etiology. If a patient presents with tearing severe chest pain along with physical exam findings such as variation in blood pressure between the right and left extremities, consider aortic dissection as a cause. If the patient presented with a history of streptococcal infection along with fevers, swollen and tender joints, skin nodules, new onset of rash, then rheumatic heart disease would be high on the differential.

[Lassa fever associated with effusive constrictive pericarditis and bilateral atrioventricular annular constriction: a case report].

A case of Lassa fever associated with effusive constrictive pericarditis and bilateral atrioventricular annular constriction was reported. A 49-year-old man, who had been diagnosed by indirect fluorescent antibody test as the first case of Lassa fever in Japan, was referred to the Hiroo Hospital because of syncope, progressive hepatomegaly, ascites and pericardial effusion in spite of pericardiocentesis and corticosteroid therapy. On admission, his blood pressure was 92/60 mmHg and he had a paradoxical pulse. Two-dimensional echocardiography revealed a localized pericardial effusion adjacent to the right ventricular wall and behind the left ventricular posterior wall. Bilateral atrioventricular annular constriction was also present. On pulsed Doppler echocardiography, the peak inflow velocities of the right and left ventricles increased during atrial systole. Right heart catheterization revealed a mean diastolic pressure gradient of 8 mmHg across the tricuspid valve. After pericardiectomy, a diastolic dip and plateau pattern became evident in the right ventricular pressure tracing, suggesting the presence of residual constriction. However, the atrioventricular annular constriction was no longer evident on two-dimensional echocardiography. This is considered the first reported case of subacute effusive constrictive pericarditis caused by Lassa fever.

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Additional clues to the etiology and importance of a heart murmur can be gleaned from the history and other physical examination findings. Symptoms suggestive of cardiovascular, neurologic, or pulmonary disease help focus the differential diagnosis, as do findings relevant to the jugular venous pressure and waveforms, the arterial pulses, other heart sounds, the lungs, the abdomen, the skin, and the extremities. In many instances, laboratory studies, an ECG, and/or a chest x-ray may have been obtained earlier and may contain valuable information. A patient with suspected infective endocarditis, for example, may have a murmur in the setting of fever, chills, anorexia, fatigue, dyspnea, splenomegaly, petechiae, and positive blood cultures. A new systolic murmur in a patient with a marked fall in blood pressure after a recent MI suggests myocardial rupture. By contrast, an isolated grade 1 or 2 mid-systolic murmur at the left sternal border in a healthy, active, and asymptomatic young

Pericarditis

Physical examinations The classic sign of pericarditis is a friction rub heard with a stethoscope on the cardiovascular examination, usually on the lower left sternal border. Other physical signs include a person in distress, positional chest pain, diaphoresis (excessive sweating); possibility of heart failure in form of pericardial tamponade causing pulsus paradoxus, and the Beck's triad of low blood pressure (due to decreased cardiac output), distant (muffled) heart sounds, and distension of the jugular vein (JVD).

Kussmaul's sign

Causes The differential diagnoses of Kussmaul's sign includes constrictive pericarditis, restrictive cardiomyopathy, pericardial effusion, and severe right-sided heart failure. With cardiac tamponade, jugular veins are distended and typically show a prominent x descent and an absent y descent as opposed to patients with constrictive pericarditis (prominent x and y descent), see Beck's triad. Other possible causes of Kussmaul's sign include: Right ventricular infarction - low ventricular compliance Right heart failure Cardiac tumours Tricuspid stenosis Restrictive cardiomyopathy Pulmonary embolism Constrictive pericarditis History Kussmaul's sign is named after the German doctor who first described it, Adolph Kussmaul (1822-1902). He is also credited with describing Kussmaul breathing. See also Pulsus paradoxus References Symptoms and signs: Vascular

[A case of subacute effusive-constrictive pericarditis].

A 30-year-old female with effusive-constrictive pericarditis was admitted to our hospital because of dyspnea, ascites and edema. On examination, her blood pressure was 118/94 mmHg and her pulse rate was 90 bpm. Physical examination revealed pulsus paradoxus, markedly raised venous pressure and pericardial knock sound. Chest X-ray showed marked cardiomegaly and bilateral pleural effusion. After cardiac catheterization there was elevation of mean right atrial pressure, right ventricular end-diastolic pressure, pulmonary-capillary-wedge pressure, and their pressures during diastole were approximately 30 mmHg. After successful pericardiocentesis, their diastolic pressures still remained at 15 mmHg. Additionally, pressure wave of the right ventricle showed distinct diastolic dip and plateau pattern, and that of the right atrium showed deep x and y descents. The pressure pattern suggested that not only pericardial effusion but also decreased compliance of the pericardium was the main factor contributing to the cardiac diastolic dysfunction. Histological examination of the pericardium showed diffuse lymphocyte infiltration and fibrosis. These findings strongly suggested that there might have been viral infection.

Heart

Pericardial disease The sac which surrounds the heart, called the pericardium, can become inflamed in a condition known as pericarditis. This condition typically causes chest pain that may spread to the back, and is often caused by a viral infection (glandular fever, cytomegalovirus, or coxsackievirus). Fluid can build up within the pericardial sac, referred to as a pericardial effusion. Pericardial effusions often occur secondary to pericarditis, kidney failure, or tumours, and frequently do not cause any symptoms. However, large effusions or effusions which accumulate rapidly can compress the heart in a condition known as cardiac tamponade, causing breathlessness and potentially fatal low blood pressure. Fluid can be removed from the pericardial space for diagnosis or to relieve tamponade using a syringe in a procedure called pericardiocentesis. Congenital heart disease

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Viral or idiopathic acute pericarditis occurs at all ages but is more common in young adults and is often associated with pleural effusions and pneumonitis. The almost simultaneous development of fever and precordial pain, often 10–12 days after a presumed viral illness, constitutes an important feature in the differentiation of acute pericarditis from AMI, in which chest pain precedes fever. The constitutional symptoms are usually mild to moderate, and a pericardial friction rub is often audible. The disease ordinarily runs its course in a few days to 4 weeks. The ST-segment alterations in the ECG usually disappear after 1 or more weeks, but the abnormal T waves may persist for several years and be a source of confusion in persons without a clear history of pericarditis. Pleuritis and pneumonitis frequently accompany viral or idiopathic acute pericarditis. Accumulation of some pericardial fluid is common, and both tamponade and constrictive pericarditis are possible, but infrequent,

[Acute nonspecific pericarditis].

In order to learn the natural history of nonspecific acute pericarditis in our environment, we studied retrospectively 50 patients seen at The Instituto Nacional de Cardiología Ignacio Chávez, between 1972-1985. The clinical history, electrocardiogram, chest x ray, laboratory findings, as well as the outpatient follow-up were analyzed. There was a history of a respiratory or gastrointestinal infection, probably viral in origin, in almost half of the cases (46%). Chest pain was present in 96% of the patients and was the most common symptom. In only half of the patients a pericardial friction rub was heard. A typical S-T elevation was found in 90% of the electrocardiograms. Arrhythmias and conduction disorders were unusual. The echocardiogram showed a pericardial effusion in seven patients and six had a pleural effusion. Only one patient developed signs of cardiac tamponade. None of the patients in this study developed a chronic constrictive pericarditis and there were no deaths. Before or after hospitalization, 14 patients (28%) had multiple episodes of chest pain suggestive of recurrent pericarditis. This study shows that nonspecific acute pericarditis seems to be a self-limited illness with a good prognosis, few recurrences and practically no complications.

InternalMed_Harrison

Diagnosis Due to the unstable condition of these patients, supportive therapy must be initiated simultaneously with diagnostic evaluation (Fig. 326-2). A focused history and physical examination should be performed, blood specimens sent to the laboratory, and an electrocardiogram (ECG) and chest x-ray obtained. Etiologies of Cardiogenic Shock or Pulmonary Edema Acute myocardial infarction/ischemia LV failure Ventricular septal rupture Papillary muscle/chordal rupture–severe MR Ventricular free wall rupture with subacute tamponade Other conditions complicating large MIs Post-cardiac arrest Post-cardiotomy Refractory sustained tachyarrhythmias Acute fulminant myocarditis End-stage cardiomyopathy LV apical ballooning Takotsubo’s cardiomyopathy Hypertrophic cardiomyopathy with severe outflow obstruction Aortic dissection with aortic insufficiency or tamponade Severe valvular heart disease Other Etiologies of Cardiogenic Shockb RV failure due to:

Acute pericarditis

Corticosteroids are usually used in those cases that are clearly refractory to NSAIDs and colchicine and a specific cause has not been found. Systemic corticosteroids are usually reserved for those with autoimmune disease. Prognosis One of the most feared complications of acute pericarditis is cardiac tamponade. Cardiac tamponade is accumulation of enough fluid in the pericardial space --- pericardial effusion --- to cause serious obstruction to the inflow of blood to the heart. Signs of cardiac tamponade include distended neck veins, muffled heart sounds when listening with a stethoscope, and low blood pressure (together known as Beck's triad). This condition can be fatal if not immediately treated.

Jugular venous pressure

An exaggerated "y" wave or diastolic collapse of the neck veins from constrictive pericarditis is referred to as Friedreich's sign. Raised JVP, normal waveform Bradycardia Fluid overload Heart failure Raised JVP, absent pulsation Superior vena cava syndrome Large 'a' wave (increased atrial contraction pressure) Tricuspid stenosis Right heart failure Pulmonary hypertension Cannon 'a' wave (atria contracting against closed tricuspid valve) Atrial flutter Premature atrial rhythm (or tachycardia) Third degree heart block Ventricular ectopics Ventricular tachycardia Absent 'a' wave (no unifocal atrial depolarisation) Atrial fibrillation Large 'v' wave (c–v wave) Tricuspid regurgitation Absent 'x' descent Tricuspid regurgitation (sometimes 'x' wave is replaced by a positive wave) Prominent 'x' descent Cardiac tamponade Slow 'y' descent Tricuspid stenosis Cardiac tamponade Prominent & deep 'y' descent Constrictive pericarditis

Constrictive pericarditis impressing and narrowing the ascending aorta.

A 77-year-old male patient was admitted to our institution with 1-year history of progressive dyspnea on exertion, and lower extremity edema. His chest x-ray showed a circumferential pericardial calcification and right-sided pleural effusion. The electrocardiography revealed atrial fibrillation with low voltage in all derivations and diffuse nonspecific T-wave inversions. The transesophageal echocardiography showed a thickened pericardium with biatrial enlargement and normal right and left ventricular systolic functions. A thick echogenic structure that caused impression and narrowing of the ascending aorta was observed. Simultaneous right and left heart catheterization showed elevation and equalization of right-sided and left-sided diastolic filling pressures, with characteristic dip and plateau. Aortic angiogram showed the ascending aorta was impressed and narrowed by calcified pericardium. Cine magnetic resonance imaging showed pericardial calcifications impressing and narrowing of the ascending aorta. All these findings were consistent with constrictive pericarditis. The patient had no history of tuberculosis, cardiac surgery, or mediastinal irradiation. His HIV antibody test was negative. Marked pericardial thickening and calcifications were evident during pericardiectomy. Histological analysis of the pericardium showed dense collageneous matrix, mild chronic inflammation and calcification. The culture of pericardial tissue revealed no identifiable cause including tuberculosis. The patient was diagnosed as idiopathic constrictive pericarditis. The patient's symptoms and edema decreased remarkably after pericardial stripping. He remained well at 1-year follow-up.

InternalMed_Harrison

or absence of a third heart sound (S3). Accurate characterization of cardiac murmurs provides important insight into the natural history of many valvular and congenital heart lesions. Finally, the important role played by the physical examination in enhancing the clinician-patient relationship cannot be overestimated. THE GENERAL PHYSICAL EXAMINATION Any examination begins with an assessment of the general appear-ance of the patient, with notation of age, posture, demeanor, and 267 SEC Tion 2 DiAgnoSiS oF CARDiovASCulAR DiSoRDERS overall health status. Is the patient in pain or resting quietly, dyspneic or diaphoretic? Does the patient choose to avoid certain body positions to reduce or eliminate pain, as might be the case with suspected acute pericarditis? Are there clues indicating that dyspnea may have a pulmonary cause, such as a barrel chest deformity with an increased anterior-posterior diameter, tachypnea, and pursed-lip breathing? Skin pallor, cyanosis, and jaundice can be

Diagnostic Challenges in Chronic Constrictive Pericarditis.

Chronic constrictive pericarditis (CCP) is a disease that has multiple possible causes and is associated with variable clinical findings, depending on its severity. It develops insidiously, and in many cases, particularly in developed countries, no antecedent diagnosis can be found. These cases are termed idiopathic. Tuberculosis is the leading cause of constrictive pericarditis in developing nations but represents only a small minority in developed countries. Here the authors describe two different case reports where tuberculosis was the probable cause of CCP. A 21-year-old man born in Cape Verde living in Europe for 4 years and a 24-year-old man born in Guiné Bissau were both admitted due to intense precordial pain and syncope after exertion. Interestingly both had fatigability, dyspnea, chest discomfort and palpitations on exertion, as well as progressive involuntary weight loss and decubitus cough. On physical examination they had tachycardia, jaundice, cachexia, elevated jugular venous pressure, hepatomegaly and ascites. Both electrocardiograms showed prominent P waves and chest X-ray showed bilateral pulmonary interstitial infiltrates and enlargement of the right cavities. Analytically, elevated bilirubin, leukopenia and thrombocytopenia was also found in both. Echocardiography revealed findings, in both cases, compatible with CCP including less common signs as annulus reversus and annulus paradoxus. Thoraco-abdomino-pelvic CT from both patients revealed chronic liver disease with congestion, pleural effusion, pericardial calcifications, ascites and massive mediastinal and abdominal adenopathies. Blood cultures and IGRA test were negative. However, given the presumptive diagnosis of tuberculosis (TB), anti-TB therapy was started. Despite the diagnosis of "end-stage" CCP with very high operative risk multidisciplinary team decided after informed consent, to perform total anterior pericardiectomy, that occurred without complications. Pericardial and mediastinal biopsies, pericardial/pleural fluid cultures/ immune-phenotyping were inconclusive. Anti- tuberculosis therapy was maintained. After surgery, the patients had a remarkable clinical improvement (NYHA I) that persisted in 6- month follow-up. These two case reports illustrate that despite the markedly elevated operative risk of pericardiectomy in "end-stage" forms of disease after patients informed consent must be a considered option. The other point to consider is that, despite rare, tuberculosis still is a possible diagnosis to consider in CCP in Portugal.

Constrictive pericarditis following hemopericardium due to ascending aortic dissection: A case report.

A 79-year-old woman, who had had no history of trauma, tuberculosis, or collagen diseases, was referred for examination of general fatigue and shortness of breath on exertion. Physical examination revealed engorged neck veins, hepatomegaly, and ascites with abdominal distention. On chest x-ray the cardiac shadow was slightly enlarged and bilateral pleural effusion was present. An electrocardiogram showed low voltage of the QRS complex. Computed tomographic scans revealed two lumens in the remarkably dilated ascending aorta and the severely thickened pericardium. Cardiac catheterization showed elevated right atrial pressure and elevated right and left ventricular end-diastolic pressures, in addition to a pressure record of early diastolic dip and end-systolic plateau in the right ventricle. Aortography demonstrated aortic dissection localized to the ascending aorta. On the basis of these findings, the diagnosis of chronic ascending aortic dissection complicated with constrictive pericarditis was made. After subtotal pericardiectomy, graft replacement of the ascending aorta and proximal aortic arch was performed with successful results. Her postoperative recovery was uneventful. Histological studies of the pericardium showed fibrosis and marked infiltration of the inflammatory cells. No findings of specific pericarditis such as tuberculosis or collagen diseases were detected.

Cardiac Syncope -- History and Physical

A careful physical exam will assess heart rate and rhythm. Any abnormalities will increase suspicion of cardiac arrhythmia. In addition, an elevated respiratory rate or hypoxia will increase suspicion of a pulmonary embolism. Jugular venous distention and hypotension are suggestive signs of an obstructive mechanical cardiac etiology. Pathological cardiac murmurs, specifically new ones, will clue one into a valvular etiology, hypertrophic cardiomyopathy, or an obstructive intracardiac lesion. Muffled sounds can be heard with pericardial tamponade. Pedal edema or other evidence of deep venous thrombosis increases a patient's risk of pulmonary embolism. [10]

Myocardial infarction diagnosis

Physical examination The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate. A cool and pale skin is common and points to vasoconstriction. Some patients have low-grade fever (38–39 °C). Blood pressure may be elevated or decreased, and the pulse can become irregular. If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on precordial examination. Various abnormalities can be found on auscultation, such as a third and fourth heart sound, systolic murmurs, paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung. Electrocardiogram

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Suspected severe valve disease in symptomatic patients—dyspnea, angina, heart failure, syncope Infective endocarditis with need for cardiac surgery Asymptomatic patients with aortic regurgitation and cardiac enlargement or Prior to cardiac surgery in patients with suspected coronary artery disease New onset with angina or suspected undiagnosed coronary artery disease New-onset cardiomyopathy of uncertain cause or suspected to be due to coronary artery disease Prior to surgical correction, when symptoms or noninvasive testing suggests coronary disease Symptomatic patients with suspected cardiac tamponade or constrictive pericarditis Hypertrophic cardiomyopathy with angina Diseases of the aorta when knowledge of coronary artery involvement is necessary for management

Acquired Immune Deficiency Syndrome -- History and Physical -- Cardiac System [8]

HIV infection and ART likely contribute to increased cardiovascular disease in patients. Common presenting symptoms may include chest pain, shortness of breath, or fatigue. The examination should proceed as one would when assessing for acute coronary syndrome or valvular disease, palpating for chest wall pain, observing for jugular venous distension and peripheral edema, and auscultating for abnormal heart sounds, murmurs, or evidence of pulmonary edema. Cardiovascular AIDS-related illnesses could include purulent pericarditis or cardiac tamponade caused by Mycobacterium tuberculosis . If these conditions are suspected, observing for Beck’s triad of low blood pressure, jugular venous distension, and muffled heart sounds may confirm a compressive pericardial effusion.

A case of dilated cardiomyopathy.

Dilated cardiomyopathy is a significant health problem in Africa. Diagnosis and treatment can be challenging as it frequently affects young patients and those without risk factors for cardiac disease. A previously well HIV negative 17 year old boy presented to Mseleni hospital in December 2011 with a short history of worsening shortness of breath on exertion. The history had been preceded by a brief upper respiratory tract infection with general malaise and headache, from which he had recovered fully. On examination, he was clammy, peripherally shut down and clearly in respiratory distress. He had a raised jugular venous pressure (JVP) and palpable displaced apex beat. He had a loud P2, third heart sound and pansystolic murmur over the apex. He had scattered inspiratory crepitations bibasally. Routine blood tests on admission, including malaria and viral serology, were unremarkable. A chest x-ray showed a grossly dilated cardiac shadow and enlarged pulmonary trunk. A cardiac ultrasound ruled out pericardial effusion but did show a dilated and hypokinetic left ventricle. He was diagnosed with dilated cardiomyopathy secondary to a viral infection and managed accordingly. Dilated cardiomyopathy, although rare worldwide, is a significant problem throughout Africa. It has been shown to account for up to 48% of admissions with heart failure. Its aetiology is multifactorial and includes exposure to toxins and infectious agents. Presenting symptoms can be vague but improved prognosis and outcomes require prompt diagnosis and appropriate management.

Cardiac Tamponade -- History and Physical

Patients with cardiac tamponade present similar to patients with other forms of cardiogenic or obstructive shock. They may endorse vague symptoms of chest pain, palpitations, shortness of breath, or in more severe cases, dizziness, syncope, and altered mental status.  They may also present in a pulseless electrical activity cardiac arrest. The classic physical findings in cardiac tamponade included in Beck’s triad are hypotension, jugular venous distension, and muffled heart sounds. Pulsus paradoxus, which is a decrease in systolic blood pressure by more than 10 mm Hg with inspiration is an important physical exam finding that suggests a pericardial effusion is causing cardiac tamponade. Pulsus paradoxus may be absent in patients with ASD, elevated diastolic pressures, pulmonary hypertension and aortic regurgitation. The Kussmaul sign - a paradoxical elevated in JVP and pressure during inspiration is sometimes seen in cardiac tamponade.

Dilated cardiomyopathy

Signs and symptoms Dilated cardiomyopathy develops insidiously, and may not initially cause symptoms significant enough to impact on quality of life. Nevertheless, many people experience significant symptoms. These might include: Shortness of breath Syncope (fainting) Angina, but only in the presence of ischemic heart disease A person suffering from dilated cardiomyopathy may have an enlarged heart, with pulmonary edema and an elevated jugular venous pressure and a low pulse pressure. Signs of mitral and tricuspid regurgitation may be present.

Pulsus Paradoxus -- History and Physical

Intracardiac shunts or moderate to severe valvular insufficiency Co-existing disease that significantly increases left or right ventricular diastolic pressure such severe systemic hypertension, aortic stenosis, or cor pulmonale Aortic dissection resulting in pericardial effusion/tamponade Cardiac tamponade in hypovolemia

Jugular venous pressure

Prominent 'x' descent Cardiac tamponade Slow 'y' descent Tricuspid stenosis Cardiac tamponade Prominent & deep 'y' descent Constrictive pericarditis Parodoxical JVP (Kussmaul's sign: JVP rises with inspiration, drops with expiration) Pericardial effusion Constrictive pericarditis Pericardial tamponade

Combined multiple-valve procedures. Factors influencing the early and late results.

The early and late results were retrospectively evaluated in 57 cases of double or triple valve replacement or repair performed in 1970-1983. The causes of the valvular lesions were rheumatic fever (43 cases), bacterial endocarditis (6), syphilis (1) and unknown (7 cases). The preoperative NYHA classification was III in 29 patients and IV in 28, due mainly to dyspnea of effort. Cardiomegaly (mean radiologic volume 880 cm3/m2) and atrial fibrillation were the dominant clinical findings. Surgery was on emergency indications in five cases. Cold cardioplegia combined with external cardiac cooling has been used for myocardial protection since 1977. The valve replacements were 56 aortic, 50 mitral and 2 tricuspid. In addition there were three closed and two open mitral commissurotomies, two mitral plastic repairs, three tricuspid valve anuloplasties (DeVega) and one aortic anuloplasty. Follow-up (0.3-13, mean 3.5 years) was supplemented with a check-up including two-dimensional echophonocardiography and hematologic tests. The operative mortality (10/57 patients) fell from 26% in 1970-1976 to 12% in 1977-1983. The causes of death were low cardiac output in preoperatively ill patients (5), myocardial infarction (2), technical failure (2) and sepsis (1 case). There were 11 late deaths (6.7/100 patient-years of observation), the commonest cause (5 patients) being congestive heart failure. The respective incidences of thromboembolism, paravalvular leak and postoperative endocarditis were 2.1, 4.2 and 2.1 episodes/100 patient-years.(ABSTRACT TRUNCATED AT 250 WORDS)

[Pericardial tuberculosis in Madagascar. 23 cases].

A 56 months retrospective study, from October 1990 to May 1995, at the Centre Hospitalier de Soavinandriana in Antananarivo pointed out 29 tuberculous pericarditis among the 97 pericardial effusions discovered by the echocardiography of 5600 patients. The sex-ratio was 0,81 and the mean age 38,6 years old (+/- 14,3). Hospitalization was justified by dyspnea (18 cases), thoracic pain (18 cases), lower limbs edema (6 cases) and ascitis (3 cases). Moreover, electrocardiography showed microvoltage in 18 cases and thoracic radiography showed one heart enlargement. Even if for 15 cases a pleural effusion was associated, only 2 patients had a pulmonary image suggestive of tuberculosis. Tuberculous pericarditis has been proved by the following examinations: pericardium puncture (21 cases), pericardium and pleural biopsy (respectively 11 and 13 cases), ganglionic biopsy and search of alcohol-acid-fast bacilli in sputum: 1 case. Histologic proof has been obtained 8 times out of 9 pericardial biopsies and 6 times out of 7 pleural biopsies. Bacteriological proof has been obtained 11 times by pathological samples cultivation: twice from fresh caseous material taken from the pericardium, once from 13 pleural fluids, 5 times from 6 pericardial biopsies, 3 times from 3 pleural biopsies. The patients have been put under antituberculous treatment associated with prednisone. 20 patients have been declared cured at the end of the treatment, 5 were dead and 4 were lost out of sight. Tuberculous pericarditis has become rare in developed countries but it is still challenging in Madagascar. In spite of the antituberculous treatment associated with corticoids, prognosis is severe (evolution towards pericardial constriction death.

InternalMed_Harrison

Echocardiography should be performed in patients with a history of cardiac disease or if abnormalities are found on physical examination or the ECG. Echocardiographic diagnoses that may be responsible for syncope include aortic stenosis, hyper-trophic cardiomyopathy, cardiac tumors, aortic dissection, and pericardial tamponade. Echocardiography also has a role in risk stratification based on the left ventricular ejection fraction. Treadmill exercise testing with ECG and blood pressure monitoring should be performed in patients who have experienced syncope during or shortly after exercise. Treadmill testing may help identify exercise-induced arrhythmias (e.g., tachycardia-related AV block) and exercise-induced exaggerated vasodilation.

Postpericardiotomy syndrome

Complications Complications include pericarditis, pericardial effusion, pleuritis, pulmonary infiltration, and very rarely pericardial tamponade. Of these cardiac tamponade is the most life-threatening complication. The pericardial fluid increases intra-pericardial pressure therefore preventing complete expansion of the atria and the ventricles upon the diastole. This causes equilibration of the pressure in all four heart chambers, and results in the common findings of the tamponade which are pulsus paradoxus, Beck's triad of hypotension, muffled heart sounds, and raised jugular venous pressure, as well as EKG or Holter monitor findings such as electrical alternans. Physically the patients who progress to severe pericardial tamponade obtundate, become mentally altered, and lethargic. If left untreated, severe decrease in cardiac output, vascular collapse, and hypoperfusion of body including the brain results in death.

Constrictive-Effusive Pericarditis -- History and Physical

In effusive-constrictive pericarditis, patients commonly present with chronic symptoms that mimic volume overload. These include jugular venous distension, ascites, hepatomegaly, peripheral edema, and pleural effusions. Tachycardia occurs reflexively due to decreased cardiac output. Other signs and symptoms of decreased cardiac output include increased fatigue, hypotension, altered mental status, dyspnea, and tachypnea. Signs of active pericarditis may also ensue, including fever, pleuritic substernal chest pain, and a pericardial friction rub. Jugular venous distention also occurs due to decreased right heart filling and subsequent backup into the venous system.


Blood gases can be misleading since a normal pH may suggest that there is no disturbance of acid-base balance, instead it is masking a double disturbance in opposite directions as in this case. The patient presents with respiratory acidosis (PaCO2 60 mmHg; normal to 50) and compensatory metabolic alkalosis (bicarbonate 36 mmol/l; normal to 28). This is the typical blood gas of the patient with COPD and compensated chronic respiratory failure.

A patient's arterial blood gas result is: pH: 7.40, PaCO2 60 mmHg; bicarbonate 36 mM/L. What is the presenting disturbance:

Respiratory acidosis and metabolic alkalosis.

Respiratory acidosis

Diagnosis Diagnoses can be done by doing an ABG (Arterial Blood Gas) laboratory study, with a pH <7.35 and a PaCO2 >45 mmHg in an acute setting. Patients with COPD and other Chronic respiratory diseases will sometimes display higher numbers of PaCO2 with HCO3- >30 and normal pH. Terminology Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial pH < 7.36. See also Acidosis Alkalosis Arterial blood gas Chemical equilibrium pCO2 pH pKa Metabolic acidosis Metabolic alkalosis Respiratory alkalosis References External links Acid–base disturbances

Arterial blood gas test

In general, it is much easier to correct acute pH derangement by adjusting respiration. Metabolic compensations take place at a much later stage. However, in a critical setting, a person with a normal pH, a high CO2, and a high bicarbonate means that, although there is a high carbon dioxide level, there is metabolic compensation. As a result, one must be careful as to not artificially adjust breaths to lower the carbon dioxide. In such case, lowering the carbon dioxide abruptly means that the bicarbonate will be in excess and will cause a metabolic alkalosis. In such a case, carbon dioxide levels should be slowly diminished. See also Anion gap Radial artery puncture Chemical equilibrium Hemoximetry Arteriovenous oxygen difference References External links Online arterial blood gas calculator Diagnostic intensive care medicine Respiratory physiology Blood tests Respiratory therapy

Respiratory alkalosis

pH Alkalosis refers to the process due to which there is elevation of blood pH. Alkalemia refers to an arterial blood pH of greater than 7.45. Treatment Respiratory alkalosis is very rarely life-threatening, though pH level should not be 7.5 or greater. The aim in treatment is to detect the underlying cause. When PaCO2 is adjusted rapidly in individuals with chronic respiratory alkalosis, metabolic acidosis may occur. If the individual is on a mechanical ventilator then preventing hyperventilation is done via monitoring ABG levels. In popular culture In The Andromeda Strain, one of the characters is exposed to contamination, but saves himself by increasing his respiratory rate to induce alkalosis. See also References Further reading External links Acid–base disturbances

Arterial Blood Gas -- Results, Reporting, and Critical Findings

Example 1 [28] : ABG: pH = 7.39, PaCO 2 = 51 mm Hg, PaO 2 = 59 mm Hg, HCO 3 = 30 mEq/L and SaO 2 = 90%, on room air. pH is in the normal range, so use 7.40 as a cutoff point, in which case it is < 7.40, and acidosis is present. The elevated PaCO 2 indicates respiratory acidosis, and the elevated HCO 3 indicates a metabolic alkalosis. The value consistent with the pH is PaCO 2 . Therefore, this is a primary respiratory acidosis. The acid-base that is inconsistent with the pH is the elevated HCO3, indicating a metabolic alkalosis, so there is compensation signifying a non-acute primary disorder because it takes days for metabolic compensation to be effective. Last, the decreased PaO 2 indicates an abnormality with oxygenation. However, a history and physical will help delineate the severity and urgency of required interventions, if any. Example 2 [28] : ABG: pH = 7.45, PaCO 2 = 32 mm Hg, PaO 2 = 138 mm Hg, HCO 3 = 23 mEq/L, the base deficit = 1 mEq/L, and SaO 2 is 92%, on room air.

Base excess

Interpretation Base excess beyond the reference range indicates metabolic alkalosis if too high (more than +2 mEq/L) metabolic acidosis if too low (less than −2 mEq/L) Blood pH is determined by both a metabolic component, measured by base excess, and a respiratory component, measured by PaCO2 (partial pressure of carbon dioxide). Often a disturbance in one triggers a partial compensation in the other. A secondary (compensatory) process can be readily identified because it opposes the observed deviation in blood pH. For example, inadequate ventilation, a respiratory problem, causes a buildup of CO2, hence respiratory acidosis; the kidneys then attempt to compensate for the low pH by raising blood bicarbonate. The kidneys only partially compensate, so the patient may still have a low blood pH, i.e. acidosis. In summary, the kidneys partially compensate for respiratory acidosis by raising blood bicarbonate.

Respiratory alkalosis

Diagnosis The diagnosis of respiratory alkalosis is done via test that measure the oxygen and carbon dioxide levels (in the blood), chest x-ray and a pulmonary function test of the individual. The Davenport diagram allows clinicians or investigators to outline blood bicarbonate concentrations (and blood pH) after a respiratory or metabolic acid-base disturbance Classification There are two types of respiratory alkalosis: chronic and acute as a result of the 3–5 day delay in kidney compensation of the abnormality. Acute respiratory alkalosis occurs rapidly, have a high pH because the response of the kidneys is slow. Chronic respiratory alkalosis is a more long-standing condition, here one finds the kidneys have time to decrease the bicarbonate level. pH Alkalosis refers to the process due to which there is elevation of blood pH. Alkalemia refers to an arterial blood pH of greater than 7.45.

The first step is to look at the pH and assess for the presence of acidemia (pH < 7.35) or alkalemia (pH > 7.45). If the pH is in the normal range (7.35-7.45), use a pH of 7.40 as a cutoff point. In other words, categorize a pH of 7.37 as acidosis and a pH of 7.42 as alkalemia. Next, evaluate the respiratory and metabolic components of the ABG results, the PaCO 2 and HCO 3 , respectively. The PaCO 2 indicates whether the acidosis or alkalemia is primarily from a respiratory or metabolic acidosis/alkalosis. PaCO 2 > 40 with a pH < 7.4 indicates a respiratory acidosis, while PaCO 2 < 40 and pH > 7.4 indicates a respiratory alkalosis (but is often from hyperventilation from anxiety or compensation for a metabolic acidosis). Next, assess for evidence of compensation for the primary acidosis or alkalosis by looking for the value (PaCO 2 or HCO 3 ) inconsistent with the pH. Lastly, assess the PaO2 for any abnormalities in oxygenation. [29]

Arterial blood gas test

Respiratory alkalosis (Pa CO2 < 35 mmHg) occurs when there is too little carbon dioxide in the blood. This may be due to hyperventilation or else excessive breaths given via a mechanical ventilator in a critical care setting. The action to be taken is to calm the person and try to reduce the number of breaths being taken to normalize the pH. The respiratory pathway tries to compensate for the change in pH in a matter of 2–4 hours. If this is not enough, the metabolic pathway takes place. Under normal conditions, the Henderson–Hasselbalch equation will give the blood pH where: 6.1 is the acid dissociation constant (pKa) of carbonic acid () at normal body temperature [] is the concentration of bicarbonate in the blood in mEq/L PaCO2 is the partial pressure of carbon dioxide in the arterial blood in mmHg

Simple acid-base disorders.

The body regulates pH closely to maintain homeostasis. The pH of blood can be represented by the Henderson-Hasselbalch equation: pH = pK + log [HCO3-]/PCO2 Thus, pH is a function of the ratio between bicarbonate ion concentration [HCO3-] and carbon dioxide tension (PCO2). There are four simple acid base disorders: (1) Metabolic acidosis, (2) respiratory acidosis, (3) metabolic alkalosis, and (4) respiratory alkalosis. Metabolic acidosis is the most common disorder encountered in clinical practice. The respiratory contribution to a change in pH can be determined by measuring PCO2 and the metabolic component by measuring the base excess. Unless it is desirable to know the oxygenation status of a patient, venous blood samples will usually be sufficient. Metabolic acidosis can result from an increase of acid in the body or by excess loss of bicarbonate. Measurement of the "anion-gap" [(Na+ + K+) - (Cl- + HCO3-)], may help to diagnose the cause of the metabolic acidosis. Treatment of all acid-base disorders must be aimed at diagnosis and correction of the underlying disease process. Specific treatment may be required when changes in pH are severe (pH less than 7.2 or pH greater than 7.6). Treatment of severe metabolic acidosis requires the use of sodium bicarbonate, but blood pH and gases should be monitored closely to avoid an "overshoot" alkalosis. Changes in pH may be accompanied by alterations in plasma potassium concentrations, and it is recommended that plasma potassium be monitored closely during treatment of acid-base disturbances.

Acidosis

Mutations to the V-ATPase 'a4' or 'B1' isoforms result in distal renal tubular acidosis, a condition that leads to metabolic acidosis, in some cases with sensorineural deafness. Arterial blood gases will indicate low pH, low blood HCO3, and normal or low PaCO2. In addition to arterial blood gas, an anion gap can also differentiate between possible causes. The Henderson-Hasselbalch equation is useful for calculating blood pH, because blood is a buffer solution. In the clinical setting, this equation is usually used to calculate HCO3 from measurements of pH and PaCO2 in arterial blood gases. The amount of metabolic acid accumulating can also be quantitated by using buffer base deviation, a derivative estimate of the metabolic as opposed to the respiratory component. In hypovolemic shock for example, approximately 50% of the metabolic acid accumulation is lactic acid, which disappears as blood flow and oxygen debt are corrected. Treatment

Hydrochloric acid infusion for treatment of metabolic alkalosis associated with respiratory acidosis.

Hypercapnia due to respiratory failure can be more severe when accompanied by coexistent metabolic alkalosis. We therefore tested the hypothesis that hydrochloric acid (HCl) infusion could improve PaCO2 in 15 critically ill patients admitted with mixed respiratory acidosis and metabolic alkalosis, and a pH of between 7.35 and 7.45. HCl was infused at a constant rate of 25 mmol/h until the bicarbonate concentration decreased less than 26 mmol/L, or until the pH decreased less than 7.35 (initial pH greater than 7.40) or 7.30 (initial pH less than 7.40). Administration of 170 +/- 53 mmol of HCl decreased the bicarbonate concentration from 34 +/- 3 to 25 +/- 2 mmol/L (p less than .001), the pH from 7.41 +/- 0.03 to 7.33 +/- 0.02 (p less than .001), and the PaCO2 from 54 +/- 8 to 48 +/- 8 torr (p less than .001). Postinfusion PaCO2 could be predicted accurately from the initial status of the patients (r = .95, p less than .001) except in one patient with fixed hypercapnia. PaCO2 increased from 77 +/- 19 to 94 +/- 24 torr (p less than .001) and PaO2/PAO2 increased from 59 +/- 17 to 66 +/- 17% (p less than .001). The effects of HCl were still present 12 h after the end of the infusion. No complications related to the acid infusion were noted. These results indicate that, even in the absence of alkalemia, active correction of metabolic alkalosis by HCl infusion can improve CO2 and oxygen exchange in critically ill patients with mixed respiratory acidosis and metabolic alkalosis.

Chronic respiratory alkalosis. The effect of sustained hyperventilation on renal regulation of acid-base equilibrium.

In normal subjects, chronic hyperventilation lowers plasma bicarbonate concentration, primarily by inhibiting the urinary excretion of net acid. The quantitative relation between reduced arterial carbon dioxide tension (PaCO2) and the plasma bicarbonate concentration in the chronic steady state has not been studied in humans, however, and the laboratory criteria for the diagnosis of chronic respiratory alkalosis therefore remain undefined. We wished to provide such reference data for clinical use. Moreover, because chronic hyperventilation paradoxically lowers blood pH still further in dogs with metabolic acidosis, we desired to study the effect of chronic hypocapnia on the plasma bicarbonate concentration (and blood pH) in normal human subjects in whom acidosis had been induced with ammonium chloride. Under metabolic-balance conditions, we used altitude-induced hypobaric hypoxia to produce chronic hypocapnia in nine normal young men, five of whom received ammonium chloride daily to cause metabolic acidosis (the mean [+/- SE] steady-state plasma bicarbonate level in these five was 12.0 +/- 0.5 mmol per liter). For each decrease of 1 mm Hg (0.13 kPa) in the PaCO2, the plasma bicarbonate concentration decreased by 0.41 mmol per liter in the subjects who started with a normal plasma bicarbonate concentration and by 0.42 mmol per liter in the subjects with acidosis. In contrast to the findings in previous studies of dogs, hypocapnia increased blood pH similarly in both groups; the blood hydrogen ion concentration decreased by about 0.4 nmol per liter for every decrease of 1 mm Hg (0.13 kPa) in PaCO2. These results provide reference data for the diagnosis of chronic respiratory alkalosis in humans. Although chronic hypocapnia decreased plasma bicarbonate levels similarly in normal subjects with acidosis and without acidosis, the percent reduction in PaCO2 was always greater than the corresponding percent reduction in the plasma bicarbonate concentration. Therefore, as was not true of the response in dogs, the subjects' blood pH always increased with hyperventilation, regardless of the initial plasma bicarbonate concentration.

The metabolic and respiratory alterations of heat stroke.

The metabolic and respiratory changes of 21 patients with heat stroke were studied. Admission arterial blood gas levels were measured, and serum bicarbonate, lactate, calcium, phosphorus, and anion gap determinations were performed. Seven patients had a metabolic acidosis (pH 7.20 +/- 0.04, PCO2 32 +/- 2 mm Hg, and bicarbonate 12 +/- 1 mEq/L), seven a combined metabolic acidosis and respiratory alkalosis (pH 7.39 +/- 0.01, PCO2 25 +/- 1 mm Hg, and bicarbonate 15 +/- 1 mEq/L), four a respiratory alkalosis (pH 7.45 +/- 0.01, PCO2 30 +/- 1 mm Hg, and bicarbonate 20 +/- 1 mEq/L), one a metabolic and respiratory acidosis (pH 7.13, PCO2 52 mm Hg, and bicarbonate 17 mEq/L), and one a respiratory acidosis (pH 7.30, PCO2 56 MM Hg, and bicarbonate 27 mEq/L). The 15 patients with a metabolic acidosis had a pH of 7.28 +/- 0.03, PCO2 of 30 +/- 2 mm Hg, bicarbonate level of 14 +/- 1 mEq/L, lactate concentration of 6.5 +/- 1.0 mEq/L, and an anion gap of 26 +/- 4 mEq/L. Nine patients were hypocalcemic (7.8 +/- 0.3 mg/dL), and five patients were hypophosphatemic (2.0 +/- 0.2 mg/dL). The predominant metabolic change in heat stroke is a metabolic acidosis secondary to increased lactate content and/or a respiratory alkalosis. Hypocalcemia is common and hypophosphatemia is not infrequent.

Arterial blood gas test

The normal range for pH is 7.35–7.45. As the pH decreases (< 7.35), it implies acidosis, while if the pH increases (> 7.45) it implies alkalosis. In the context of arterial blood gases, the most common occurrence will be that of respiratory acidosis. Carbon dioxide is dissolved in the blood as carbonic acid, a weak acid; however, in large concentrations, it can affect the pH drastically. Whenever there is poor pulmonary ventilation, the carbon dioxide levels in the blood are expected to rise. This leads to a rise of carbonic acid, leading to a decrease in pH. The first buffer of pH will be the plasma proteins, since these can accept some H+ ions to try to maintain acid-base homeostasis. As carbon dioxide concentrations continue to increase (PaCO2 > 45 mmHg), a condition known as respiratory acidosis occurs. The body tries to maintain homeostasis by increasing the respiratory rate, a condition known as tachypnea. This allows much more carbon dioxide to escape the body through the

Metabolic acidosis

Diagnostic approach and causes Metabolic Acidosis is defined as a reduced serum pH, and an abnormal serum bicarbonate concentration of <22 mEq/L, below the normal range of 22 to 29 mEq/L. However, if a patient has other coexisting acid-base disorders, the pH level may be low, normal or high in the setting of metabolic acidosis. In the absence of chronic respiratory alkalosis, metabolic acidosis can be clinically diagnosed by measuring serum bicarbonate levels in the blood, which is generally a standard component of blood panels. Imperatively, when weighing a metabolic acidosis diagnosis, the change in serum bicarbonate levels over time should be considered; if baseline bicarbonate results are unknown, a single set of values may be misinterpreted. Causes Generally, metabolic acidosis occurs when the body produces too much acid (e.g., lactic acidosis, see below section), there is a loss of bicarbonate from the blood, or when the kidneys are not removing enough acid from the body.

Pulmonary gas pressures

The alveolar pO2 is not routinely measured but is calculated from blood gas measurements by the alveolar gas equation. Partial pressure of carbon dioxide Pathology The partial pressure of carbon dioxide, along with the pH, can be used to differentiate between metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. Hypoventilation exists when the ratio of carbon dioxide production to alveolar ventilation increases above normal values – greater than 45mmHg. If pH is also less than 7.35 this is respiratory acidosis. Hyperventilation exists when the same ratio decreases – less than 35mmHg. If the pH is also greater than 7.45 this is respiratory alkalosis. See also Alveolar-arterial gradient Diffusing capacity Pulmonary alveolus References Respiratory physiology

Metabolic alkalosis

To calculate the expected pCO2 in the setting of metabolic alkalosis, the following equations are used: pCO2 = 0.7 [HCO3] + 20 mmHg ± 5 pCO2 = 0.7 [HCO3] + 21 mmHg Treatment To effectively treat metabolic alkalosis, the underlying cause(s) must be corrected. A trial of intravenous chloride-rich fluid is warranted if there is a high index of suspicion for chloride-responsive metabolic alkalosis caused by loss of gastrointestinal fluid (e.g., due to vomiting). Terminology Alkalosis refers to a process by which the pH is increased. Alkalemia refers to a pH which is higher than normal, specifically in the blood. See also Hypokalemia Metabolic acidosis Respiratory acidosis Respiratory alkalosis References External links Acid–base disturbances

pH is in the normal range. Using 7.40 as a cutoff point, it is >7.40, so alkalemia is present. The decreased PaCO 2 indicates a respiratory alkalosis, and the HCO 3 is normal but on the low end of normal. The value consistent with the pH is PaCO 2 . Therefore, this is a primary respiratory alkalosis. The HCO 3 is in the normal range and, thus, not inconsistent with the pH, so there is a lack of compensation. Last, the PaO 2 is within the normal range, so there is no abnormality in oxygenation.

Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low Plasma Bicarbonate Using the Urine Anion Gap.

Hypobicarbonatemia, or a reduced bicarbonate concentration in plasma, is a finding seen in 3 acid-base disorders: metabolic acidosis, chronic respiratory alkalosis and mixed metabolic acidosis and chronic respiratory alkalosis. Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy. Proper diagnosis of the cause of hypobicarbonatemia requires integration of the laboratory values, arterial blood gas, and clinical history. The information derived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of urine anion gap, as a surrogate marker of urine ammonium excretion, in the evaluation of a patient with low plasma bicarbonate concentration to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of urine acid-base indexes at bedside (urine pH, urine bicarbonate, and urine anion gap) to evaluate urine acidification are discussed.

Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease.

Variation of the arterial carbon dioxide partial pressure (PaCO2) is not uncommon in anesthetic practice. However, little is known about the myocardial consequences of respiratory alkalosis and acidosis, particularly in patients with coronary artery disease. The aim of the current study was to investigate the effects of variation in PaCO2 on myocardial blood flow (MBF), metabolism, and systemic hemodynamics in patients before elective coronary artery bypass graft surgery. In 10 male anesthetized patients, measurements of MBF, myocardial contractility, metabolism, and systemic hemodynamics were made in a randomized sequence at PaCO2 levels of 30, 40, and 50 mmHg, respectively. The MBF was measured using the Kety-Schmidt technique with argon as a tracer. End-diastolic left ventricular pressure and the maximal increase of left ventricular pressure were assessed using a manometer-tipped catheter. The cardiac index significantly changed with varying PaCO2 levels (hypocapnia, - 9%; hypercapnia, 13%). This reaction was associated with inverse changes in systemic vascular resistance index levels. The MBF significantly increased by 15% during hypercapnia, whereas no change was found during hypocapnia. Myocardial oxygen and glucose uptake and the maximal increase of left ventricular pressure were not affected by varying PaCO2 levels. In anesthetized patients with coronary artery disease, short-term variations in PaCO2 have significant effects on MBF but do not influence global myocardial oxygen and glucose uptake. Changes in systemic hemodynamics associated with respiratory alkalosis and acidosis are caused by changes in systemic vascular resistance rather than by alterations in myocardial contractility.

Respiratory compensation

In metabolic alkalosis, chemoreceptors sense a deranged acid-base balance with a plasma pH of greater than normal (>7.4). The chemoreceptors send afferent fibers to the brainstem respiratory centers. The brainstem respiratory centers decrease alveolar ventilation (hypoventilation) to create a rise in arterial carbon dioxide () tension, resulting in a decrease of plasma pH. The respiratory brainstem centers can only compensate for metabolic acid-base disturbances (metabolic acidosis and metabolic alkalosis). Renal compensation is needed to balance respiratory acid-base syndromes (respiratory acidosis and respiratory alkalosis). The kidneys can compensate for both, respiratory and metabolic acid-base imbalances. References Acid–base disturbances

[Gas acidosis and alkalosis].

Arterial concentration of CO2 (PaCO2) is dependent of pulmonary excretion. When this excretion is lower than cellular production respiratory acid-basis occurs: rise in PaCO2 which lowers pH and produces secondary increases in bicarbonate (HCO3-) plasma concentration. Respiratory alkalosis, generated by a CO2 pulmonary excretion greater than metabolic production is characterized by a fall in PaCO2 which raises pH and induces secondary reduction of plasmatic HCO3- concentration. Attention to the possibility of serious hypoxemia, cause or consequence, should always be regarded and treated in respiratory acid-base disorders.

[Characteristics of acid-base balance in patients with chronic severe hepatitis: analysis of 126 cases].

To investigate the characteristics of acid-base balance in patients with chronic severe hepatitis. Samples of venous blood and arterial blood were collected from 126 patients with chronic severe hepatitis, 106 males and 20 females, aged 44 +/- 13 (25 - 74), to undergo measurement of the potassium, sodium, and chloride ions, and urea nitrogen and creatine, blood electrolytes and blood gas analysis respectively. Acid-base disturbance (ABD) was found in 115 of the 126 patients (91.3%). 40 of the 115 patients with ABD (31.7%) had respiratory alkalosis combined with metabolic alkalosis, 32 of them (25.4%) had respiratory alkalosis combined with metabolic acidosis; 28 of them (22.2%) had pure respiratory alkalosis, and 8 (6.3%) had pure metabolic acidosis. Five patients had triple acid-base disturbance, 4 of which had respiratory alkalosis (combined with metabolic alkalosis and metabolic acidosis, 3.2%), and 1 of which had respiratory acidosis (combined with metabolic alkalosis and metabolic acidosis, 0.8%). There was no significantly difference in the prevalence rates of pure acid-base disturbance and multiple acid-base disturbances between the patients with cirrhosis-base chronic severe hepatitis and those with chronic hepatitis-based chronic severe hepatitis. Hypoxia symptoms were seen in 34 patients (27%). 103 patients died. All the 15 patients with their blood pH < 7.35 died. ABD in the patients with chronic severe hepatitis is mainly alkalosis with respiratory alkalosis as the basic ABD type. The appearance of ABD is not associated with the underlying illness. Patients of chronic severe hepatitis often suffer from hypoxia. Low blood pH is an important factor causing death.

Acid–base homeostasis

Acidemia and alkalemia unambiguously refer to the actual change in the pH of the extracellular fluid (ECF). Two other similar sounding terms are acidosis and alkalosis. They refer to the customary effect of a component, respiratory or metabolic. Acidosis would cause an acidemia on its own (i.e. if left "uncompensated" by an alkalosis). Similarly, an alkalosis would cause an alkalemia on its own. In medical terminology, the terms acidosis and alkalosis should always be qualified by an adjective to indicate the etiology of the disturbance: respiratory (indicating a change in the partial pressure of carbon dioxide), or metabolic (indicating a change in the Base Excess of the ECF). There are therefore four different acid-base problems: metabolic acidosis, respiratory acidosis, metabolic alkalosis, and respiratory alkalosis. One or a combination of these conditions may occur simultaneously. For instance, a metabolic acidosis (as in uncontrolled diabetes mellitus) is almost always partially

Blood gas test

Blood gas tests also measure the levels of bicarbonate and of standard bicarbonate, of base excess, of oxygen saturation, and of pH. An arterial blood gas test is more often used. Clinical significance Blood gas tests can be used in the diagnosis of a number of acidosis conditions such as lactic, metabolic, and respiratory acidosis, diabetic ketoacidosis, and also of respiratory alkalosis. Particularly, umbilical cord blood gas analysis can give an indication of preceding fetal hypoxic stress. In combination with other clinical information, normal paired arterial and venous cord blood gas results can usually provide a robust defence against a suggestion that an infant had an intrapartum hypoxic‐ischaemic event.

Partial Pressure of Carbon Dioxide -- Clinical Significance

There are differences in the acute and chronic stages of respiratory acidosis or alkalosis. Acute respiratory acidosis from increased PCO2 will result in immediate changes to serum bicarbonate levels due to the bicarbonate buffer system; however, this is limited in its ability to achieve homeostasis. The kidney will gradually increase the serum bicarbonate levels in chronic cases. Chronic respiratory acidosis is when the acidemia exists for 3 to 5 days, which is approximately how long it will take the kidney to buffer the acidemia. In acute respiratory acidosis, normally, the serum bicarbonate will increase by 1 mEq/L for every 10 mmHg increase in PCO2. For chronic respiratory acidosis, the serum bicarbonate will increase by 4 to 5 mEq/L for every 10 mmHg rise in PCO2. [6] [5] The result typically causes a mild chronic acidosis or low-normal pH near 7.35. [6] In regards to respiratory alkalosis, the same timeframe applies to acute versus chronic. In acute respiratory alkalosis, for every decrease in PCO2 by 10 mmHg, the serum bicarbonate will also decrease by 2 mEq/L. In chronic respiratory alkalosis, or alkalosis lasting 3 to 5 days, for every 10mmHg drop in PCO2, it is expected that serum bicarbonate will decrease by 4 to 5 mEq/L. [5] [6]

[Meeting point Stewart. Buffer bases, base excess and strong ions].

Development of a two-buffer model which simulates the acid-base properties of blood and allows comparison of the different acidbase concepts according to Stewart and to Siggaard-Andersen. The two-buffer model consisted of different aqueous solutions of bicarbonate/CO(2) (pCO(2), sCO(2), pK(1)), HEPES buffer (A(tot), pK(a)) and electrolytes. These were used to calculate the pH from the independent variables according to Stewart - strong ion difference (SID), pCO(2) and total concentration of the weak acids (A(tot)) - from which all other dependent variables (cHCO(3)(-), cA(-), BB, BE) were obtained and compared with the measured values. The normal pH (7.408) was calculated from the normal values for SID (48 mmol/l), pCO(2) (40 mmHg) and A(tot) (45.2 mmol/l) and agreed perfectly with the measured value (7.409+/-0.001). This was also valid for all calculated and measured pH values when the SID was varied: non-respiratory alkalosis ( upward arrow) or acidosis ( downward arrow), pCO(2):respiratory acidosis ( upward arrow) or alkalosis ( downward arrow) and A(tot):hyperproteinemic acidosis ( upward arrow) or hypoproteinemic alkalosis ( downward arrow) were varied and the sum of the buffer bases (BB) was always equal to the SID. All changes and hence BE were also equal, providing that A(tot) was normal. This was not the case, however, if A(tot) was outside the normal range, when BE was then the difference from the normal BB at the respective reference point. Whereas the deviation of the measured pCO(2) was acceptable (1.74+/-0.86 mmHg), this was not the case for the SID (-6.18+/-3.58 mmol/l) calculated from the measured ion concentrations (Na, K, Ca, Cl). Despite controversial discussions, both concepts are much closer than might be expected. Whereas in the Stewart approach the focus of analysis is on plasma, with the Siggaard-Andersen approach it is on blood. Hence, a combined analysis of the blood gases (pH, pCO(2), pO(2), sO(2), cHb, BE) and of the strong ion gap (SIG) may be useful.

[Preclinical blood gas analysis. 1. The value of preclinical blood gas analysis].

Prehospital blood gas analysis is a new method in out-of-hospital emergency care. In a prospective pilot study we evaluated the feasibility of prehospital compensation of severe acidosis relying on different monitoring systems to evaluate patients oxygen, carbon dioxide or acid-base status, respectively. With the help of arterial blood gas checks taken at the site of the emergency, the acid base status of patients undergoing out of hospital cardiopulmonary resuscitation was analysed. The values derived from the first arterial puncture were used to determine the presence and the type of acidosis. The data of the arterial blood gas checks were set into relation with the time elapsed since the beginning of resuscitation and they were compared with end-tidal CO2. During the observation period 26 blood gas analyses from patients who had out-of-hospital resuscitation because of cardiac arrest were done. Twenty three patients had severe acidosis (pH range < 6.9 to 7.31), one had alkalosis (pH 7.51). Only two had an arterial pH within normal range. The pCO2 was variable (range: 24 to 97 mm Hg). The correlation of pH with time from the beginning of resuscitation to arterial puncture was poor (r = 0.407, p < 0.05). There was no correlation between pH and BE (r = 0.267) or pH and pCO2, (r = 0.016) respectively. Prehospital capnometry had a poor correlation with arterial pCO2 in most emergency patients. Only patients with respiratory disturbances of extrapulmonary origin showed a good correlation between end-tidal CO2 and the arterial pCO2. In severely ill patients the arterio-alveolar CO2-difference was unexpectedly high (> 15 mm Hg). In four patients resuscitation was not successful until compensation of an unexpectedly severe acidosis based upon the findings from blood-gas analysis had been performed. Arterial blood gas analysis proved to be helpful in the optimal management of out of hospital cardiac arrest. The incidence of severe acidosis in patients undergoing cardiopulmonary resuscitation was 80%. The probability of developing acidosis was found to increase slightly depending on the time elapsed since the beginning of CPR. The application of a calculated buffering of acidosis with sodium bicarbonate showed a good outcome in selected cases. In emergency patients alternative methods fail to detect severe disturbances of the patients oxygen and/or carbon dioxide status and the acid-base balance. Management of prehospital cardiac arrest could be optimized by the routine use of blood gas analysis.

PCO2

Medicine In medicine, the partial pressure of carbon dioxide in arterial blood is called or PaCO2. Measurement of in the systemic circulation indicates the effectiveness of ventilation at the lungs' alveoli, given the diffusing capacity of the gas. It is a good indicator of respiratory function and the closely related factor of acid–base homeostasis, reflecting the amount of acid in the blood (without lactic acid). Normal values for humans are in the range 35–45 mmHg. Values less than this may indicate hyperventilation and (if blood pH is greater than 7.45) respiratory alkalosis. Values greater than 45 mmHg may indicate hypoventilation, and (if blood pH is less than 7.35) respiratory acidosis. Aquatic Sciences

Physiology, Metabolic Alkalosis -- Related Testing

An arterial blood gas is a laboratory test used for the measurement of arterial pH, the arterial partial pressure of oxygen (PaO2), the arterial partial pressure of carbon dioxide (PaCO2), bicarbonate (HCO3), base excess, total CO2, and O2 saturation. A venous blood gas is a laboratory test identical to an arterial blood gas measurement, except the blood is drawn from a venous site. This results in a slightly more acidic “normal” pH range. Urine chloride is a direct measurement of chloride being excreted into urine. This test is useful to help determine the etiology of metabolic alkalosis. [3] [4] [5]

Base excess or buffer base (strong ion difference) as measure of a non-respiratory acid-base disturbance.

Stewart in 1983 (Can J Physiol Pharmacol 1983: 61: 1444) reintroduced plasma buffer base under the name "strong ion difference" (SID). Buffer base was originally introduced by Singer and Hastings in 1948 (Medicine (Baltimore) 1948: 27: 223). Plasma buffer base, which is practically equal to the sum of bicarbonate and albuminate anions, may be increased due to an excess of base or due to an increased albumin concentration. Singer and Hastings did not consider changes in albumin as acid-base disorders and therefore used the base excess, i.e., the actual buffer base minus the buffer base at normal pH and pCO2, as measure of a non-respiratory acid-base disturbance. Stewart and followers, however, consider changes in albumin concentration to be acid-base disturbances: a patient with normal pH, pCO2, and base excess but with increased plasma buffer base due to increased plasma albumin concentration get the diagnoses metabolic (strong ion) alkalosis (because plasma buffer base is increased) combined with metabolic hyperalbuminaemic acidosis. Extrapolating to whole blood, anaemia and polycytaemia should represent types of metabolic alkalosis and acidosis, respectively. This reveals that the Stewart approach is absurd and anachronistic in the sense that an increase or decrease in any anion is interpreted as indicating an excess or deficit of a specific acid. In other words, a return to the archaic definitions of acids and bases as being the same as anions and cations. We conclude that the acid-base status (the hydrogen ion status) of blood and extracellular fluid is described in terms of the arterial pH, the arterial pCO2, and the extracellular base excess. It is measured with a modern pH-blood gas analyser. The electrolyte status of the plasma is a description of the most important electrolytes, usually measured in venous blood with a dedicated electrolyte analyser, i.e., Na+, Cl-, HCO3-, and K+. Albumin anions contribute significantly to the anions, but calculation requires measurement of pH in addition to albumin and is usually irrelevant. The bicarbonate concentration may be used as a screening parameter of a nonrespiratory acid-base disturbance when respiratory disturbances are taken into account. A disturbance in the hydrogen ion status automatically involves a disturbance in the electrolyte status, whereas the opposite need not be the case.

[Cardiac arrest in chronic metabolic alkalosis due to sodium bicarbonate abuse].

Moderate metabolic alkalosis has not been considered as a life-threatening situation by many authors, but when it persists and pH increases above 7.65, the situation may become critical. We present a case of a 61-yr-old alcoholic male patient, who had been consuming approximately 200 g of sodium bicarbonate daily for twenty years, due to persisitent heartburn and abdominal pains. The patient was admitted to the ITU after home cardiac arrest and resuscitation. On admission he was unconscious and in respiratory distress, with a GCS of 5. Blood gases revealed that his pH was 7.64, HCO3 44 mmol L(-1), K+ 2.4 mmol L(-1)l, Cl- 44 mmol L(-1), and lactate concentration over 15 mmol L(-1). He was treated with controlled hypercapnia, up to a PaCO2 of 63 mm Hg, sedation, and administration of a large amount of chloride (864 mmol during the first day). The patient regained consciousness after 48 h, was extubated and transferred to the internal medicine department where he died 3 days later. Chronic alkali abuse can lead to various metabolic disturbances, neurologic disturbances and cardiovascular compromise. In the described case, the exact cause of cardiac arrest remained unknown, but may have been caused by alkalosis combined with hypoxia, hypokalemia and poor general condition. The extreme metabolic alkalosis (pH 7.8) could also have been enhanced by the administration of i.v. sodium bicarbonate during resuscitation. The treatment of choice in such cases should consist of vigorous chloride containing fluid resuscitation, ammonium chloride and hemodialysis.