Loading

Trihexyphenidyl

Trihexyphenidyl (Artane generic) 2mg

By C. Copper. Purdue University.

There may be AV dissociation cheap trihexyphenidyl 2 mg with amex, or retrograde atrial capture may occur order trihexyphenidyl 2mg without a prescription. Ischemia (usually from right coronary artery occlusion in acute inferior MI patients) and digoxin intoxication are the two common causes trihexyphenidyl 2mg low cost. Ventricular Arrhythmias  Premature Ventricular Complexes (PVCs)  PVCs may be unifocal buy generic trihexyphenidyl 2mg line, multifocal or multiformed trusted trihexyphenidyl 2 mg. Multifocal PVCs have different sites of origin and different coupling intervals (from previous QRS complexes). Multiformed PVCs usually have the same coupling intervals (because they originate in the same ectopic site but their conduction through the ventricular myocardium varies. Multiformed PVCs used to be common in digoxin intoxication, but dig-toxicity is rarely seen today due to infrequent use and lower doses. PVCs can occur as isolated, single events or as couplets, triplets, and salvos (4-6 PVCs in a row) which are actually short runs of nonsustained ventricular tachycardia. Analyzing the direction of the QRS in various ECG leads usually enables one to determine the ventricle of origin and even the approximate location in the ventricle. They are also common in various heart diseases and may be precursors to more malignant ventricular arrhythmias, cardiac arrest, and sudden death episodes. R-on-T PVCs may be especially dangerous in acute ischemic settings, because the ventricles are more vulnerable to ventricular tachycardia or fibrillation. For fusion to occur the sinus P wave must have already entered the ventricles to initiate the ventricular activation sequence. Before ventricular activation is completed, however, the "late" PVC occurs resulting in a QRS looking a bit like the normal QRS, and a bit like the PVC; i. In contrast, PACs are usually followed by an incomplete pause because the PAC resets the sinus node timing; this enables the next sinus P wave to appear earlier than expected. These concepts are illustrated in the diagram below as well as in the ECG strip seen on the bottom of p20. If a PVC occurs early enough (especially when the sinus rate is slow), it can be “sandwiched” between two normal sinus beats. Often the retrograde P wave can be seen hiding in the ST-T wave of the PVC. The "ladder" diagram under the ECG helps us understand the mechanism. The P wave following the PVC is in fact the next sinus P wave, but the PR interval is too short for it to have caused the next QRS. Note the timing of the sinus P waves is not interrupted. Appropriate modifications and additions from the original have been made for the 21st Century. A thorough understanding of its mechanism and recognition is essential to all persons (and computers) who interpret ECGs. Before we can understand aberrant ventricular conduction we must first review how normal conduction of the electrical impulse occurs in the heart (Figure 1). The AV node provides sufficient conduction delay to allow atrial contraction to contribute to ventricular filling. Following slow AV node conduction high velocity conduction tracts deliver the electrical impulse to the right and left ventricles (through the His bundle, bundle branches and fascicles, and into the Purkinje network). Near- simultaneous activation of the two ventricles results in a NORMAL, NARROW QRS COMPEX (60-109 ms QRS duration). Should conduction delay or block occur in one of the two bundle branches an ABNORMAL WIDE QRS COMPLEX will reflect sequential activation of the ventricles. Figure 1 (note: the left bundle often has a third branch called the septal fascicle, not shown in the above figure) The next ECG strip (Figure 2) illustrates a basic principle of AVC. AVC refers to a temporary alteration of QRS morphology when one might expect a normal QRS complex. Permanent or rate- dependent bundle branch block (BBB) is NOT AVC. The ECG illustrated in Figure 2 from lead V1 begins with two normal sinus beats followed by a premature atrial complex (PAC, first arrow). The narrow QRS complex of the PAC resembles the QRS morphology of the sinus beats. After an incomplete pause, another sinus beat is followed by a slightly earlier PAC. If not careful one might mistake this wide funny looking beat (FLB) as a PVC and attach a different clinical significance (and possible therapy). The diagram and examples on p19-20 also illustrate the different “fates” of PACs. The important clues to recognizing AVC in Figure 2 are: 1.

cheap trihexyphenidyl 2mg free shipping

buy trihexyphenidyl 2 mg free shipping

Nonsteroidal Increased plasma lithium level due to decreased Removing lithium from the body as soon as possible the is the anti-inflammatory drugs renal lithium clearance (exceptions are aspirin mainstay of treating lithium intoxication generic trihexyphenidyl 2 mg visa. W ith preserved renal func- and sulindac) tion purchase trihexyphenidyl 2mg line, excretion can be increased by use of furosemide buy 2 mg trihexyphenidyl otc, up to 40 mg/h generic trihexyphenidyl 2 mg mastercard, Bronchodilators (amino- Decreased plasma lithium level due to increased phylline generic trihexyphenidyl 2 mg on line, theophylline) obviously under close monitoring for excessive losses of sodium and renal lithium clearance water induced by this loop diuretic. W hen renal function is impaired Angiotensin-converting May increase plasma lithium level enzyme inhibitors in association with severe toxicity, extracorporeal extraction is the Cyclosporine most efficient way to decrease serum lithium levels. One should, Decreased lithium clearance however, remember that lithium leaves the cells slowly and that plas- ma levels rebound after hemodialysis is stopped, so that longer dialy- sis treatment or treatment at more frequent intervals is required. Inhibitors of the Renin-Angiotensin System efferent arteriolar vascular tone and in Pre-kallikrein general is reversible after withdrawing the angiotensin-converting enzym e (ACE) inhibitor. Angiotensinogen Kininogen Activated factor XII Inhibition of the ACE kinase II results in at least two im portant effects: depletion Renin + + Kallikrenin of angiotensin II and accum ulation of +: stimulation bradykinin. The role of the latter effect Angiotensin I Angiotensin Bradykinin converting on renal perfusion pressure is not clear, A. W hen renal per- Potentiation of sympathetic activity fusion drops, renin is released into the plas- m a and lym ph by the juxtaglom erular cells Increased Ca2+ current Prostaglandins of the kidneys. Renin cleaves angiotensino- gen to form angiotensin I, which is cleaved further by converting enzym e to form Cough? Angiotensin II partici- pates in glom erular filtration rate regulation in a least two ways. First, angiotensin II FIGURE 11-16 increases arterial pressure— directly and Soon after the release of this useful class of antihypertensive drugs, the syndrom e of func- acutely by causing vasoconstriction and tional acute renal insufficiency was described as a class effect. This phenom enon was first m ore “chronically” by increasing body fluid observed in patients with renal artery stenosis, particularly when the entire renal m ass was volum es through stim ulation of renal sodi- affected, as in bilateral renal artery stenosis or in renal transplants with stenosis to a soli- um retention; directly through an effect on tary kidney. Acute renal dysfunction appears to be related to loss of postglom erular the tubules, as well as by stim ulating thirst (Continued on next page) 11. Normal condition depletion as during diuretic therapy, con- Autoregulation gestive heart failure, cirrhosis, and +– +– nephrotic syndrom e. W hen activated, this Afferent Efferent reninangiotensin system plays an im por- arteriole Glomerulus arteriole tant role in the m aintenance of glom erular pressure and filtration through preferen- M yogenic reflex (Laplace) tial angiotensin II–m ediated constriction Tubuloglomerular feedback of the efferent arteriole. Thus, under such Tubule conditions the kidney becom es sensitive B2. Perfusion pressure reduced to the effects of blockade of the renin- but still within autoregulatory range PGE2 (congestive heart failure, angiotensin system by angiotensin I–con- – renal artery stenosis, verting enzym e inhibitor or angiotensin II diuretic therapy, receptor antagonist. Perfusion pressure com prom ised renal function and congestive seriously reduced PGE2 heart failure, the incidence of serious (prerenal azotemia) – changes in serum creatinine during ACE Intra- glomerular inhibition depends on the severity of the pressure pretreatm ent heart failure and renal failure. Second, angiotensin II preferentially constricts the efferent am ong the appropriate m easures for arteriole, thus helping to preserve glom erular capillary hydrostatic pressure and, conse- patients at risk. Acute interstitial nephritis associated with W hen arterial pressure or body fluid volum es are sensed as subnorm al, the renin- angiotensin I–converting enzym e inhibition angiotensin system is activated and plasm a renin activity and angiotensin II levels has been described. This m ay occur in the context of clinical settings such as renal artery stenosis, O pie; with perm ission. M ost of the renal abnorm alities encountered clinically as a result of N SAIDs can be attributed to the action of these com pounds on prostaglandin production in the kidney. Renal vasoconstriction Sodium chloride and water retention are the m ost com m on side ↓Renal function effects of N SAIDs. This should not be considered drug toxicity because it represents a m odification of a physiologic control "Normalized" renal function m echanism without the production of a true functional disorder in the kidney. Inhibition – – by NSAID Compensatory vasodilation induced by renal prostaglandin synthesis Renal Injury Due To Environmental Toxins, Drugs, and Contrast Agents 11. N SAIDs can induce acute renal decom pensation in patients with various renal and extrarenal clinical conditions that cause a decrease in blood perfu- Severe heart disease (congestive heart failure) sion to the kidney. Renal prostaglandins play an im portant Severe liver disease (cirrhosis) role in the m aintenance of hom eostasis in these patients, so disrup- tion of counter-regulatory m echanism s can produce clinically Nephrotic syndrome (low oncotic pressure) im portant, and even severe, deterioration in renal function. Chronic renal disease Age 80 years or older Protracted dehydration (several days) FIGURE11-19 Physiologic stimulus Inflammatory stimuli Inhibition by nonsteroidal anti-inflam m atory drugs (N SAIDs) on pathways of cyclo-oxygenase (CO X) and prostaglandin synthesis Inhibition - by NSAID -. The recent dem onstration of the existence of functionally dis- tinct isoform s of the cox enzym e has m ajor clinical significance, as COX-1 it now appears that one form of cox is operative in the gastric COX-2 constitutive inducible m ucosa and kidney for prostaglandin generation (CO X-1) whereas Stomach Kidney Inflammatory sites an inducible and functionally distinct form of cox is operative in Intestine Platelets (macrophages, the production of prostaglandins in the sites of inflam m ation and Endothelium synoviocytes) pain (CO X-2). The clinical therapeutic consequence is that an N SAID with inhibitory effects dom inantly or exclusively upon the - cox isoenzym e induced at a site of inflam m ation m ay produce the PGE2 TxA2 PGI2 Inflamma- Proteases O2 tory PGs desired therapeutic effects without the hazards of deleterious effects on the kidneys or gastrointestinal tract. A focal diffuse inflam m atory infiltrate Renal Syndrome Mechanism Risk Factors Prevention/Treatment can be found around the proxim al and dis- Sodium retension ↓ Prostaglandin NSAID therapy (most Stop NSAID tal tubules. The infiltrate consists prim arily and edema common side effect) of cytotoxic T lym phocytes but also con- Hyperkalemia ↓ Prostaglandin Renal disease Stop NSAID tains other T cells, som e B cells, and plasm a ↓ Potassium to Heart failure Avoid use in high-risk patients cells. Changes in the glom eruli are m inim al distal tubule Diabetes and resem ble those of classic m inim al- ↓ Aldosterone/renin- Multiple myeloma change glom erulonephritis with m arked angiotensin Potassium therapy epithelial foot process fusion. Potassium-sparing H yperkalem ia, an unusual com plication diuretic of N SAIDs, is m ore likely to occur in Stop NSAID Acute deterioration of ↓ Prostaglandin and Liver disease patients with pre-existing renal im pairm ent, Avoid use in high-risk patients renal function disruption of Renal disease cardiac failure, diabetes, or m ultiple m yelo- hemodynamic bal- m a or in those taking potassium supple- Heart failure ance m ents, potassium -sparing diuretic therapy, Dehydration Stop NSAID or intercurrent use of an angiotensin-con- Old age Dialysis and steroids (?

generic trihexyphenidyl 2 mg without a prescription

trihexyphenidyl 2mg on line

These results were interpreted as indicating that the predom inant cause of resistance to AN P in dogs with low-output congestive heart failure is a reduction in RPP discount 2 mg trihexyphenidyl otc. Fluid intake 20 20 A prim ary decrease in cardiac output (indi- Net volume intake cated by dark blue arrow) leads to a Nonrenal 10 10 decrease in arterial pressure generic trihexyphenidyl 2mg visa, which decreas- fluid loss – + es pressure natriuresis and volum e excre- 0 0 tion cheap trihexyphenidyl 2mg with mastercard. These decreases expand the ECF vol- 0 10 20 30 um e quality trihexyphenidyl 2 mg. The inset graph shows that the ratio ECF volume trihexyphenidyl 2mg on-line, L of interstitial volum e (solid line) to plasm a + – Rate of change + volum e (dotted line) increases as the ECF Arterial Kidney volume Extracellular of extracellular pressure output fluid volume volum e expands because the interstitial fluid volume com pliance increases. Thus, although + expansion of the ECF volum e increases Total peripheral blood volum e and venous return, thereby + resistance Blood volume + restoring cardiac output toward norm al, + Autoregulation this occurs at the expense of a dispropor- + + M ean circulatory tionate expansion of interstitial volum e, Cardiac output Venous return filling pressure often m anifested as edem a. H epatic venous outflow obstruction leads to portal hypertension. Hepatic venous SVR – Hepatic venous According to the underfill theory, transudation from the liver leads outflow obstruction outflow obstruction to reduction of the blood volum e, thereby stim ulating sodium (N a) retention by the kidney. As indicated by the question m ark near the + term blood volum e, a low blood volum e is rarely detected in clini- cal or experim ental cirrhosis. Furtherm ore, this theory predicts that ascites would develop before renal N a retention, when the reverse Transudation Transudation generally occurs. According to the overflow theory, increased por- tal pressure stim ulates renal N a retention through incom pletely + defined m echanism s. The vasodilation theory suggests that Renin portal hypertension leads to vasodilation and relative arterial ↓ Blood volume ↑ ECF volume hypotension. Evidence for vasodilation in cirrhosis that precedes? UNaV FIGURE 2-31 Vasodilators Vasoconstrictors Alterations in cardiovascular hem odynam ics in hepatic cirrhosis. H epatic dysfunction and Nitric oxide portal hypertension increase the production and im pair the m etabolism of several vasoac- Glucagon CGRP tive substances. The overall balance of vasoconstriction and vasodilation shifts in favor of ANP SNS dilation. Vasodilation m ay also shift blood away from the central circulation toward the VIP RAAS periphery and away from the kidneys. Som e of the vasoactive substances postulated to Substance P Vasopressin ET-1 participate in the hem odynam ic disturbances of cirrhosis include those shown here. Prostaglandin E2 AN P— atrial natrivretic peptide; ET-1— endothelin-1; CGRP— calcitonin gene related Encephalins TNF peptide; RAAS— renin/angiotensin/aldosterone system ; TN F— tum or necrosis factor; Andrenomedullin VIP— vasoactive intestinal peptide. Com pared with control subjects (A), patients with cirrhosis (B) have decreased central and increased non- 1. The higher cardiac output (CO ) results from peripheral vasodila- 1. Perfusion of the kidney is reduced significantly in patients with cirrhosis. Com pared with control rats, rats having cir- Cirrhosis & L-name rhosis induced by carbon tetrachloride and phenobarbital exhibited increased plasm a renin activity (PRA) and plasm a arginine vaso- 10 10 pressin (AVP) concentrations. At steady state, the urinary N a excre- tion (UN aV) was sim ilar in both groups. After treatm ent with L- N AM E for 7 days, plasm a renin activity decreased to norm al lev- els, AVP concentrations decreased toward norm al levels, and urinary N a excretion increased by threefold. These changes were 5 5 associated with a norm alization of m ean arterial pressure and car- diac output. A prim ary decrease in system ic + 20 Fluid intake 20 vascular resistance (indicated by dark blue Net volume arrow), induced by m ediators shown in intake 10 10 Figure 2-31, leads to a decrease in arterial Nonrenal fluid loss – pressure. The reduction in system ic vascular + 0 0 resistance, however, is not uniform and 0 10 20 30 favors m ovem ent of blood from the central ECF volume, L (“effective”) circulation into the peripheral + – Rate of change + circulation, as shown in Figure 2-32. Arterial Kidney volume Extracellular of extracellular H ypoalbum inem ia shifts the interstitial to pressure output fluid volume fluid volume blood volum e ratio upward (com pare the + interstitial volum e with norm al [dashed Total peripheral line], and low [solid line], protein levels in Central Peripheral + resistance blood volume blood volume the inset graph). Because cardiac output increases and venous return m ust equal car- + + diac output, dram atic expansion of the + M ean circulatory extracellular fluid (ECF) volum e occurs. Cardiac output Venous return filling pressure M echanisms of Extracellular Fluid Volume Expansion in Nephrotic Syndrome FIGURE 2-35 14 Changes in plasm a protein concentration affect the net oncotic pressure difference across 12 capillaries ( c - i) in hum ans. N ote that m oderate reductions in plasm a protein concen- tration have little effect on differences in transcapillary oncotic pressure. O nly when plas- 10 m a protein concentration decreases below 5 g/dL do changes becom e significant. N ote that urinary N a excretion (squares) increases Plasm a renin activity (PRA) and atrial natriuretic peptide (AN P) before serum album in concentration increases.