An ejection fraction (EF) is one of the measurements used by physicians to

assess how well a patients heart is functioning. Ejection refers to the amount
of blood that is pumped out of the hearts main pumping chamber during each
heartbeat. Fraction refers to the fact that, even in a healthy heart, some blood
always remains within this chamber after each heartbeat. Therefore an ejection
fraction is a percentage of the blood within the chamber that is pumped out
with every heartbeat. An EF of 55 to 75 percent is considered normal. A higher
than normal ejection fraction could indicate the presence of certain heart
conditions, such as hypertrophic cardiomyopathy. A low ejection fraction could
be a sign that the heart is weakened.

Systolic failure- most common cause

*Dec. in left ventricular ejection fraction (EF); Dec. contractility left ventricle;
unable to generate enough pressure to eject blood forward through high-pressure aorta
*EF- percentage of end-diastolic blood volume that is ejected during systole (reflects
left ventricular function) (Lewis p. 757) normal-approx 60%; less than 40% = heart
failure (determined by ECHO)

Diastolic heart failure

Impaired ability of ventricles to relax and fill during diastole > dec. stroke volume and
CO
Due to left ventricular hypertrophy from chronic hypertension, aortic stenosis (Lewis,
p. 880), hypertrophic cardiomyopathy (Lewis p. 888) or isolated right ventricular
diastolic failure from pulmonary hypertension (*recall cor pulmonale- how affect
afterload ?)
Diagnosis based on presence of pulmonary congestion, pulmonary hypertension,
ventricular hypertrophy, *normal EF-not much blood to eject!

Mixed systolic and diastolic failure

Disease states as dilated cardiomyopathy (DCM), poor EFs (<35%), high pulmonary
pressures
Biventricular failure (both ventricles may be dilated, poor filling and emptying
capacity)

BNP belongs to a family of protein hormones called natriuretic peptides, which

includes ANP, BNP, CNP, and DNP. Natriuretic peptides are part of the bodys
natural defense mechanisms designed to protect the heart from stress and play
an important role in regulating circulation. They promote urine excretion, relax
blood vessels, lower blood pressure, and reduce the hearts workload. Most
scientific study has focused on ANP and BNP.
Measurement of BNP helps doctors diagnose and treat congestive heart failure.
In this condition, the heart is unable to pump blood efficiently, and the heart
chambers swell with blood. As the heart cells stretch, they produce extra BNP,
which pours into the bloodstream. By measuring blood levels of BNP, doctors
can spot signs of congestive heart failure in its early stages, when it may be
hard to distinguish from other disorders. A normal BNP level is about 98%
accurate in ruling out heart failure. And, in general, the higher the level, the

Compensatory Mechanisms (Lewis 823-824) (goal-maintain adequate CO!)

*Important to understand-basis of management/control
Sympathetic nervous system activation-first line response; least
effective, release epinephrine, norepinephrine
Inc. heart rate (HR), myocardial contractility and peripheral vasoconstriction
*Overtime-detrimental- inc. failing myocardiums need for oxygen and workload
Neurohormonal response
Kidneys- release rennin (Lewis, p. 1139, Fig 45-4)
Renin- converts angiotensinogen to angiotensin I; Angiotensin I converted to
angiotensin II by converting enzyme made in lungs
Angiotensin II- > adrenal cortex > release aldosterone (sodium and water retention),

Renin-angiotensin-aldosterone system
Neurohormonal responses (Low CO >dec. in cerebral perfusion pressurecompensatory mechanisms- maintain CO)
Antidiuretic hormone (ADH) secreted >inc. water reabsorption in renal tubules >
water retention and inc. blood volume
Endothelin- stimulated by ADH, catecholamines, and angiotensin II > arterial
vasoconstriction, inc. in cardiac contractility, cardiac hypertrophy
Neurohormonal responses >release proinflammatory cytokines (e.g., tumor necrosis
factor) by cardiac myocytes in response to cardiac injury; depress cardiac function >
cardiac hypertrophy, contractile dysfunction, and myocyte cell death

Counter-regulatory mechanisms (counteract negative effects)

*Natriuretic peptides: atrial natriuretic peptide (ANP) and b-type natriuretic peptide
(BNP) (*hormones secreted by heart muscle) *Prolonged HF- depletes these factors.
*(*BNP-note measure in CHF-secreted by ventricles due to fluid volume overload)
(Lewis p. 752. Tab. 32-7)
Released in response to inc. in atrial volume and ventricular pressure
Promote venous and arterial vasodilation (reduce preload and afterload) diuresis
Natriuretic peptides- endothelin and aldosterone antagonists; Enhance dieresis, block
effects of RAAS; inhibit development cardiac hypertrophy, possible
antiinflammatory (*What drug has this effect- p. 832)
Nitric oxide (NO)- Released from vascular endothelium in response to compensatory
mechanisms; relaxes arterial smooth muscle > results in vasodilation and dec.