Oliguria and anuria are the decreased or absent production of urine, respectively. The decreased production of urine may be a sign of dehydration, renal failure or urinary obstruction/urinary retention.
Contents[hide]
1 Definition
2 Pathophysiology
2.1 Postoperative oliguria
3 Oliguria in infants
4 References
//
[edit] Definition
Oliguria is defined as a urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL/day in adults.[1]
[edit] Pathophysiology
The pathophysiologic mechanisms causing oliguria can be categorized globally in three different categories:
Prerenal: in response to hypoperfusion of the kidney (e.g. as a result of dehydration by poor oral intake, diarrhea, massive bleeding or sepsis)
Renal: due to kidney damage (severe hypoperfusion, rhabdomyolysis, medication)
Postrenal: as a consequence of obstruction of the urine flow (e.g. enlarged prostate, tumour compression urinary outflow, expanding hematoma or fluid collection)
[edit] Postoperative oliguria
Patients usually have decrease in urine output after a major operation that may be a normal physiological response to:
fluid/ blood loss – decreased glomerular filtration rate secondary to hypovolemia and/or hypotension
response of adrenal cortex to stress -increase in aldosterone (Na and water retention) and antidiuretic hormone (ADH) release
[edit] Oliguria in infants
Oliguria, when defined as less than 1 mL/kg/h, in infants is not considered to be a reliable sign of renal failure.
Friday, November 30, 2007
nephrotic syndrome
Nephrotic syndrome is a disorder where the kidneys have been damaged, causing them to leak protein from the blood into the urine.
Contents[hide]
1 Presentation
1.1 Maltese cross
2 Investigations
3 Pathogenesis
4 Causes of nephrotic syndrome
5 Differential diagnosis of gross edema
6 Treatment
6.1 A) General measures (supportive)
6.2 B) Specific treatment of underlying cause
6.3 C) Dietary recommendations
7 Complications
8 Prognosis
9 References
10 External links
//
[edit] Presentation
It is characterised by proteinuria (>3.5g/day), hypoalbuminemia, hyperlipidemia and edema. A few other characteristics are:
The most common sign is excess fluid in the body. This may take several forms:
Puffiness around the eyes, characteristically in the morning.
Edema over the legs which is pitting (i.e. leaves a little pit when the fluid is pressed out, which resolves over a few seconds).
Fluid in the pleural cavity causing pleural effusion.
Fluid in the peritoneal cavity causing ascites.
Hypertension (rarely)
Some patients may notice foamy urine, due to a lowering of the surface tension by the severe proteinuria. Actual urinary complaints such as hematuria or oliguria are uncommon, and are seen commonly in nephritic syndrome.
May have features of underlying cause, such rash associated with SLE, or neuropathy with diabetes.
Examination should also exclude other causes of gross edema- especially the cardiovascular and hepatic system.
[edit] Maltese cross
The classic Maltese cross pattern is evident in fatty casts with polarized microscopy because of the birefringence of the lipid.[1] Maltese crosses are due to cholesterol, which is increased in nephrotic syndrome.
[edit] Investigations
The following are baseline, essential investigations
Urine sample shows proteinuria. It is also examined for active casts; which is more a feature of active nephritis.
Hypoalbuminemia: albumin levels in blood < 30g/L
High levels of cholesterol (hypercholesterolemia), specifically elevated LDL, usually with concomitantly elevated VLDL
Electrolytes, urea and creatinine (EUCs): to evaluate renal function
Furher investigations are indicated if the cause is not clear
Biopsy of kidney (not usually done in children)
Auto-immune markers (ANA, ASOT, C3, cryoglobulins, serum electrophoresis)
[edit] Pathogenesis
The glomeruli of the kidneys are the parts that normally filter the blood. They consist of capillaries that are fenestrated (leaky, due to little holes called fenestrae or windows) and that allow fluid, salts, and other small solutes to flow through, but normally not proteins.
In nephrotic syndrome, the glomeruli become damaged due to inflammation and hyalinisation so that small proteins, such as albumins immunoglobulins and anti-thrombin can pass through the kidneys into urine.
Albumin is the major protein in the blood which maintains colloid osmotic pressure- this prevents leakage of blood from vessels into tissue. However, experiments show that the edema formation in nephrotic syndrome is more so due to microvascular damage and intense salt and water retention by the damaged kidneys (due to increased angiotensin secretion). The mechanism is very complex and still not fully understood.
In response to leakage of albumin, the liver begins to make more of all its proteins, and levels of large proteins (such as alpha 2-macroglobulin and lipoproteins) increase. The excess lipoproteins end up in the urine filtrate, which is then rebsorbed by the tubular cells, which end up shedding and forming oval fat bodies or fatty casts.
[edit] Causes of nephrotic syndrome
A) Primary renal diseases
Any of the glomerulonephritides can cause nephrotic syndrome; but in adults the most common ones are membranous, FSGS, and minimal change disease. In children 95% of cases are due to minimal change disease.
B) Secondary renal diseases
Many and varied. Causes include
Diabetes
SLE
Amyloidosis
However, Idiopathic Nephritic syndrome, has no known causes.
[edit] Differential diagnosis of gross edema
When someone presents with generalised edema, the following causes should be excluded
1) Heart failure: The patient is older, with a history of heart disease.
Jugular venous pressure is elevated on examination, might hear heart murmurs
An echocardiogram is the gold standard investigation
2) Liver failure: History suggestive of hepatitis/ cirrhosis: alcoholic, IV drug user, some hereditary causes
Stigmata of liver disease are seen: dilated veins over umbilicus (caput medusae), scratch marks, enlarged spleen, spider angiomata, encephalopathy, bruising, nodular liver
3) Acute fluid overload in someone with kidney failure: These people are known to have kidney failure, and have either drunk too much or missed their dialysis.
4) Metastatic cancer: When cancer seeds the lungs or abdomen it causes effusions and fluid accumulation due to obstruction of lymphatics and veins as well as serous exudation.
[edit] Treatment
Treatment includes:
[edit] A) General measures (supportive)
Monitoring and maintaining euvolemia (the correct amount of fluid in the body)
- monitoring urine output, BP regularly
- fluid restrict to 1L
- diuretics (IV furosemide)
Monitoring kidney function
-do EUCs daily and calculating GFR
Prevent and treat any complications [see below]
Albumin infusions are generally not used because their effect lasts only transiently.
[edit] B) Specific treatment of underlying cause
Immunosupression for the glomerulonephritides (steroids,[2] cyclosporin)
Achieving stricter blood glucose control if diabetic
BP control. ACE inhibitors are the drug of choice. Independent of their blood pressure lowering effect, they have been shown to decrease protein loss.
[edit] C) Dietary recommendations
Limit high protein animal foods to 1 oz per meal (prefferably lean cuts of meat, fish, and poultry)
Limit high phosphorous foods such as cheese, cooked dried beans and peas, nut butters, soy, tofu, and yogurt, including cokes and colas.
Limit high potassium vegetables and fruits such as artichokes, avocado, bamboo shoots, beets, brussels sprouts, chard, greens (such as beet and collards), kohlrabi, okra, parsnips, potatoes, pumpkin, rutabagas, spinach, sweet potatoes, tomatoes, tomato juice, tomato sauce, wax beens, winter squash, yams. Fruits include, apricots, bananas, dates, honey dew, nectarines, orange juice, oranges, prune juice.
Avoid saturated fats and eat unsaturated fats in moderation.
Eat low-fat desserts only.
Monitor fluid intake which includes all fluids and foods that are liquid at room temperature.
[edit] Complications
Venous thrombosis: due to leak of anti-thrombin 3, which helps prevent thrombosis. This often occurs in the renal veins. Treatment is with heparin.
Infection: due to leakage of immunoglobulins, encapsulated bacteria such as Haemophilus influenzae and Streptococcus pneumonia can cause infection.
Acute renal failure is due to hypovolemia. Despite the excess of fluid in the tissues, there is less fluid in the vasculature. Decreased blood flow to the kidneys causes them to shutdown. Thus it is a tricky task to get rid of excess fluid in the body while maintaining ciculalatory euvolemia.
Pulmonary edema: again due to fluid leak, sometimes it leaks into lungs causing hypoxia and dyspnoea.
Do not give diuretics.
[edit] Prognosis
The prognosis depends on the cause of nephrotic syndrome. It is usually good in children, because minimal change disease responds very well to steroids and does not cause chronic renal failure. However other causes such as focal segmental glomerulosclerosis frequently lead to end stage renal disease. Factors associated with a poorer prognosis in these cases include level of proteinuria, blood pressure control and kidney function (GFR).
Contents[hide]
1 Presentation
1.1 Maltese cross
2 Investigations
3 Pathogenesis
4 Causes of nephrotic syndrome
5 Differential diagnosis of gross edema
6 Treatment
6.1 A) General measures (supportive)
6.2 B) Specific treatment of underlying cause
6.3 C) Dietary recommendations
7 Complications
8 Prognosis
9 References
10 External links
//
[edit] Presentation
It is characterised by proteinuria (>3.5g/day), hypoalbuminemia, hyperlipidemia and edema. A few other characteristics are:
The most common sign is excess fluid in the body. This may take several forms:
Puffiness around the eyes, characteristically in the morning.
Edema over the legs which is pitting (i.e. leaves a little pit when the fluid is pressed out, which resolves over a few seconds).
Fluid in the pleural cavity causing pleural effusion.
Fluid in the peritoneal cavity causing ascites.
Hypertension (rarely)
Some patients may notice foamy urine, due to a lowering of the surface tension by the severe proteinuria. Actual urinary complaints such as hematuria or oliguria are uncommon, and are seen commonly in nephritic syndrome.
May have features of underlying cause, such rash associated with SLE, or neuropathy with diabetes.
Examination should also exclude other causes of gross edema- especially the cardiovascular and hepatic system.
[edit] Maltese cross
The classic Maltese cross pattern is evident in fatty casts with polarized microscopy because of the birefringence of the lipid.[1] Maltese crosses are due to cholesterol, which is increased in nephrotic syndrome.
[edit] Investigations
The following are baseline, essential investigations
Urine sample shows proteinuria. It is also examined for active casts; which is more a feature of active nephritis.
Hypoalbuminemia: albumin levels in blood < 30g/L
High levels of cholesterol (hypercholesterolemia), specifically elevated LDL, usually with concomitantly elevated VLDL
Electrolytes, urea and creatinine (EUCs): to evaluate renal function
Furher investigations are indicated if the cause is not clear
Biopsy of kidney (not usually done in children)
Auto-immune markers (ANA, ASOT, C3, cryoglobulins, serum electrophoresis)
[edit] Pathogenesis
The glomeruli of the kidneys are the parts that normally filter the blood. They consist of capillaries that are fenestrated (leaky, due to little holes called fenestrae or windows) and that allow fluid, salts, and other small solutes to flow through, but normally not proteins.
In nephrotic syndrome, the glomeruli become damaged due to inflammation and hyalinisation so that small proteins, such as albumins immunoglobulins and anti-thrombin can pass through the kidneys into urine.
Albumin is the major protein in the blood which maintains colloid osmotic pressure- this prevents leakage of blood from vessels into tissue. However, experiments show that the edema formation in nephrotic syndrome is more so due to microvascular damage and intense salt and water retention by the damaged kidneys (due to increased angiotensin secretion). The mechanism is very complex and still not fully understood.
In response to leakage of albumin, the liver begins to make more of all its proteins, and levels of large proteins (such as alpha 2-macroglobulin and lipoproteins) increase. The excess lipoproteins end up in the urine filtrate, which is then rebsorbed by the tubular cells, which end up shedding and forming oval fat bodies or fatty casts.
[edit] Causes of nephrotic syndrome
A) Primary renal diseases
Any of the glomerulonephritides can cause nephrotic syndrome; but in adults the most common ones are membranous, FSGS, and minimal change disease. In children 95% of cases are due to minimal change disease.
B) Secondary renal diseases
Many and varied. Causes include
Diabetes
SLE
Amyloidosis
However, Idiopathic Nephritic syndrome, has no known causes.
[edit] Differential diagnosis of gross edema
When someone presents with generalised edema, the following causes should be excluded
1) Heart failure: The patient is older, with a history of heart disease.
Jugular venous pressure is elevated on examination, might hear heart murmurs
An echocardiogram is the gold standard investigation
2) Liver failure: History suggestive of hepatitis/ cirrhosis: alcoholic, IV drug user, some hereditary causes
Stigmata of liver disease are seen: dilated veins over umbilicus (caput medusae), scratch marks, enlarged spleen, spider angiomata, encephalopathy, bruising, nodular liver
3) Acute fluid overload in someone with kidney failure: These people are known to have kidney failure, and have either drunk too much or missed their dialysis.
4) Metastatic cancer: When cancer seeds the lungs or abdomen it causes effusions and fluid accumulation due to obstruction of lymphatics and veins as well as serous exudation.
[edit] Treatment
Treatment includes:
[edit] A) General measures (supportive)
Monitoring and maintaining euvolemia (the correct amount of fluid in the body)
- monitoring urine output, BP regularly
- fluid restrict to 1L
- diuretics (IV furosemide)
Monitoring kidney function
-do EUCs daily and calculating GFR
Prevent and treat any complications [see below]
Albumin infusions are generally not used because their effect lasts only transiently.
[edit] B) Specific treatment of underlying cause
Immunosupression for the glomerulonephritides (steroids,[2] cyclosporin)
Achieving stricter blood glucose control if diabetic
BP control. ACE inhibitors are the drug of choice. Independent of their blood pressure lowering effect, they have been shown to decrease protein loss.
[edit] C) Dietary recommendations
Limit high protein animal foods to 1 oz per meal (prefferably lean cuts of meat, fish, and poultry)
Limit high phosphorous foods such as cheese, cooked dried beans and peas, nut butters, soy, tofu, and yogurt, including cokes and colas.
Limit high potassium vegetables and fruits such as artichokes, avocado, bamboo shoots, beets, brussels sprouts, chard, greens (such as beet and collards), kohlrabi, okra, parsnips, potatoes, pumpkin, rutabagas, spinach, sweet potatoes, tomatoes, tomato juice, tomato sauce, wax beens, winter squash, yams. Fruits include, apricots, bananas, dates, honey dew, nectarines, orange juice, oranges, prune juice.
Avoid saturated fats and eat unsaturated fats in moderation.
Eat low-fat desserts only.
Monitor fluid intake which includes all fluids and foods that are liquid at room temperature.
[edit] Complications
Venous thrombosis: due to leak of anti-thrombin 3, which helps prevent thrombosis. This often occurs in the renal veins. Treatment is with heparin.
Infection: due to leakage of immunoglobulins, encapsulated bacteria such as Haemophilus influenzae and Streptococcus pneumonia can cause infection.
Acute renal failure is due to hypovolemia. Despite the excess of fluid in the tissues, there is less fluid in the vasculature. Decreased blood flow to the kidneys causes them to shutdown. Thus it is a tricky task to get rid of excess fluid in the body while maintaining ciculalatory euvolemia.
Pulmonary edema: again due to fluid leak, sometimes it leaks into lungs causing hypoxia and dyspnoea.
Do not give diuretics.
[edit] Prognosis
The prognosis depends on the cause of nephrotic syndrome. It is usually good in children, because minimal change disease responds very well to steroids and does not cause chronic renal failure. However other causes such as focal segmental glomerulosclerosis frequently lead to end stage renal disease. Factors associated with a poorer prognosis in these cases include level of proteinuria, blood pressure control and kidney function (GFR).
Wednesday, November 28, 2007
mitral regurgitation
Mitral regurgitation (MR), a valvular heart disease also known as mitral insufficiency, is the abnormal leaking of blood through the mitral valve, from the left ventricle into the left atrium of the heart.
Contents[hide]
1 Etiology
2 Pathophysiology
2.1 Acute phase
2.2 Chronic compensated phase
2.3 Chronic decompensated phase
3 Symptoms
4 Diagnostic studies
4.1 Chest x-ray
4.2 Echocardiography
5 Quantification of mitral regurgitation
6 Treatment
6.1 Indication for surgery
7 References
8 See also
9 External links
//
[edit] Etiology
The mitral valve is composed of the valve leaflets, the mitral valve annulus (which forms a ring around the valve leaflets), the papillary muscles (which tether the valve leaflets to the left ventricle, preventing them from prolapsing into the left atrium), and the chordae tendineae (which connect the valve leaflets to the papillary muscles). A dysfunction of any of these portions of the mitral valve apparatus can cause mitral regurgitation.
Primary mitral regurgitation is due to any disease process that affects the mitral valve apparatus itself. The causes of primary mitral regurgitation include:
Myxomatous degeneration of the mitral valve
Ischemic heart disease / Coronary artery disease
Infective endocarditis
Collagen vascular diseases (ie: SLE, Marfan's syndrome)
Rheumatic heart disease
Trauma
Balloon valvulotomy of the mitral valve
Certain forms of medication (e.g. fenfluramine)
The most common cause of primary mitral regurgitation in the United States (causing about 50% of primary mitral regurgitation) is myxomatous degeneration of the valve. Myxomatous degeneration of the mitral valve is more common in males, and is more common in advancing age. It is due to a genetic abnormality that results in a defect in the collagen that makes up the mitral valve. This causes a stretching out of the leaflets of the valve and the chordae tendineae. The elongation of the valve leaflets and the chordae tendineae prevent the valve leaflets from fully coapting when the valve is closed, causing the valve leaflets to prolapse into the left atrium, thereby causing mitral regurgitation.
Ischemic heart disease causes mitral regurgitation by the combination of ischemic dysfunction of the papillary muscles, and the dilatation of the left ventricle that is present in ischemic heart disease, with the subsequent displacement of the papillary muscles and the dilatation of the mitral valve annulus.
Secondary mitral regurgitation is due to the dilatation of the left ventricle, causing stretching of the mitral valve annulus and displacement of the papillary muscles. This dilatation of the left ventricle can be due to any cause of dilated cardiomyopathy, including aortic insufficiency, nonischemic dilated cardiomyopathy and Noncompaction Cardiomyopathy.
[edit] Pathophysiology
Comparison of acute and chronic mitral regurgitation
Acute mitral regurgitation
Chronic mitral regurgitation
Electrocardiogram
Normal
P mitrale, atrial fibrillation, left ventricular hypertrophy
Heart size
Normal
Cardiomegaly, left atrial enlargement
Systolic murmur
Heard at the base, radiates to the neck, spine, or top of head
Heard at the apex, radiates to the axilla
Apical thrill
May be absent
Present
Jugular venous distension
Present
Absent
The pathophysiology of mitral regurgitation can be broken into three phases of the disease process: the acute phase, the chronic compensated phase, and the chronic decompensated phase.
[edit] Acute phase
Acute mitral regurgitation (as may occur due to the sudden rupture of a chordae tendineae or papillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle. The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta (the forward cardiac output or forward stroke volume), but also the blood that regurgitates into the left atrium (the regurgitant volume). The combination of the forward stroke volume and the regurgitant volume is known as the total stroke volume of the left ventricle.
In the acute setting, the stroke volume of the left ventricle is increased (increased ejection fraction), but the forward cardiac output is decreased. The mechanism by which the total stroke volume is increased is known as the Frank-Starling mechanism.
The regurgitant volume causes a volume overload and a pressure overload of the left atrium. The increased pressures in the left atrium inhibit drainage of blood from the lungs via the pulmonary veins. This causes pulmonary congestion.
[edit] Chronic compensated phase
If the mitral regurgitation develops slowly over months to years or if the acute phase can be managed with medical therapy, the individual will enter the chronic compensated phase of the disease. In this phase, the left ventricle develops eccentric hypertrophy in order to better manage the larger than normal stroke volume. The eccentric hypertrophy and the increased diastolic volume combine to increase the stroke volume (to levels well above normal) so that the forward stroke volume (forward cardiac output) approaches the normal levels.
In the left atrium, the volume overload causes enlargement of the chamber of the left atrium, allowing the filling pressure in the left atrium to decrease. This improves the drainage from the pulmonary veins, and signs and symptoms of pulmonary congestion will decrease.
These changes in the left ventricle and left atrium improve the low forward cardiac output state and the pulmonary congestion that occur in the acute phase of the disease. Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerances.
[edit] Chronic decompensated phase
An individual may be in the compensated phase of mitral regurgitation for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mitral regurgitation. It is currently unclear what causes an individual to enter the decompensated phase of this disease. However, the decompensated phase is characterized by calcium overload within the cardiac myocytes.
In this phase, the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of mitral regurgitation, and the stroke volume of the left ventricle will decrease. The decreased stroke volume causes a decreased forward cardiac output and an increase in the end-systolic volume. The increased end-systolic volume translates to increased filling pressures of the ventricular and increased pulmonary venous congestion. The individual may again have symptoms of congestive heart failure.
The left ventricle begins to dilate during this phase. This causes a dilatation of the mitral valve annulus, which may worsen the degree of mitral regurgitation. The dilated left ventricle causes an increase in the wall stress of the cardiac chamber as well.
While the ejection fraction is less in the chronic decompensated phase than in the acute phase or the chronic compensated phase of mitral regurgitation, it may still be in the normal range (ie: > 50 percent), and may not decrease until late in the disease course. A decreased ejection fraction in an individual with mitral regurgitation and no other cardiac abnormality should alert the physician that the disease may be in its decompensated phase.
[edit] Symptoms
The symptoms associated with mitral regurgitation are dependent on which phase of the disease process the individual is in. Individuals with acute mitral regurgitation will have the signs and symptoms of decompensated congestive heart failure (ie: shortness of breath, pulmonary edema, orthopnea, paroxysmal nocturnal dyspnea), as well as symptoms suggestive of a low cardiac output state (ie: decreased exercise tolerance). Cardiovascular collapse with shock (cardiogenic shock) may be seen in individuals with acute mitral regurgitation due to papillary muscle rupture or rupture of a chordae tendineae.
Individuals with chronic compensated mitral regurgitation may be asymptomatic, with a normal exercise tolerance and no evidence of heart failure. These individuals may be sensitive to small shifts in their intravascular volume status, and are prone to develop volume overload (congestive heart failure).
[edit] Diagnostic studies
There are many diagnostic tests that have abnormal results in the presence of mitral regurgitation. These tests suggest the diagnosis of mitral regurgitation and may indicate to the physician that further testing is warranted. For instance, the electrocardiogram (ECG) in long standing mitral regurgitation may show evidence of left atrial enlargement and left ventricular hypertrophy. Atrial fibrillation may also be noted on the ECG in individuals with chronic mitral regurgitation. The ECG may not show any of these finding in the setting of acute mitral regurgitation.
The quantification of mitral regurgitation usually employs imaging studies such as echocardiography or magnetic resonance angiography of the heart.
[edit] Chest x-ray
The chest x-ray in individuals with chronic mitral regurgitation is characterized by enlargement of the left atrium and the left ventricle. The pulmonary vascular markings are typically normal, since pulmonary venous pressures are usually not significantly elevated.
[edit] Echocardiography
transesophageal echocardiogram of mitral valve prolapse
The echocardiogram is commonly used to confirm the diagnosis of mitral regurgitation. Color doppler flow on the transthoracic echocardiogram (TTE) will reveal a jet of blood flowing from the left ventricle into the left atrium during ventricular systole.
Because of the inability in getting accurate images of the left atrium and the pulmonary veins on the transthoracic echocardiogram, a transesophageal echocardiogram may be necessary to determine the severity of the mitral regurgitation in some cases.
Factors that suggest severe mitral regurgitation on echocardiography include systolic reversal of flow in the pulmonary veins and filling of the entire left atrial cavity by the regurgitant jet of MR.
[edit] Quantification of mitral regurgitation
Determination of the degree of mitral regurgitation
Degree of mitral regurgitation
Regurgitant fraction
Regurgitant Orifice area
Mild mitral regurgitation
< 20 percent
Moderate mitral regurgitation
20 - 40 percent
Moderate to severe mitral regurgitation
40 - 60 percent
Severe mitral regurgitation
> 60 percent
> 0.3 cm2
The degree of severity of mitral regurgitation can be quantified by the percentage of the left ventricular stroke volume that regurgitates into the left atrium (the regurgitant fraction).
Methods that have been used to assess the regurgitant fraction in mitral regurgitation include echocardiography, cardiac catheterization, fast CT scan, and cardiac MRI.
The echocardiographic technique to measure the regurgitant fraction is to determine the forward flow through the mitral valve (from the left atrium to the left ventricle) during ventricular diastole, and comparing it with the flow out of the left ventricle through the aortic valve in ventricular systole. This method assumes that the aortic valve does not suffer from aortic insufficiency. The regurgitant fraction would be described as:
Another way to quantify the degree of mitral regurgitation is to determine the area of the regurgitant flow at the level of the valve. This is known as the regurgitant orifice area, and correlates with the size of the defect in the mitral valve. One particular echocardiographic technique used to measure the orifice area is measurement of the proximal isovelocity surface area (PISA). The flaw of using PISA to determine the mitral valve regurgitant orifice area is that it measures the flow at one moment in time in the cardiac cycle, which may not reflect the average performance of the regurgitant jet.
[edit] Treatment
The treatment of mitral regurgitation depends on the acuteness of the disease and whether there are associated signs of hemodynamic compromise.
In acute mitral regurgitation secondary to a mechanical defect in the heart (ie: rupture of a papillary muscle or chrordae tendineae), the treatment of choice is urgent mitral valve replacement. If the patient is hypotensive prior to the surgical procedure, an intra-aortic balloon pump may be placed in order to improve perfusion of the organs and to decrease the degree of mitral regurgitation.
If the individual with acute mitral regurgitation is normotensive, vasodilators may be of use to decrease the afterload seen by the left ventricle and thereby decrease the regurgitant fraction. The vasodilator most commonly used is nitroprusside.
Individuals with chronic mitral regurgitation can be treated with vasodilators as well. In the chronic state, the most commonly used agents are ACE inhibitors and hydralazine. Studies have shown that the use of ACE inhibitors and hydralazine can delay surgical treatment of mitral regurgitation1,2. The current guidelines for treatment of mitral regurgitation limit the use of vasodilators to individuals with hypertension, however.
There are two surgical options for the treatment of mitral regurgitation: mitral valve replacement and mitral valve repair.
[edit] Indication for surgery
Indications for surgery for chronic mitral regurgitation3
Symptoms
LV EF
LVESD
NYHA II - IV
> 60 percent
< 45 mm
Asymptomatic or symptomatic
50 - 60 percent
≥ 45 mm
Asymptomatic or symptomatic
< 50 percent or ≥ 45 mm
Pulmonary artery systolic pressure ≥ 50 mmHg
Indications for surgery for chronic mitral regurgitation include signs of left ventricular dysfunction. These include an ejection fraction of less than 60 percent and a left ventricular end systolic dimension (LVESD) of greater than 45 mm.
Contents[hide]
1 Etiology
2 Pathophysiology
2.1 Acute phase
2.2 Chronic compensated phase
2.3 Chronic decompensated phase
3 Symptoms
4 Diagnostic studies
4.1 Chest x-ray
4.2 Echocardiography
5 Quantification of mitral regurgitation
6 Treatment
6.1 Indication for surgery
7 References
8 See also
9 External links
//
[edit] Etiology
The mitral valve is composed of the valve leaflets, the mitral valve annulus (which forms a ring around the valve leaflets), the papillary muscles (which tether the valve leaflets to the left ventricle, preventing them from prolapsing into the left atrium), and the chordae tendineae (which connect the valve leaflets to the papillary muscles). A dysfunction of any of these portions of the mitral valve apparatus can cause mitral regurgitation.
Primary mitral regurgitation is due to any disease process that affects the mitral valve apparatus itself. The causes of primary mitral regurgitation include:
Myxomatous degeneration of the mitral valve
Ischemic heart disease / Coronary artery disease
Infective endocarditis
Collagen vascular diseases (ie: SLE, Marfan's syndrome)
Rheumatic heart disease
Trauma
Balloon valvulotomy of the mitral valve
Certain forms of medication (e.g. fenfluramine)
The most common cause of primary mitral regurgitation in the United States (causing about 50% of primary mitral regurgitation) is myxomatous degeneration of the valve. Myxomatous degeneration of the mitral valve is more common in males, and is more common in advancing age. It is due to a genetic abnormality that results in a defect in the collagen that makes up the mitral valve. This causes a stretching out of the leaflets of the valve and the chordae tendineae. The elongation of the valve leaflets and the chordae tendineae prevent the valve leaflets from fully coapting when the valve is closed, causing the valve leaflets to prolapse into the left atrium, thereby causing mitral regurgitation.
Ischemic heart disease causes mitral regurgitation by the combination of ischemic dysfunction of the papillary muscles, and the dilatation of the left ventricle that is present in ischemic heart disease, with the subsequent displacement of the papillary muscles and the dilatation of the mitral valve annulus.
Secondary mitral regurgitation is due to the dilatation of the left ventricle, causing stretching of the mitral valve annulus and displacement of the papillary muscles. This dilatation of the left ventricle can be due to any cause of dilated cardiomyopathy, including aortic insufficiency, nonischemic dilated cardiomyopathy and Noncompaction Cardiomyopathy.
[edit] Pathophysiology
Comparison of acute and chronic mitral regurgitation
Acute mitral regurgitation
Chronic mitral regurgitation
Electrocardiogram
Normal
P mitrale, atrial fibrillation, left ventricular hypertrophy
Heart size
Normal
Cardiomegaly, left atrial enlargement
Systolic murmur
Heard at the base, radiates to the neck, spine, or top of head
Heard at the apex, radiates to the axilla
Apical thrill
May be absent
Present
Jugular venous distension
Present
Absent
The pathophysiology of mitral regurgitation can be broken into three phases of the disease process: the acute phase, the chronic compensated phase, and the chronic decompensated phase.
[edit] Acute phase
Acute mitral regurgitation (as may occur due to the sudden rupture of a chordae tendineae or papillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle. The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta (the forward cardiac output or forward stroke volume), but also the blood that regurgitates into the left atrium (the regurgitant volume). The combination of the forward stroke volume and the regurgitant volume is known as the total stroke volume of the left ventricle.
In the acute setting, the stroke volume of the left ventricle is increased (increased ejection fraction), but the forward cardiac output is decreased. The mechanism by which the total stroke volume is increased is known as the Frank-Starling mechanism.
The regurgitant volume causes a volume overload and a pressure overload of the left atrium. The increased pressures in the left atrium inhibit drainage of blood from the lungs via the pulmonary veins. This causes pulmonary congestion.
[edit] Chronic compensated phase
If the mitral regurgitation develops slowly over months to years or if the acute phase can be managed with medical therapy, the individual will enter the chronic compensated phase of the disease. In this phase, the left ventricle develops eccentric hypertrophy in order to better manage the larger than normal stroke volume. The eccentric hypertrophy and the increased diastolic volume combine to increase the stroke volume (to levels well above normal) so that the forward stroke volume (forward cardiac output) approaches the normal levels.
In the left atrium, the volume overload causes enlargement of the chamber of the left atrium, allowing the filling pressure in the left atrium to decrease. This improves the drainage from the pulmonary veins, and signs and symptoms of pulmonary congestion will decrease.
These changes in the left ventricle and left atrium improve the low forward cardiac output state and the pulmonary congestion that occur in the acute phase of the disease. Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerances.
[edit] Chronic decompensated phase
An individual may be in the compensated phase of mitral regurgitation for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mitral regurgitation. It is currently unclear what causes an individual to enter the decompensated phase of this disease. However, the decompensated phase is characterized by calcium overload within the cardiac myocytes.
In this phase, the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of mitral regurgitation, and the stroke volume of the left ventricle will decrease. The decreased stroke volume causes a decreased forward cardiac output and an increase in the end-systolic volume. The increased end-systolic volume translates to increased filling pressures of the ventricular and increased pulmonary venous congestion. The individual may again have symptoms of congestive heart failure.
The left ventricle begins to dilate during this phase. This causes a dilatation of the mitral valve annulus, which may worsen the degree of mitral regurgitation. The dilated left ventricle causes an increase in the wall stress of the cardiac chamber as well.
While the ejection fraction is less in the chronic decompensated phase than in the acute phase or the chronic compensated phase of mitral regurgitation, it may still be in the normal range (ie: > 50 percent), and may not decrease until late in the disease course. A decreased ejection fraction in an individual with mitral regurgitation and no other cardiac abnormality should alert the physician that the disease may be in its decompensated phase.
[edit] Symptoms
The symptoms associated with mitral regurgitation are dependent on which phase of the disease process the individual is in. Individuals with acute mitral regurgitation will have the signs and symptoms of decompensated congestive heart failure (ie: shortness of breath, pulmonary edema, orthopnea, paroxysmal nocturnal dyspnea), as well as symptoms suggestive of a low cardiac output state (ie: decreased exercise tolerance). Cardiovascular collapse with shock (cardiogenic shock) may be seen in individuals with acute mitral regurgitation due to papillary muscle rupture or rupture of a chordae tendineae.
Individuals with chronic compensated mitral regurgitation may be asymptomatic, with a normal exercise tolerance and no evidence of heart failure. These individuals may be sensitive to small shifts in their intravascular volume status, and are prone to develop volume overload (congestive heart failure).
[edit] Diagnostic studies
There are many diagnostic tests that have abnormal results in the presence of mitral regurgitation. These tests suggest the diagnosis of mitral regurgitation and may indicate to the physician that further testing is warranted. For instance, the electrocardiogram (ECG) in long standing mitral regurgitation may show evidence of left atrial enlargement and left ventricular hypertrophy. Atrial fibrillation may also be noted on the ECG in individuals with chronic mitral regurgitation. The ECG may not show any of these finding in the setting of acute mitral regurgitation.
The quantification of mitral regurgitation usually employs imaging studies such as echocardiography or magnetic resonance angiography of the heart.
[edit] Chest x-ray
The chest x-ray in individuals with chronic mitral regurgitation is characterized by enlargement of the left atrium and the left ventricle. The pulmonary vascular markings are typically normal, since pulmonary venous pressures are usually not significantly elevated.
[edit] Echocardiography
transesophageal echocardiogram of mitral valve prolapse
The echocardiogram is commonly used to confirm the diagnosis of mitral regurgitation. Color doppler flow on the transthoracic echocardiogram (TTE) will reveal a jet of blood flowing from the left ventricle into the left atrium during ventricular systole.
Because of the inability in getting accurate images of the left atrium and the pulmonary veins on the transthoracic echocardiogram, a transesophageal echocardiogram may be necessary to determine the severity of the mitral regurgitation in some cases.
Factors that suggest severe mitral regurgitation on echocardiography include systolic reversal of flow in the pulmonary veins and filling of the entire left atrial cavity by the regurgitant jet of MR.
[edit] Quantification of mitral regurgitation
Determination of the degree of mitral regurgitation
Degree of mitral regurgitation
Regurgitant fraction
Regurgitant Orifice area
Mild mitral regurgitation
< 20 percent
Moderate mitral regurgitation
20 - 40 percent
Moderate to severe mitral regurgitation
40 - 60 percent
Severe mitral regurgitation
> 60 percent
> 0.3 cm2
The degree of severity of mitral regurgitation can be quantified by the percentage of the left ventricular stroke volume that regurgitates into the left atrium (the regurgitant fraction).
Methods that have been used to assess the regurgitant fraction in mitral regurgitation include echocardiography, cardiac catheterization, fast CT scan, and cardiac MRI.
The echocardiographic technique to measure the regurgitant fraction is to determine the forward flow through the mitral valve (from the left atrium to the left ventricle) during ventricular diastole, and comparing it with the flow out of the left ventricle through the aortic valve in ventricular systole. This method assumes that the aortic valve does not suffer from aortic insufficiency. The regurgitant fraction would be described as:
Another way to quantify the degree of mitral regurgitation is to determine the area of the regurgitant flow at the level of the valve. This is known as the regurgitant orifice area, and correlates with the size of the defect in the mitral valve. One particular echocardiographic technique used to measure the orifice area is measurement of the proximal isovelocity surface area (PISA). The flaw of using PISA to determine the mitral valve regurgitant orifice area is that it measures the flow at one moment in time in the cardiac cycle, which may not reflect the average performance of the regurgitant jet.
[edit] Treatment
The treatment of mitral regurgitation depends on the acuteness of the disease and whether there are associated signs of hemodynamic compromise.
In acute mitral regurgitation secondary to a mechanical defect in the heart (ie: rupture of a papillary muscle or chrordae tendineae), the treatment of choice is urgent mitral valve replacement. If the patient is hypotensive prior to the surgical procedure, an intra-aortic balloon pump may be placed in order to improve perfusion of the organs and to decrease the degree of mitral regurgitation.
If the individual with acute mitral regurgitation is normotensive, vasodilators may be of use to decrease the afterload seen by the left ventricle and thereby decrease the regurgitant fraction. The vasodilator most commonly used is nitroprusside.
Individuals with chronic mitral regurgitation can be treated with vasodilators as well. In the chronic state, the most commonly used agents are ACE inhibitors and hydralazine. Studies have shown that the use of ACE inhibitors and hydralazine can delay surgical treatment of mitral regurgitation1,2. The current guidelines for treatment of mitral regurgitation limit the use of vasodilators to individuals with hypertension, however.
There are two surgical options for the treatment of mitral regurgitation: mitral valve replacement and mitral valve repair.
[edit] Indication for surgery
Indications for surgery for chronic mitral regurgitation3
Symptoms
LV EF
LVESD
NYHA II - IV
> 60 percent
< 45 mm
Asymptomatic or symptomatic
50 - 60 percent
≥ 45 mm
Asymptomatic or symptomatic
< 50 percent or ≥ 45 mm
Pulmonary artery systolic pressure ≥ 50 mmHg
Indications for surgery for chronic mitral regurgitation include signs of left ventricular dysfunction. These include an ejection fraction of less than 60 percent and a left ventricular end systolic dimension (LVESD) of greater than 45 mm.
cardiac arrest
A cardiac arrest, also known as cardiorespiratory arrest, cardiopulmonary arrest or circulatory arrest, is the abrupt cessation of normal circulation of the blood due to failure of the heart to contract effectively during systole.[1]
"Arrested" blood circulation prevents delivery of oxygen to all parts of the body. Cerebral hypoxia, or lack of oxygen supply to the brain, causes victims to lose consciousness and to stop normal breathing. Brain injury is likely if cardiac arrest is untreated for more than 5 minutes,[2] although new treatments such as induced hypothermia have begun to extend this time.[3][4] To improve survival and neurological recovery immediate response is paramount.[5]
Cardiac arrest is a medical emergency that, in certain groups of patients, is potentially reversible if treated early enough (See "Reversible causes" below). When unexpected cardiac arrest leads to death this is called sudden cardiac death (SCD).[1] The primary first-aid treatment for cardiac arrest is cardiopulmonary resuscitation (commonly known as CPR) to provide circulatory support until availability of definitive medical treatment, which will vary dependant on the rhythm the heart is exhibiting, but often requires defibrillation.
Contents[hide]
1 Characteristics and diagnosis
2 Causes of cardiac arrest
2.1 Reversible causes
2.1.1 H's
2.1.2 T's
3 Treatment
3.1 Out of hospital arrest
3.2 Hospital treatment
3.3 Peri-arrest period
4 Prognosis
5 Prevention
6 Implantable cardioverter defibrillators
7 Ethical issues
8 See also
9 References
10 External links
//
[edit] Characteristics and diagnosis
Cardiac arrest is an abrupt cessation of pump function (evidenced by absence of a palpable pulse) of the heart that with prompt intervention could be reversed, but without it will lead to death.[1]
Due to inadequate cerebral perfusion, the patient will be unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest (as opposed to respiratory arrest, which shares many of the same features) is lack of circulation, however there are a number of ways of determining this.
In many cases, lack of carotid pulse is the gold standard for diagnosing cardiac arrest, but lack of a pulse (particularly in the peripheral pulses) may be a result of other conditions (e.g. shock), or simply an error on the part of the rescuer. Studies have shown that rescuers often make a mistake when checking the carotid pulse in an emergency, whether they are healthcare professionals[6][7] or lay persons.[8]
Owing to the inaccuracy in this method of diagnosis, some bodies such as the European Resuscitation Council (ERC) have de-emphasised its importance. The Resuscitation Council (UK), in line with the ERC's recommendations and those of the American Heart Association,[9] have suggested that the technique should be used only by healthcare professionals with specific training and expertise, and even then that it should be viewed in conjunction with other indicators such as agonal respiration.[10]
Various other methods for detecting circulation have been proposed. Guidelines following the 2000 International Liaison Committee on Resusciation (ILCOR) recommendations were for rescuers to look for "signs of circulation", but not specifically the pulse [9]. These signs included coughing, gasping, colour, twitching and movement.[11] However, in face of evidence that these guidelines were ineffective, the current recommendation of ILCOR is that cardiac arrest should be diagnosed in all casualties who are unconscious and not breathing normally.[9]
Following initial diagnosis of cardiac arrest, healthcare professionals further categorise the diagnosis based on the ECG/EKG rhythm. There are 4 rhythms which result in a cardiac arrest. Ventricular fibrillation (VF/VFib) and pulseless ventricular tachycardia (VT) are both responsive to a defibrillator and so are colloquially referred to as "shockable" rhythms, whereas asystole and pulseless electrical activity (PEA) are non-shockable. The nature of the presenting hearth rhythm suggests different causes and treatment, and is used to guide the rescuer as to what treatment may be appropriate[10] (see Advanced life support and Advanced cardiac life support, as well as the causes of arrest below).
[edit] Causes of cardiac arrest
Cardiac arrest is synonymous with Clinical death. All disease processes leading to death have a period of (potentially) reversible cardiac arrest: the causes of arrest are, therefore, numerous. However, many of these conditions, rather than causing an arrest themselves, promote one of the "Reversible causes" (see below), which then triggers the arrest (e.g. choking leads to hypoxia which in turn leads to an arrest). In some cases, the underlying mechanism cannot be overcome, leading to an unsuccessful resuscitation.
Among adults, ischemic heart disease is the predominant cause of arrest.[12] At autopsy 30% of victims show signs of recent myocardial infarction[citation needed]. Other cardiac conditions potentially leading to arrest include structural abnormalities, arrhythmias and cardiomyopathies. Non-cardiac causes include infections, overdoses, trauma and cancer, in addition to many others.
[edit] Reversible causes
Cardiopulmonary resuscitation (CPR), including adjunctive measures such as defibrillation, intubation and drug administration, is the standard of care for initial treatment of cardiac arrest. However, most cardiac arrests occur for a reason, and unless that reason can be found and overcome, CPR is often ineffective, or if it does result in a return of spontaneous circulation, this is short lived. [10]. As highlighted above, a variety of disease processes can lead to a cardiac arrest, however they usually boil down to one or more of the "Hs and Ts" (see below).
[edit] H's
Hypovolemia - A lack of circulating body fluids, principally blood volume. This is usually (though not exclusively) caused by some form of bleeding, anaphylaxis, or pregnancy with gravid uterus. Peri-arrest treatment includes giving IV fluids and blood transfusions, and controlling the source of any bleeding - by direct pressure for external bleeding, or emergency surgical techniques such as esophagogastroduodenoscopy (i.e. esophageal varices) and thoracotomy for internal bleeding.
Hypoxia - A lack of oxygen to the heart, brain and other vital organs. This can be identified through a careful assessment of breath sounds and tuble placement. Treatment may include providing oxygen, proper ventilation, and good CPR technique.
Hydrogen ions (Acidosis) - An abnormal pH in the body as a result of shock, diabetic ketoacidosis, renal failure, or tricyclic antidepressant overdose. This can be treated with proper ventilation, good CPR technique, and buffers like sodium bicarbonate.
Hyperkalemia or Hypokalemia - The most life threatening electrolyte derangement is hyperkalemia (too much potassium). The classic presentation is the chronic renal failure patient who has missed a dialysis appointment and presents with weakness, nausea, and broad QRS complexes on the electrocardiogram. The most important initial therapy is the administration of calcium, either with calcium gluconate or calcium chloride. Other therapies may include nebulized albuterol, sodium bicarbonate, glucose, and insulin. The diagnosis of hypokalemia (not enough potassium) can be suspected when there is a history of diarrhoea or malnutrition. Loop diuretics may also contribute. The electrocardiogram may show depressed T waves and prominent U waves. Hypokalemia is an important cause of acquired long QT syndrome, and may predispose the patient to torsades de pointes. Digitalis use may increase the risk that hypokalemia will produce life threatening arrhythmias.
Hypothermia - A low core body temperature, defined clinically as a temperature of less than 35 degrees Celsius. The patient is re-warmed either by using a cardiac bypass or by irrigation of the body cavities (such as thorax, peritoneum, bladder) with warm fluids; or warmed IV fluids. CPR only is given until the core body temperature reached 30 degrees Celsius, as defibrillation is ineffective at lower temperatures. Patients have been known to be successfully resuscitated after periods of hours in hypothermia and cardiac arrest, and this has given rise to the often-quoted medical truism, "You're not dead until you're warm and dead."
Hypoglycemia or Hyperglycemia - Low blood glucose from insulin reactions, DKA, nonketotic hyperosmolar coma. This condition can be suspected when the patient is known to be a diabetic. The treatment may include fluids, potassium, glucose (for hypoglycemia), and insulin (for hyperglycemia).
[edit] T's
Tablets or Toxins - Tricyclic antidepressants, phenothiazines, beta blockers, calcium channel blockers, cocaine, digoxin, aspirin, acetominophen. This may be evidenced by items found on or around the patient, the patient's medical history (i.e. drug abuse, medication) taken from family and friends, checking the medical records to make sure no interacting drugs were prescribed, or sending blood and urine samples to the toxicology lab for report. Treatment may include specific antidotes, fluids for volume expansion, vasopressors, sodium bicarbonate (for tricyclic antidepressants), glucagon or calcium (for calcium channel blockers), benzodiazepines (for cocaine), or cardiopulmonary bypass.
Cardiac Tamponade - Blood or other fluids building up in the pericardium can put pressure on the heart so that it is not able to beat. This condition can be recognized by the presence of a narrowing pulse pressure, muffled heart sounds, distended neck veins, electrical alternans on the electrocardiogram, or echocardiogram. This is treated in an emergency by inserting a needle into the pericardium to drain the fluid (pericardiocentesis), or if the fluid is too thick then an emergency thoracotomy is performed to cut the pericardium and release the fluid.
Tension pneumothorax - The build up of air into one of the pleural cavities, which causes a mediastinal shift. When this happens, the great vessels (particularly the superior vena cava) become kinked, which limits blood return to the heart. The condition can be recognized by severe air hunger, hypoxia, jugular venous distension, hyperressonance to percussion on the effected side, and a tracheal shift away from the effected side. The tracheal shift often requires a chest x-ray to appreciate. This is relieved in an emergency by a needle thoracotomy (inserting a needle catheter) into the 2nd intercostal space at the mid-clavicular line, which relieves the pressure in the pleural cavity.
Thrombosis (Myocardial infarction) - If the patient can be successfully resuscitated, there is a chance that the myocardial infarction can be treated, either with thrombolytic therapy or percutaneous coronary intervention.
Thromboembolism (Pulmonary embolism) - Usually diagnosed at autopsy. Patients in asystole or pulseless electrical activity have a poor prognosis. If this can be detected early, the patient may receive dopamine, heparin, and thrombolytics.
Trauma (Hypovolemia) - Reduced blood volume from acute injury or primary damage to the heart or great vessels. Cardiac arrest secondary to trauma, particularly blunt trauma, has a very poor prognosis.
Checking respiration.
Checking carotid pulse.
Insulfation mouth-to-mouth.
[edit] Treatment
[edit] Out of hospital arrest
Most out-of-hospital cardiac arrests occur following a myocardial infarction (heart attack), and present initially with a heart rhythm of ventricular fibrillation. The patient is therefore likely to be responsive to defibrillation, and this has become the focus of pre-hospital interventions. Several organisations promote the idea of a "chain of survival", of which defibrillation is a key step. The links are:
Early recognition - If possible, recognition of illness before the patient develops a cardiac arrest will allow the rescuer to prevent its occurrence. Early recognition that a cardiac arrest has occurred is key to survival - for every minute a patient is in cardiac arrest, their chances of survival drop by roughly 10% [10]
Early CPR - This buys time by keeping vital organs perfused with oxygen whilst waiting for equipment and trained personnel to reverse the arrest. In particular, by keeping the brain supplied with oxygenated blood, chances of neurological damage are decreased.
Early defibrillation - This is the only effective for ventricular fibrillation, and also has benefit in ventricular tachycardia[10]. If defibrillation is delayed, then the rhythm is likely to degenerate into asystole, for which outcomes are markedly worse.
Early post-resuscitation care - Treatment and rehabillitation in a hospital by specialist staff helps to prevent further complications, attempts to fully reverse the underlying cause, and promotes quality of life.
If one or more links in the chain are missing or delayed, then the chances of survival drop significantly. In particular, bystander CPR is an important indicator of survival: if it has not been carried out, then resuscitation is associated with very poor results. Paramedics in some jurisdictions are authorised to abandon resuscitation altogether if the early stages of the chain have not been carried out in a timely fashion prior to their arrival.
Because of this, considerable effort has been put into educating the public on the need for CPR. In addition, there is increasing use of public access defibrillation. This involves placing automated external defibrillators in public places, and training key staff in these areas how to use them. This allows defibrillation to take place prior to the arrival of emergency services, and has been shown to lead to increased chances of survival. In addition, it has been shown that those who suffer arrests in remote locations have worse outcomes following cardiac arrest [13]: these areas often have first responder schemes, whereby members of the community receive training in resuscitation and are given a defibrillator, and called by the emergency medical services in the case of a collapse in their local area.
[edit] Hospital treatment
Treatment within a hospital usually follows advanced life support protocols. Depending on the diagnosis, various treatments are offered, ranging from defibrillation (for ventricular fibrillation or ventricular tachycardia) to surgery (for cardiac arrest which can be reversed by surgery - see causes of arrest, above) to medication (for asystole and PEA). All will include CPR.
[edit] Peri-arrest period
The period (either before or after) surrounding a cardiac arrest is known as the peri-arrest period. During this period the patient is in a highly unstable condition and must be constantly monitored in order to halt the progression or repeat of a full cardiac arrest. The preventative treatment used during the peri-arrest period depends on the causes of the impending arrest and the likelihood such an event occurring.
[edit] Prognosis
The out-of-hospital cardiac arrest (OHCA) has a worse survival rate (2-8% at discharge and 8-22% on admission), than an in-hospital cardiac arrest (15% at discharge). The principal determining factor is the initially documented rhythm. Patients with VF/VT have 10-15 times more chance of surviving than those suffering from pulseless electrical activity or asystole (as they are sensitive to defibrillation, whereas asystole and PEA are not).[citation needed]
Since mortality in case of OHCA is high, programs were developed to improve survival rate. A study by Bunch et al. showed that, although mortality in case of ventricular fibrillation is high, rapid intervention with a defibrillator increases survival rate to that of patients that did not have a cardiac arrest.[12][14]
Survival is mostly related to the cause of the arrest (see above). In particular, patients who have suffered hypothermia have an increased survival rate, possibly because the cold protects the vital organs from the effects of tissue hypoxia. Survival rates following an arrest induced by toxins is very much dependent on identifying the toxin and administering an appropriate antidote. A patient who has suffered a myocardial infarction due to a blood clot in the left coronary artery has a lower chance of survival as it cuts of the blood supply to most of the left ventricle (the chamber which must pump blood to the whole of the systemic circulation).
Cobbe et al (1996) conducted a study into survival rates from out of hospital cardiac arrest. 14.6% of those who had received resuscitation by ambulance staff survived as far as admission to an acute hospital ward. Of these, 59.3% died during that admission, half of these within the first 24 hours. 46.1% survived to hospital discharge (this is 6.75% of those who had been resuscitated by ambulance staff), however 97.5% suffered a mild to moderate neurological disability, and 2% suffered a major neurological disability. Of those who were successfully discharged from hospital, 70% were still alive 4 years after their discharge.[15]
Ballew (1997) performed a review of 68 earlier studies into prognosis following in-hospital cardiac arrest. They found a survival to discharge rate of 14% (this roughly double the rate for out of hospital arrest found by Cobbe et al (see above)), although there was a wide range (0-28%).[16]
Several high profile organisations (such as St John Ambulance and the British Heart Foundation) have promoted the "Chain of Survival", which is made up of 4 links, as a way to maximise prognosis following arrest:
Early access - Identifying patients at risk of cardiac arrest early is the best way of improving prognosis, as it is often possible to prevent the arrest. Similarly, if the arrest is witnessed there is a much greater chance of survival, as treatment can begin straight away before tissue hypoxia sets in.
Early CPR - CPR is unlikely to revive the patient, but it does buy some time by keeping a (limited) circulation going until it is possible to reverse the arrest, thereby increasing the chances of this reversal being successful, and minimising the risk of cerebral hypoxia (which can lead to neurological impairment following return of circulation).
Early defibrillation - Patients who present with VF/VT can be defibrillated, and the earlier this happens the better, as VF/VT often degenerate into asystole (which is unshockable).
Early hospital care - Many patients suffer further arrests within the first 24 hours of admission, so it is better that they are in hospital where their chances of survival are a little higher.
[edit] Prevention
With positive outcomes following cardiac arrest so unlikely, a great deal of effort has been spent in finding effective strategies to prevent cardiac arrest.
As noted above, one of the prime causes of cardiac arrest outside of hospital is ischemic heart disease. Vast resources have been put into trying to reduce cardiovascular risks across much of the developed world. In particular schemes have been put in place to promote a healthy diet and exercise. For people considered to be particularly at risk of heart disease, measures such as blood pressure control, prescription of cholesterol lowering medications, and other medico-therapeutic interventions, have been widely used. A magnesium deficiency, or lower levels of magnesium, can contribute to heart disease and a healthy diet that contains adequte magnesium may help prevent heart disease.[17] Magnesium can be used to enhance long term treatment, so it may be effective in long term prevention.
Patients in hospital are far less likely to have a cardiac arrest caused of primary cardiac origin, and hence present in asystole or PEA, and have bleak outcomes.[citation needed] Extensive research has shown that patients in general wards often deteriorate for several hours or even days before a cardiac arrest occurs [18][19]. This has been attributed to a lack of knowledge and skill amongst ward based staff, in particular a failure to carry out measurement of the respiratory rate, which is often the major predictor of a deterioration [18]and can often change up to 48 hours prior to a cardiac arrest. In response to this, many hospitals now have increased training for ward based staff. A number of "early warning" systems also exist which aim to quantify the risk which patients are at of deterioration based on their vital signs and thus provide a guide to staff. In addition, specialist staff are being utilised more effectively in order to augment the work already being done at ward level. These include:
Crash teams (also known as code teams) - These are designated staff members who have particular expertise in resuscitation, who are called to the scene of all arrests within the hospital.
Medical emergency teams - These teams respond to all emergencies, with the aim of treating the patient in the acute phase of their illness in order to prevent a cardiac arrest.
Critical care outreach - As well as providing the services of the other two types of team, these teams are also responsible for educating non-specialist staff. In addition, they help to facilitate transfers between intensive care/high dependency units and the general hospital wards. This is particularly important, as many studies have shown that a significant percentage of patients discharged from critical care environments quickly deteriorate and are re-admitted - the outreach team offers support to ward staff to prevent this from happening.
[edit] Implantable cardioverter defibrillators
A technically based intervention to prevent further cardiac arrest episodes is the use of an implantable cardioverter-defibrillator (ICD). This device is implanted in to the patient and can offer a 'pacemaker' effect to the heart as well as acting as an instant defibrillator in the event of arrhythmia. A recent study by Birnie et al. at the University of Ottawa Heart Institute has demonstrated that ICDs are underused in both the United States and Canada.[20] An accompanying editorial by Simpson explores some of the economic, geographic, social and political reasons for this.[21]
[edit] Ethical issues
Cardiopulmonary resuscitation and advanced cardiac life support are not always in a person's best interest. This is particularly true in the case of terminal illnesses when resuscitation will not alter the outcome of the disease. Properly performed CPR often fractures the rib cage, especially in older patients or those suffering from osteoporosis. Defibrillation, especially repeated several times as called for by ACLS protocols, may also cause electrical burns.
Some people with a terminal illness choose to avoid such measures and die peacefully. People with views on the treatment they wish to receive in the event of a cardiac arrest should discuss these views with both their doctor and with their family. A patient may ask their doctor to record a do not resuscitate (DNR) order in the medical record. Alternatively, in many jurisdictions, a person may formally state their wishes in an advance directive or advance health directive.
"Arrested" blood circulation prevents delivery of oxygen to all parts of the body. Cerebral hypoxia, or lack of oxygen supply to the brain, causes victims to lose consciousness and to stop normal breathing. Brain injury is likely if cardiac arrest is untreated for more than 5 minutes,[2] although new treatments such as induced hypothermia have begun to extend this time.[3][4] To improve survival and neurological recovery immediate response is paramount.[5]
Cardiac arrest is a medical emergency that, in certain groups of patients, is potentially reversible if treated early enough (See "Reversible causes" below). When unexpected cardiac arrest leads to death this is called sudden cardiac death (SCD).[1] The primary first-aid treatment for cardiac arrest is cardiopulmonary resuscitation (commonly known as CPR) to provide circulatory support until availability of definitive medical treatment, which will vary dependant on the rhythm the heart is exhibiting, but often requires defibrillation.
Contents[hide]
1 Characteristics and diagnosis
2 Causes of cardiac arrest
2.1 Reversible causes
2.1.1 H's
2.1.2 T's
3 Treatment
3.1 Out of hospital arrest
3.2 Hospital treatment
3.3 Peri-arrest period
4 Prognosis
5 Prevention
6 Implantable cardioverter defibrillators
7 Ethical issues
8 See also
9 References
10 External links
//
[edit] Characteristics and diagnosis
Cardiac arrest is an abrupt cessation of pump function (evidenced by absence of a palpable pulse) of the heart that with prompt intervention could be reversed, but without it will lead to death.[1]
Due to inadequate cerebral perfusion, the patient will be unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest (as opposed to respiratory arrest, which shares many of the same features) is lack of circulation, however there are a number of ways of determining this.
In many cases, lack of carotid pulse is the gold standard for diagnosing cardiac arrest, but lack of a pulse (particularly in the peripheral pulses) may be a result of other conditions (e.g. shock), or simply an error on the part of the rescuer. Studies have shown that rescuers often make a mistake when checking the carotid pulse in an emergency, whether they are healthcare professionals[6][7] or lay persons.[8]
Owing to the inaccuracy in this method of diagnosis, some bodies such as the European Resuscitation Council (ERC) have de-emphasised its importance. The Resuscitation Council (UK), in line with the ERC's recommendations and those of the American Heart Association,[9] have suggested that the technique should be used only by healthcare professionals with specific training and expertise, and even then that it should be viewed in conjunction with other indicators such as agonal respiration.[10]
Various other methods for detecting circulation have been proposed. Guidelines following the 2000 International Liaison Committee on Resusciation (ILCOR) recommendations were for rescuers to look for "signs of circulation", but not specifically the pulse [9]. These signs included coughing, gasping, colour, twitching and movement.[11] However, in face of evidence that these guidelines were ineffective, the current recommendation of ILCOR is that cardiac arrest should be diagnosed in all casualties who are unconscious and not breathing normally.[9]
Following initial diagnosis of cardiac arrest, healthcare professionals further categorise the diagnosis based on the ECG/EKG rhythm. There are 4 rhythms which result in a cardiac arrest. Ventricular fibrillation (VF/VFib) and pulseless ventricular tachycardia (VT) are both responsive to a defibrillator and so are colloquially referred to as "shockable" rhythms, whereas asystole and pulseless electrical activity (PEA) are non-shockable. The nature of the presenting hearth rhythm suggests different causes and treatment, and is used to guide the rescuer as to what treatment may be appropriate[10] (see Advanced life support and Advanced cardiac life support, as well as the causes of arrest below).
[edit] Causes of cardiac arrest
Cardiac arrest is synonymous with Clinical death. All disease processes leading to death have a period of (potentially) reversible cardiac arrest: the causes of arrest are, therefore, numerous. However, many of these conditions, rather than causing an arrest themselves, promote one of the "Reversible causes" (see below), which then triggers the arrest (e.g. choking leads to hypoxia which in turn leads to an arrest). In some cases, the underlying mechanism cannot be overcome, leading to an unsuccessful resuscitation.
Among adults, ischemic heart disease is the predominant cause of arrest.[12] At autopsy 30% of victims show signs of recent myocardial infarction[citation needed]. Other cardiac conditions potentially leading to arrest include structural abnormalities, arrhythmias and cardiomyopathies. Non-cardiac causes include infections, overdoses, trauma and cancer, in addition to many others.
[edit] Reversible causes
Cardiopulmonary resuscitation (CPR), including adjunctive measures such as defibrillation, intubation and drug administration, is the standard of care for initial treatment of cardiac arrest. However, most cardiac arrests occur for a reason, and unless that reason can be found and overcome, CPR is often ineffective, or if it does result in a return of spontaneous circulation, this is short lived. [10]. As highlighted above, a variety of disease processes can lead to a cardiac arrest, however they usually boil down to one or more of the "Hs and Ts" (see below).
[edit] H's
Hypovolemia - A lack of circulating body fluids, principally blood volume. This is usually (though not exclusively) caused by some form of bleeding, anaphylaxis, or pregnancy with gravid uterus. Peri-arrest treatment includes giving IV fluids and blood transfusions, and controlling the source of any bleeding - by direct pressure for external bleeding, or emergency surgical techniques such as esophagogastroduodenoscopy (i.e. esophageal varices) and thoracotomy for internal bleeding.
Hypoxia - A lack of oxygen to the heart, brain and other vital organs. This can be identified through a careful assessment of breath sounds and tuble placement. Treatment may include providing oxygen, proper ventilation, and good CPR technique.
Hydrogen ions (Acidosis) - An abnormal pH in the body as a result of shock, diabetic ketoacidosis, renal failure, or tricyclic antidepressant overdose. This can be treated with proper ventilation, good CPR technique, and buffers like sodium bicarbonate.
Hyperkalemia or Hypokalemia - The most life threatening electrolyte derangement is hyperkalemia (too much potassium). The classic presentation is the chronic renal failure patient who has missed a dialysis appointment and presents with weakness, nausea, and broad QRS complexes on the electrocardiogram. The most important initial therapy is the administration of calcium, either with calcium gluconate or calcium chloride. Other therapies may include nebulized albuterol, sodium bicarbonate, glucose, and insulin. The diagnosis of hypokalemia (not enough potassium) can be suspected when there is a history of diarrhoea or malnutrition. Loop diuretics may also contribute. The electrocardiogram may show depressed T waves and prominent U waves. Hypokalemia is an important cause of acquired long QT syndrome, and may predispose the patient to torsades de pointes. Digitalis use may increase the risk that hypokalemia will produce life threatening arrhythmias.
Hypothermia - A low core body temperature, defined clinically as a temperature of less than 35 degrees Celsius. The patient is re-warmed either by using a cardiac bypass or by irrigation of the body cavities (such as thorax, peritoneum, bladder) with warm fluids; or warmed IV fluids. CPR only is given until the core body temperature reached 30 degrees Celsius, as defibrillation is ineffective at lower temperatures. Patients have been known to be successfully resuscitated after periods of hours in hypothermia and cardiac arrest, and this has given rise to the often-quoted medical truism, "You're not dead until you're warm and dead."
Hypoglycemia or Hyperglycemia - Low blood glucose from insulin reactions, DKA, nonketotic hyperosmolar coma. This condition can be suspected when the patient is known to be a diabetic. The treatment may include fluids, potassium, glucose (for hypoglycemia), and insulin (for hyperglycemia).
[edit] T's
Tablets or Toxins - Tricyclic antidepressants, phenothiazines, beta blockers, calcium channel blockers, cocaine, digoxin, aspirin, acetominophen. This may be evidenced by items found on or around the patient, the patient's medical history (i.e. drug abuse, medication) taken from family and friends, checking the medical records to make sure no interacting drugs were prescribed, or sending blood and urine samples to the toxicology lab for report. Treatment may include specific antidotes, fluids for volume expansion, vasopressors, sodium bicarbonate (for tricyclic antidepressants), glucagon or calcium (for calcium channel blockers), benzodiazepines (for cocaine), or cardiopulmonary bypass.
Cardiac Tamponade - Blood or other fluids building up in the pericardium can put pressure on the heart so that it is not able to beat. This condition can be recognized by the presence of a narrowing pulse pressure, muffled heart sounds, distended neck veins, electrical alternans on the electrocardiogram, or echocardiogram. This is treated in an emergency by inserting a needle into the pericardium to drain the fluid (pericardiocentesis), or if the fluid is too thick then an emergency thoracotomy is performed to cut the pericardium and release the fluid.
Tension pneumothorax - The build up of air into one of the pleural cavities, which causes a mediastinal shift. When this happens, the great vessels (particularly the superior vena cava) become kinked, which limits blood return to the heart. The condition can be recognized by severe air hunger, hypoxia, jugular venous distension, hyperressonance to percussion on the effected side, and a tracheal shift away from the effected side. The tracheal shift often requires a chest x-ray to appreciate. This is relieved in an emergency by a needle thoracotomy (inserting a needle catheter) into the 2nd intercostal space at the mid-clavicular line, which relieves the pressure in the pleural cavity.
Thrombosis (Myocardial infarction) - If the patient can be successfully resuscitated, there is a chance that the myocardial infarction can be treated, either with thrombolytic therapy or percutaneous coronary intervention.
Thromboembolism (Pulmonary embolism) - Usually diagnosed at autopsy. Patients in asystole or pulseless electrical activity have a poor prognosis. If this can be detected early, the patient may receive dopamine, heparin, and thrombolytics.
Trauma (Hypovolemia) - Reduced blood volume from acute injury or primary damage to the heart or great vessels. Cardiac arrest secondary to trauma, particularly blunt trauma, has a very poor prognosis.
Checking respiration.
Checking carotid pulse.
Insulfation mouth-to-mouth.
[edit] Treatment
[edit] Out of hospital arrest
Most out-of-hospital cardiac arrests occur following a myocardial infarction (heart attack), and present initially with a heart rhythm of ventricular fibrillation. The patient is therefore likely to be responsive to defibrillation, and this has become the focus of pre-hospital interventions. Several organisations promote the idea of a "chain of survival", of which defibrillation is a key step. The links are:
Early recognition - If possible, recognition of illness before the patient develops a cardiac arrest will allow the rescuer to prevent its occurrence. Early recognition that a cardiac arrest has occurred is key to survival - for every minute a patient is in cardiac arrest, their chances of survival drop by roughly 10% [10]
Early CPR - This buys time by keeping vital organs perfused with oxygen whilst waiting for equipment and trained personnel to reverse the arrest. In particular, by keeping the brain supplied with oxygenated blood, chances of neurological damage are decreased.
Early defibrillation - This is the only effective for ventricular fibrillation, and also has benefit in ventricular tachycardia[10]. If defibrillation is delayed, then the rhythm is likely to degenerate into asystole, for which outcomes are markedly worse.
Early post-resuscitation care - Treatment and rehabillitation in a hospital by specialist staff helps to prevent further complications, attempts to fully reverse the underlying cause, and promotes quality of life.
If one or more links in the chain are missing or delayed, then the chances of survival drop significantly. In particular, bystander CPR is an important indicator of survival: if it has not been carried out, then resuscitation is associated with very poor results. Paramedics in some jurisdictions are authorised to abandon resuscitation altogether if the early stages of the chain have not been carried out in a timely fashion prior to their arrival.
Because of this, considerable effort has been put into educating the public on the need for CPR. In addition, there is increasing use of public access defibrillation. This involves placing automated external defibrillators in public places, and training key staff in these areas how to use them. This allows defibrillation to take place prior to the arrival of emergency services, and has been shown to lead to increased chances of survival. In addition, it has been shown that those who suffer arrests in remote locations have worse outcomes following cardiac arrest [13]: these areas often have first responder schemes, whereby members of the community receive training in resuscitation and are given a defibrillator, and called by the emergency medical services in the case of a collapse in their local area.
[edit] Hospital treatment
Treatment within a hospital usually follows advanced life support protocols. Depending on the diagnosis, various treatments are offered, ranging from defibrillation (for ventricular fibrillation or ventricular tachycardia) to surgery (for cardiac arrest which can be reversed by surgery - see causes of arrest, above) to medication (for asystole and PEA). All will include CPR.
[edit] Peri-arrest period
The period (either before or after) surrounding a cardiac arrest is known as the peri-arrest period. During this period the patient is in a highly unstable condition and must be constantly monitored in order to halt the progression or repeat of a full cardiac arrest. The preventative treatment used during the peri-arrest period depends on the causes of the impending arrest and the likelihood such an event occurring.
[edit] Prognosis
The out-of-hospital cardiac arrest (OHCA) has a worse survival rate (2-8% at discharge and 8-22% on admission), than an in-hospital cardiac arrest (15% at discharge). The principal determining factor is the initially documented rhythm. Patients with VF/VT have 10-15 times more chance of surviving than those suffering from pulseless electrical activity or asystole (as they are sensitive to defibrillation, whereas asystole and PEA are not).[citation needed]
Since mortality in case of OHCA is high, programs were developed to improve survival rate. A study by Bunch et al. showed that, although mortality in case of ventricular fibrillation is high, rapid intervention with a defibrillator increases survival rate to that of patients that did not have a cardiac arrest.[12][14]
Survival is mostly related to the cause of the arrest (see above). In particular, patients who have suffered hypothermia have an increased survival rate, possibly because the cold protects the vital organs from the effects of tissue hypoxia. Survival rates following an arrest induced by toxins is very much dependent on identifying the toxin and administering an appropriate antidote. A patient who has suffered a myocardial infarction due to a blood clot in the left coronary artery has a lower chance of survival as it cuts of the blood supply to most of the left ventricle (the chamber which must pump blood to the whole of the systemic circulation).
Cobbe et al (1996) conducted a study into survival rates from out of hospital cardiac arrest. 14.6% of those who had received resuscitation by ambulance staff survived as far as admission to an acute hospital ward. Of these, 59.3% died during that admission, half of these within the first 24 hours. 46.1% survived to hospital discharge (this is 6.75% of those who had been resuscitated by ambulance staff), however 97.5% suffered a mild to moderate neurological disability, and 2% suffered a major neurological disability. Of those who were successfully discharged from hospital, 70% were still alive 4 years after their discharge.[15]
Ballew (1997) performed a review of 68 earlier studies into prognosis following in-hospital cardiac arrest. They found a survival to discharge rate of 14% (this roughly double the rate for out of hospital arrest found by Cobbe et al (see above)), although there was a wide range (0-28%).[16]
Several high profile organisations (such as St John Ambulance and the British Heart Foundation) have promoted the "Chain of Survival", which is made up of 4 links, as a way to maximise prognosis following arrest:
Early access - Identifying patients at risk of cardiac arrest early is the best way of improving prognosis, as it is often possible to prevent the arrest. Similarly, if the arrest is witnessed there is a much greater chance of survival, as treatment can begin straight away before tissue hypoxia sets in.
Early CPR - CPR is unlikely to revive the patient, but it does buy some time by keeping a (limited) circulation going until it is possible to reverse the arrest, thereby increasing the chances of this reversal being successful, and minimising the risk of cerebral hypoxia (which can lead to neurological impairment following return of circulation).
Early defibrillation - Patients who present with VF/VT can be defibrillated, and the earlier this happens the better, as VF/VT often degenerate into asystole (which is unshockable).
Early hospital care - Many patients suffer further arrests within the first 24 hours of admission, so it is better that they are in hospital where their chances of survival are a little higher.
[edit] Prevention
With positive outcomes following cardiac arrest so unlikely, a great deal of effort has been spent in finding effective strategies to prevent cardiac arrest.
As noted above, one of the prime causes of cardiac arrest outside of hospital is ischemic heart disease. Vast resources have been put into trying to reduce cardiovascular risks across much of the developed world. In particular schemes have been put in place to promote a healthy diet and exercise. For people considered to be particularly at risk of heart disease, measures such as blood pressure control, prescription of cholesterol lowering medications, and other medico-therapeutic interventions, have been widely used. A magnesium deficiency, or lower levels of magnesium, can contribute to heart disease and a healthy diet that contains adequte magnesium may help prevent heart disease.[17] Magnesium can be used to enhance long term treatment, so it may be effective in long term prevention.
Patients in hospital are far less likely to have a cardiac arrest caused of primary cardiac origin, and hence present in asystole or PEA, and have bleak outcomes.[citation needed] Extensive research has shown that patients in general wards often deteriorate for several hours or even days before a cardiac arrest occurs [18][19]. This has been attributed to a lack of knowledge and skill amongst ward based staff, in particular a failure to carry out measurement of the respiratory rate, which is often the major predictor of a deterioration [18]and can often change up to 48 hours prior to a cardiac arrest. In response to this, many hospitals now have increased training for ward based staff. A number of "early warning" systems also exist which aim to quantify the risk which patients are at of deterioration based on their vital signs and thus provide a guide to staff. In addition, specialist staff are being utilised more effectively in order to augment the work already being done at ward level. These include:
Crash teams (also known as code teams) - These are designated staff members who have particular expertise in resuscitation, who are called to the scene of all arrests within the hospital.
Medical emergency teams - These teams respond to all emergencies, with the aim of treating the patient in the acute phase of their illness in order to prevent a cardiac arrest.
Critical care outreach - As well as providing the services of the other two types of team, these teams are also responsible for educating non-specialist staff. In addition, they help to facilitate transfers between intensive care/high dependency units and the general hospital wards. This is particularly important, as many studies have shown that a significant percentage of patients discharged from critical care environments quickly deteriorate and are re-admitted - the outreach team offers support to ward staff to prevent this from happening.
[edit] Implantable cardioverter defibrillators
A technically based intervention to prevent further cardiac arrest episodes is the use of an implantable cardioverter-defibrillator (ICD). This device is implanted in to the patient and can offer a 'pacemaker' effect to the heart as well as acting as an instant defibrillator in the event of arrhythmia. A recent study by Birnie et al. at the University of Ottawa Heart Institute has demonstrated that ICDs are underused in both the United States and Canada.[20] An accompanying editorial by Simpson explores some of the economic, geographic, social and political reasons for this.[21]
[edit] Ethical issues
Cardiopulmonary resuscitation and advanced cardiac life support are not always in a person's best interest. This is particularly true in the case of terminal illnesses when resuscitation will not alter the outcome of the disease. Properly performed CPR often fractures the rib cage, especially in older patients or those suffering from osteoporosis. Defibrillation, especially repeated several times as called for by ACLS protocols, may also cause electrical burns.
Some people with a terminal illness choose to avoid such measures and die peacefully. People with views on the treatment they wish to receive in the event of a cardiac arrest should discuss these views with both their doctor and with their family. A patient may ask their doctor to record a do not resuscitate (DNR) order in the medical record. Alternatively, in many jurisdictions, a person may formally state their wishes in an advance directive or advance health directive.
acute pericarditis
Acute pericarditis is an inflammation of the sac surrounding the heart --- the pericardium --- usually lasting < 6 weeks. It is by far the most common condition affecting the pericardium.
Contents[hide]
1 Causes
2 Symptoms and Signs
2.1 Complications
3 Diagnostic tests, imaging
4 Treatment
5 References
//
[edit] Causes
According to a recent article[1], the most common causes of acute pericarditis includes:
(35%) Neoplastic
(23%) Autoimmune
(21%) Viral - adenovirus, enterovirus, cytomegalovirus, influenza virus, hepatitis B virus, and herpes simplex virus, etc
( 6%) Bacterial (other than tuberculosis)
( 6%) Uremia
( 4%) Tuberculosis
( 4%) Idiopathic
(remaining) trauma, drugs, post-AMI, myocarditis, dissecting aortic aneurysm, radiation
[edit] Symptoms and Signs
Chest pain is one of the common symptoms of acute pericarditis. It is usually of sudden onset, occurring in the anterior chest and may be pleuritic in nature --- that is, sharp and worsens with inspiration, due to concomitant pleural inflammation. The pain may be alleviated with sitting up and leaning forward while worsened with lying down, and also may radiate to the back, to one or both trapezius ridges. However, the pain can also be dull and steady, resembling the chest pain in an acute myocardial infarction. As with any chest pain, other causes must also be ruled out, such as GERD, pulmonary embolism, muscular pain, etc.
Main article: chest pain
Pericardial rub is a very specific sign of acute pericarditis, meaning the presence of this sign invariably indicates presence of disease. However, absence of this sign does not rule out disease. This rub can be best heard by the diaphragm of the stethoscope at the left sternal border arising as a squeaky or scratching sound, resembling the sound of leather rubbing against each other. This sound should be distinguished from the sound of a murmur, which is similar but sounds more like a "swish" sound than a scratching sound. The pericardial rub is said to be generated from the friction generated by the two inflamed layers of the pericardium; however, even a large pericardial effusion does not necessarily prevent a rub. The rub is best heard during the maximal movement of the heart within the pericardial sac, namely, during atrial systole, ventricular systole, and the filling phase of early ventricular diastole.
Fever may be present since this is an inflammatory process.
[edit] Complications
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. This condition is fatal if not treated promptly.
[edit] Diagnostic tests, imaging
Inflammatory markers. A CBC may show an elevated white count and a serum C-reactive protein may be elevated.
Molecular markers. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB)[2][3] and cardiac troponin I (cTnI)[4][5], both of which are also markers for myocardial injury. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances is related to inflammation of the myocardium. Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 µg/L[5]. Coronary angiography in those patients should indicated normal vascular perfusion. The elevation of these biomarkers are typically transient and should return to normal within a week. Persistence may indicated myopericarditis.
Electrocardiogram (EKG). EKG changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes[6][2]
stage 1 -- diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury.
stage 2 -- normalization of ST and PR deviations
stage 3 -- diffuse T wave inversions (may not be present in all patients)
stage 4 -- EKG becomes normal OR T waves may be indefinitely inverted
Because the most common cause of ST elevation is an acute myocardial infarction, and since acute pericarditis can also be a short term complication after an acute myocardial infarction, steps must be taken to differentiate the two EKG readings.
Rarely, electrical alternans may be seen, depending on the size of the effusion.
Chest X-ray. Usually normal in acute pericarditis, but can reveal cardiomegaly (enlarged heart) if the pericardial effusion is more than 200 mL. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.
Echocardiogram. Usually normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis.
[edit] Treatment
Patients with uncomplicated acute pericarditis can generally be treated and followed up in an outpatient clinic. However, those with high risk factors for developing complications (see above) will need to be admitted to an inpatient service, most likely an ICU setting. High risk patients include:[7]
subacute onset
high fever (> 100.4 F) and leukocytosis
development of cardiac tamponade
large pericardial effusion (echo-free space > 20 mm) resistant to NSAID treatment
immunocompromised
history of oral anticoagulation therapy
acute trauma
failure to respond to seven days of NSAID treatment
Pericardiocentesis is a procedure whereby the fluid in a pericardial effusion is removed through a needle. It is performed under the following conditions:[8]
presence of moderate or severe cardiac tamponade
diagnostic purpose for suspected purulent, tuberculosis, or neoplastic pericarditis
persistent symptomatic pericardial effusion
NSAIDs in viral or idiopathic pericarditis. In patients with underlying causes other than viral, the specific etiology should be treated. With idiopathic or viral pericarditis, NSAID is the mainstay treatment. Goal of therapy is to reduce pain and inflammation. The course of the disease may not be affected. The preferred NSAID is ibuprofen because of rare side effects, better effect on coronary flow, and larger dose range.[8] Depending on severity, dosing is between 300-800 mg every 6-8 hours for days or weeks as needed. An alternative protocol is aspirin 800 mg every 6-8 hours.[7] Dose tapering of NSAIDs may be needed. In pericarditis following acute myocardial infarction, NSAIDs other than aspirin should be avoided since they can impair scar formation. As with all NSAID use, GI protection should be engaged. Failure to respond to NSAIDs within one week (indicated by persistence of fever, worsening of condition, new pericardial effusion, or continuing chest pain) likely indicates that a cause other than viral or idiopathic is in process.
Colchicine can be used alone or in conjunction with NSAIDs in prevention of recurrent pericarditis and treatment of recurrent pericarditis. For patients with a first episode of acute idiopathic or viral pericarditis, they should be treated with an NSAID plus colchicine 1-2 mg on first day followed by 0.5 daily or BID for three months. [9][10][11]
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.
Contents[hide]
1 Causes
2 Symptoms and Signs
2.1 Complications
3 Diagnostic tests, imaging
4 Treatment
5 References
//
[edit] Causes
According to a recent article[1], the most common causes of acute pericarditis includes:
(35%) Neoplastic
(23%) Autoimmune
(21%) Viral - adenovirus, enterovirus, cytomegalovirus, influenza virus, hepatitis B virus, and herpes simplex virus, etc
( 6%) Bacterial (other than tuberculosis)
( 6%) Uremia
( 4%) Tuberculosis
( 4%) Idiopathic
(remaining) trauma, drugs, post-AMI, myocarditis, dissecting aortic aneurysm, radiation
[edit] Symptoms and Signs
Chest pain is one of the common symptoms of acute pericarditis. It is usually of sudden onset, occurring in the anterior chest and may be pleuritic in nature --- that is, sharp and worsens with inspiration, due to concomitant pleural inflammation. The pain may be alleviated with sitting up and leaning forward while worsened with lying down, and also may radiate to the back, to one or both trapezius ridges. However, the pain can also be dull and steady, resembling the chest pain in an acute myocardial infarction. As with any chest pain, other causes must also be ruled out, such as GERD, pulmonary embolism, muscular pain, etc.
Main article: chest pain
Pericardial rub is a very specific sign of acute pericarditis, meaning the presence of this sign invariably indicates presence of disease. However, absence of this sign does not rule out disease. This rub can be best heard by the diaphragm of the stethoscope at the left sternal border arising as a squeaky or scratching sound, resembling the sound of leather rubbing against each other. This sound should be distinguished from the sound of a murmur, which is similar but sounds more like a "swish" sound than a scratching sound. The pericardial rub is said to be generated from the friction generated by the two inflamed layers of the pericardium; however, even a large pericardial effusion does not necessarily prevent a rub. The rub is best heard during the maximal movement of the heart within the pericardial sac, namely, during atrial systole, ventricular systole, and the filling phase of early ventricular diastole.
Fever may be present since this is an inflammatory process.
[edit] Complications
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. This condition is fatal if not treated promptly.
[edit] Diagnostic tests, imaging
Inflammatory markers. A CBC may show an elevated white count and a serum C-reactive protein may be elevated.
Molecular markers. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB)[2][3] and cardiac troponin I (cTnI)[4][5], both of which are also markers for myocardial injury. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances is related to inflammation of the myocardium. Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 µg/L[5]. Coronary angiography in those patients should indicated normal vascular perfusion. The elevation of these biomarkers are typically transient and should return to normal within a week. Persistence may indicated myopericarditis.
Electrocardiogram (EKG). EKG changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes[6][2]
stage 1 -- diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury.
stage 2 -- normalization of ST and PR deviations
stage 3 -- diffuse T wave inversions (may not be present in all patients)
stage 4 -- EKG becomes normal OR T waves may be indefinitely inverted
Because the most common cause of ST elevation is an acute myocardial infarction, and since acute pericarditis can also be a short term complication after an acute myocardial infarction, steps must be taken to differentiate the two EKG readings.
Rarely, electrical alternans may be seen, depending on the size of the effusion.
Chest X-ray. Usually normal in acute pericarditis, but can reveal cardiomegaly (enlarged heart) if the pericardial effusion is more than 200 mL. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.
Echocardiogram. Usually normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis.
[edit] Treatment
Patients with uncomplicated acute pericarditis can generally be treated and followed up in an outpatient clinic. However, those with high risk factors for developing complications (see above) will need to be admitted to an inpatient service, most likely an ICU setting. High risk patients include:[7]
subacute onset
high fever (> 100.4 F) and leukocytosis
development of cardiac tamponade
large pericardial effusion (echo-free space > 20 mm) resistant to NSAID treatment
immunocompromised
history of oral anticoagulation therapy
acute trauma
failure to respond to seven days of NSAID treatment
Pericardiocentesis is a procedure whereby the fluid in a pericardial effusion is removed through a needle. It is performed under the following conditions:[8]
presence of moderate or severe cardiac tamponade
diagnostic purpose for suspected purulent, tuberculosis, or neoplastic pericarditis
persistent symptomatic pericardial effusion
NSAIDs in viral or idiopathic pericarditis. In patients with underlying causes other than viral, the specific etiology should be treated. With idiopathic or viral pericarditis, NSAID is the mainstay treatment. Goal of therapy is to reduce pain and inflammation. The course of the disease may not be affected. The preferred NSAID is ibuprofen because of rare side effects, better effect on coronary flow, and larger dose range.[8] Depending on severity, dosing is between 300-800 mg every 6-8 hours for days or weeks as needed. An alternative protocol is aspirin 800 mg every 6-8 hours.[7] Dose tapering of NSAIDs may be needed. In pericarditis following acute myocardial infarction, NSAIDs other than aspirin should be avoided since they can impair scar formation. As with all NSAID use, GI protection should be engaged. Failure to respond to NSAIDs within one week (indicated by persistence of fever, worsening of condition, new pericardial effusion, or continuing chest pain) likely indicates that a cause other than viral or idiopathic is in process.
Colchicine can be used alone or in conjunction with NSAIDs in prevention of recurrent pericarditis and treatment of recurrent pericarditis. For patients with a first episode of acute idiopathic or viral pericarditis, they should be treated with an NSAID plus colchicine 1-2 mg on first day followed by 0.5 daily or BID for three months. [9][10][11]
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.
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