Cardiovascular System – Pathophysiology, Risk Factors, Complications

In the cardiovascular system, Heart failure

TYPES OF HEART FAILURE (cardiovascular system)

  1. Myocardial, caused by damage to myocardiocytes by toxic, infectious, immune or ischemic factors.
  2. Overload, arising from overload or increased blood volume.
  3. Mixed.

In cardiovascular system, Myocardial ischemia is an insufficient supply of oxygen with the blood that does not provide global (general) or local (local) needs of the heart.

American cardiologists define myocardial ischemia as a condition with a decrease in arterial blood flow, leading to a change in the metabolism of cardiomyocytes from aerobic to anaerobic.

PHASES OF TOTAL MYOCARDIAL ISCHEMIA (cardiovascular system)

  • Latent period. Heart function does not change. It coincides in time with the period of aerobic metabolism of the myocardium (utilization of oxygen from the available reserves – oxyhemoglobin and oxymyoglobin). Normally, these reserves are enough for 1-20 s.
  • The period of survival, i.e. the one when reperfusion or reoxygenation leads to a rapid restoration of heart function to its original level. Biochemically, this period is characterized by a transition to anaerobic metabolism. The duration of the hypothermia phase is 5 minutes;
  • The period of possibility of revitalization (from the onset of ischemia to the onset of limiting reversible changes). The duration of the phase is 20-40 minutes.

In cardiovascular system, Coronary insufficiency is a condition caused by the inability of the coronary blood supply to provide the metabolic oxygen requirements of the myocardium due to spasm, thrombosis, embolism, etc. It can be absolute (with a true decrease in volumetric blood flow in the heart) and relative (with unchanged blood flow in the heart, but reduced functional capabilities due to a drop in the partial pressure of oxygen with severe anemia or increased myocardial oxygen demand with significant hypertrophy).


 

RISK FACTORS FOR ISCHEMIC HEART DAMAGE (cardiovascular system)

  1. Primary, directly affecting health: unbalanced diet, smoking, alcohol abuse, physical inactivity, stress.
  2. Secondary, i.e. diseases or syndromes of pathological disorders that contribute to the development of cardiovascular diseases: hypercholesterolemia, arterial hypertension, diabetes, rheumatism, etc.

PATHOGENESIS OF ISCHEMIC HEART DISEASE ACCORDING TO F.Z.? MERSON (cardiovascular system)

  1. stress hypercholesterolemia and hyperlipidemia;
  2. primary stress damage to the myocardium (pronounced metabolic and structural changes in the myocardium);
  3. hypercatecholaminemia with subsequent coronary spasm and secondary ischemic injury;
  4. activation by excess of catecholamines of the blood coagulation system and the formation of blood clots;
  5. decrease in myocardial resistance to hypoxia and ischemia due to prolonged stress response;
  6. adrenergic increase in vascular resistance and increased load on the heart;
  7. a decrease in the tone of the capacitive vessels, mainly of the portal system, leading to pathological blood deposition and a decrease in the volume of circulating blood;
  8. hyperventilation, leading to the development of alkalosis and a decrease in coronary blood flow.

Complications of myocardial infarction (cardiovascular system)

  1. Parietal thrombosis (in the first 7-10 days).
  2. Fibrinous pericarditis.
  3. Acute and chronic aneurysm.
  4. Heart rupture with tamponade of the pericardial cavity.
  5. Cardiogenic shock
  6. Pulmonary edema.
  7. Arrhythmias (up to fibrillation).

In the cardiovascular system, Cardiac reactions to toxic damage can be classified according to whether they are:

  1. a consequence of direct exposure to toxic substances;
  2. the result of an excessive pharmacological effect of the substance either on the myocardium itself, or on the coronary or systemic circulation;
  3. a consequence of hypersensitivity or allergic reaction.

TOXIC DAMAGE TO THE MYOCARDIAL ARE MANIFESTED (cardiovascular system):

  1. hypertrophy (with an excess of STH, thyroid hormones, norepinephrine, isoproterenol);
  2. cardiomyopathies (chronic alcohol intoxication, viral infections, antineoplastic drugs, calcium antagonists, antidepressants);
  3. myocardial infarction as a reaction to toxic substances (amphetamines, oral contraceptives, carbon monoxide, thyroid drugs, catecholamines);
  4. myocarditis as a manifestation of myocardial hypersensitivity (sulfonamides, methyldOPA, chloramphenicol, PASK, butadion, etc.);
  5. toxic myocarditis (catecholamines, antineoplastic drugs, heavy metal salts, oral hyperglycemic drugs, etc.).

In cardiovascular system, Heart failure with an overload of an increased blood volume usually develops with heart defects (valve insufficiency or congenital defects of the heart septa), less often with anemia and thyrotoxicosis. The compensation mechanism is heterometric.

In cardiovascular system, Heart failure due to pressure overload occurs with stenosis of the valves of the heart and blood vessels, with hypertension of the large and pulmonary circulation, pulmonary emphysema. The compensation mechanism is homeometric, energetically more expensive than heterometric.

In cardiovascular system, Myocardial hypertrophy is the process of increasing the mass of individual cardiomyocytes without increasing their number under conditions of increased stress.


 

STAGES OF MYOCARDIAL HYPERTROPHY ACCORDING TO F.Z.? MERSON

  1. “Emergency”, or the period of development of hypertrophy.
  2. The stage of completed hypertrophy and relatively stable hyperfunction of the heart, when the normalization of myocardial functions occurs.
  3. Stage of progressive cardiosclerosis and myocardial depletion.

Pathology of the cardiac membrane (pericardium) is most often represented by pericarditis: acute or chronic, dry or exudative.

Etiology: viral infections (Coxsackie A and B, influenza, etc.), staphylococci, pneumo-, strepto- and meningococci, tuberculosis, rheumatism, collagenoses, allergic lesions – serum sickness, drug allergy, metabolic lesions (in chronic renal failure , gout, myxedema, thyrotoxicosis), radiation damage, myocardial infarction, heart surgery.

In cardiovascular system, Pathogenesis: 1) hematogenous route of infection is typical – ren for viral infections and septic conditions, 2) lymphogenous – with tuberculosis, diseases of the pleura, lung, mediastinum.

Cardiac tamponade syndrome is the accumulation of a large amount of exudate in the pericardial cavity. The severity of tamponade is affected by the rate of fluid accumulation in the pericardium. The rapid accumulation of 300-500 ml of exudate leads to acute cardiac tamponade.

Arrhythmias are any heart rhythm that is not a regular sinus rhythm of a normal frequency.


 

PATHOGENESIS OF STRESS ARRHYTHMIAS (cardiovascular system)

  1. hyperactivity of sympathetic centers of blood circulation regulation; an increase in sympathetic influences on the myocardium and an increase as a result of this ectopic automatism of the atria and ventricles;
  2. spasm of the coronary arteries;
  3. hypoxia of the myocardium due to insufficiency of the coronary circulation, excessive stimulation of the heart, dissociation of the processes of oxidative phosphorylation, the occurrence of an energy deficit, accompanied by an increase in myocardial heterogeneity;
  4. violation of microcirculation, the appearance of hemorrhages, including with a violation of the structure of the conducting system of the heart;
  5. the occurrence of dystrophic and necrotic changes in the myocardium;
  6. violation of the reciprocity of the states of the nerve centers, as well as the transition from sympathetic to parasympathetic hyperactivity.

CLASSIFICATION OF ARRHYTHMIAS (cardiovascular system)

  1. Arrhythmias associated with dysfunction of automatism:
    1. sinus tachycardia;
    2. sinus bradycardia;
    3. sinus arrhythmia;
    4. atrioventricular rhythm;
    5. dissociation with interference;
    6. idioventricular rhythm;
    7. weakness of the sinus node.
  2. Arrhythmias caused by dysfunction of the excitability of the heart:
    1. extrasystoles;
    2. paroxysmal tachycardia.
  3. Arrhythmias caused by impaired conduction function:
    1. sinoauricular block;
    2. intra-atrial block;
    3. atrioventricular block – complete and incomplete;
    4. intraventricular block:
      1. atrioventricular bundle;
      2. the legs of the bundle of His;
      3. Wolff-Parkinson-White syndrome.
  4. Arrhythmias associated with impaired contractility function:
    1. alternating pulse.
  5. Arrhythmias caused by dysfunction of excitability and contractility:
    1. atrial fibrillation;
    2. atrial flutter;
    3. fibrillation and flutter of the ventricles.

In cardiovascular system, Ectopic rhythm is a rhythm for which impulses come from a focus located outside the sinus node.

In cardiovascular system, Extrasystole is a premature excitement and contraction of the whole heart or its parts as a result of an impulse emanating from various parts of the conducting system.


 

THEORY OF THE ORIGIN OF EXTRASYSTOLIES

  1. The theory of re-entry of excitation (“micro- and macrorientry”). It is assumed that there is a local blockade of impulse conduction, causing later excitation of a certain small area of ​​the myocardium of the atria or ventricles, where the impulse enters in a roundabout way. In this case, a circular motion of the excitation wave occurs along the myocardium, causing the formation of an extrasystole.
  2. Theory of increasing the amplitude of trace potentials remaining after the previous excitation.
  3. Theory of non-simultaneous repolarization of individual myocardial structures. The potential difference between cells that have not yet left the state of depolarization and cells with already completed repolarization provides extrasystole.
  4. The theory of increased automatism of “latent pacemakers”.
  5. The theory of the occurrence of extrasystoles by the type of parasystole. It assumes the existence of an ectopic center in the atria or ventricles, which generates impulses with a certain frequency and periodically initiates premature excitation of the heart.

THEORY OF THE OCCURRENCE OF ATIBLE ARRHYTHMIA

  1. Circular motion of a wave of excitation along the atria with high speed. Additional waves depart from the circular wave, causing the excitation of individual atrial fibers. For the occurrence of such a phenomenon, it is necessary: ​​a shortened refractoriness of atrial myocytes, a relative slowdown in the conduction of impulses in them and a local disturbance of conduction in some area.
  2. The presence of one or two ectopic foci in the atria, generating impulses with a high frequency, causing re-excitation of individual atrial fibers.
  3. The theory of “small waves”: the origin of atrial fibrillation – a consequence of the inequality of the refractory periods of individual atrial fibers.