High blood pressure cardiac patient

Improving the diagnosis and management of high blood pressure in the cardiac patient... 

Cardiac arrhythmia can arise due to exposure to chemicals, but also due to certain deficiencies in the body. A magnesium deficiency, for example (common among MCS patients), can lead to heart palpitations and arrhythmia. Cardiac arrhythmia can also arise as a reaction to a food item or additive to which you have become sensitive or as a result of high blood pressure. A clinical specialist or therapist can test you for deficiencies. 

An example of the correct documentation of the generic and brand name of a dmg is furosemide (Lasix). This drug is a diuretic used for many patients with hypertension (high blood pressure) or cardiac (heart) disease. 

Potassium is often prescribed for people with high blood pressure who are required to take diuretics to reduce excess water in the body because of the belief that diuretics deplete the body of potassium. However, newer knowledge indicates that diuretics do not seriously deplete natural potassium levels of the great majority of patients taking these drugs for high blood pressure. Since high blood potassium concentration can cause cardiac arrest (a heart attack) and death, potassium supplements should be taken with caution and only on the advice of a physician. 

Oral decongestants are not strongly associated with rhinitis medicamentosa but are associated with systemic adverse effects, e.g., blood pressure elevation, palpitations, tremor, appetite loss, and insomnia. Oral decongestants should be used with caution in patients with cardiac disease (arrhythmias, high blood pressure, coronary heart disease), hyperthyroidism, glaucoma, diabetes, and urinary dysfunction. Pseudoephedrine is less likely to elevate blood pressure than phenyl propanolamine (64). 

Upon stabilization, placement of a pulmonary artery (PA) catheter may be indicated based on the need for more extensive cardiovascular monitoring than is available from non-invasive measurements such as vital signs, cardiac rhythm, and urine output.9,10 Key measured parameters that can be obtained from a PA catheter are the pulmonary artery occlusion pressure, which is a measure of preload, and CO. From these values and simultaneous measurement of HR and blood pressure (BP), one can calculate the left ventricular SV and SVR.10 Placement of a PA catheter should be reserved for patients at high risk of death due to the severity of shock or preexisting medical conditions such as heart failure.11 Use of PA catheters in broad populations of critically ill patients is somewhat controversial because clinical trials have not shown consistent benefits with their use.12-14 However, critically ill patients with a high severity of illness may have improved outcomes from PA catheter placement. It is not clear why this was... 

Vasopressin levels are increased during hypotension to maintain blood pressure by vasoconstriction. However, there is a vasopressin deficiency in septic shock. Low doses of vasopressin increase MAP, leading to the discontinuation of vasopressors. However, routine use of vasopressin is not recommended because of lack of evidence of efficacy. Vasopressin is a direct vasoconstrictor without inotropic or chronotropic effects and may result in decreased cardiac output and hepatosplanchnic flow. Vasopressin use may be considered in patients with refractory shock despite adequate fluid resuscitation and high-dose vasopressors.24,27-28... 

The net cardiovascular effects of moderate doses of cholinesterase inhibitors therefore consist of modest bradycardia, a fall in cardiac output, and an increased vascular resistance that result in a rise in blood pressure. (Thus, in patients with Alzheimer s disease who have hypertension, treatment with cholinesterase inhibitors requires that blood pressure be monitored to adjust antihypertensive therapy.) At high (toxic) doses of cholinesterase inhibitors, marked bradycardia occurs, cardiac output decreases significantly, and hypotension supervenes. 

The authors reviewed the biphasic effect of marijuana on the autonomic nervous system. At low to moderate doses it causes increased sympathetic activity, producing a tachycardia and increase in cardiac output blood pressure therefore increases. At high doses it causes increased parasympathetic activity, leading to bradycardia and hypotension. They thought that this patient most probably had adrenergic atrial flutter. 

Intermediate dose (3-5 l.g/min per kg body weight) High dose (5-20 (ig/min per kg body weight) Also stimulates cardiac 3i adrenoceptors Also stimulates peripheral a, adrenoceptors May further increase RBF by increasing cardiac output May improve blood pressure in hypotensive patients Peripheral vasoconstriction may decrease RBF Even greater risk of inducing arrhythmias... 

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