7 Principles of Pharmacology - Congestive Heart Failure & its Pharmacological Management
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Course
Pharmacology
Institution
Pharmacology
The object of the course is to teach students an approach to the study of pharmacologic agents. It is not intended to be a review of the pharmacopoeia. The focus is on the basic principles of biophysics, biochemistry, and physiology as to the mechanisms of drug action, biodistribution and metabolis...
Harvard-MIT Division of Health Sciences and Technology
HST.151: Principles of Pharmocology
Instructor: Prof. Keith Baker
1
Congestive Heart Failure
& its Pharmacological Management
Keith Baker, M.D., Ph.D.
Department of Anesthesia and Critical Care, MGH
HST 151 – Spring 2005
The physiological framework for understanding CHF: The Pressure-Volume Loop of the LV
ESPVR = Emax = Es
Ea
3 SV
Pressure 2
EDPVR
1
4
LVEDP
Volume
Key:
1 = End diastole, just prior to LV contraction. The pressure at 1 is known as the left ventricular
end diastolic pressure (LVEDP)
(1 to 2 = isovolemic contraction)
2 = Opening of the aortic valve and beginning of ejection into the aorta
(2 to 3 is the volume ejected from the LV into the aorta which is the stroke volume
(SV))
3 = End systole. The pressure at 3 is known as the end-systolic pressure (ESP). The aortic
valve shuts just after 3.
(3 to 4 is isovolumic relaxation)
4 = Beginning of passive diastolic filling.
4 to 1 is diastolic filling along the dotted curve. This dotted curve is the end-diastolic
pressure volume relation (EDPVR).
ESPVR = End-systolic pressure volume relation. This also called Emax or Es which stand for
maximal elastance or elastance at end-systole, respectively. This characterizes the
strength of the LV irrespective of the systolic load it faces.
Ea = Effective arterial elastance. This is characterizes the arterial tree and the load it presents
to the LV during systole. Ea is primarily determined by arterial resistance but arterial
compliance effects it too.
Ea and ESPVR “Couple” to exactly determine the stroke volume.
, 2
What is meant by “congestive heart failure” (CHF)?
Congestive heart failure simply means that the pulmonary blood volume is expanded and,
therefore, the pulmonary circulation is congested with blood. The congestion arises because
of elevated left ventricular end-diastolic pressure (LVEDP). An elevated LVEDP is a
hallmark of uncompensated congestive heart failure. Common symptoms include shortness
of breath, fatigue, orthopnea and paroxysmal nocturnal dyspnea (PND). Once a patient is
treated for CHF they may become asymptomatic. This is termed compensated CHF and does
NOT imply that the underlying disease process has gone away! It is entirely reasonable and
even common for patients who are well medically managed to have a markedly reduced
ejection fraction (EF) yet be capable of most normal activities. This handout pertains
primarily to LEFT ventricular failure. Although RIGHT ventricular failure occurs, it is less
common and not the focus of this handout.
How long do people live if they have congestive heart failure?
For all comers, the mortality is 50% in five years. However, if a patient is symptomatic,
despite treatment, one-year mortality can approach 50%. Approximately five million people
have congestive heart failure (CHF) in the United States at any given time. The great
majority of these patients have primarily left ventricular failure.
There are FIVE main physiologic ways to get CHF
1. Decrease the strength of the LV and thereby decrease its ejection – this causes the LVEDP
to rise (CHF). This is characterized by a reduction in the slope of the ESPVR line.
Acute causes include: myocardial ischemia, myocardial infarction, sepsis
syndrome, myocardial contusions, excess beta blockers or excess calcium
channel blockers.
Chronic causes include: dilated cardiomyopathy due to certain viral illnesses,
multiple myocardial infarctions or large territory myocardial infarctions,
excessive alcohol consumption and certain chemotherapeutic agents such as
adriamycin. Prolonged pressure overload (hypertension and aortic stenosis)
also causes a weak heart after initially causing hypertrophy. With continued
overload, the compensation of hypertrophy progresses to a failing myocardium
(a low ESPVR)
2. Provide much too much venous return (and hence filling) to the LV– this causes the
LVEDP to rise (CHF).
Acute causes include: excessive volume administration or large increased in
venous tone as with some vasoconstrictors. Exercise causes a large increase in
venous return and if the LV cannot eject all that it receives, there is an
elevation in the LVEDP (CHF).
Chronic causes include profound chronic anemia, longstanding mitral
regurgitation or aortic regurgitation. Poor compliance with diuretic therapy or
with high salt intake can cause a rise in the plasma volume which in turn
elevates the venous return.
3. Alter the passive filling characteristics of the LV such that a normal filling volume is
associated with a high pressure – this causes the LVEDP to rise (CHF). This is called
diastolic CHF.
Acute causes include: myocardial ischemia
Chronic causes include: prolonged pressure overload (hypertension and aortic
stenosis) which cause this problem by initially causing hypertrophy of the
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