What medications are contraindicated in aortic stenosis?
May 19, 2020 · Why is aortic stenosis afterload dependent? The patient with severe aortic stenosis is relatively "afterload fixed and preload dependent" -- meaning cardiac output does not increase with after-load reduction. Thus all afterload reducing agents (angiotensin-converting enzyme inhibitors, calcium channel blockers, blockers) are contraindicated.
What are the end stages of aortic stenosis?
The patient with severe aortic stenosis is relatively “afterload fixed and preload dependent” — meaning cardiac output does not increase with after-load reduction. Thus all afterload reducing agents (angiotensin-converting enzyme inhibitors, calcium channel blockers, blockers) are contraindicated.
Why is nitroglycerin contraindicated in aortic stenosis?
Jul 01, 2015 · Aortic valve area is measured as an index to body surface area, and is represented as cm 2 /m 2. Mild stenosis is compensated for by LV hypertrophy, as the LV is expected to generate an increasing pressure to drive blood across the narrowing valve. Moderate stenosis (an aortic valve index below 0.7cm 2 /m 2) results in some degree of LV failure ...
What is the prognosis for severe aortic stenosis?
Jun 22, 2018 · Antihypertensive treatment in severe AS is safe and may be important for reducing the LV pressure overload and retarding the progression of severe valvular aortic stenosis. To date, no randomized clinical trial has been performed and no definite treatment guideline for antihypertensive regimens. However, RAS inhibitors and β-blockers are safe ...
Is aortic stenosis afterload dependent?
The patient with severe aortic stenosis is relatively "afterload fixed and preload dependent" -- meaning cardiac output does not increase with after-load reduction. Thus all afterload reducing agents (angiotensin-converting enzyme inhibitors, calcium channel blockers, blockers) are contraindicated.
How does afterload affect aortic stenosis?
This leads to an increase in ventricular wall stress (afterload), a decrease in stroke volume, and an increase in end-systolic volume. Stroke volume (width of PV loop) decreases because the velocity of fiber shortening is decreased by the increased afterload (see force-velocity relationship).
Why is as afterload dependent?
Afterload is the pressure that the heart must work against to eject blood during systole (ventricular contraction). Afterload is proportional to the average arterial pressure. As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles respectively.
Does aortic stenosis increase preload or afterload?
During the asymptomatic latent period, left ventricular hypertrophy and atrial augmentation of preload compensate for the increase in afterload caused by aortic stenosis. As the disease worsens, these compensatory mechanisms become inadequate, leading to symptoms of heart failure, angina, or syncope.Sep 15, 2008
Why does ventricular dilation increase afterload?
At a given intraventricular pressure, wall stress and therefore afterload are increased by an increase in ventricular inside radius (ventricular dilation). A hypertrophied ventricle, which has a thickened wall, has less wall stress and reduced afterload.
Is aortic stenosis preload dependent?
[3] Patients with aortic stenosis often have ventricular tachycardia during syncopal episodes. [4] It is critical to remember that patients with aortic stenosis are preload dependent and require aggressive fluid support to maintain their cardiac output.
Why would you want to increase afterload?
An increase in afterload causes a decrease in stroke volume and the velocity of left-ventricular shortening. The resulting stress-shortening and stress–velocity curves are analogous to those obtained from variably afterloaded isotonic contractions in isolated muscle.
What causes low afterload?
The afterload can be decreased by any process that lowers blood pressure. Mitral regurgitation also decreases afterload since blood has two directions to leave the left ventricle. Chronic elevation of the afterload leads to pathologic cardiac structural changes including left ventricular hypertrophy.
Why does afterload decrease stroke volume?
The effect of afterload on stroke colume is due to the fact that the maximum pressure that the heart can develop is smaller at lower ventricular volumes. Therefore, if the systolic pressure is lower, the heart will be able to contract to a smaller volume at the end of systole.
Does aortic stenosis cause increased cardiac output?
In most patients with aortic stenosis, LV systolic function is preserved and cardiac output is maintained for many years despite an elevated LV systolic pressure. Although cardiac output is normal at rest, it often fails to increase appropriately during exercise, which may result in exercise-induced symptoms.
How does aortic stenosis affect cardiac output?
Aortic stenosis can reduce ventricular stroke volume due to increased afterload (which decreases ejection velocity). The reduced stroke volume decreases the aortic pulse pressure, and the mean aortic pressure will fall if the reduced cardiac output is not offset by an increase in systemic vascular resistance.
What is the purpose of an arterial catheter?
An arterial catheter shortens the detection time for hemodynamic abnormalities and is mandatory in severe cases of AS. EKG findings are often obscured by the LVH, making myocardial infarction difficult to detect. Pulmonary artery catheters are often used, however keep in mind that the wedge pressure is not a good indicator of ventricular filling, as ventricular compliance is greatly reduced. Vasodilators should be avoided unless a PA catheter is in place. TEE can be a useful adjunct as well. Always have a defibrillator available because external compressions are essentially useless with significant stenosis.
Is AS congenital or rheumatic?
AS can be divided into congenital (bicuspid), rheumatic, or degenerative (calcific). If in concert with rheumatic fever, is almost always associated with mitral pathology. These patients have an increased incidence of sudden death as compared to the general population.
What are the vital signs of a 90 year old male?
His vital signs are as follows: HR 112, BP 85/60, RR 28, SpO2 85% on room air. Bedside ultrasound reveals diffuse B lines consistent with pulmonary edema, and he is placed on non-invasive positive pressure ventilation.
Does phenylephrine increase blood pressure?
As a pure alpha-1 agonist, phenylephrine increases diastolic blood pressure and thus improves coronary perfusion. Phenylephrine also may result in a reflex bradycardia — a favorable pharmacodynamic property for its use in aortic stenosis. 9 Norepinephrine is, similarly, a reasonable choice.
What is critical aortic stenosis?
Critical aortic stenosis (AS) is the single most problematic valvular disease we encounter in the emergency department. Patients with critical AS have a fixed cardiac output and cannot meaningfully increase cardiac output to meet the physiologic demands of critical illness. Avoiding systemic hypotension, maintaining sinus rhythm, ...
Does a tight aortic valve cause pulmonary congestion?
The tight aortic valve increases left-sided pressures and can lead to pulmonary congestion. However, patients with AS also have diastolic dysfunction and depend on preload to fill the left ventricle and maintain cardiac output. Decisions on fluid administration are challenging in this patient population and should be made in the context of the clinical scenario.
What is the prevalence of AS?
AS is the third most common cardiovascular disease in the developed world, eclipsed only by systemic hypertension and coronary artery disease. The prevalence in the general population is 0.4%, but increases to 9.8% in octogenarians, with an overall prevalence of 2.8% in adults older than 75 years of age. 1,2 Valve replacement, either surgical or catheter directed (ie, transcatheter aortic valve replacement, or TAVR), is the mainstay of treatment for advanced disease.
What is the best vasopressor for a hypotensive patient?
Phenylephrine is the vasopressor of choice in treating the hypotensive patient with AS. Using an agent that solely increases afterload is initially counterintuitive. It is important to recognize that the massive afterload of aortic stenosis is at the level of the aortic valve, with little contribution from the systemic vasculature. As a pure alpha-1 agonist, phenylephrine increases diastolic blood pressure and thus improves coronary perfusion. Phenylephrine also may result in a reflex bradycardia — a favorable pharmacodynamic property for its use in aortic stenosis. 9 Norepinephrine is, similarly, a reasonable choice. Avoid epinephrine as a first line agent given its strong beta-1 agonism and propensity to promote tachycardia and increase myocardial oxygen demand.
What causes afterload?
Factors that affect afterload include : 1 Increased or decreased aortic pressure—when the blood pressure is increased, there is a natural increase in the pressure the ventricle must press against and increased Similarly, when the blood pressure is reduced, there is less force to be pressed against by the ventricles and a reduction in afterload. 2 Increased or decreased systemic vascular resistance (SVR)—the systemic vascular resistance will affect the overall pressure and will change the resistance to outflow of the ventricles. Increased SVR will increase the afterload, while decreased SVR will decrease the afterload. 3 Aortic valve stenosis—this will not affect the aortic pressure but will, of course, change the force that the heart needs to push against, increasing the afterload. 4 Ventricular dilation—this will increase the afterload by increasing the radius of the heart chamber. The wall stress, as you know, is proportional to the radius of the chamber so it will increase the end-diastolic volume because the ventricle will not be able to push blood out to the extent it needs to. This decreases the stroke volume or the amount of blood that is pushed out of the ventricle with each beat.
What is the preload of a drug?
The preload is the amount of stretch or pressure left in the left ventricle at the end of diastole—when the heart is the most relaxed. It is also referred to as the left ventricular end-diastolic pressure ...
Does Nitroprusside lower blood pressure?
By relaxing arterial smooth muscle, the systemic vascular resistance will decrease and blood pressure will be reduced. The major effect of nitroprusside is on the arteries, meaning that it affects afterload more than preload. It does, however, relax venous smooth muscle, reducing the preload to a lesser degree.
What is the afterload of the left ventricle?
The afterload is the amount of vascular resistance that must be overcome by the left ventricle to allow blood to flow out of the heart. It is also referred to as the systemic ...
What happens when blood pressure is increased?
Increased or decreased aortic pressure—when the blood pressure is increased, there is a natural increase in the pressure the ventricle must press against and increased Similarly, when the blood pressure is reduced, there is less force to be pressed against by the ventricles and a reduction in afterload.
What happens to the left ventricular afterload?
Anytime the afterload is increased, the stroke volume will be decreased and the left-ventricular end-diastolic volume (the preload) will be increased. Increased afterload will decrease the speed of myocardial muscle fiber shortening. Because the time frame for ventricular ejection is only 200 milliseconds, a shorter velocity translates ...
What is preload in cardiac muscle?
The preload is directly related to the stretch of the sarcomeres (or muscle fiber units) of the ventricular cardiac muscle. This, of course, is impossible to actually determine in a living person so it is indirectly measured as the left ventricular pressure during diastole or the ventricular end-diastolic volume.
Causes
Epidemiology
Prognosis
- Normal valve area is 2.53.5 cm2 (2-4 cm2 in Barash). Hemodynamically significant stenosis occurs when area < 1.2 cm2 but these patients are not necessarily symptomatic. Symptomatic stenosis usually occurs when area falls below 0.8-0.9 cm2. Symptoms include angina (heart), dyspnea on exertion (lungs), and orthostatic or exertional syncope (brain). Non-surgical survival …
Clinical significance
- Critical aortic stenosis occurs when the valve area is < 0.7 cm2, at which point the transvalvular gradient will be 50 mm Hg at rest (ie with a normal cardiac output) at 0.7 cm2/50 mm Hg, patients cannot appreciably increase their cardiac output.
Mechanism
- Left ventricle becomes concentrically thickened due to increased afterload, which has the dual effects of increasing myocardial demand and reducing ventricular compliance (thus, sinus rhythm and atrial kick are CRITICAL, providing 30-40% of LVEDV). Increased systolic pressures further increase demand. Early in the disease, LVEDP will increase (lead...
Treatment
- Tachycardia and hypertension, which are poorly tolerated, should be treated by increasing anesthetic depth. If an adrenergic blocking agent is used, esmolol is preferable. Hypotension should generally be treated with small doses (2550 ucg) of phenylephrine. Amiodarone is effective for both supraventricular and ventricular arrhythmias, although if hemodynamic instabil…
Medical uses
- Central neuraxial analgesia can be used (with extreme caution) in mild cases, but is otherwise to be avoided as it may lead to excessive decreases in SVR and consequently DBP/myocardial perfusion. If used, epidural analgesia is preferable to spinal analgesia.
Prevention
- Keep systolic pressures < ~ 100 mm Hg in order to protect the aortic suture line. Remember that while the valve has been replaced, the LV is still dysfunctional (ex. decreased compliance) and these patients may need relatively high LVEDP (i.e., they can be preload dependent).
Assessment
- For quantitative assessment of AS, the ASE recommends measuring jet velocity, mean pressure gradient, and valve area (using the Continuity Equation). If additional information is needed, the dimensionless index (VTI_LVOT/VTI_valve, severe if < 0.25) and valve area via 2D planimetry can be assessed.
Specifications
- ASE Recommendations for AS Quantification 1. Jet Velocity ( > 4 m/s is severe) 2. Mean Pressure Gradient (> 40 mm Hg is severe) 3. Valve Area (by Continuity Equation, < 1.0 cm2 is severe)
Epidemiology
Pathophysiology
Significance
Clinical significance
Medical uses
- Phenylephrine is the vasopressor of choice in treating the hypotensive patient with AS. Using an agent that solely increases afterload is initially counterintuitive. It is important to recognize that the massive afterload of aortic stenosis is at the level of the aortic valve, with little contribution from the systemic vasculature. As a pure alpha-...
Risks
Preparation
Diagnosis
Treatment
Management