After screening to identify a patient as being at risk for OH, an accurate assessment of the underlying cause s is required to determine the appropriate treatment recommendation. A stepwise approach is recommended for diagnosis of nOH, specifically starting with measurement of orthostatic blood pressure and heart rate, followed by more detailed autonomic testing in select cases Fig. However, in facilities in which this method is impractical, a seated-to-standing blood pressure can be performed as an acceptable alternative. If the test is positive i.
However, if the test is negative but symptoms are strongly suggestive of OH, a supine-to-standing blood pressure test or HUT should be considered. As some individuals with OH are at risk for falls when standing suddenly, testing staff should be aware of this possibility and take appropriate precautions. Even this appropriate testing of blood pressure will not identify all patients with OH, since variability in meals, hydration, time of day, and medications can affect the orthostatic change in blood pressure.
Additionally, there is a subgroup of patients who manifest symptoms of OH beyond the 3-min interval, defined as delayed OH [ 34 ], which may be a manifestation of early autonomic failure. Further discussion of this group is outside the scope of this paper. These compensatory changes are induced primarily by augmentation of norepinephrine output by sympathetic autonomic peripheral nerve endings. The heart rate information is acquired during the measurement of orthostatic vital signs as described above.
It should be noted that without a fall in blood pressure, the heart rate criteria for nOH do not apply. In addition, monitoring of postural heart rate changes for diagnostic purposes requires that there is no confounding medication effect e. In a similar fashion, volume depletion e. In addition to in-clinic blood pressure monitoring, patients should be asked to check their blood pressure and heart rate at home and record the values in a diary.
The following timings are our recommendations for at-home blood pressures and heart rate monitoring: 1 first thing in the morning before taking morning medications, 2 when a patient feels symptomatic, and 3 at bedtime for several days. With any change in therapy, an additional week of blood pressure monitoring is required to determine the effectiveness of the change. An example patient diary for blood pressure and heart rate is provided in Appendix I.
There are numerous medications that can diminish the normal compensatory postural increase in heart rate, e. Cardiac disorders e.
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Due to variability among patients, including age, disease status, and current medication usage, the lack of heart rate increase on standing may not always be an accurate indicator of nOH in patients with OH; therefore, clinical scenario and specific presentation need to be considered. If standard orthostatic blood pressure testing does not reveal OH in an at-risk individual with unexplained postural symptoms, falls, or syncope, then any of the following are appropriate as next steps: 1 conducting extended at-home blood pressure monitoring with results recorded by the patient or caregiver, 2 implementing h ambulatory blood pressure monitoring where the patient can annotate times when supine or standing to determine a typical range of blood pressures during the day and, with patient annotation of position, help to understand fluctuations , or 3 use of autonomic function tests.
The specialized tests described below are considered by the panel to be beyond the scope of many primary care clinicians and usually require referral to a center specializing in autonomic disorders. Specialized tests for a definitive diagnosis of nOH include autonomic reflex testing including heart rate variability to paced breathing, heart rate and blood pressure response to a Valsalva maneuver, and continuous blood pressure response to a prolonged HUT.
In addition, cardiovascular reflex testing, tilt table testing, and the Valsalva maneuver may help discriminate multiple system atrophy with predominant parkinsonism MSA-P from PD [ 40 ]. Supine and standing plasma fractionated catecholamine levels can aid in making a diagnosis, but have somewhat low sensitivity [ 6 , 41 ]. It is useful to differentiate between OH and nOH because of the significantly greater morbidity and mortality associated with nOH [ 3 , 6 ].
Many of the diagnosis and management points noted throughout this paper are appropriate for use in all individuals with OH. Readers are referred to several comprehensive reviews for further information [ 22 , 33 , 42 ]. A full review of the diagnosis and management of non-neurogenic OH is outside the scope of this paper. After making a diagnosis of nOH, it is was the opinion of the panel that it is important to establish its severity.
A proposed grading scale for nOH is based on the total drop in systolic blood pressure, duration of standing time, and the number and severity of symptoms that affect activities of daily living [ 29 ]. The purpose of the grading scale is to help clinicians decide when to refer a patient to a specialist. For example, depending on comfort level, a patient presenting with Grade 1 or 2 may not require referral; whereas, consideration of referral for a patient presenting with Grade 3 or 4 nOH is reasonable.
Proposed grading scale for nOH [ 27 ]. A patient with grade 3 or 4 nOH should be treated by a healthcare provider with experience in managing nOH. It should be noted that large meals, particularly those high in carbohydrates or associated with alcohol, can magnify the drop in blood pressure.
Elderly persons are more susceptible to these effects [ 8 ]. If symptoms are more prominent postprandially, then measurement of orthostatic blood pressures before and after meals should be considered. Once a patient is diagnosed with nOH, the goal of treatment should not be to normalize standing blood pressure, but the principal treatment goals should serve to reduce the burden of symptoms especially falls , prolong standing time, and improve the physical capabilities of the patient to restore independence in activities of daily living.
A treatment algorithm for nOH that encompasses a 4-step hierarchical process is proposed Fig. At each step, it is recommended that the patient undergo a 2-week assessment to establish whether sufficient symptomatic benefit has been achieved before moving onto successive steps.
Each facet of the algorithm is described in detail below. After establishment of a diagnosis of symptomatic nOH, it is imperative to first consider pharmacologic simplification by reducing or discontinuing medication that exacerbate nOH. One of the keys to initial success is to complete a comprehensive medication review so that adjustments in regimens can be made as needed. Discontinuation or dose reduction of medications which can potentially aggravate orthostatic symptoms such as diuretics, vasodilators, and medications with negative chronotropic properties such as beta blockers may be sufficient to resolve symptoms of nOH in some patients.
Once a medication review has been conducted, it is recommended that any planned changes be discussed with the prescribing clinician such as: taking the patient off a particular drug, lowering current doses, or changing the dosing schedule. While there is limited published literature supporting this recommendation there is strong expert opinion underlying this approach. The next step in the treatment algorithm is to have the patient incorporate a number of simple non-pharmacological measures into their daily routines to address symptoms due to nOH.
From a practical perspective, these measures are often incorporated into a treatment plan in parallel to the changes to pharmacology outlined in step 1 above. For patients who are experiencing syncope, near-syncope, or falls, there is some urgency to eliminating destabilizing postural changes. Hence, non-pharmacologic measures may be used individually, but are most effective when used in combination or while concomitantly titrating pharmacologic treatments. Patients with nOH require interventions which are aimed at ensuring normal or even expanded blood volume. Many patients with nOH, especially older patients, are often blood volume depleted due to inadequate oral fluid intake [ 44 ].
This may be due to voluntary restriction of intake for self-management of common conditions causing urinary urgency and urinary frequency including benign prostatic hyperplasia BPH , overactive bladder, neurogenic bladder, stress incontinence or similar bladder dysfunctions as are commonly seen in many neurodegenerative disorders. However, the most common identifiable and readily treatable problem is decreased daily water intake. Most patients are unaware of the volume of water intake necessary during a typical day.
Modifications in fluid volume recommendations also need to be considered in geographic areas with warmer weather or during the summer season. The effect is due to a hypo-osmolar reflex in the portal circulation and can last for an hour to help alleviate the symptoms of nOH experienced on standing [ 46 , 47 ]. Liquids other than water do not provide the same blood pressure response [ 48 , 49 ]. Thus, proper hydration can produce both acute and long-lasting significant clinical benefits to patients with nOH [ 46 , 50 — 53 ]. Another non-pharmacologic treatment is to monitor and adjust as needed the amount of salt that the patient is ingesting.
Because salt is typically seen as a negative dietary component, patients may try to remove or at least reduce salt from their diet. However, many patients who suffer orthostatic symptoms have an inadequate intake of salt. For the patient with nOH, it is recommended that they add up to 1—2 teaspoons 2. Patients at risk for heart failure or severe peripheral edema must be closely monitored for worsening symptoms and salt intake adjusted downward accordingly [ 43 , 57 ]. The long-term risks associated with greater salt intake e. The long-term risks of high sodium diets in individuals with orthostatic hypotension have not been well studied.
Lower body strength training and moderate, non-strenuous activities may be incorporated into standard treatment for patients with nOH [ 58 , 59 ].
Deconditioning occurs very quickly in bed bound or hospitalized patients and will exacerbate the magnitude of the blood pressure drop in patients with nOH. We advocate the use of exercise that is not gravitationally challenging, such as a stationary recumbent bicycle, rowing machine, or water-based activities. Upright exercise, such as treadmill walking or running, should be avoided in some patients because of the risk of falls due to nOH. Patients should be cautioned that strenuous activity may temporarily exacerbate symptoms of nOH due to increased core body temperature and peripheral vasodilation as described below.
To help mitigate against this occurring, patients should be well hydrated prior to exercise and should be careful when standing after an exercise session. Elevation in body temperature causes peripheral vasodilation. Patients with nOH should avoid situations that could increase core body temperature, such as excessive high-intensity exercise, exercise when ambient temperature and humidity are high, utilization of hot tubs, spas, or saunas, prolonged hot showers, etc.
Simple safety adjustments, such as using a shower chair, will help prevent complications. Additionally, individuals with autonomic failure may have impaired thermoregulatory capacity and may be at increased risk for hyperthermia. An example of impaired thermoregulation in autonomic failure is shown by the lack of the expected nocturnal decrease of body core temperature that has been described in patients with MSA [ 61 ]. Supine hypertension commonly leads to a pressure diuresis that occurs resulting in nocturia and blood volume depletion overnight.
This nocturnal forced diuresis can be decreased by elevating the head of the bed. In addition, the modest effects of gravity in the head-up position will maintain activation of the renin—angiotensin—aldosterone system and maintain higher blood pressure in the morning. The net result is a diminished magnitude of blood pressure drop in the morning [ 63 ]. Compression garments are another mechanism to combat blood pressure changes due to postural venous pooling [ 64 , 65 ]. Because most of the pooling occurs in the splanchnic—mesenteric bed, waist-high compression garments are the most effective, followed by thigh-high compression stockings.
Knee-high stockings are not effective, although they are widely used for treatment of orthostatic hypotension and many patients are convinced of their effectiveness. Unfortunately, compliance with the use of compression stockings is low because they require fitting, are difficult to put on, and uncomfortable in hot climates.
Abdominal binders offer an effective alternative [ 66 ], and arguably should be tried first, alone or if necessary in combination with leg compression. In individuals with postprandial hypotension, smaller, more frequent meals are recommended [ 69 , 70 ]. Finally, postprandial hypotension can be reduced with caffeine [ 73 ] or acarbose [ 74 ].
B12 deficiency and anemia should be corrected and ongoing observation is necessary to prevent recurrence. Thus, changes in diet as well as vitamin and iron supplementation may be helpful for some patients with nOH. If the implementation of non-pharmacologic measures does not adequately improve the symptoms of nOH, then it becomes necessary to initiate pharmacotherapy.
For patients who are experiencing syncope, near-syncope, or falls, the potential consequences are so grave that some clinicians believe that institution of pharmacotherapy at the outset of management is appropriate. Clinicians must individualize treatment based upon the urgency of the symptoms. Until , the two drugs primarily used to treat nOH were fludrocortisone and midodrine of which only midodrine has received FDA approval for treatment of OH.
The selection of one drug over the other, in many situations, was related to clinician preference and experience. Below, we present an overview of the key drugs used to treat nOH and the recommendations for usage. One of the challenges associated with treating nOH pharmacologically is the limited availability of clinical evidence and lack of comparative effectiveness studies. Typical dosing is between 2. The dose is typically up-titrated to symptomatic relief.
In multiple clinical trials, midodrine resulted in a significant increase in systolic and diastolic blood pressure, as well as modest improvements in orthostatic symptoms [ 11 — 13 ]. A high supine blood pressure seen shortly after midodrine administration should not cause the drug dose to be decreased or stopped, but managed by avoiding the supine posture.
A meta-analysis of seven trials with midodrine total subjects found an increased incidence of supine hypertension and that the pooled risk ratio was 6. Other side effects with midodrine include piloerection, scalp itching, and urinary retention [ 79 ].
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Caution should also be exercised in patients with congestive heart failure and chronic renal failure [ 79 ]. Droxidopa is an orally administered norepinephrine pro-drug that is converted into norepinephrine both in the central nervous system and in peripheral tissues, including sympathetic peripheral nerve endings. Replenishment of neural norepinephrine is believed to be the primary mechanism of action for improvement of standing blood pressure with droxidopa.
A recommended dosing schedule would be at 8 AM, noon, and 4 PM. Clinically, droxidopa has been evaluated in Phase 3 studies and has demonstrated significant improvement in the symptoms of nOH such as dizziness, lightheadedness, weakness, fatigue, and in improvements to activities of daily living [ 15 — 17 ]. Additionally, in studies of droxidopa for the treatment of nOH, the rate of falls and fall-related adverse events demonstrated a favorable trend but not statistically significant in the groups of patients receiving droxidopa versus those receiving placebo [ 15 — 17 ].
Side effects observed with droxidopa included headache, dizziness, nausea, fatigue, and supine hypertension [ 15 — 17 ]. Caution should be exercised in patients with congestive heart failure and chronic renal failure. It acts by increasing renal sodium and water reabsorption, thus expanding intravascular blood volume. Fludrocortisone is typically dosed at 0. The main side effects of fludrocortisone include supine hypertension, hypokalemia, and edema. It should be used with caution in patients with congestive heart failure [ 22 ]. Pyridostigmine is thought to work in OH by amplifying the increased sympathetic nerve activity in response to orthostatic stress.
Therefore, it is likely more useful in less severe patients with residual sympathetic function, and has the advantage of not worsening supine hypertension. Several small studies have reported a modest improvement in OH and orthostatic symptoms [ 14 , 18 — 21 ]. Patients may experience adverse side effects associated with cholinergic stimulation, including abdominal cramps, diarrhea, sialorrhea, excessive sweating, and urinary incontinence. Many patients with nOH also have autonomic failure resulting in constipation and anhidrosis, so these side effects may be salutary for some patients.
There have been no head-to-head comparison studies to guide the initial choice of nOH treatments. An individualized treatment regimen should consider severity, co-morbid disease especially cardiac or renal failure , and treatment goals. Midodrine has an FDA-approved indication for the treatment of symptomatic OH; FDA approval was based on studies showing an improvement in upright blood pressure as a surrogate for symptom relief.
In contrast, the FDA-approved droxidopa with an orphan designation for the treatment of nOH based on studies showing improvement in symptoms of nOH. Patients receiving droxidopa reported a decrease in dizziness, lightheadedness, feeling faint, or feeling as if they might black out compared with those receiving placebo.
There have been no long-term studies on the durability of the treatment effect for either midodrine or droxidopa.
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Once initial therapy has begun, symptomatic benefit, including impact on activities of daily living, and changes in blood pressure need to be assessed frequently. If symptoms do not improve after reaching maximum labeled dose, it is recommended that the treatment be changed and symptomatic benefit be assessed once more.
This process is iterative until either symptomatic benefit is achieved or maximum tolerable dose of the therapy is reached. Little data exists to determine efficacy and safety of different combinations of therapy compared to monotherapy for nOH. Based on the experience of the consensus panel, the recommendation is to appropriately titrate to maximum tolerable dose of a single agent and then, if symptomatic benefit is not obtained, consider switching to a different therapy or adding a second agent and titrate from its lowest starting dose.
Assessment of treatment success needs to be a multifaceted approach involving predominantly the measurement of symptomatic improvements as well as ongoing blood pressure measurements. It is critical that patients are educated on the various symptoms and about how to keep a diary of symptoms. Similarly, it is necessary for the patient to conduct a period of home monitoring of blood pressure after implementing new or additional non-pharmacologic measures or after a change in treatment or dose.
We recommend that patients check their blood pressures at home in the supine head-up position at bedtime, prior to arising in the morning, and while the patient is in their normal head-up sleeping position. We recommend checking blood pressures first thing in the morning prior to taking any morning medications, when symptomatic, and at bedtime for several days. An example patient diary for blood pressure and heart rate monitoring is provided in Appendix I. If blood pressure measurements have been stable, a reduction in monitoring frequency can be considered, but reinstituted if symptoms worsen or if medications are changed.
Lastly, h ambulatory blood pressure monitoring can be considered so that there is an ongoing record of the impact of treatment on blood pressure. Additional clinical assessments will be largely driven by symptom frequency and severity. However, re-assessment of the clinical condition should occur at every visit via symptom review and orthostatic blood pressure measurements. It helps you apply the most recent knowledge in personalized medicine, imaging techniques, pharmacology, interventional cardiology, electrophysiology, and much more!
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Thanks in advance for your time. Skip to content. About Elsevier. Search for books, journals or webpages All Pages Books Journals. Hardcover ISBN: Imprint: Saunders. Published Date: 18th September Page Count: Free Shipping Free global shipping No minimum order. Locate the answers you need fast thanks to a user-friendly, full-color design with more than 1, color illustrations. Part 1 Fundamentals of Cardiovascular Disease 1.
Global Burden of Cardiovascular Disease 2. Heart Disease in Varied Populations 3. Ethics in Cardiovascular Medicine 4. Clinical Decision Making and Cost Effectiveness 5.
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Measurement and Improvement of Quality of Cardiovascular Care 6. Overview of Personalized Cardiovascular Medicine 8. Principles of Cardiovascular Genetics and Genomics 9. Hemodynamic stabilization: inotropes e. Hemodialysis if volume overload is symptomatic pulmonary edema , pleural effusion , ascites and resistant to treatment ECLS may temporarily substitute pulmonary function. The prognosis depends on the patient, type and severity of heart disease, medication regimens, and lifestyle changes.
The prognosis for patients with preserved EF is similar to or better than for patients with decreased EF Risk stratification scales may be used to evaluate the prognosis e. Prepare and succeed on your medical exams. Find hundreds of Learning Cards covering all clinical subjects Practice answering thousands of USMLE-formatted multiple choice questions in the Qbank Explore concepts in depth with interactive images, videos and charts Fill knowledge gaps with the help of supportive features and an analysis of your progress.
Dyspnea , orthopnea Pulmonary edema in severe cases or acute decompensated heart failure see below Bilateral basilar rales may be audible on auscultation.
Paroxysmal nocturnal dyspnea : nocturnal bouts of coughing and acute shortness of breath Cardiac asthma : increased pressure in the bronchial arteries results in airway compression, leading to bronchospasm  Laterally displaced apical heart beat precordial palpation beyond the midclavicular line. Forward failure less pronounced. Slight limitations of moderate or prolonged physical activity e.
Marked limitations of physical activity symptoms during daily activities like dressing, walking across rooms ; comfortable only at rest. Confined to bed, discomfort during any form of physical activity; symptoms present at rest. No corresponding NYHA class. Structural damage to the heart e.
NYHA I. Heart failure at its terminal stage. Begin treatment with loop diuretics furosemide to treat volume overload Thiazides may be added for a synergistic effect. Monitor for hypokalemia and hyponatremia , weight gain, and volume status. Improve symptoms.
Initiate treatment with ACE inhibitors to reduce preload , afterload , and improve cardiac output If the patient does not tolerate drug e. Improve symptoms and prognosis. Add a beta blocker once the patient is stable on ACE inhibitor Particularly beneficial for patients with hypertension and post- myocardial infarction. Contraindicated in acute decompensated heart failure! In select patients, an aldosterone antagonist may be beneficial. Monitor for hyperkalemia. Contraindicated in severe bradycardia. Monitor for volume depletion and hypotension.
Improves symptoms; may improve prognosis. In heart failure with reduced ejection fraction If symptoms persist despite treatment with beta blocker , ACE inhibitor , diuretics , and aldosterone antagonists May be given to control ventricular rate in atrial fibrillation if beta blockers are contraindicated.
Related Complete Medical Guide and Prevention for Heart Disease Volume XVI; Hypotension
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