18.

atrial kick

when relaxation impairs, early diastolic filling decreases

progressively and a vigorous compensatory atrial contraction (atrial kick) occurs. (Fig. 2).
Schematic representation of transmitral and pulmonary venous flow pattern according to
Appelton and Hatle [21]. With increasing age the E/A ratio decreases. In elderly patients the ratio
is less than 1 (impaired relaxation pattern) and the pulmonary venous flow shows a decrease in
diastolic flow (PVd). In subjects with impaired LV relaxation (e.g. myocardial hypertrophy,
ischemia) the filling pattern shows a further decrease in thee E-wave, whereas with a decrease in
LV compliance the filling pattern changes towards normal (pseudo-normalization) and even
shows enhanced early diastolic filling with an E/Aratio>2 (restrictive filling pattern). With the
progressive decrease in LV compliance pulmonary venous flow shows a diminution of systolic
flow with an enhanced early diastolic flow and a reversal of atrial flow.

Lazar Mandinov et al. Cardiovasc Res 2000;45:813-825

[sumber : http://cardiovascres.oxfordjournals.org/content/45/4/813]

17.

Cardiac Cycle - Isovolumetric Relaxation (Phase 5)

SUMBER : http://www.cvphysiology.com/

All Valves Closed (S2)

When the intraventricular pressures fall sufficiently at the end of phase 4, the aortic
and pulmonic valves abruptly close (aortic precedes pulmonic) causing
the second heart sound (S2) and the beginning of isovolumetric relaxation. Valve
closure is associated with a small backflow of blood into the ventricles and a
characteristic notch (incisura or dicrotic notch) in the aortic and pulmonary artery
pressure tracings.

After valve closure, the aortic and pulmonary artery pressures rise slightly
(dicrotic wave) following by a slow decline in pressure.

The rate of pressure decline in the ventricles is determined by the rate of

relaxation of the muscle fibers, which is termed lusitropy. This relaxation is
regulated largely by the sarcoplasmic reticulum that are responsible for rapidly resequestering calcium following contraction (see excitation-contraction

coupling).

Although ventricular pressures decrease during this phase, volumes do not change
because all valves are closed. The volume of blood that remains in a ventricle is called

the end-systolic volume and is ~50 ml in the left ventricle. The difference between the
end-diastolic volume and the end-systolic volume is ~70 ml and represents the stroke
volume.

Left atrial pressure (LAP) continues to rise because of venous return from the lungs.
The peak LAP at the end of this phase is termed the v-wave.

Cardiac Cycle - Isovolumetric Contraction (Phase 2)

All Valves Closed (S1)

This phase of the cardiac cycle begins with the appearance of the QRS complex of
the ECG, which represents ventricular depolarization. This triggersexcitationcontraction coupling, myocyte contraction and a rapid increase in intraventricular
pressure. Early in this phase, the rate of pressure development becomes
maximal. This is referred to as maximal dP/dt.

The AV valves close when intraventricular pressure exceeds atrial

pressure. Ventricular contraction also triggers contraction of the papillary muscles
with their chordae tendineae that are attached to the valve leaflets. This tension on
the the AV valve leaflets prevent them from bulging back into the atria and
becoming incompetent (i.e., leaky). Closure of the AV valves results in the first
heart sound (S1). This sound is normally split (~0.04 sec) because mitral valve
closure precedes tricuspid closure.

During the time period between the closure of the AV valves and the opening of the
aortic and pulmonic valves, ventricular pressure rises rapidly without a change in
ventricular volume (i.e., no ejection occurs). Ventricular volume does not change
because all valves are closed during this phase. Contraction, therefore, is said to be
"isovolumic" or "isovolumetric." Individual myocyte contraction, however, is not
necessarily isometric because individual myocyte are undergoing length changes.
Some individual fibers contract isotonically (i.e., concentric, shortening contraction),
whereas others contract isometrically (i.e., no change in length) or eccentrically (i.e.,
lengthening contraction). Therefore, ventricular chamber geometry changes
considerably as the heart becomes more spheroid in shape; circumference increases
and atrial base-to-apex length decreases.

The rate of pressure increase in the ventricles is determined by the rate of contraction
of the muscle fibers, which is determine by mechanisms governingexcitationcontraction coupling. The maximal rate of pressure change during this phase is termed
"dP/dtmax."

The "c-wave" noted in the LAP may be due to bulging of mitral valve leaflets back into
left atrium. Just after the peak of the c wave is the x'-descent.

Cardiac Cycle - Rapid Filling (Phase 6)

A-V Valves Open (S3)

As the ventricles continue to relax at the end of phase 5, the intraventricular

pressures will at some point fall below their respective atrial pressures. When this
occurs, the AV valves rapidly open and passive ventricular filling begins. Despite
the inflow of blood from the atria, intraventricular pressure continues to briefly fall
because the ventricles are still undergoing relaxation. Once the ventricles are
completely relaxed, their pressures will slowly rise as they fill with blood from the
atria.

The opening of the mitral valve causes a rapid fall in LAP. The peak of the LAP
just before the valve opens is the "v-wave." This is followed by the y-descent of
the LAP. A similar wave and descent are found in the right atrium and in the jugular
vein.

Ventricular filling is normally silent. When a third heart sound (S3) is audible
during rapid ventricular filling, it may represent tensing of chordae tendineae and
AV ring during ventricular relaxation and filling. This heart sound is normal in
children; but is often pathological in adults and caused by ventricular dilation..

19. The appearance of crackles has been considered to be an early sign of pulmonary
impairment in Asbestosis [1, 10, 72]; in early disease, crackles have been described to appear
first in the basal pulmonary areas, later successively higher up on the thorax [73]. On
rare occasions, e.g. in severe heart insufficiency, crackles are audible at the mouth [5].

Sumber :
https://www.researchgate.net/publication/14535385_Crackles_Recording_analysis
_and_clinical_significance

23. aku kirim bentuk pdfnya lengkap

24. The Right Ventricle in Pulmonary Hypertension
The right ventricle is exposed to pressure overload by pulmonary valve stenosis or by chronic
pulmonary hypertension from any cause (Table 1). An initial adaptive response of myocardial
hypertrophy2 is followed by progressive contractile dysfunction. Chamber dilatation ensues to
allow compensatory preload and maintain stroke volume despite reduced fractional
shortening. As contractile weakening progresses, clinical evidence of decompensated right
ventricular failure occurs, characterized by rising filling pressures, diastolic dysfunction, 3 and
diminishing cardiac output, which is compounded by tricuspid regurgitation due to annular
dilatation and poor leaflet coaptation. The increased size and pressure overload of the right
ventricle also produce diastolic dysfunction of the left ventricle. 4,5 Thus, the function and size
of the right ventricle are not only indicators of the severity and chronicity of pulmonary
hypertension but impose an additional cause of symptoms and reduced longevity. Right
ventricular function is the most important determinant of longevity in patients with pulmonary
arterial hypertension.69

he specific mechanisms underlying the development of right ventricular failure secondary to

pulmonary hypertension are unclear. For example, it is uncertain whether some patients
develop right ventricular myocardial ischemia, whether there is microvascular endothelial cell
dysfunction, and whether or not myocytes undergo apoptosis. In severe, end-stage pulmonary
hypertension, the shape of the right ventricle is changed from the normal
conformation,10,11 and right ventricular wall stress and right ventricular free wall thickness
appear to be inversely related12(Figure 2). The mechanism by which a severely dilated endstage right ventricle repairs itself after lung transplantation is also uncertain.13,14

Plasma levels of brain natriuretic peptide1519 and troponin T20 correlate with pulmonary arterial
pressure and pulmonary vascular resistance in patients with pulmonary arterial hypertension.
Increases in brain natriuretic peptide plasma levels during serial follow-up visits are
associated with increased mortality in idiopathic pulmonary arterial hypertension patients.
Paradoxically, however, atrial natriuretic peptides may promote cardiomyocyte survival.21

SUMBER : http://circ.ahajournals.org/

Special Report
Right Ventricular Function and Failure
Report of a National Heart, Lung, and Blood Institute Working Group on Cellular and
Molecular Mechanisms of Right Heart Failure

1.
2.
3.
4.

Norbert F. Voelkel, MD;

Robert A. Quaife, MD;
Leslie A. Leinwand, PhD;
Robyn J. Barst, MD;

5.
6.
7.
8.
9.
10.
11.
12.
13.
14.

Michael D. McGoon, MD;

Daniel R. Meldrum, MD;
Jocelyn Dupuis, MD, PhD;
Carlin S. Long, MD;
Lewis J. Rubin, MD;
Frank W. Smart, MD;
Yuichiro J. Suzuki, PhD;
Mark Gladwin, MD;
Elizabeth M. Denholm, PhD;
Dorothy B. Gail, PhD