Download Left Ventricular Assist Device (LVAD)

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Management of acute coronary syndrome wikipedia , lookup

Cardiac contractility modulation wikipedia , lookup

Coronary artery disease wikipedia , lookup

Mitral insufficiency wikipedia , lookup

Heart failure wikipedia , lookup

Antihypertensive drug wikipedia , lookup

Lutembacher's syndrome wikipedia , lookup

Jatene procedure wikipedia , lookup

Electrocardiography wikipedia , lookup

Myocardial infarction wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Heart arrhythmia wikipedia , lookup

Dextro-Transposition of the great arteries wikipedia , lookup

Transcript
Left Ventricular Assist Device (LVAD)
LVAD uses an external pump outside the body to bypass the left ventricle. The blood is drained from the apex of
the left ventricle via an intake cannula and ejected into the aorta via an output cannula. BiVAD bypasses both
ventricles. The development of LVAD began in the 1960s as a bridge to cardiac transplant. It has evolved into a
“destination therapy,” meaning a permanent therapy rather than a transitional stage until another therapy. The
indication for LVAD candidates is New York Heart Association class 4 heart failure, ejection fraction <25%,
VO2 max (the maximum rate of oxygen consumption) less than 15, among other criteria. All VADs are preload
dependent, but ECG independent, unlike ICDs. VADs have 3 major variables: speed, flow, and power.
Four Key Variables for the Cardiac Function
Preload is affected by the end diastolic pressure that stretches the right or left ventricle of the heart to its greatest
geometric dimensions under variable physiologic demand. In other words, it is the initial stretching of the
sarcomeres in cardiomyocytes prior to contraction. Preload is affected by venous blood pressure and the rate of
venous return. Regulation of the preload is related to the atrial natriuretic peptide (ANP) and the kidney function.
Afterload is the resistance that the ventricle of the heart has to overcome to eject the blood from the ventricle
chamber during systole. The resistance comes from the blood in the vessels and the constriction of the vessel
walls.
Contractility represents the intrinsic ability of the heart/myocardium to contract. Changes in the ability to
produce force during contraction result from incremental degrees of binding between myosin (thick) and actin
(thin) filaments.
Heart rate is the speed of the heartbeat measured by the number of beats of the heart per minute (bpm). The
normal resting adult human heart rate ranges from 60–80 bpm. Bradycardia is a slow heart rate, defined as below
60 bpm. Tachycardia is a fast heart rate, defined as above 100 bpm at rest. The heart rate can vary according to
the body's physical needs, including the need to absorb oxygen and excrete carbon dioxide. Activities that can
provoke change include physical exercise, sleep, anxiety, stress, illness, ingesting, and drugs. The maximum
heart (MHR) achieved by exercise can be age-dependent; a rough estimate is MHR = 220 – age.