notes dr Claudio Italiano
Pulmonary heart is defined as the pathology manifested by the dilatation of the right ventricle in response to the increase of the afterload, ie an increase in cardiac work resulting in an increase in the resistance of the pulmonary circulation, thus resulting in diseases of the thorax, lungs and pulmonary circulation.
Thus patients suffering from chronic obstructive pulmonary disease (see chronic bronchitis).
The passage of blood into the pulmonary circulation serves for the exchange of gases, for the filtering of the particles and for the chemical conditioning of the blood (for example to the transformation of the angiotensiona I into II).
During inhalation the lung expands and allows a better blood circulation. The range of the right ventricle is a function of preload, of contractility of the heart and of the resistances (post-load), but the right ventricle does not have great ability to increase the pressure and the post-load is a function of the pulmonary arterial pressure which is always kept low.
Indeed the difference between the pressure in the left atrium and pulmonary artery is 5 cm of H20, being 15 cm in the pulmonary artery and 10 in the atrium and this low pressure allows a flow of 5 liters of blood at rest up to 25 liters under stress for every minutes.
The dilatation of the right ventricle in the pulmonary heart depends on the
fact that the bloodstream resistance in the lung during chronic
bronchopneumopathy is impaired, both because the vessels are stretched and,
therefore, smaller in diameter, and because the pulmonary capillaries are
compressed. But the same thing also happens in restrictive forms, where the
vessels are compressed and distorted or in hypoxia, where there is
vasoconstriction.
Conditions that cause acute pulmonary heart are pulmonary embolism (see pulmonary embolism), an event that is widespread in the USA where at least 50,000 people die from pulmonary embolism, due to the low cardiac output resulting from the obstructed pulmonary blood flow.
The patient is prey to violent chest pain that resembles a heart attack (see Chest pain Chest pain: unstable angina myocardial infarction), sweaty, pale, hypotensive, with accelerated pulse, dyspnoea (see dyspnea), he observes the jugular turgidity because the blood coming from the hollow vein system does not discharge into the right atrium as it should, since the right ventricle pushes against an embolized pulmonary circle, ie with clots that block the vessels.
A systolic murmur from tricuspid insufficiency and a cantering rhythm appears in the auscultation. The hemogas (cf. acid-base balance) almost always shows hypoxemia, secondary to imbalances in the ventilation / perfusion ratio, as well as a decrease in Pa C02. If the cardiac output holds for 2-3 hours, then naturally the thrombus is blurred and the patient survives, so thrombolytic therapy is more indicated than simple heparin.
The chronic pulmonary heart is secondary, however, to chronic diseases affecting the lung. In this case the increase in resistance of the pulmonary circle is gradual and there is a hypertrophy of the right ventricle. The increase in resistance of the pulmonary circulation recognizes different causes:
- Repeated microemboliation with organization of the emboli
- Administration of intravenous powders, eg, in the addict (see opiates)
- Parasites
-Tumori
- Primitive essential causes.
- Collagen vasculopathy
Wegener's rheumatoid arthritis granulomatosis
The presence of dyspnoea, (cf. dyspnoea), characterizes pulmonary hypertension,
which is very evident even after mild efforts, which is associated with
non-productive cough (see Patient with cough, diagnosis and treatment),
sometimes even chest pain occurs ( cfr Pain in the chest) for cardiac ischemic
events. Second tone splitting may be present, hypocarbia for alveolar
hyperventilation, with partial pressure of reduced oxygen and constant doubling
of the second tone, with murmur insufficiency.
The diagnosis can be made with the chest X-ray (see rx_torace) which demonstrates a dilatation of the common trunk of the pulmonary artery and ilari vessels. The echocardiogram demonstrates the right hypertrophic ventricle and the pressure of the right ventricle can be studied by the colordoppler studying the peak of the flow of tricuspid and pulmonary regurgitation.