Clin med 1 ,Exam 2 ( MPAS 541-21 Shock,hypotension, pots, vasovagal syncop) Starting at ppt 33

Hypotension Definition

▪Extreme low BP seen with shock

▪Hypovolemic, cardiogenic, obstructive, and distributive

▪Lower BP compensated by faster heart rate

▪Correction of underlying cause always part of therapy

▪Signs include elevated jugular venous pressure, peripheral edema, pulmonary rales, cold and mottled extremities, and hypotension

Hypotension Criteria

▪Symptomatic

▪Drop in Systolic

▪Increase of HR

▪*** <90/60

Epidemiology of hypotension

▪Cardiogenic Shock is 2/3 of cases

▪Distributive Shock is 7%

▪Hypovolemic Shock is 3%

▪Mixed Shock is 20%

▪4% is noncategorizable

Etiology of Hypotension

•Emotional stress, fear, insecurity or pain (the most common causes of fainting)

•Dehydration, which reduces blood volume.

•The body's reaction to heat, which is to shunt blood into the vessels of the skin, leading to dehydration.

•Blood donation.

•Internal bleeding, such as a perforated stomach ulcer.

▪

Hypotension Risk Factors

•Age. Drops in blood pressure on standing or after eating occur primarily in adults older than 65. ...

•Medications. Certain medications, including some blood pressure drugs, increase the risk of low blood pressure.

▪Sudden shift in position

▪Standing for long periods

▪Sudden blood loss

Hypotension Pathology

Reduces blood flow and therefore oxygen delivery to organs and tissues, which may cause cellular damage and dysfunction.

Blood pressure is continuously regulated via the autonomic nervous system as a balance of the sympathetic nervous system and the parasympathetic nervous system.

▪The sympathetic nervous system acts to raise blood pressure by increasing heart rate and constricting arterioles.

▪The parasympathetic nervous system lowers blood pressure by decreasing heart rate and relaxing arterioles to increase vessel diameter.

▪

Hypotension Physical Exam

▪Vital Signs

•For most individuals, a healthy blood pressure lies from 90/50 mmHg to 135/90 mmHg. A small drop in blood pressure, even as little as 20 mmHg, can result in transient hypotension.

•Evaluating neurocardiogenic syncope is done with a tilt table test.

Clinical History/Presentation

▪Most common is lightheadedness or dizziness.

▪In extremely low pressures, syncope may occur. Other symptoms are possible which typically begin from the underlying etiology rather than hypotension itself. They may include chest pain, shortness of breath, irregular heartbeat, fever higher than 101 degrees Fahrenheit, headache, stiff neck, severe upper back pain, cough with sputum, diarrhea, vomiting, dysuria, acute allergic reactions, fatigue, or vision aberrations.

Laboratory Workup or Diagnostics of Hypotension

▪CBC

▪TSH

▪Free T4

▪Cortisol

▪EKG

▪Echo

▪CT angiogram Chest

Hypotension Diagnosed

▪90/60 or less is recognized as hypotensive

▪Benign condition usually

▪Easily missed due to no symptoms

Hypotension Differential Dx

•Benign hypotension

•Distributive shock

•Cardiogenic shock

•Hypovolemic shock

•Obstructive shock

•Combined-type hypotensive shock

Imaging

▪CT angiogram

▪TEE

Management Approach of hypotension

▪Underlying etiology

▪Monitor fluid electrolytes and replace

▪Trauma-replace blood if indicated

▪D/C and suspected medication

▪Vasopressors may be utilized

Goal Directed Treatment of HYpotension

▪Raise BP and keep patient asymptomatic

Monitor Treatment Response Hypotension

▪Ambulatory BP monitoring

▪If applicable, HH to monitor patient at home 3-5 times per week.

Hypotension Clinical Management

▪Asymptomatic hypotension should not receive drastic interventions. However, if symptoms are present, the treatment of hypotension should focus on reversing the underlying etiology.

▪Noninvasive imaging or hemodynamic indices of low cardiac output or systemic vascular resistance are not diagnostic but may help to classify hypotension.

Hypotension Prognosis

▪Good in mild disease

▪Complications of untreated hypotension with poor cardiac output are severe and can ultimately lead to death. In impending shock or fulminant shock, untreated hypotension can lead to multi-organ failure.

Hypotension on the long term

▪Risk of Falls

▪Heart Failure

▪Stroke

Cardiogenic Shock Criteria

occurs when the heart is unable to pump as much blood as the body needs. It can happen even if there hasn't been a heart attack if one of these problems occurs and your heart function drops suddenly.

Cardiogenic Epidemiology

▪Heterogeneous population of patients

▪The incidence of cardiogenic shock is in decline, which can be attributed to increased rates of use of primary percutaneous coronary intervention (PCI) for acute MI. However, approximately 5% to 8% of STEMI and 2% to 3% of NON-STEMI cases can result in cardiogenic shock. This can translate to 40,000 to 50,000 cases per year in the United States.

Cardiogenic shock Risk factors

▪Certain factors may increase your risk for cardiogenic shock.

•Age: People who are 75 or older have increased risk.

•Race or ethnicity: Asian Americans and Pacific Islanders have a higher risk of cardiogenic shock than other racial or ethnic groups. Hispanics and African Americans are not typically at higher risk for cardiogenic shock, but they are less likely than whites to receive emergency lifesaving treatment to restore blood flow when they do have cardiogenic shock.

•Sex: Cardiogenic shock may be more common in women than men. Women are also less likely than men to receive emergency treatment to restore blood flow when they have cardiogenic shock.

•Heart and blood vessel problems, such as coronary heart disease, heart failure, and high blood pressure

•Diabetes and prediabetes

•Overweight and obesity

•Past coronary artery bypass grafting (CABG)

•Pneumothorax, a type of pleural disorder that can lead to a collapsed lung

•sepsis, a life-threatening inflammatory response to an infection

▪

Cardiogenic shock Pathologic is

▪Complex and not fully understood

Cardiogenic shock Physical Exam

▪The presenting symptoms of cardiogenic shock are variable.

▪most common clinical manifestations of shock, such as hypotension, altered mental status, oliguria, and cold, clammy skin, can be seen in patients with cardiogenic shock.

•Altered mental status, cyanosis, cold and clammy skin, mottled extremities

•Peripheral pulses are faint, rapid, and sometimes irregular if there is an underlying arrhythmia.

•Jugular venous distension

•Diminished heart sounds, S3 or S4, may be present, murmurs in the presence of valvular disorders such as mitral regurgitation or aortic stenosis.

•Pulmonary vascular congestion may be associated with rales.

•Peripheral edema may be present in the setting of fluid overload

Cardiogenic shock Clinical History/Presentation

▪History plays a very important role in understanding the etiology of the shock and thus helps in the management of cardiogenic shock

Workup-Laboratory Testing or Diagnostics

•Complete blood picture, comprehensive metabolic panel, magnesium, phosphorous, coagulation profile, thyroid-stimulating hormone

•Arterial blood gas

•Lactate

•Brain natriuretic peptide

•Cardiac enzyme test

•Chest x-ray

•Electrocardiogram

•Two-dimensional echocardiography

•Ultrasonography to guide fluid management

•Coronary angiography

▪Due to the poor prognosis associated with cardiogenic shock, medical therapy is often inadequate, and mechanical circulatory support (MCS) therapy to improve end-organ perfusion may be required. An experienced interprofessional team should evaluate MCS.

Diagnostic Studies in Shock

▪Serum lactate levels followed serially

▪Venous and arterial blood gases

▪Complete blood count

▪BMP to assess for kidney perfusion/damage/hyperkalemia

▪EKG for acute coronary syndrome (ACS) evaluation

▪Chest film/echocardiogram

Dissection, pulmonary edema, pulmonary embolism, pericarditis, cardiac tamponade

Cardiogenic Shock Differential Diagnoses

▪Takotsubo cardiomyopathy

▪Acute myocarditis

▪Exercise-induced ventricular dysfunction

▪Pulmonary embolism

▪Hypotension

▪Obstructive shock

▪Distributive shock

▪Hypovolemic shock

▪Septic shock

cardiogenic shock Management Approach

▪Improve myocardial oxygenation, peripheral tissue perfusion, and control of tissue congestion

▪Medicine can help increase blood flow and protect against organ damage.

Cardiogenic Shock : Medical Management

Current Management Guidelines

1.Immediate transfer for PCI

2.Consider open heart surgery if PCI not available

3.Start fibrinolytic therapy if PCI and open surgery not available

4.Do not start beta-blockers

5.May use an IABP to stabilize the patient

6.Consider LV assist device if no contraindications

Cardiogenic Shock Clinical Management

•Medicines to restore a regular heartbeat are called anti-arrhythmia medicines.

•Blood thinners or antiplatelet medicines can dissolve blood clots and reduce platelets that may be blocking the coronary arteries.

•Medicines that increase blood pressure and blood flow out of the heart are called vasopressors and inotropes, including norepinephrine and dobutamine.

cardiogenic shock Goal Directed Treatment

▪Extracorporeal membrane oxygenation (ECMO) in veno-arterial configuration provides circulatory support. ECMO in cardiogenic shock provides rapid improvement of circulatory status and a significant increase in tissue perfusion.

▪An intra-aortic balloon pump (IABP) may improve survival when used with ECMO device.

▪Percutaneous circulatory assist devices (PCADs), including ventricular assist devices (VADs), can help support the heart until it recovers or while waiting for a heart transplant.

▪

Cardiogenic Shock Monitor Treatment Response

•Continuous kidney dialysis filters waste out of the blood if the kidneys are damaged.

•Fluids given through an intravenous (IV) line inserted in one of the blood vessels can maintain normal blood volumes.

•Mechanical breathing support, such as a ventilator, can protect the airway and provide extra oxygen.

•Oxygen therapy can help more oxygen reach the lungs, the heart, and the rest of the body.

Cardiogenic Shock Prognosis

Cardiogenic shock has the potential for significant morbidity and mortality if not recognized early.

Cardiogenic shock carries a poor prognosis and is the leading cause of death in patients with an acute MI. Close to 80% of patients die despite optimal treatment.

Complications associated with cardiogenic shock include:

•Dysrhythmias

•Cardiac arrest

•Renal failure

•Ventricular aneurysm

•Stroke

•Thromboembolism

•Death

Cardiogenic Shock Factors Affecting Prognosis

▪Six factors have been identified as independent predictors for 30-day mortality rate in the setting of cardiogenic shock: age older than 73, prior stroke, glucose on admission >191 mg/dL, creatinine >1.5 mg/dL, thrombosis in MI (TIMI) flow grades <3 after percutaneous coronary intervention (PCI), and arterial blood lactate being >5 mmol/L. Higher scores based on these risk factors have an increased mortality risk and these scores can help to risk stratify patients for short-term mortality and help with clinical decision-making

Cardiogenic Shock Long Term

▪Despite advances in therapy, shock continues to have a high mortality rate, even when identified early and treated appropriately in an ICU environment. Hospital mortality rate of cardiogenic shock can be as high as 60%.

▪Patients with shock are continually monitored in an ICU setting. Management of shock is performed in a hospital setting so patient education is done in order to prevent a recurrence of this condition. In a trauma setting leading to massive bleeding and injury, common sense counseling such as seatbelt and helmet use are emphasized. Because cardiogenic shock is a frequent cause of shock overall, aggressive secondary preventive strategies are employed in order to prevent cardiac decline over time.

Cardiogenic Shock Therapy

▪Done to improve myocardial oxygenation, peripheral tissue perfusion, and control of tissue congestion

Treatments attempt to optimize oxygen delivery and reverse poor perfusion by providing volume resuscitation in the form of crystalloid administration, packed RBCs for bleeding

▪ACS not responding to treatment may need intra-aortic balloon counterpulsation, extracorporeal membrane oxygenation, left ventricular assist device, vasopressors to maintain blood pressure after fluids are given

Cardiogenic Shock Key points

▪Mortality rate high

▪Treat underlying cause

▪More than just hypotension

•Poor perfusion

Hypertrophic cardiomyopathy

Left ventricular outflow tract obstruction causing decreased cardiac output and increased risk of ventricular dysrhythmia leading to loss of consciousness and sudden death.

Severe aortic stenosis

Fixed left ventricular outflow tract obstruction leading to decreased cardiac output and loss of conscousness

Long QT syndrome

Genetic channelopathy increasing the risk of sudden development of ventricular tachycardia/ventricular fibrillation leading to loss of consciousness and sudden death

Wolff-Parkinson-White (WPW) syndrome

Palpitations due to development of supraventricular tachycardia (SVT). Fast conducting accessory pathway may lead to development of ventricular dysrhythmia and loss of consciousness. If atrial fibrillation develops in these patients, it can be fatal.

Neurologic disorders (seizure)

Loss of consciousness with bowel/bladder incontinence or postictal amnesia.

Metabolic disorders (hypoglycemia/thyroid disease)

Hypoglycemia causing dizziness. Thyroid disease, causing changes in heart rate

Vasovagal Syncope

▪Type of reflex syncope, is a transient loss of consciousness due to a sudden drop in heart rate and blood pressure.

▪Triggers include prolonged periods of standing, excessive heat, or pain.

▪Treated conservatively with positional change and improving hydration.

▪Cerebral hypoperfusion occurring after several minutes in an upright position causing transient loss of consciousness and loss of postural tone.

▪3 P's-posture, Provoking, Prodromal

Vasovagal Criteria

▪Systolic blood pressure drops more than 20 mm Hg, and /or the heart rate increases by 30 beats per minute (bpm) or more.

▪Determine if the syncopal event/symptoms

consistent with a "vasovagal syncope" or due to another cause.

Vasovagal Epidemiology

▪There is a bimodal distribution in the incidence of vasovagal syncope with peaks during adolescence and senior age groups. Females are twice as likely as males to experience reflex-mediated syncope during adolescence.

Vasovagal Etiology

▪What is the most common etiology of syncope in adults?

▪It most often occurs when blood pressure is too low (a condition called hypotension) and the heart doesn't pump enough oxygen to the brain. It can be harmless or a symptom of an underlying medical condition.

▪ Vasovagal reaction is an exaggeration of an adaptive response meant to assist in hemostasis in times of trauma

Vasovagal Risk Factors

High‐risk factors for cardiogenic syncope included:

▪ age ≥60

▪male

▪hypertension

▪palpitation

▪troponin T‐positive

▪abnormal ECG

▪CHD history

▪syncope‐related trauma

Vasovagal Pathology

▪When Standing initially, decrease in central blood volume, decreased stroke volume, and decreased cardiac output despite increase in heart rate.

▪Blood pressure variability during this stage

mean systolic pressure may be preserved by an increase in systemic vascular resistance.

▪Circulatory instability occurs after continued decrease in both cardiac output and central blood volume.

▪Hypotension and vasovagal loss of consciousness occur with an increase in lower body negative pressure inducing a fall in heart rate and cardiac output

Vasovagal Physical Exam

Orthostatic vital signs

▪Experiences symptoms during the testing

▪Systolic blood pressure drops more than 20 mm Hg

▪and /or the heart rate increases by 30 beats per minute (bpm) or more.

Thyroid

▪Palpated and assessed for underlying thyroid disease.

Respiratory examination unremarkable

Cardiac examination unremarkable

▪Not uncommon to appreciate a marked increase in the patient's heart rate by auscultation with positional changes.

Consider further workup for structural heart disease if a murmur is present. (what test?)

Abdominal examination unremarkable.

Peripheral examination should reveal normally palpable pulses in all extremities with brisk capillary refill. No Peripheral edema should be present.

Vasovagal Clinical History/Presentation

•Dizziness with positional changes (typically described as lightheadedness not "the room is spinning")

•Palpitations (typically not with sudden onset)

•Paresthesia

•Visual changes (tunnel vision, seeing spots)

•Pallor

•Diaphoresis

•Nausea/vomiting

Vasovagal Syncope Signs and Symptoms

▪Dizziness with positional changes (typically described as lightheadedness, not "the room is spinning")

▪Palpitations (typically not with sudden onset)

▪Paresthesia

▪Visual changes (tunnel vision, seeing spots)

▪Pallor

▪Diaphoresis

▪Nausea/vomiting

Vasovagal Syncope Differential Diagnoses

Hypertrophic cardiomyopathy

Severe aortic stenosis

Long QT syndrome

•Congenital or acquired

Wolff-Parkinson-White

Neurologic disorders

•Seizures

Metabolic disease

•Hypoglycemia

•Thyroid disease

Differential Diagnosis for Vasovagal Syncope

Hypertrophic cardiomyopathy

Severe aortic stenosis

Long QT syndrome

Wolff-Parkinson-White (WPW) syndrome

Neurologic disorders (seizure)

Metabolic disorders (hypoglycemia/thyroid disease)

Vasovagal workup

•24-hour Holter monitor: Performed if there is a concern for cardiac dysrhythmia.

•Echocardiogram: Performed if the syncopal event or family history raises concerns for structural heart disease.

•Exercise stress test: Performed if the syncopal event or family history raises concerns for structural heart disease. Will also be considered if the syncopal event is related to exercise.

•Tilt table testing (rarely performed): May be performed by a cardiology electrophysiologist if other testing is inconclusive or there is a suspicion of genetic cardiac dysrhythmia that was not able to be identified by other testing.

Differential Diagnosis of vasovagal

•Dehydration

•Diabetic neuropathy

•Diuresis

•Drug-induced orthostasis

•Dysautonomia

•Ectopic pregnancy

•Hemorrhage

•Hypotension

•Hypovolemia

•Multisystem atrophy

•Peripheral polyneuropathy

•Postural hypotension

•Subclavian steal

•Vasomotor insufficiency

Laboratory Testing or Diagnostics of Vasovagal

Diagnostic studies are performed to rule out other disorders.

▪EKG: Done as a screening tool for all syncope.

▪The EKG should show normal sinus rhythm with normal QTc interval and no pre-excitation (delta wave) or shortening of the QT interval.

Syncope Evaluation

▪EKG

screen; identifies pre-excitation, prolonged QT, conduction disorders

▪Twenty-four-hour Holter monitor/cardiac event monitor

Done if cardiac dysrhythmia suspected

▪Echocardiogram

Structural disease

▪Exercise stress test

*Tilt table testing

▪postural orthostatic tachycardia syndrome (POTS)

Syncope Management Approach

▪Initial treatment involves optimizing hydration, increasing salt intake to further improve intravascular volume, and decreasing or eliminating caffeine (a diuretic that decreases intravascular volume). Extensive time should be spent educating patients on potential triggers and avoidance of known triggers if possible. Triggers include hot/humid environments, rapid positional changes, prolonged standing, poor sleep quality, fasting (hypoglycemia), emotional/physical stress/anxiety, pain, or hormonal fluctuations during menstrual cycle.

Syncope Treatment

▪Optimize hydration

▪Decrease caffeine

▪Avoid known precipitants/triggers

▪Compression stockings

▪Supplemental salt tablets if needed

▪Mineralocorticoid fludrocortisone

▪Beta-blockers if need prolonged filling times

▪Midodrine as vasoconstrictor

Goal Directed Treatment of vasovagal syncope

•Compression stockings may be considered to aid in centralizing intravascular volume during periods of standing.

•Supplemental salt tablets may be utilized to optimize salt intake if patient is unable to adequately obtain salt from dietary means alone.

•If lifestyle modifications are inadequate to control the patient's symptoms, pharmacologic therapy is considered.

vasovagal syncope Clinical Management

•Typical first-line agent is fludrocortisone 0.1 to 0.4 mg per day. Typical dose is 0.2 mg orally (PO) daily either as a single dose or divided twice daily. Mechanism of action is sodium retention by the kidneys promoting shift of water from the renal tubules back to the vasculature. This medication should be taken with water to increase effectiveness.

•Secondary pharmacologic therapy (if patient fails fludrocortisone) includes beta blockade therapy or vasoconstrictive agents such as midodrine.

•❍ Consider beta blockade therapy in patients with complaints of palpitations or tachycardia with minimal exertion. Start with a small dose and slowly uptitrate to desired effect. Be mindful that beta blockers may cause hypotension and worsening dizziness.

•❍ Consider midodrine in patients whose primary complaint is dizziness and hypotension is noted on physical examination. Midodrine is typically dosed three times per day but can be used twice daily as well. Blood pressure should be monitored closely for significant hypertension. Counsel patients to avoid lying supine for at least 30 minutes after receiving a dose of midodrine to avoid sudden elevation in systolic blood pressure.

Vasovagal syncope prognosis

appears to have a benign prognosis

Factors Affecting Prognosis of vasovagal syncope

▪Prognosis is determined by the underlying etiology, specifically the presence and severity of cardiac disease.

▪Untreated, mortality can be >10% at 6 months, whereas vasovagal and other reflex mediated syncope have a generally favorable prognosis.

Long term aspect of vasovagal syncope

Can be chronic and can cause flare-ups

▪Falls

▪Immobility, due to fainting

Postural Orthostatic Tachycardia Syndrome(POTS)

is a form of dysautonomia — a disorder of the autonomic nervous system. This branch of the nervous system regulates functions we don't consciously control, such as heart rate, blood pressure, sweating and body temperature. The key characteristics of POTS are the specific symptoms and the exaggerated increase in heart rate when standing

POTS is characterized by two factors

•A specific group of symptoms that frequently occur when standing upright

•A heart rate increase from horizontal to standing (or as tested on a tilt table) of at least 30 beats per minute in adults, or at least 40 beats per minute in adolescents, measured during the first 10 minutes of standing

True or false : ▪**Most common form of orthostatic intolerance in young people

True

Types and Causes of POTS

▪Causes of postural tachycardia syndrome (PoTS)

•feeling hot.

•eating, especially refined carbohydrates like white bread.

•not drinking enough fluids.

•drinking alcohol.

•resting too much.

•exercise.

•being on your period.

POTS Criteria

▪To diagnose excessive orthostatic tachycardia (required for POTS), patients should have a sustained heart rate increase of at least 30 beats/min (for adults) or at least 40 beats/min (for patients aged 12-19 yr) on at least 2 of the readings taken when standing.

Table 1. Criteria for the Postural Tachycardia Syndrome

Heart rate increases ≥30 bpm from supine to standing (10 min)

Symptoms worsen with standing and improved with recumbence

Symptoms last ≥6 mo

Absence of other overt cause of orthostatic symptoms or tachycardia (eg, active bleeding, acute dehydration, medications)

POTS Pathology

▪Complex pathophysiology of postural tachycardia syndrome (POTS)

▪The mechanisms of orthostatic intolerance in POTS include:

▪impaired sympathetic vasoconstriction leading to venous pooling

▪Hypovolemia

▪Deconditioning

hyperadrenergic state

Why POTS is a syndrome and not a disease?

Many disorders with the common key clinical presentation of orthostatic tachycardia have been described. Much has been learned about specific features or subtypes within POTS, although a simple test to categorize the individual patient remains elusive.

POTS symptoms vary from person to person

•Severe and/or long-lasting fatigue

•Lightheadedness with prolonged sitting or standing that can lead to fainting

•Brain fog: trouble focusing, remembering or paying attention

•Forceful heartbeats or heart palpitations (a feeling of the heart pounding or skipping a beat)

•Nausea and vomiting

•Headaches

•Excessive sweating

•Shakiness

•Intolerance of exercise or a prolonged worsening of general symptoms after increased activity

•A pale face and purple discoloration of the hands and feet if the limbs are lower than the level of the heart

POTS Epidemiology

POTS is a disorder affecting predominantly young women

POTS Etiology

The complex heterogeneous etiologies of POTS generally classify as neuropathic, hyperadrenergic, hypovolemic, autoimmune, and physical deconditioning with significant overlap between the various etiologies.

POTS risk factors

•Faster supine HR, less water intake and shorter sleeping hours were identified as risk factors for POTS.

POTS Physical exam

▪Vital Signs-For orthostatic vital signs, BP and HR should ideally be measured after the patient has been supine for at least 5 minutes, and again after 1, 3, 5, and 10 minutes of standing to capture the sustained orthostatic tachycardia.

POTS Clinical History/Presentation

•Dizziness or lightheadedness, especially when standing up, during prolonged standing in one position or on long walks.

•Fainting or near fainting.

•Forgetfulness and trouble focusing (brain fog).

•Heart palpitations or racing heart rate.

•Exhaustion/fatigue.

•Feeling nervous or anxious.

•Shakiness and excessive sweating.

•Shortness of breath (dyspnea).

•Chest pain.

•Headaches.

•Feeling sick.

•Bloating.

•A pale face and purple discoloration of your hands and feet if they're lower than the level of your heart.

•Disrupted sleep from chest pain, racing heart rate and excessive sweating during sleep.

POTS Laboratory Workup or Diagnostics

▪ECG-resting 12-lead ECG

▪Holter Monitor-exclude re-entrant dysrhythmia in patients with history of paroxysmal tachycardia with sudden onset/offset.

▪Plasma norepinephrine

▪CBC with diff (reflex to iron studies)

▪TSH/free T4

▪CMP

POTS DIAGNOSED

▪can be complicated.

▪In most instances, symptoms have been present for months before the diagnosis is made.

▪Provider will perform a physical exam, order bloodwork and arrange a standing test or a head-up tilt table test to confirm POTS.

POTS as Differential Dx

▪acute dehydration, diabetes mellitus, cardiomyopathy, heavy-metal poisoning, Sjögren's syndrome, systemic lupus erythematosus, deconditioning, inappropriate sinus tachycardia, pheochromocytoma, thyrotoxicosis, or manifestations of a paraneoplastic syndrome

POTS Imaging

▪MRI and other imaging tests to rule out tumors or other abnormalities.

POTS Management Approach

▪should be tailored to each individual, because the symptoms and underlying conditions may vary widely. No therapy is uniformly successful, and combinations of approaches are often needed. Efforts should initially focus on treating any reversible causes.

▪Although there is no known cure for POTS, the condition can be managed in most patients with diet, exercise and medications.

POTS Goal Directed Treatment

•Improving blood volume

•Helping the kidneys retain sodium (e.g., fludrocortisone)

•Reducing heart rate or blocking the effect of adrenal hormones on the heart (e.g., beta blockers)

•Improving blood vessel constriction (e.g., midodrine)

▪

POTS Monitor Treatment Response

▪frequently monitoring your pulse and blood pressure

▪check your blood pressure and pulse when you aren't feeling well.

POTS Clinical Management

Unfortunately, there's no cure for POTS. Instead, manage the symptoms of POTS.

Treatment is highly individualized based on your symptoms and what works best for you.

The main forms of treatment include:

•Exercise and physical activity.

•Diet and nutrition.

▪Medical compression stockings can also help push blood up from your legs to reduce POTS symptoms.

Presence of hypovolemia is either known or strongly suspected, fludrocortisone (aldosterone analog) is often used. Another volume-expanding agent that may be helpful for short-term use is desmopressin (DDAVP).

▪

▪

POTS Prognosis

▪While POTS can be life-changing, it is not life-threatening

▪The prognosis (outlook) for POTS is generally good, although it can severely disrupt daily living. POTS symptoms may come and go for years. In approximately 80% of cases, the condition improves, but many people have residual symptoms.

▪The biggest risk to people with POTS is getting hurt if they faint and fall.

▪

POTS Long terms impact

▪Activities of daily living such as bathing or doing housework may greatly exacerbate symptoms, with resultant fatigue.