Hypotension Focus: “It’s not ACS or HF, but it will be on

the PANRE”Andrea Applegate, PA-C

Question #1

Which of the following “pains” is associated with orthostatic hypotension?

A. “toe box” pain

B. “coat hanger” pain

C. “hat band” pain

D. “saddle” pain

Question #2

If a patient complains of nausea and dizziness 5 times in the past year, which they believe is associated with “low pressure”, they are ___

A. Class I

B. Class II

C. Class III

D. Faking it

Question #3VA ECMO does which of the following?

A. Oxygenates blood while allowing the heart to pump naturally

B. Contains ghosts after they are lassoed by a Proton Pack.

C. Circulates blood during routine open heart surgery.

D. Oxygenates and circulates the blood.

Hypotension Focus: Orthostatic Hypotension

Orthostatic intoleranceOrthostatic hypotension (primary vs secondary)

Structural (neurogenic): chronic autonomic failure. Multiple system atrophy, Parkinson’s disease. Can also be secondary to diabetes, amyloidosis, or advanced renal failure.

Functional (non-neurogenic): treatment with vasodilators, TCA, chemo, diuretics, blood volume loss, heart failure with chronotropic or inotropic changes.

Neutrally mediated (reflex) syncope

Postural tachycardia syndrome

Blood pressure regulation

Clinical PresentationNormal response to standing:

Pooling of blood in lower extremities and splanchnic circulation (500-1000 ml)

Venous return to the heart decreases, resulting in diminished cardiac output and BP.

Compensatory reflex with nervous system increases sympathetic stimulation and decreases parasympathetic (baroreceptor reflex).

Peripheral vascular resistance is raised with SNS stimulation, increasing venous return and reversing above changes in vitals, limiting BP drop.

Symptoms include dizziness, syncope, TIA, angina, “coat hanger” pain, visual changes.

Exacerbated by venous pooling and dehydration; heat, fever, alcohol, urination, post-exercise, and immobilization. Nocturnal polyuria can occur due to fluid shifts, causing overnight volume loss.

Can occur after eating (postprandial hypotension) and worse in those with autonomic failure.

Etiology20% of those aged >65 were found to have postural hypotension.

Some studies associate it with vasodilators including nitrates and CCB, antidepressants, opiates, and alcohol.

Most do not have underlying neurogenic cause.

Consider adrenal insufficiency, central nervous system dysfunction, arrhythmia, spinal cord origin, myocardial ischemia, autonomic neuropathy, sepsis, hypovolemia, and acute autonomic neuropathy.

In young, usually occurs in volume depletion or chronic autonomic failure.

Criteria, updated 2011Classic: Drop in SBP 20 mmHg or DBP 10 mmHg within 3 minutes or stand or tilt.

Initial: rapid drop in SBP 40 mmHg and/or DBP of 20 mmHg within 15 seconds.

With hypertension: drop of SBP of 30 mmHg or more (higher baseline).

Delayed: reduction occurring after 3 minutes of standing, may progress up to 45 minutes.

Tilt Table TestingIndicated in high probability despite negative eval, motor impairment, and monitoring response to therapy.

Patient is supine for 5 minutes, then table is slowly elevated 60-80 degrees for three minutes.

Positive if blood pressure falls or if patient becomes symptomatic.

Evaluation

Classes of OH

TreatmentConservative Treatment:

Compression hose (30-50 mmHg) hip height.

Abdominal binding (20-30 mmHg): may increase tolerance of BP drop by 40%. Remember “the higher, the better” due to volume of venous circulation in abdomen.

Physical counter-maneuvers: avoiding sudden changes, 5 minute “dangle”, 2 L of fluid per day, avoiding hot environments, calf exercises, squats.

Head of bed height elevated 10-30 degrees

Neurogenic OH may improve with bolus water intake and eating smaller more frequent meals.

Comprehensive Geriatric Assessment (CGA)

Medications to consider decreasing or stopping: Diuretics, sympatholytics, vasodilators, antihypertensives, antidepressants, anti-parkinsonism medications.

Consider nighttime administration of antihypertensive drugs (to avoid sleep-time hypertension >160/90)

Treatment, cont.Fludrocortisone: synthetic mineralocorticoid, expands plasma volume with sodium intake.

Midodrine: alpha-adrenoceptor agonist. Should be taken 1 hour before rising, last dose 4 hours before bed to avoid nocturnal hypertension. Half life of 3 hours.

Droxidopa: prodrug metabolized to noradrenaline. Administer during the day to avoid NOC HTN.

Pyridostigmine: peripheral acetylcholinesterase inhibitor.

Emerging agents:

Atomoxetine: noradrenaline reuptake inhibitor (vasopressor effect)

Miragegron: beta-3 adrenergic receptor (stimulatory effect)

TD-9855: noradrenaline and serotonin reuptake inhibitor. Still in clinical trials.

PrognosisIncreasingly found in patients with hypertension and diabetes. Also more common in renal failure and autoimmune disease.

Increased 5-year mortality and incidence of cardiovascular disease and heart failure.

Stronger association with mortality and OH in <65 than those older.

>50% delayed OH progressed to OH within 3 minutes.

1/3 developed an alpha-synuclieopathy

Hypotension Focus: Cardiogenic Shock

Shock

Cellular hypoxia (supply vs demand)

Hypotension: circulatory failure, reduced perfusion

Elevated serum lactate

May result in multi-system organ failure and can become irreversible.

Types of Shock

Distributive

Hypovolemic

Obstructive

Cardiogenic

Cardiogenic ShockDecreased cardiac output and hypoperfusion despite adequate volume status.

Signs: poor UOP, tachycardia, mental status changes, cyanosis, increased respirations. May have normal BP, JVD, rales, clammy appearance.

Eventually develop systemic hypotension.

Systolic blood pressure <90 mm Hg, cardiac index <2.2 L/min/m2, and the presence of normal or elevated pulmonary capillary occlusion pressure [>15 mm Hg], or right ventricular [RV] end-diastolic pressure [RVEDP; >10 mm Hg])

Who to suspect

STEMI (chest pain, EKG changes)

Acute aortic or mitral valve insufficiency (chest pain, new murmur, pulmonary edema)

Dissection (hypertension, tearing chest and/or back pain)

Arrhythmia (abnormal EKG, syncope)

Myocardial infarction

Loss of perfusion to myocardium resulting in inability to contract. Can lead to necrosis or stunned myocardium.

Reduces contractility, coronary filling pressures, stroke volume.

Leads to increased end systolic volume, diastolic filling and volume, leading to increased oxygen demands and cardiac work.

Eventually leads to poor systemic perfusion, sympathetic stimulation, salt and fluid retention, lactic acidosis, and death.

Acute structural dysfunction

Papillary muscle rupture, usually caused by ischemia, causing valvular insufficiency

Obstruction due to thrombus, causing cardiac output decrease.

Septum rupture due to ischemia, causing decreased output due to shunting.

Aortic dissection

Can result in acute aortic insufficiency.

Blood may leak into pericardial sack, resulting in pericardial effusion.

Cardiac tamponade may result, causing restrictive reduction in cardiac output.

What will you find?Patient will appear gray or ashen, with cool skin.

May seem confused

Will have not gone to the restroom or had much urine output in the past few hours.

Pulses will be faint, heart sounds distant. May have murmur or gallop.

Breathing and heart rates will increase.

May sound “wet” and have low SpO2.

What do you needAirway

Ventilation (or O2)

Venous access for volume

• Labs: CBC, CMP, lactate, cardiac enzymes, BNP, coags, VBG

ABG with arterial line (maybe)

PA catheter (maybe)

IABP (maybe)

ImagingChest radiograph

Abdominal radiograph

CT head, chest, abd, pelvis

CTA aorta/pulmonary vasculature

US at bedside

TTE or TEE

EKG

Cardiac cath

Treatment

#1 volume (typically 500 to 1000 ml boluses, crystalloids)

Then vasopressors

Adrenergic agonists: Norepinephrine, epinephrine, and phenylephrine.

Inotropes: dobutamine, dopamine, milrinone.

Intra-aortic balloon pump

Placed in cath lab or at bedside in ICU with fluoro.

Increases coronary perfusion

Decreases afterload and cardiac oxygen demands.

ECMO and VAD

Extracorporeal membrane oxygenation

Bedside “bypass” that allows the body time to heal

VA ECMO circulates and oxygenates the blood

VV ECMO oxygenates the blood

Ventricular assist device - implantable “pump”

Interventions and surgical repair

Balloon angioplasty

PCI with stenting (DES vs BMS)

Coronary artery bypass grafting

Valve replacement or repair

Thoracic aortic repair or replacement

Bentall procedure (AVR, thoracic aorta, and re-implant coronaries)

Prevention and after-care

Early identification is key to reducing morbidity and mortality.

Cardioprotective medications (ASA, statin, beta-blocker) are guideline therapies.

ReferencesUpToDate: Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock. Accessed 2/24/2018.

UpToDate: Mechanisms, causes, and evaluation of orthostatic hypotension. Accessed 04/30/2018

Current Medical Diagnosis & Treatment 2017. Papadakis et. al. 56th edition, McGraw Hill Education.

Cardiogenic Shock. https://emedicine.medscape.com/article/152191-overview. Accessed 02/24/2018.

“Orthostatic Hypotension: Epidemiology, Prognosis, and Treatment” Fabrizio Ricci et al. Journal of the American College of Cardiology: 66 (7):848-860. Accessed 04/30/2018.

“New Horizons in Orthostatic Hypotension” Age Ageing. 2017; 46 (2): 168-174. Medscape accessed 04/30/2018.

“Postural and Postprandial Hypotension: Approach to Management” Geriatrics and Aging 2007; 10(5):298-304. Medscape accessed 04/30/2018.

“Evaluation and Management of Orthostatic Hypotension” American Family Physician. 2011 September; 84(5):527-536. Accessed online 04/30/2018.

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