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ADVANTAGES OF MODERN CLINICAL DIAGNOSTIC METHODS FOR
CARDIOVASCULAR DISEASES
¹Baxrillayev Yusufxon
²Komilova Mohinur
³Salimova Malika
¹'²'³Samarkand State Medical University, DKTF, Department of Internal Medicine, Cardiology
and Functional Diagnostics, 2nd year clinical residents
https://doi.org/10.5281/zenodo.14866770
Introduction
Cor pulmonale results from pathology of the lungs or their vessels; it does not include left
ventricular (LV) failure, congenital heart defects (eg, ventricular septal defect), or secondary right
ventricular (RV) dilatation due to acquired valvular pathology. Cor pulmonale is usually a chronic
condition, but it can be acute and reversible. Primary pulmonary hypertension (i.e., not caused by
lung or heart disease) is discussed elsewhere.
Research methods and materials:
Pulmonary hypertension increases RV load, which
leads to a cascade of events that occur in the left ventricular heart rate, including increased end-
diastolic and central venous pressures, ventricular hypertrophy, and dilation. RV load may be
increased by increased blood viscosity due to hypoxia-induced polycythemia. Sometimes RV
failure leads to LV pathology, with the interventricular septum bulging into the LV cavity,
preventing LV filling, thereby creating its diastolic dysfunction. The heart should be visualized
with echocardiography or radionuclide scanning to assess LV and RV function. Echocardiography
can help assess RV systolic pressure, but its feasibility is often limited in patients with pulmonary
disease; cardiac MRI may be useful in some patients to assess the chambers of the heart and their
function. Right heart catheterization may be necessary to confirm the diagnosis.
Research results:
Pulmonary heart disease is difficult to treat; it is aimed at the cause (see table of causes of
heart failure), in particular, to alleviate or alleviate hypoxia. Early diagnosis and treatment are
important, because Later structural changes in the lungs become irreversible.
Diuretics may be prescribed in the presence of peripheral edema, but they are effective only
in the presence of LV failure and pulmonary fluid overload. Diuretics should be used with caution,
as even a small reduction in preload often worsens cor pulmonale. Pulmonary vasodilators (eg,
hydralazine, calcium channel blockers, nitric oxide, prostacyclin, phosphodiesterase inhibitors),
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although effective in primary pulmonary hypertension, are ineffective in cor pulmonale. Bosentan
(an endothelin receptor blocker) may be used in patients with primary pulmonary hypertension,
although its use in cor pulmonale has not been adequately studied. Digoxin is effective only in the
presence of concomitant LV dysfunction. This drug should be used with caution, as patients with
COPD are particularly sensitive to its effects.
Phlebotomy has been suggested as necessary in hypoxic cor pulmonale, but the effect of
reducing blood viscosity, except in cases of significant polycythemia, is unlikely to counteract the
adverse effects of reduced oxygen carrying capacity. Long-term use of anticoagulants in patients
with chronic cor pulmonale reduces the risk of venous thromboembolism.
Cor pulmonale (heart lung) is a lung disease characterized by right ventricular enlargement
and subsequent failure, secondary to pulmonary artery hypertension.
Cor pulmonale is usually asymptomatic, but common physical findings include a left
parasternal systolic rise, a loud pulmonary component of S2, functional tricuspid regurgitation,
and pulmonary bruit; later, jugular vein edema, hepatomegaly, and lower extremity edema.
Diagnosis usually requires echocardiography or radionuclide imaging, and in some cases,
right heart catheterization.
It is important to identify and treat the causes of the disease early, before systemic changes
in the heart become irreversible.
Although patients may have significant peripheral edema, diuretic therapy is not indicated
and may be harmful; even a modest reduction in preload often worsens cor pulmonale (pulmonary
heart disease).
Heart failure (HF) is a syndrome of dysfunction of the ventricles of the heart. Left
ventricular failure leads to the development of shortness of breath and rapid fatigue, while right
ventricular failure leads to peripheral edema and fluid accumulation in the abdominal cavity. Both
ventricles or each ventricle may be involved in the process. The diagnosis is made clinically and
confirmed by chest radiography, echocardiography, and plasma natriuretic peptide levels.
Treatment includes patient education, diuretics, angiotensin-converting enzyme (ACE) inhibitors,
angiotensin II receptor blockers, beta-blockers, aldosterone antagonists, sodium-glucose
cotransporter type 2 inhibitors, neprilysin inhibitors, sinus node inhibitors, or other specialized
H/implantable pacemakers. Afterload is the force of resistance to contraction of myocardial fibers
at the beginning of systole. It is determined by the pressure in the LV, the volume and thickness
of the wall at the time of aortic valve opening. From a clinical point of view, the systemic systolic
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blood pressure measured at or immediately after aortic valve opening is related to the peak systolic
stress of the ventricular wall and approximates the afterload value.
The Frank-Starling law describes the relationship between preload and cardiac output.
Typically, the systolic work (contractile capacity) of the heart, expressed as stroke volume or CO2,
is proportional to preload within the normal physiologic range (see Frank-Starling law diagram).
Contractility is difficult to measure clinically (because it requires cardiac catheterization with
pressure-volume analysis), but is best reflected by the ejection fraction (EF), which is the ratio of
stroke volume after ejection during contraction to end-diastolic volume (stroke volume/end-
diastolic). Noninvasive techniques such as echocardiography, nuclear tomography, or MRI are
usually used to adequately assess EF.
Force-frequency relationship refers to the phenomenon whereby repeated stimulation of a
muscle over a given frequency range results in an increase in the force of contraction. Normal
cardiac muscle at a normal heart rate exhibits a positive force-frequency relationship, so that higher
heart rates result in more forceful contractions (and correspond to greater substrate demand). In
some types of heart failure, the force-frequency relationship may be negative, so that myocardial
contractility decreases when the heart rate exceeds a certain level.
Cardiac reserve is the ability of the heart to produce more than its resting level in response
to emotional or physical stress. The div can increase oxygen consumption from 250 to ≥ 1500
ml/min at maximum exertion. Developmental mechanisms include:
Increased tissue oxygen extraction (the difference between the oxygen content in arterial
blood and mixed venous or pulmonary artery blood)
In well-trained young adults, during maximal exercise, the heart rate can increase from 55–
70 beats per minute (at rest) to 180 beats per minute, and CO 6 can increase to ≥ 25 l/min or more.
At rest, arterial blood contains approximately 18 ml of oxygen per dL of blood, and mixed venous
or pulmonary arterial blood contains approximately 14 ml/dL. Thus, oxygen extraction is
approximately 4 ml/dL. As demand increases, oxygen extraction can increase to 12–14 ml/dL.
This mechanism also helps to compensate for the decreased tissue blood flow in heart failure.
Conclusion
: In heart failure associated with left ventricular dysfunction, CO is reduced
and pulmonary venous pressure is increased. Since pulmonary capillary pressure exceeds the
oncotic pressure of plasma proteins (approximately 24 mmHg), the liquid part of the blood flows
from the capillaries into the interstitial space and alveoli, reducing lung function and increasing
respiratory rate. In compensation, lymphatic drainage of the lungs increases, but this does not
compensate for the increase in fluid volume in the lungs. A large accumulation of fluid in the
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alveoli ( pulmonary edema ) significantly disrupts the ventilation-perfusion (V / Q) relationship:
deoxygenated pulmonary arterial blood passes through poorly ventilated alveoli, which leads to a
decrease in the partial pressure of oxygen (PaO2) in arterial blood and leads to the development
of dysplasia. However, shortness of breath may occur before the V / P disorder, possibly due to an
increase in pulmonary venous pressure and an increase in the work of breathing; The exact
mechanism of this phenomenon is unclear.
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