Download Heart and work Cardiac reserve - Energy Energy Force and pressure

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Heart and work
dW=F·ds
Zdroje: Atlas patofyziologie
(Silbernagl); Essentials of
pathophysiology (Porth): web a další
Cardiac reserve • The difference between resting and
maximal cardiac output; non-athletes have
a cardiac reserve about 4 times their
normal cardiac output while trained
athletes and our astronaut corps have
cardiac reserves up to 7 times their normal
cardiac output.
Energy
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The heart can use a variety of substrates to oxidatively regenerate ATP
depending upon availability.
Several hours after a meal, the heart utilizes fatty acids (60-70%) and
carbohydrates (~30%).
Following a high carbohydrate meal, the heart can adapt itself to utilize
carbohydrates (primarily glucose) almost exclusively.
Lactate can be used in place of glucose, and becomes a very important substrate
during exercise.
The heart can also utilize amino acids and ketones instead of fatty acids.
Ketone bodies (e.g., acetoacetate) are particularly important in diabetic acidosis.
During ischemia and hypoxia, the coronary circulation is unable to deliver
metabolic substrates to the heart to support aerobic metabolism. Under these
conditions, the heart is able to utilize glycogen (a storage form of carbohydrate)
as a substrate for anaerobic production of ATP and the formation of lactic acid.
However, the amount of ATP that the heart is able to produce by this pathway is
very small compared to the amount of ATP that can be produced via aerobic
metabolism. Furthermore, the heart has a limited supply of glycogen, which is
rapidly depleted under severely hypoxic conditions
Energy
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Oxygen
Substrates
= energy
Energy = functions and surviving
Energy - work
Force and pressure
dW=F·ds
Pressure – force; distance - volume
PV diagram (area) - work
Possible consequences of MI depend on site, extent, and scarring
of the infarct. In addition to various arrhythmias, among them
acutely life-threatening ventricular fibrillation, there is a risk of a
number of morphological/mechanical complications :
• Tearing of the chordae tendineae resulting in acute mitral
regurgitation;
• Perforation of the interventricular septum with left-to-right
shunting;
• Fall in cardiac output that, together with
• stiffened parts of the ventricular wall (akinesia) due to scarring,
• will result in a high end-diastolic pressure. Still more harmful than
a stiff infarct scar is
• a stretchable infarct area, because it will bulge outward during
systole (dyskinesia), which will therefore—at comparably large
scar area—be more likely to reduce cardiac output to dangerous
levels (cardiogenic shock) than a stiff scar will;
• Finally, the ventricular wall at the site of the infarct can rupture to
the outside so that acutely life-threatening pericardial tamponade
occurs.
Heart failure (HF)
• due to reduced systolic ejection (systolic or
forward failure), resulting from either an
– increased volume load,
– myocardial disease,
– an increased pressure load, or
– impaired diastolic filling of the heart,
• HF in which diastolic filling is impaired
(diastolic or backward failure), for example as
a result of
– greater ventricular wall stiffness.
HF caused by volume load
• In forward HF the stroke volume, and thus cardiac
output, can no longer adequately meet the organism’s
requirements.
• In backward HF this can be counteracted only by
increasing the diastolic filling pressure.
• Usually HF only becomes manifest initially on severe
physical work (whenmaximal O2 uptake and maximal
cardiac utput is decreased, but otherwise without
symptoms;
– stage I of the NYHA [New York Heart Association]
classification).
– However, symptoms later develop progressively, at first
only on ordinary physical activity, later even at rest (NYHA
stages II–IV).
• Aortic and mitral regurgitation, for example, are
characterized by the regurgitant volume that is added
to the effective stroke volume. The enddiastolic
volume, and therefore the radius (r) of the left
ventricle, are increased so that, according to
Laplace’s law the wall tension (T), i.e., the force that
has to be generated per myocardial cross-sectional
area, must rise to achieve a normal, effective stroke
volume.
• As this succeeds only inadequately, stroke volume
and thus CO (= heart rate · stroke volume) decrease
and the blood pressure falls. Sympathetic stimulation
occurs as a counterregulatory mechanism, resulting in
increased heart rate and peripheral vasoconstriction.
HF caused by volume load
• If chronic volume load develops, the dilated ventricle reacts
with hypertrophy to compensate, i.e., with an increased wall
thickness (d). However, r remains elevated (eccentric
hypertrophy), and this form of HF usually has a less favorable
course than one with concentric hypertrophy . If the
underlying condition (e.g., valvar defect) is not removed
early, HF gets worse relatively rapidly because of the
resulting myocardial remodeling . Stiffening of the ventricle,
caused by the hypertrophy, is involved in this development.
• Because of its steeper compliance (= lusitropic = relaxation)
curve,it has a diminished enddiastolic volume and thus a
small stroke volume (backward HF). A vicious circle arises, in
that the dilated ventricular wall gives way even more (dilation
with myocardial restructuring) and r rises steeply.
• This decompensation is characterized by a life-threatening fall
in stroke volume despite an enormously elevated
enddiastolic volume.
HF caused by myocardial disease.
• In coronary heart disease (ischemia) and after myocardial
infarction the load on the uninvolved myocardium
increases, i.e., forward HF develops due to diminished
contractility. This is reflected by a shift of the contractility
(C) curve of the ventricular work diagram. The endsystolic
volume and, to a lesser extent, the EDV also rises, while
stroke volume falls.
• Hypertrophy of the remaining myocardium, a stiff
myocardial scar as well as the diminished effect of ATP on
actin–myosin separation in the ischemic myocardium will
lead to additional backward HF.
• Finally, a compliant infarct scar may bulge outward during
systole (dyskinesia) , resulting in additional volume load
(regurgitant volume). Cardio-myopathies can also lead to
HF, volume load being prominent in the dilated form,
backward HF in the hypertrophic and restrictive forms.
HF due to pressure load
• The wall tension (T) of the left ventricle also rises in hypertension
or aortic stenosis, because an increased left ventricular pressure
(PLV) is required (Laplace’s law). Forward HF with diminished
contractility develops. An analogous situation exists regarding the
right ventricle in pulmonary hypertension. Compensatory
hypertrophy will also develop when there is an increased pressure
load, but it will be “concentric” , because in this case the
ventricular volume is not enlarged and may in some circumstances
actually be decreased. However, even in concentric hypertrophy
the enddiastolic volume will be reduced and thus also the stroke
volume (backward HF). When there is a high pressure load,
myocardial remodeling (see below), and unfavorable capillary
blood supply (relative coronary ischemia), a “critical heart weight”
of ca. 500 g may be attained, at which the myocardial structure
gives way, causing decompensation.
Left Heart Failure Symptoms
• Dyspnea
– on exertion
– at rest
• Orthopnea
– redistribution of peripheral edema fluid
– graded by number of pillows needed
• Paroxysmal Nocturnal Dyspnea (PND)
Right Sided Heart Failure
• Etiology
– left heart failure
– cor pulmonale
• Symptoms and signs
– Liver and spleen
• passive congestion (nutmeg liver)
• congestive spleenomegaly
• ascites
– Kidneys
– Pleura/Pericardium
• pleural and pericardial effusions
• transudates
– Peripheral tissues
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Oxygen demand rises as a consequence of increased cardiac work (= pressure times
volume; orange area).
The diastolic pressure (important for coronary perfusion), is reduced and simultaneously
the wall tension of the left ventricle is relatively high — both causes of a lowered
transmural coronary artery pressure and hence underperfusion which, in the presence of
the simultaneously increased oxygen demand, damages the left ventricle by hypoxia. Left
ventricular failure and angina pectoris or myocardial infarction are the result.
Finally, decompensation occurs and the situation deteriorates relatively rapidly (vicious
circle): as a consequence of the left ventricular failure the endsystolic volume rises, while
at the same time total stroke volume decreases at the expense of effective endsystolic
volume (red area), so that blood pressure falls (left heart failure) and the myocardial
condition deteriorates further. Because of the high ESV, both the diastolic PLV and the
PLA rise. This can cause pulmonary edema and pulmonary hypertension , especially when
dilation of the left ventricle has resulted in functional mitral regurgitation.
LEFT Heart Failure
Dyspnea
Orthopnea
PND (Paroxysmal Nocturnal Dyspnea)
Blood tinged sputum
Cyanosis
Elevated pulmonary “WEDGE”
pressure (PCWP) (nl = 2-15 mm Hg)
RIGHT Heart Failure
FATIGUE
“Dependent” edema
JVD
Hepatomegaly (congestion)
ASCITES, PLEURAL EFFUSION
GI
Cyanosis
Increased peripheral venous pressure (CVP)
(nl = 2-6 mm Hg)
Congestive Heart Failure
• heart valve disease caused by past rheumatic fever
or other infections
• infections of the heart valves and/or heart muscle
(i.e., endocarditis)
• cardiac arrhythmias (irregular heartbeats)
• cardiomyopathy, or another primary disease of the
heart muscle
• chronic lung disease
• anemia
• high blood pressure (hypertension)
• hemorrhage (excessive bleeding)
Congestive Heart Failure
Dilated Cardiomyopathy
Dilated Cardiomyopathy
• Dilated cardiomyopathy involves enlargement
of the heart muscle and is the most common
type of cardiomyopathy. The heart muscle is
weakened and cannot pump blood efficiently.
Decreased heart function affects the lungs,
liver, and other body systems.
Cor Pulmonale
Hypertrophic Cardiomyopathy
Definition:
Stimulus:
WHO: left and/or right ventricular
hypertrophy, usually asymmetric and
involves the interventricular septum.
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Unknown
Disorder of intracellular calcium metabolism
Neural crest disorder
Papillary muscle malpositioned and
misoriented
Genetic abnormality:
Pathophysiology of HCM
• Autosomal dominant.
• Mutations in genes for cardiac sarcomeric
proteins.
• Polymorphism of ACE gene.
• ß-myosin heavy chain gene on chromosome
14.
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• Left ventricular outflow tract gradient
• ↑ with decreased preload, decreased
afterload, or increased contractility.
• Venturi effect: anterior mitral valve leaflets &
chordae sucked into outflow tract →
↑ obstruction, eccentric jet of MR in mid-late
systole.
Maneuvers that ↓ end-diastolic volume
(↓ venous return & afterload, ↑ contractility)
• Vasodilators
• Inotropes
• Dehydration
• Valsalva
• Amyl nitrite
• Exercise
→ ↑ HCM murmur
Dynamic LV outflow tract obstruction
Diastolic dysfunction
Myocardial ischemia
Mitral regurgitation
Arrhythmias