Hypertension is one of the most common worldwide diseases afflicting humans. Because of the associated morbidity and mortality and the cost to society, hypertension is an important public health challenge. Over the past several decades, extensive research, widespread patient education, and a concerted effort on the part of health care professionals have led to decreased mortality and morbidity rates from the multiple organ damage arising from years of untreated hypertension.
Defining abnormally high blood pressure is extremely difficult and arbitrary. Furthermore, the relationship between systemic arterial pressure and morbidity appears to be quantitative rather than qualitative. A level for high blood pressure must be agreed upon in clinical practice for screening patients with hypertension and for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about aggressiveness of treatment or therapeutic interventions.
Based on recommendations of the Seventh Report of the Joint National Committee of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII), the classification of blood pressure (expressed in mm Hg) for adults aged 18 years or older is as follows:
N Normal - Systolic lower than 120, diastolic lower than 80
N Prehypertension - Systolic 120-139, diastolic 80-99
N Stage 1 - Systolic 140-159, diastolic 90-99
N Stage 2 - Systolic equal to or more than 160, diastolic equal to or more than 100
Non-modifiable risk factors for hypertension includes family history, age in which primary hypertension typically appears between ages of 30-50 years, gender in which overall incidence is higher in men than in women until about the age 55 years and ethnicity where blacks are at high risks.
On the other hand, modifiable factors includes diabetes, stress, obesity, excessive sodium consumption and substance abuse such as cigarette smoking, heavy alcohol consumption and some illicit drugs are risks for having hypertension.
This is based on the average of 2 or more readings taken at each of 2 or more visits after initial screening. Normal blood pressure with respect to cardiovascular risk is less than 120/80 mm Hg. However, unusually low readings should be evaluated for clinical significance.
Prehypertension, a new category designated in the JNC VII report, emphasizes that patients with prehypertension are at risk for progression to hypertension and that lifestyle modifications are important preventive strategies. Hypertension may be either essential or secondary. Essential hypertension is diagnosed in the absence of an identifiable secondary cause. Approximately 95% of American adults have essential hypertension, while secondary hypertension accounts for fewer than 5% of the cases.
Blacks have a higher prevalence and incidence of hypertension than whites. The prevalence of hypertension was increased by 50% in African Americans. In Mexican Americans, the prevalence and incidence of hypertension is similar to or lower than in whites. The National Health and Nutrition Examination Survey (NHANES) III reported an age-adjusted prevalence of hypertension at 20.6% in Mexican Americans and 23.3% in non-Hispanic whites.
A progressive rise in blood pressure with increasing age is observed. The third NHANES survey reported that the prevalence of hypertension grows significantly with increasing age in all sex and race groups. National health surveys in various countries have shown a high prevalence of poor control of hypertension. These studies have reported that prevalence of hypertension is 22% in Canada, of which 16% is controlled; 26.3% in Egypt, of which 8% is controlled; and 13.6% in China, of which 3% is controlled. Hypertension is a worldwide epidemic; in many countries, 50% of the population older than 60 years has hypertension. Overall, approximately 20% of the world's adults are estimated to have hypertension. The 20% prevalence is for hypertension defined as blood pressure in excess of 140/90 mm Hg. The prevalence dramatically increases in patients older than 60 years.
Potassium, the most abundant intracellular cation, is essential for the life of the organism. Potassium is obtained through the diet, and common potassium-rich foods include meats, beans, fruits, and potatoes. Gastrointestinal absorption is complete, resulting in daily excess intake of approximately 1 mEq/kg/d (60-100 mEq). Ninety percent of this excess is excreted through the kidneys, and 10% is excreted through the gut. Potassium homeostasis is maintained predominantly through the regulation of renal excretion.
Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a very poor indicator of total body stores. Because potassium moves easily across cell membranes, serum potassium levels reflect movement of potassium between intracellular and extracellular fluid compartments, as well as total body potassium homeostasis.
Muscle contains the bulk of body potassium, and the notion that muscle could play a prominent role in the regulation of serum potassium concentration through alterations in sodium pump activity has been promoted for a number of years. Insulin stimulated by potassium ingestion increases the activity of the sodium pump in muscle cells, resulting in an increased uptake of potassium. Studies in a model of potassium deprivation demonstrate that acutely, skeletal muscle develops resistance to insulin-stimulated potassium uptake even in the absence of changes in muscle cell sodium pump expression. However, long term potassium deprivation results in a decrease in muscle cell sodium-pump expression, resulting in decreased muscle uptake of potassium.
Thus, there appears to be a well-developed system for sensing potassium by the pancreas and adrenal glands, resulting in rapid adjustments in immediate potassium disposal and for long-term potassium homeostasis. High potassium states stimulate cellular uptake via insulin-mediated stimulation of sodium-pump activity in muscle and stimulate potassium secretion by the kidney via aldosterone-mediated enhancement of distal renal expression of secretory potassium channels (ROMK). Low potassium states result in insulin resistance, impairing potassium uptake into muscle cells, and cause decreased aldosterone release, lessening renal potassium excretion.
In the general population, data are difficult to estimate; however, probably fewer than 1% of people on no medications have a serum potassium level of lower than 3.5 mEq/L. Potassium intake varies according to age, sex, ethnic background, and socioeconomic status. Whether these differences in intake produce different degrees of hypokalemia or different sensitivities to hypokalemic insults is not known. Up to 21% of hospitalized patients have serum potassium levels lower than 3.5 mEq/L, with 5% of patients achieving potassium levels lower than 3 mEq/L. Of elderly patients, 5% demonstrate potassium levels lower than 3 mEq/L.
Hypokalemia generally is associated with higher morbidity and mortality, especially due to cardiac arrhythmias or sudden cardiac death. However, an independent contribution of hypokalemia to increased morbidity/mortality has not been conclusively established.
Patients who develop hypokalemia often have multiple medical problems, making the separation and quantitation of the contribution by hypokalemia, per se, difficult. Some suggestion is observed of increased frequency of diuretic-induced hypokalemia in African Americans. The higher frequency of hypokalemia in this group may be due to the lower intake of potassium among African American men (approximately 25 mEq/d) than in their white counterparts (70-100 mEq/d).
Some suggestion also is observed of increased frequency of diuretic-induced hypokalemia in women. With age, frequency increases, due to increased use of diuretics and poor diet, which often is low in potassium.
Serum sodium concentration and serum osmolarity normally are maintained under precise control by homeostatic mechanisms involving stimulation of thirst, secretion of antidiuretic hormone (ADH), and renal handling of filtered sodium. Clinically significant hyponatremia is relatively uncommon and is nonspecific in its presentation; therefore, the physician must consider the diagnosis in patients presenting with vague constitutional symptoms or with altered level of consciousness. Irreparable harm can befall the patient when abnormal serum sodium levels are corrected too quickly or too slowly. The physician must have a thorough understanding of the pathophysiology of hyponatremia to initiate safe and effective corrective therapy. The patient's fluid status must be accurately assessed upon presentation, as it guides the approach to correction.
Though clearly not indicative of the overall prevalence internationally, hyponatremia has been observed in as high as 42.6% of patients in a large acute care hospital in Singapore and in 30% of patients hospitalized in an acute care setting in Rotterdam.
Pathophysiologic differences between patients with acute and chronic hyponatremia engender important differences in their morbidity and mortality.
Patients with acute hyponatremia (developing over 48 h or less) are subject to more severe degrees of cerebral edema for a given serum sodium level. The primary cause of morbidity and death is brainstem herniation and mechanical compression of vital midbrain structures. Rapid identification and correction of serum sodium level is necessary in patients with severe acute hyponatremia to avert brainstem herniation and death.
Patients with chronic hyponatremia (developing over more than 48 h) experience milder degrees of cerebral edema for a given serum sodium level. Brainstem herniation has not been observed in patients with chronic hyponatremia. The principal causes of morbidity and death are status epilepticus (when chronic hyponatremia reaches levels of 110 mEq/L or less) and cerebral pontine myelinolysis (an unusual demyelination syndrome that occurs in association with chronic hyponatremia).
The distinction between acute hyponatremia and chronic hyponatremia has critical implications in terms of morbidity and mortality and in terms of proper corrective therapy. Overall incidence of hyponatremia is approximately equal in males and females, though postoperative hyponatremia appears to be more common in menstruant females. Hyponatremia is most common in the extremes of age; these groups are less able to experience and express thirst and less able to regulate fluid intake autonomously.