Hypoperfusion

FIGURE 2.6 Dynamic susceptibility contrast imaging. Axial images of the brain are acquired repeatedly, in this case every 1.5 seconds. As a bolus of intravenously injected contrast material enters the brain, first arteries, then brain parenchyma, and finally veins demonstrate a transient loss of signal intensity. In this acute stroke patient, hypoperfusion of the left middle cerebral artery territory results in delayed arrival of the contrast bolus and prolonged stasis of contrast within the tissue. 

With modest impairment of blood flow, this mechanism allows for preservation of oxidative metabolism without alteration in electrical function. However, when CPP and therefore CBF are sufficiently low, OEF reaches a maximum and cannot increase further. Brain tissue ceases to function electrically, resulting in a neurologic deficit. Microvascular collapse occurs, and CBV falls. If the oxygen supply falls low enough, the tissue dies. Of critical clinical importance is the observation that the amount of time it takes for tissue to suffer irreversible damage is inversely related to the severity of the ischemic insult. Tissue that is completely deprived of blood will die within a few minutes, but less severely hypoperfused tissue may survive for many hours, and may be saved by timely thrombolysis that restores perfusion, or perhaps by another therapeutic intervention. 

Dissection of the internal carotid and vertebral arteries is a common cause of stroke, particularly in young patients. Although many occur due to trauma, it is estimated that over half occur spontaneously. The mechanism of stroke following arterial dissection is either by artery-to-artery embolism, by thrombosis in situ, or by dissection-induced lumenal stenosis with secondary cerebral hypoperfusion and low-flow watershed infarction. Occasionally, dissection may lead to the formation of a pseudoaneurysm as a source of thrombus formation. Vertebrobasilar dissections that extend intracranially have a higher risk of rupture leading to subarachnoid hemorrhage (SAH). ° ... 

Schurer, L., Grogaard, B., Gerdin, B. and Arfors, K.-E. (1990). Effects of neutrophil depletion and superoxide dismutase on postischemic hypoperfusion of rat brain. Adv. Neurol. 52, 57-62. 

Hepatic reperfusion injury is not a phenomenon connected solely to liver transplantation but also to situations of prolonged hypoperfusion of the host s own liver. Examples of this occurrence are hypovolemic shock and acute cardiovascular injur) (heart attack). As a result of such cessation and then reintroduction of blood flow, the liver is damaged such that centrilobular necrosis occurs and elevated levels of liver enzymes in the serum can be detected. Particularly because of the involvement of other organs, the interpretation of the role of free radicals in ischaemic hepatitis from this clinical data is very difficult. The involvement of free radicals in the overall phenomenon of hypovolemic shock has been discussed recently by Redl et al. (1993). More specifically. Poll (1993) has reported preliminary data on markers of free-radical production during ischaemic hepatitis. These markers mostly concerned indices of lipid peroxidation in the serum and also in the erythrocytes of affected subjects, and a correlation was seen with the extent of liver injury. The mechanisms of free-radical damage in this model will be difficult to determine in the clinical setting, but the similarity to the situation with transplanted liver surest that the above discussion of the role of XO activation, Kupffer cell activation and induction of an acute inflammatory response would be also relevant here. It will be important to establish whether oxidative stress is important in the pathogenesis of ischaemic hepatitis and in the problems of liver transplantation discussed above, since it would surest that antioxidant therapy could be of real benefit. 

Bradycardia (heart rate <60 bpm), systolic blood pressure <100 mmHg, severe left ventricular dysfunction with pulmonary edema, second- or third-degree heart block, PR interval >0.24 s, evidence of hypoperfusion, active asthma... 

Potentially useful in resuscitated patients with persistent evidence of systemic or organ hypoperfusion... 

Heart failure is a clinical syndrome characterized by a history of specific signs and symptoms related to congestion and hypoperfusion. As HF can occur in the presence or absence of fluid overload, the term heart failure is preferred over the former term congestive heart failure. Heart failure results from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.1 Many disorders such as those of the pericardium, epicardium, endocardium, or great vessels may lead to HF, but most patients develop symptoms due to impairment in left ventricular (LV) myocardial function. 

Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the central nervous system (CNS) is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. This results from several factors, including loss of appetite, malabsorption due to gastrointestinal edema, elevated metabolic rate, and elevated levels of proinflammatory cytokines. 

Serum creatinine May be increased owing to hypoperfusion preexisting renal dysfunction can contribute to volume overload. 

Patients can experience a variety of symptoms related to buildup of fluid in the lungs. Dyspnea, or shortness of breath, can result from pulmonary congestion or systemic hypoperfusion due to LVF. Exertional dyspnea occurs when patients describe breathlessness induced by physical activity or a lower level of activity than previously known to cause breathlessness. Patients often state that activities such as stair climbing, carrying groceries, or walking a particular distance cause shortness of breath. Severity of HF is inversely proportional to the amount of activity required to produce dyspnea. In severe HF, dyspnea will be present even at rest. 

Hypoperfusion leads to increased mortality, elevating death rates four-fold compared to those who are adequately perfused... 

Pathophysiology Muscle cramps can occur with up to 20% of dialysis sessions.48 The cause is often related to excessive ultrafiltration, which causes hypoperfusion of the muscles. Other contributing factors to the development of muscle cramps include hypotension and electrolyte and acid-base imbalances that occur during hemodialysis sessions. 

Sepsis is a continuum of physiologic stages characterized by infection, systemic inflammation, and hypoperfusion with widespread tissue injury.1 The American College of Chest Physicians and the Society of Critical Care Medicine developed definitions to utilize for sepsis (Table 79—l).2 They provide physiologic parameters categorizing patients as having bacteremia, infection, systemic inflammatory response syndrome (SIRS), sepsis, severe sepsis, septic shock, or multiple-organ-dysfunction syndrome (MODS).2 Standardized definitions have been developed for infections in critically ill patients.3... 

Sepsis The systemic inflammatory response syndrome and documented infection (culture or Gram stain of blood, sputum, urine, or normally sterile body fluid positive for pathogenic microorganisms Severe sepsis Sepsis associated with organ dysfunction, hypoperfusion, or hypotension (systolic blood pressure less than 90 mm Hg). Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria, or acute alteration in mental status. 

Treatment for sepsis focuses on infection, inflammation, hypoperfusion, and widespread tissue injury. Septic patients may require... 

An elevated serum lactate concentration may be an early marker for tissue hypoperfusion. 

Early goal-directed resuscitation decreases 28-day mortality in septic patients. The treatment goals of sepsis-induced hypoperfusion (hypotension or lactic acidosis) during the first 6 hours include 24,27-29... 

Gansler DA, Harris GJ, Oscar-Berman M, Streeter C, Lewis RF, Ahmed I and Achong D (2000). Hypoperfusion of inferior frontal brain regions in abstinent alcoholics A pilot SPECT study. Journal of Studies on Alcohol, 61, 32-37. 

Brain SPECT of AD patients typically shows bilateral posterior temporal and parietal hypoperfusion. The areas of reduced perfusion are secondary to the reduced brain metabolism in areas of neuronal depletion. This scintigraphic pattern of bilateral decreased posterior parietal-temporal perfusion has a predictive value of greater than 80% for AD [63], The sensitivity and specificity of brain SPECT for the diagnosis of AD are 86% and 96%, respectively [127],... 

The term decompensated HF refers to patients with new or worsening signs or symptoms that are usually caused by volume overload and/or hypoperfusion and lead to the need for additional medical care, such as emergency department visits and hospitalizations. 

Sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria, or acute alteration in mental status. 

Immediate initial resuscitation of a patient in severe sepsis or sepsis-induced tissue B hypoperfusion should be instituted to achieve central venous pressure 8-12 mm Hg mean arterial pressure >65 mm Hg urine output >0.5 mt/kj hour, central venous or mixed venous oxygen saturation >70%... 

Isolated renal hypoperfusion Bilateral renal artery stenosis (unilateral renal artery stenosis in solitary kidney) Emboli Cholesterol Thrombotic Medications Cyclosporine Angiotensin-converting enzyme inhibitors Nonsteroidal antiinflammatory drugs Radiocontrast media... 

White matter hyperintesities in magnetic resonance imaging (MRI) scans reflecting cerebrovascnlar damage and brain hypoperfusion are more severe in ACE-D/D subjects (638). Association of ACE-D/D with vascular dementia has also been reported (615,639), although in some stndies no association of ACE-I/D indel variant with vascnlar dementia was fonnd (640). 

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