Learning Issues PRIN Week 11 1.

Normal ranges of vitals -- relevance of deviation of each (focus: systolic and diastolic) 120/80 BP = normal Clinician's Pocket Reference The indirect explanation is that the low diastolic pressure is not harmful per se, but is a marker for generalized cardiovascular disease, or more particularly increased arterial stiffness. It is generally accepted that the age-related increase of systolic and decrease of diastolic pressure that is seen in the brachial artery is largely the result of accelerated wave reflection in stiff arteries. Hurst's The Heart 2. Pathophysiology of fainting and diff types (keep general). 3. Orthostatic hypotension (mechanism, effects, cause) - how BP controlled.

Table 162. Causes of Orthostatic Hypotension.

Drug-induced Phenothiazines (chlorpromazine, etc.) Tricyclic antidepressants (amitriptyline, etc.) Antihypertensives Diuretics Nitrates (nitroglycerine, etc.) Levodopa Monoamine oxidase inhibitors Peripheral neuropathies (see Chapter 16) Diabetic Amyloid Hypovolemia or hemorrhage Addison's disease Acute or chronic spinal cord injury Degenerative diseases of the central nervous system

Parkinsonism Shy-Drager syndrome (anhidrosis, sphincter dysfunction, impotence) Posterior fossa tumors Sequelae of surgical sympathectomy
Patients usually describe lightheadedness, dimming of vision, weakness, and a fainting sensation. True vertigo does not occur. Blood pressure that is significantly lower (>20 mm Hg systolic difference) when the patient is standing than when he or she is supine is diagnostic. Orthostatic tachycardia (abnormally large increase in heart rate) may be present as well. A stool sample should be evaluated for the presence of blood. CBC may reveal anemia or hemoconcentration due to blood loss or dehydration, respectively. Electrolyte determinations should be made to detect abnormalities produced by dehydration or drugs. Serum drug levels should be obtained as indicated. Current Emergency Med: 6th Edition In the standing position, as a result of the effect of gravity on the blood (see Chapter 30: Dynamics of Blood & Lymph Flow), the mean arterial blood pressure in the feet of a normal adult is 180200 mm Hg and venous pressure is 8590 mm Hg. The arterial pressure at head level is 6075 mm Hg, and the venous pressure is zero. If the individual does not move, 300500 mL of blood pools in the venous capacitance vessels of the lower extremities, fluid begins to accumulate in the interstitial spaces because of increased hydrostatic pressure in the capillaries, and stroke volume is decreased. Symptoms of cerebral ischemia develop when the cerebral blood flow decreases to less than about 60% of the flow in the recumbent position. If no compensatory cardiovascular changes occurred, the reduction in cardiac output due to pooling on standing would lead to a reduction of cerebral flow of this magnitude, and consciousness would be lost. In a sense, the fainting is a "homeostatic mechanism," because falling to the horizontal position promptly restores venous return, cardiac output, and cerebral blood flow to adequate levels. It is common in patients receiving sympatholytic drugs. It also occurs in diseases such as diabetes and syphilis, in which there is damage to the sympathetic nervous system. This underscores the importance of the sympathetic vasoconstrictor fibers in compensating for the effects of gravity on the circulation. Another cause of postural hypotension is primary autonomic failure (Table 331). Autonomic failure occurs in a variety of diseases. One form is caused by a congenital deficiency of dopamine -hydroxylase (see Chapter 4: Synaptic & Junctional Transmission) with little or no production of norepinephrine and epinephrine.

The effects of gravity on the circulation are multiplied during acceleration or deceleration in vehicles that in modern civilization range from elevators to rockets. Lange Physiology 4. Prazosin and HCTZ (moa, indication, contraindication, drug int.) Prazosin Use Treatment of hypertension Concerns related to adverse effects: Orthostatic hypotension/syncope: May cause significant orthostatic hypotension and syncope, especially with first dose; anticipate a similar effect if therapy is interrupted for a few days, if dosage is rapidly increased, or if another antihypertensive drug (particularly vasodilators) or a PDE-5 inhibitor is introduced. Patients should be cautioned about performing hazardous tasks when starting new therapy or adjusting dosage upward. Adverse Reactions >10%: Central nervous system: Dizziness (10%) Interactions Ethanol: Avoid ethanol (may increase vasodilation). MOA Competitively inhibits postsynaptic alpha-adrenergic receptors which results in vasodilation of veins and arterioles and a decrease in total peripheral resistance and blood pressure AccessMedicine Drug Monographs HCTZ Use Management of mild to moderate hypertension; treatment of edema in congestive heart failure and nephrotic syndrome Concerns related to adverse effects: Electrolyte disturbances: Hypokalemia, hypochloremic alkalosis, and hyponatremia can occur. Mechanism of Action Inhibits sodium reabsorption in the distal tubules causing increased excretion of sodium and water as well as potassium and hydrogen ions AccessMedicine Drug Monographs