Pressure sinus

The regulation of the total peripheral resistance also involves the complex interactions of several mechanisms. These include baroreflexes and sympathetic nervous system activity response to neurohumoral substances and endothelial factors myogenic adjustments at the cellular level, some mediated by ion channels and events at the cellular membrane and intercellular events mediated by receptors and mechanisms for signal transduction. As examples of some of these mechanisms, there are two major neural reflex arcs (Fig. 1). Baroreflexes are derived from high-pressure barorecep-tors in the aortic arch and carotid sinus and low-pressure cardiopulmonary baroreceptors in ventricles and atria. These receptors respond to stretch (high pressure) or... 

Cardiovascular-peripheral vasodilation,decreased peripheral resistance, inhibition of baroreceptors (pressure receptors located in the aortic arch and carotid sinus that regulate blood pressure), orthostatic hypotension and fainting... 

Decongestants are used to treat the congestion associated with rhinitis, hay fever, allergic rhinitis, sinusitis, and the common cold. In addition, they are used in adjunctive therapy of middle ear infections to decrease congestion around the eustachian tube Nasal inhalers may relieve ear block and pressure pain during air travel. Many can be administered orally as well as topically, but topical application is more effective than the oral route. 

Tsai FY, Wang AM, Matovich VB, Lavin M, Berberian B, Simonson TM, Yuh W. MR staging of acute dural sinus thrombosis correlation with venous pressure measurements and implications for treatment and prognosis. Am J Neuroradiol 1995 16 1021-1029. 

Drugs related to PCP are known to alter the carotid sinus reflex. Mechanical stimulation of the carotid sinus in the neck normally results in a slowing of heart rate and a decrease in blood pressure. Carotid sinus stimulation, coupled with the effects of PCP on blood vessels, might result in a marked fall in the blood pressure that could lead, ultimately, to death. Individuals intoxicated with PCP may be at a higher risk to complications of carotid compression neck holds. Hence, additional cases would be expected to become medicolegal issues. 

Monitor the patient for return of pulse and blood pressure, and for termination of VF and restoration of normal sinus rhythm. 

Adults Nasal congestion or obstruction, nasal/postnasal discharge or purulence, facial pain or pressure (especially unilateral in a sinus area), diminished sense of smell, fever, cough, maxillary dental pain, fatigue, ear fullness or pain... 

Clinical improvement should be evident by 72 hours of therapy, as demonstrated by defervescence, reduction in nasal congestion and discharge, and improvements in facial pain or pressure and other symptoms. Patients should be monitored for common adverse events and referred to a specialist if clinical response is not obtained with first- or second-line therapy. Referral is also important for recurrent or chronic sinusitis or acute disease in immunocompromised patients. Surgery may be indicated in complicated cases. 

Some of the participants reported health benefits such as relief from sinus congestion, reduction in the desire to smoke and drink alcohol as well as lowered blood pressure. Of the 112 participants, a total of 580 kilograms or 1,276.8 pounds were lost during the seven-day period, an average of 1.6 pounds per person daily. Two people discontinued the program complaining of side effects of hypoglycemia and another person... 

Loss of plasma volume leads to a decrease in MAP. Baroreceptors located in the aortic and carotid sinuses detect this fall in MAP and elicit reflex responses that include an increase in the overall activity of the sympathetic nervous system. Sympathetic stimulation of the heart and blood vessels leads to an increase in cardiac output (CO) and increased total peripheral resistance (TPR). These adjustments, which increase MAP, are responsible for the short-term regulation of blood pressure. Although increases in CO and TPR are effective in temporary maintenance of MAP and blood flow to the vital organs, these activities cannot persist indefinitely. Ultimately, plasma volume must be returned to normal (see Table 19.1). 

A decrease in plasma volume leads to decreased MAP, which is detected by baroreceptors in the carotid sinuses and the arch of the aorta. By way of the vasomotor center, the baroreceptor reflex results in an overall increase in sympathetic nervous activity. This includes stimulation of the heart and vascular smooth muscle, which causes an increase in cardiac output and total peripheral resistance. These changes are responsible for the short-term regulation of blood pressure, which temporarily increases MAP toward normal. 

Hypotension, tachycardia, tachypnea, confusion, and oliguria are common symptoms. Myocardial and cerebral ischemia, pulmonary edema (cardiogenic shock), and multisystem organ failure often follow. Significant hypotension (systolic blood pressure [SBP] less than 90mmHg) with reflex sinus tachycardia (greater than 120 beats/min) and increased... 

Atmospheres were within a few percent of nominal concentrations the mean oxygen concentration was approximately 20.5%. No significant or consistent differences were found between air exposure and test chemical exposure for clinical observations, blood pressure, heart rate, peak expiratory flow, or EKG recordings. During blood sampling and blood pressure measurements, all subjects showed sinus arrhythmia before and after exposure. 

Figure 8. Cardiovascular effects of clonidine (St 155) in an anaesthetized dog. Upper curve, blood pressure, heart frequency. Lower curve, nictitating membrane. At the whole dots carotid sinus occlusion reflex was elicited (11).

Aorta A familiar arterial pressure trace. Its systolic component follows the LV trace between points B and C at a slightly lower pressure to enable forward flow. During IVR, closure of the aortic valve and bulging of the sinus of Valsalva produce the dicrotic notch, after which the pressure falls to its diastolic value. 

Both physiological and metabolic factors play a role in regulation of blood pressure. The former involves the vasomotor centre at the base of the brain and the basoreceptor located in the carotid sinus and the aortic arch. These mechanisms provide short-term regulation of the blood pressure, which is not discussed in this book. 

Raised intracranial pressure could be a cause of early morning headache. Early morning headache could also be triggered by sinusitis, tension or muscle spasm. 

P-Blockers also serve to lower cardiac rate (sinus tachycardia, p. 134) and elevated blood pressure due to high cardiac output (p. 312). The mechanism underlying their antihypertensive action via reduction of peripheral resistance is unclear. 

Indications. Verapamil is used as an antiarrhythmic drug in supraventricular tachyarrhythmias. In atrial flutter or fibrillation, it is effective in reducing ventricular rate by virtue of inhibiting AV-conduction. Verapamil is also employed in the prophylaxis of angina pectoris attacks (p. 308) and the treatment of hypertension (p. 312). Adverse effects Because of verapamil s effects on the sinus node, a drop in blood pressure fails to evoke a reflex tachycardia Heart rate hardly changes bradycardia may even develop. AV-block and myocardial insufficiency can occur. Patients frequently complain of constipation. 

Propranolol is a prototype of this series of drugs and is the oldest and most widely used nonselective )3-adrenoblocker. It possesses antianginal, hypotensive, and antiarrhythmic action. Propranolol is a cardiac depressant that acts on the mechanic and electrophysio-logical properties of the myocardium. It can block atrioventricular conductivity and potential automatism of sinus nodes as well as adrenergic stimulation caused by catecholamines nevertheless, it lowers myocardial contractility, heart rate, blood pressure, and the myocardial requirement of oxygen. 

Hypertrophic cardiomyopathy (IHSS) Serious adverse effects were seen in 120 patients with IHSS (especially with pulmonary artery wedge pressure more than 20 mm Hg and left ventricular outflow obstruction) who received oral verapamil at doses up to 720 mg/day. Sinus bradycardia occurred in 11%, second-degree AV block in 4% and sinus arrest in 2%. 

Tolerance Following 12 days of dronabinol, tolerance to the cardiovascular and subjective effects developed at doses 210 mg/day or less. An initial tachycardia induced by dronabinol was replaced successively by normal sinus rhythm and then bradycardia. A fall in supine blood pressure, made worse by standing, was also observed initially. Within days, these effects disappeared, indicating development of tolerance. Tachyphylaxis and tolerance did not, however, appear to develop to the appetite stimulant effect. 

Any sudden alteration in the mean arterial blood pressure tends to produce compensatory reflex changes in heart rate, contractility, and vascular tone, which will oppose the initial pressure change and restore the homeostatic balance. The primary sensory mechanisms that detect changes in the mean arterial blood pressure are stretch receptors (baroreceptors) in the carotid sinus and aortic arch. 

Mechanism of Action An antihypertensive and antiglaucoma agent that blocks beta,-adrenergic receptors in cardiac tissue. Reduces aqueous humor production. Therapeutic Effect Slows sinus heart rate, decreases BP, and reduces intraocular pressure (lOP). 

Mechanism of Action An antihypertensive that blocks betaj-adrenergic receptors at normal doses and betaj-adrenergic receptors at large doses. Predominantly blocks betaj-adrenergic receptors in cardiac tissue. Reduces aqueous humor production. Therapeutic Effect Slows sinus heart rate, decreases cardiac output, decreases blood pressure (BP), increases airway resistance, decreases intraocular pressure (lOP). Pharmacokinetics Well absorbed from the G1 tract. Protein binding unknown. Mini-mally metabolized in liver. Primarily excreted unchanged in urine. Not removed by hemodialysis. Half-life 6 hr (increased in decreased renal function). 

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