1. CARDIAC INSUFFICIENCY
PATHOLOGY OF VASCULAR TONE
Lecturer: PhD Ivanytsa A.
Vinnytsya National Pirogov Memorial Medical
University
Pathophysiology Department
2. .
• Insufficiency of blood circulation of is the
state when the cardio-vascular system can not
provide organs and tissues of an organism
with necessary amount of blood
3. Cardiac insufficiency is the pathological
condition characterized by inability of the
heart to provide blood supply of organs and
tissues in accordance with their necessities.
4. Classification of cardiac
insufficiency
1.According to clinical course cardiac insufficiency
is divided into:
• acute;
• chronic.
2.According to clinical manifestations intensity
cardiac insufficiency is divided into:
• compensated;
• decompensated.
5. 3.According to injured parts of the heart
cardiac insufficiency is divided into:
• left ventricle cardiac insufficiency;
• right ventricle cardiac insufficiency;
• total cardiac insufficiency.
6. 4.According to pathogenesis cardiac
insufficiency is divided into:
• cardiac insufficiency due to overload of the
heart:
-overload of heart by volume (reasons: heart
disease with valvular insufficiency,
hypervolemia);
-overload of heart by resistance (reasons: heart
disease with valvular stenosis, arterial
hypertension);
7. • cardiac insufficiency due to damage of
myocardium (reasons: arrhythmias,
myocarditis, myocardiopathys);
• cardiac insufficiency due to violation of the
coronary blood circulation (reasons:
atherosclerosis, tromboembolism or spasm
of coronal vessels);
• cardiac insufficiency due to the injury of
pericardium (acute and chronic
pericarditis, cardiac tamponade);
• mixed form.
8. Cardiac insufficiency due overload
of the heart
1.overload by blood volume -
emerges when the inflow of the
blood to a definite part of the heart
is increased:
• hypervolemia
• valvular insufficiency
9. 2. overload by resistance - emerges
when the resistance to the heart
outflow is increased and develops at:
• arterial pressure increase
• valvular stenosis (the left ventricle
overload develops at aortal stenosis,
at mitral stenosis - left atrium, at
pulmonary valve artery stenosis -
right ventricle, at tricuspid stenosis -
right atrium).
10. Cardiac insufficiency due to
damage of the myocardium
Etiology:
• arrhythmias - related to the damage of the heart
conducting system;
• myocarditis - related to the damage of myocardium
of inflammatory origin (e.g., bacteria, viruses,
fungi, allergens, toxic factors);
• myocardiopathys - related to the congenital or
acquired damage of myocardium noninflammatory
origin (e.g., alcohol, anemia, intoxication, hypoxia).
11. Cardiac insufficiency due to
violation of the coronary blood
circulation
Insufficiency of coronary blood
circulation is the pathology which is
characterized by inability of
coronary vessels to supply blood to
the heart in accordance with its
requirements.
12. Coronary heart disease (CHD) is illness which
develops as a result of absolute insufficiency of
coronary circulation and characterized by the
myocardium damage.
Etiology:
• atherosclerosis of coronary vessels;
• thromboembolism of coronary vessels;
• primary thrombosis or embolism of coronary vessels
• spasm of coronary vessels
• inflammation in the coronary vessels ,(e.g.,
rheumatism); compression of coronary vessels (e.g.,
scars, tumors, ligature).
13. Main clinical forms of CHD:
1.Stenocardia (angina pectoris) is
characterized by attacks of brief (to 20
min) acute myocardium ischemia which
are accompanied by a pain syndrome,
sense of fear, vegetative reactions, pain is
relieved by nitroglycerine
2. the preceding infarction state is the
acute focal myocardium dystrophy which
develops during myocardial ischemia from
20 to 40 min;
14. 3. the myocardial infarction is the necrosis of
myocardium, caused by coronary circulation
violation. Emerges at a reversible ischemia
continued over 40-60 min, or at irreversible
coronary circulation violation , «-» effect of
nitroglycerine
4.cardiosclerosisis the sclerotic changes of cardiac
muscle. It can be diffuse (atherosclerotic
cardiosclerosis) and focal (postinfarction
atherosclerotic cardiosclerosis).
15. Clinical syndromes which characteristic for the
myocardial infarction
• pain;
• acute cardiac insufficiency - develops at the injury
of large areas of myocardium and characterized by
the cardiac asthma syndrome, pulmonary edema
or cardiogenic shock;
• arrhythmia - possibly development of all types of
arrhythmias at myocardial infarction. Appearance
of ventricular fibrillation is the most dangerous;
• reperfusion syndrome;
• resorption - necrotizing syndrome.
16. Clinical signs which characteristic
for the myocardial infarction
• Unbearable pain behind the breastbone with
irradiation in the left shoulder, arm and others.
• The skin is pale, cold.
• His face covered with sweat, with a bluish
tinge.
• Pulse is thready, weak filling, frequent,
sometimes arrhythmic.
• Pulmonary edema.
17. MI Laboratory Diagnostics:
Elevated level of enzymes !!!!:
(damage of cell membranes)
↑ CPK (creatine phosphokinase)
↑ AST, ALT
↑ LDH1,2
2. ↑ troponins
3. neutrophilic leukocytosis, left shift
of leukogramm
4. ↑ ESR
18. ECG changes
1. Zone Necrosis -
pathological Q wave or QR,
QRS, QS
2. Zone damage - domed
lifting ST, which is a sign of
acute stage and discordant
changes of the opposite
parts;
3. Zone of ischemia -
negative, high, spiky T.
19. Сomplications of myocardial
infarction
Reperfusion syndrome emerges as a result of re-
establishment blood flow in the area of myocardial
ischemia over 40 min ischemia duration.
The pathogenetic basis of the reperfusion syndrome
is so-called «oxygen paradox», because of the lipid
peroxidation activating and plenty of free radicals
formation which damage the cellular membranes.
20. Cardiogenic shock emerges as a result
of the acute falling of the pumping ability
of the heart.
Etiology:
• myocardial infarction;
• congestive heart failure;
• cardiomyopathy;
• pulmonary edema;
• cardiac tamponade;
• ineffective pumping due to cardiac dysrhythmias
and from acute disruption of valvular function.
21. Pathogenesis of cardiogenic shock:
1. The initial ↓ of arterial pressure
2. Compensatory spasm of
arterioles
3. Secondary ↓ of arterial pressure
4. Terminal changes
22. Resorption - necrotizing syndrome
at the myocardial infarction is the outcome of
the entry of necrotic products of myocardial
disintegration into blood
Signs:
• fever;
• neutrophilic leukocytosis;
• increase of ESR;
• appearance in the blood of enzymes from
damaged cardiomyocytes (creatine kinase,
AST, LDH;)
23. Dressler's syndrome
- develops as a result
of autoantibodies’
production on the
changed myocardium
proteins and
characterized by
serous membranes
inflammationnism -
polyserositis (c.g.,
pericarditis, pleurisy,
peritonitis).
24. Cardiac insufficiency due to
pathology of the pericardium
Etiology:
pathology of pericardium, as a result heart’s work is
violated during a diastole (e.g., exudate or
transudate accumulation in the cavity of
pericardium, acute cardiac tamponade).
Clinical signs:
• arterial hypotension;
• diminishing of ECG wave voltage;
• enlargement of the heart.
25. Acute cardiac tamponade
Acute cardiac tamponade is rapid
accumulation of liquid in the cavity
of pericardium because of
hemorrhage at the wound or cardiac
rupture, or at quickly developing
pericarditis
26. Mechanisms of compensation of
the heart's work
urgent mechanisms of compensation:
• the heterometric mechanism provides compensation at the
cardiac overload by a volume (reasons: heart disease with
valvular insufficiency, hypervolemia). Its essence consists in
the increase of force of the heartbeats in the case of entrance
to the heart of bigger blood volume (а law of Frank-Starling’s)
the homeometric mechanism provides compensation at the
cardiac overload by resistance (reasons: heart disease with
valvular stenosis, arterial hypertension). Its essence consists in
the increase of force of the heartbeats in case of the increase
of resistance to blood flow.
• tachycardia provides constant level of the minute blood
volume.
27.
28. Mechanism of long duration adaptation of the
heart is the myocardial hypertrophy.
myocardial hypertrophy according to F. Meerson:
• myocardial hypertrophy in sportsmen - develops at
periodically increasing loadings; it's characterized
by the increase of all parts of the heart
(myocardiocytes,vessels and nerves)
• compensotory myocardial hypertrophy:
1.hypertrophy due to overloads (develops at the
cardiac insufficiency, arterial hypertension);
2. hypertrophy due to the damage (e.g.,
atherosclerosis, myocarditis).
29. Stages of compensatory heart hypertrophy
development of according F. Meerson:
• emergency stage
• stage of complete hypertrophy and
relatively proof hyperfunction
• stage of gradual exhaustion and
progressive cardiosclerosis
30. Dilatation of myocardium
• Tonogenic dilatation - this is expansion of heart
cavities, that is accompanied by the increase of
stroke volume of blood. Develops as a result of
activating of heterometric mechanism of provides
compensation.
• Myogenic dilatation arises up at the dystrophic
changes of myocardium. It is accompanied by
expansion of cavities of heart and decrease of force
of cardiac contractions. Arises up during
decompensation of cardiac insufficiency.
31. Indicators hemodynamic:
• blood flow velocity;
• circulatory blood volume
• stroke volume of the heart
• cardiac output
• heart rate
• cardiac index
• Arterial pressure
• venous pressure
• total peripheral resistance
• rate of oxygen utilization
32. The indices of hemodynamics change during cardiac
decompensation:
• cardiac output diminishes;
• under the left ventricle cardiac insufficiency:
1)arterial hypotension in the systemic circulation;
2)common peripheral resistance increases;
3)hypertension of the pulmonary circulation, which leads to the
lungs edema;
• under the right ventricle cardiac insufficiency
1) hypotension of the pulmonary circulation;
2) resistance of the pulmonary circulation vessels increases
hereupon;
3)central venous pressure increases which leads to the
congestion in the systemic circulation;
• the circulatory blood volume increases.
33. Clinical symptoms of cardiac
insufficiency:
• circulatory hypoxia;
• shortness of breath because of acidosis and lungs edema; cyanosis
because of venous hyperemia;
• edema (under the right ventricle cardiac insufficiency edema develops on
the lower extremities, under the left ventricle cardiac insufficiency
develops lungs edema);
• portal hypertension and cardiac cirrhosis develops under the right
ventricle cardiac insufficiency;
• ABB violations: metabolic lactate acidosis because of the lactic acid
accumulation and gas alkalosis because of shortness of breath; secondary
hyperaldosteronism due to activating of the renin-angiotensin- aldosteron
system and because of diminishing of aldosteron disintegration in the liver
• Cyanosis (↑ concentration of reduced hemoglobin ).
34. • Acute cardiac insufficiency develops quickly,
at the surplus loading on a heart, when all
compensatory mechanisms are not corrected
with it , e.g., at the myocardium infarction
and its complications (cardiogenic shock,
tamponade of heart), at arrhythmias
(fibrillation of heart, paroxismal tachycardia,
complete atrioventricular blockade), acute
pericarditis, myocarditis, embolism of
pulmonary artery.
37. • Chronic (stagnant) cardiac insufficiency
develops gradually, mainly as a result of
metabolic violations in myocardium at
protracted hyperfunction of heart or
different types of myocardium damage
(e.g., arterial hypertension,
cardiomyopathys, and others).
38. • Normal AP:
-100 - 120 / 70-80 mm Hg (17 - 20 )
-120 - 140 / 80-90 mm Hg (21 - 60)
Arterial hypertension is the increase of
systolic pressure more than I40mni Hg and
diastolic more than 90mm Hg.
39. Classification of arterial
hypertension :
• primary hypertension (essential or idiopathic
hypertension) appears to be a familial disease of
unknown etiology
• secondary hypertension develops secondary to
another disease;
• hypertensive crisis is a sudden acute elevation in
arterial blood pressure
• isolated systolic hypertension refers to an elevation
in systolic blood pressure greater than 140 mm Hg
without a concurrent elevation in diastolic blood
pressure (elderly persons)
40. II. The type of high blood pressure:
1. Systolic.
2. Diastolic.
3. Mixed.
ІІІ. The value of the cardiac output (cardiac output):
Hyperkinetic: ↑cardiac output (↑ circulating blood
volume).
Hypokinetic: ↑vascular resistance(hypertension) -
↑ diastolic blood pressure.
Eukinetic.
IV. The level of renin:
hyperreninemic. Normoreninemic.Hyporeninemic
41. Etiology:
• Primary hypertension results from unknown causes,
it accounts for 80% of hypertension cases.
• Secondary hypertension 10% of hypertension cases:
• renal diseases-may cause accelerated renin release,
which, in turn, elevates blood pressure;
• Cushing's syndrome, which causes accumulation of
extracellular sodium and water;
• primary aldosteronism, which causes accumulation
of extracellular sodium and water;
• hypothyroidism and hyperthyroidism
• coarctation of the aorta
• excessive alcohol ingestion and prolonged use of oral contraceptives.
42. Risk factors of essential hypertension:
main factors:
• psycho-emotional overload (chronic stress
situations)
• Excessive consumption of salt,
• hereditary predisposition,
• low body weight at birth
• male sex; middle age ; black color of skin;
hypodynamia;
• insulin resistance;
• urban population, bad habits (e.g., cigarette
smoking).
43. Pathogenesis of primary (essential)
hypertension
• Dysregulatory theory - violations of regulatory
mechanisms of arterial vessels tone.
There are two phases:
1. Hyperkinetic
1 stage: activation of the sympathetic and adrenal
system under the action of stress factors
2 stage: activation of the rennin-angiotensin-
aldosteron system
3 stage: activation of aldosteron and vasopressin
systems
44. Pathogenesis of primary (essential)
hypertension
2. Hypokinetic - is characterized by the irreversible
structural changes of compession and resistance
vessels, peripheral vascular resistance and arterial
vessels tone grows as a result constantly. The main
significance has following factors:
• constant spasm of arterioles;
• hypertrophy of smooth muscles;
• atherosclerosis and substitution of smooth
muscles by connective tissue.
45. Pathogenesis of primary (essential)
hypertension
• Membrane theory is the hereditarily conditioned
violation of ionic pumps of membranes of smooth
muscles fibers:
• defect of Ca2+- pump- this leads to the
development of permanent contraction and the
increase of peripheral vascular resistance.
• decrease work of Na -K –pump - the outcome is the
thickening of vessel’s wall and diminishing of
diameter of vessels increase of sensitization to the
action of catecholamine, damage and necrosis of
cells, atherosclerosis).
46. Arterial hypotension
is the decrease of systolic pressure less than
100 Hg and diastolic less than 60 mm Hg.
Kinds:
• Physiological (it is not accompanied by the
symptoms of illnesses).
• Pathological:
А) acute (shock and collapse)
B) сhronic (primary and secondary):
47. • secondary (symptomatic) arterial hypotension is
a result of acute and chronic heart diseases
(congenital heart diseases, myocarditis, infarction
of myocardium); brain diseases, lungs diseases
(croupous pneumonia), liver diseases (hepatitis,
mechanical jaundice), blood diseases (anemia),
endocrine diseases (Addison’s disease) and
intoxications;
• primary arterial hypotension develops at patients
with neurocirculatory dystonia of hypotension
type (essential, primary, idiopathic hypotension).
48. Collapse
• Collapse is acute vascular insufficiency which is
characterized by the acute dicrease of arterial
vessels tone and central- venous pressure and
diminished circulatory blood volume.
Types of collapse:
• toxic and infectious collapse, - develops at intestinal infections (dysentery,
salmonellosis) due to the action of endotoxins (after death of microorganisms).
• hemorrhagic collapse - arises up at acute massive bleeding and related to the
rapid decrease, of volume of circulatory blood
• pancreatic collapse - at the mechanical trauma of pancreas or acute
pancreatitis and liberation of tripsin in blood
• orthostatic collapse - arises up in acute transition from horizontal position to
vertical position
• anoxic - arises up at the rapid decrease of partial pressure of oxygen in air, as a
result of anoxemia develops, decrease of vessels tone
49. Pathogenesis of collapse
The decrease of volume of circulatory
blood and vessels’ tone leads to the
decrease of venous return to the
heart, decrease of cardiac output
decrease of both arterial and venous
pressure and disturbance of tissues
perfusion and metabolism, which
leads to the brain hypoxia.
50. Atherosclerosis
is pathology of vascular wall, which characterize
by the sedimentation of lipids, elements of blood,
calcium and connecting tissue in its internal
membrane (tunica intima).
51. Risk factors of atherosclerosis:
• Hypertension;
• metabolic disturbances;
• hormonal violations;
• pathology of vascular wall;
• cigarette smoking
• elevated serum cholesterol
• obesity
• diabetes mellitus
• Other presumed risk factors include increasing age, physical
inactivity, and a family history of arteriosclerosis.
• Incidence is higher in men than in women.
52. Pathophysiologic processes and
manifestations
• It has two theories:
1. primary damage of vessel wall
2.secondary deposit of cholesterol and lipoproteids
of low density
• Complications of atherosclerosis:
• ischemia;
• heart attack;
• aneurism.
53.
54. Vinnytsya National Pirogov Memorial Medical University
Pathophysiology Department
PhD., Viktoriia Pylyponova
55. Normal gas composition in blood:
In arterial blood:
pO2: 80-100 mmHg.
pCO2: 40 mmHg.
In venous blood :
pO2: 40 mmHg.
pCO2: 46 mmHg.
56.
57. Raspiration – is function of the
organism, which consists in
maintaining the gas composition of the
blood, supplying tissues with oxygen
(O2) and releasing carbon dioxide
(CO2).
58. Respiratory failure – is a pathological state that is
characterized by disorder of gas exchange
between ambient air and circulating blood and
leads to inequality of blood gas composition to an
organism oxygen necessity.
59. Classification of the external respiratory
disorders :
According to the clinical caurse:
Acute (e.g. asphyxia),
Chronic
According to
the localization:
Partial
total
According to clinical manifestations:
сompensative
decompensative
60. EXTERNAL RESPIRATION is a complex of
processes occurring in the lung and providing
normal contents of oxygen (О2) and carbon
dioxide (СО2) in blood.
61. Three main processes take place in the
lungs:
alveolar ventilation,
diffusion of the oxygen and carbon
dioxide through the alveolar-capillary
membrane
perfusion (flowing of the blood
through the pulmonary capillary
vessels).
64. Classification of respiratory failure
according to VOTCHAL:
1. Centrogenic
2. Nervous-muscular
3. Thoraco-diaphragmal
4. Broncho-pulmonary
• Obstructive
• Restrictive
• Diffusive
65. Primary-dyskinetic respiratory failure:
Pathology of Respiratory center
(opression RS by morfine, craniocerebral
traumas);
Pathology of motoneurons of spinal cord
(tumors, poliomyelitis);
Disorders of the thorax motility;
Damage of the integrity of thorax and
pleural cavity (open, closed pneumothorax)
66. Obstructive – increased resistance to air passage.
Foreign bodies in the upper airways;
Thickening of walls of respiratory tracts
(inflammatory edema of mucus membranes of
nose, larynges, tracheas);
Spasm of bronci, larynx (bronchial asthma,
laryngospasm,);
Compression of respiratory tracts from outside
(by tumor, inflammatory swelling, retropharyngeal
abscess, enlarged thyroid gland, etc.)
67. Restrictive or diminishing of total volume of
alveoli (limitation of pulmonary ventilation)
Inflammation and congestion in the lungs
fluids (pneumonia, edema of the lungs)
Partial pulmonary resection
Destruction of part of the lung (cavernous Tbs,
lung’s abscess )
Pulmonary fibrosis
Complete stopping of the lungs ventilation
(lung collapse)
Violation of surfactant synthesis (atelectasis)
68. Diffusive: diminishing of total surface of alveoli-
capillary membranes for gases diffusion.
thickness of alveolar and capillary membrane
and decrease of its permeability for gases
(fibrosis; edema of capillary membrane –
pneumonia, RDS, DIC-syndrome);
decrease of summary internal surface of
alveols (lungs resection, RDS (atelectasis).
70. Disorder of perfusion of lungs (lung blood flow):
right ventricle failure of the heart (myocardium
infarction, myocarditis, exudative pericarditis and
others);
left ventricle failure of the heart (mitral
stenosis) - development of pulmonary edema;
vascular insufficiency (shock, collapse);
embolism , thrombosis of pulmonary artery.
71. Classification of respiratory failure
according to VOTCHAL:
1. Centrogenic
2. Nervous-muscular
3. Thoraco-diaphragmal
4. Broncho-pulmonary
• Obstructive
• Restrictive
• Diffusive
72. Classification of respiratory failure
according to VOTCHAL:
1.Centrogenic:
at the violation of work of the
Respiratory center (hemorrhage,
tumor, depression of CNS at shock);
depression of central regulation of
breathing as a result of poisoning by
narcotic drugs (Morphine!),
barbiturates.
74. Thoraco-diaphragmal
violation of biomechanics of breathing is related to
pathology of thorax (fractures of ribs, kyphoscoliosis);
high standing of diaphragm (paresis of stomach,
intestine, ascitis, obesity, pregnancy);
hemothorax,
pneumothorax.
75. Broncho-pulmonary - pathological
processes in lungs and respiratory tracts.
kinds
• Obstructive
• Restrictive
• Diffusive
77. Restrictive form- at reduction of respiratory
surface of alveoli:
surfactant insufficiency;
pneumonia,
pneumosclerosis,
emphysema,
resection of lungs;
78. Broncho-pulmonary
diffusive form at the thickening of
alveolar-capillary membrane
(black-lung disease, fibrosis of lungs).
The reasons that reduces
diffusion:
a - the norm;
b - alveolar wall thickening;
в - in capillary wall
thickening;
г - swelling in the alveoli
д - interstitial edema;
e - dilatation capillaries
79. The indexes of respiratory insufficiency are divided
into:
1. direct - change of gas composition of blood:
- hypoxemia (decrease of pO2 of arterial blood less
than 90 mmHg);
- hypercapnia (increase of pCO2 of arterial blood
more than 45 mmHg)
- gas acidosis
2.indirect - change of lungs volumes (RV, RVinsp.,
RVex., VLV, MVL)
80. Indexes of respiratory failure
Index Norm Respiratory
failure
RV 500 ml ↓
RVinsp 1200-1400 ml ↓
RVex 1200 ml ↓
VLV 3500-5500 ml ↓
RR 16-20 per min. ↑
81. Classification of pathological types of breathing:
1. Disorders of the breathing depth and rate:
bradypnea;
tachypnea;
dyspnea;
hyperpnea;
2. Periodic breathing.
Cheyne-Stoke’s breathing.
Biot’s breathing.
3. Terminal breathing.
Apneustic respiration.
Gasping respiration.
Kussmaul’s respiration
82. Bradypnea - is decrease of frequency of the
respiration.
inhibition of nerve impulses from baroreceptors of the
aortic arch and carotid sinus receptors to RC:
Causes
Prolonged and severe hypoxia;
The effect of narcotic drugs,
Brain damage (inflammation, stroke, edema, etc.).
83. Tachipnea – is frequent shallow respiration.
Reasons:
1. Fever.
2. Functional impairment of the CNS.
3. Damage lung (atelectasis, pneumonia, congestion).
3. Pain localized in the chest or abdomen.
84. Hyperpnea – is an increase of depth and
frequency of the respiration (develops as
adaptative reaction, can leads to
hypoventilation).
85. Dyspnea –characterized by the change of
frequency, depth and breathing rhythm
and is accompanied by feeling of air
insufficiency.
86. Reasons for dyspnea development:
Decrease of blood oxygenations in the lungs
(decrease of pO2 in the air, disorder of pulmonary
ventilation and diffusion);
Disorders of gas transport (anemia, cardiac
insufficiency);
Pathology of thorax and breathing regulation.
Acidosis
Functional and organic central nervous
system violations (stress, violations of blood
cerebral circulation)
88. Inspiratory (develops in case of excitement of
respiratory center and restrictive disorders of
ventilation)
1. in the first stage of asphyxia
2. General disorders of the CNS,
3. physical exercise in patients with heart failure,
4. pneumothorax.
Expiratory (develops in case of obstructive disorders
of ventilation);
1. broncial asthma,
2. In the second stage of asphyxia
3. emphysema (increased resistance to airflow during
exhalation).
89. PERIODICAL BREATHING – is
pathological breathing that is
characterized by the periods of
respiration and periods of absence of
breathing (apnea).
90. Cheyne-Stoke’s respiration
Reasons: brain hypoxia, cardiac failure, the diseases of
the brain and its membranes, uremia, mountain
diseases, obesity, premature babies, some drugs
(poisoning by morphine).
Characterized by growing amplitude of respiration till
the marked hyperpnoea and then it's diminishing to
apnoea followed by a cycle of the respiratory movements
also finishing with apnoea.
91. Mechanism of development Cheyne-Stoke’s
respiration: the cells of the brain cortex and
subcortical structures are inhibited due to hypoxia –
respiration stops, consciousness disappears, the
activity of the vascular motors becomes inhibited
with an acute intensification of impulses of
chemoreceptors, which leads to a high concentration
of carbon dioxide and stimulate from baroreceptors
due to decrease of the arterial pressure are sufficient
to excite the respiratory center and respiration
92. Biot’s respiration
Reasons: meningitis, encephalitis and other diseases,
accompanied by impairment of the CNS especially the
medulla oblongata.
Characterized by constant amplitude but both stop
and begin suddenly.
93. Terminal breathing – is characteristic for the
terminal states.
Apneustic respiration – is characteristic for
inhibition of respiratory center.
Kussmaul’s respiration - is characteristic for
hyperketonemic diabetes coma.
Gasping respiration – is characteristic for agony.
94. Asphyxia - life-threatening pathological
condition caused by acute respiratory failure,
which occurs when the blood does not arrive
O2, and with blood not derived CO2.
95. Causes of asphyxia:
1. Compression of airway (strangulation).
2. Obstruction of airway (foreign body,
inflammatory edema).
3. The presence of fluid in the airways and
alveoli (drowning, pulmonary edema,
aspiration of vomit).
4. Pneumothorax.
5. Strong inhibition RC.
96. Periods of asphyxia:
First period: inspiratory dyspnea.
Second period: expiratory dyspnea
Third period: the observed decrease in the frequency
and amplitude of respiration.
There Gasping respiration, followed by respiratory
arrest.
98. Atelectasis: is the collapse or closure
of a lung resulting in reduced or
absent gas exchange.
Primary: is a condition in which lung
tissue remains uninflated as a result of
insufficient surfactant production
Secondary: is caused by airway
obstruction, lung compression or
increased recoil of the ling due to
diminished pulmonary surfactant
100. HYPOXIA – reduction of oxygen
supply to a tissue below physiological
levels despite adequate perfusion of the
tissue by blood.
101. Classification of hypoxia
by etiology:
1. Exogenous (hypoxic).
2. Respiratory.
3. Circulatory.
4. Hemic.
5. Tissue.
6. Mixed.
102.
103. Exogenous (hypoxic) hypoxia –
due to a decrease pO2 in air.
with the rise in altitude, in the mountains
In blood -
Hypoxemia (↓ pO2art)
Hypocapnia (↓ pCO2art) resulting
compensatory hyperventilation of the lungs and leads
to the gas alkalosis
104. Respiratory hypoxia that due to failure to transport
sufficient oxygen because of inadequate lungs
ventilation.
alveolar hypoventilation (bronchial asthma,
pneumonia, pulmonary edema, hemothorax)
lowering blood perfusion lung (↓VBC, lack of
contractile function of the heart, pulmonary
hypertension, and others.)
violation diffusion of oxygen in the lungs
(pulmonary edema, fibrosis, pneumoconiosis, etc.).
In blood
↓ pO2art - arterial hypoxemia.
↑ pCO2 art – hypercapnia – gas acidosis
105. Anemic hypoxia that due to reduction of
the oxygen-carrying capacity of the blood owing to
decreased total hemoglobin or altered hemoglobin
constituents.
Causes
Anemia
Hemoglobin inactivation (violation of binding,
transport and give oxygen to the tissues).
106. • Reasons hemoglobin qualitative changes:
Poisoning CO (carbon monoxide) -
carboxyhemoglobin formation.
• fires
• in garages and on city highways with heavy motor
traffic,
• the premises at fault or gas furnace devices.
•Methemoglobine formated during poisoning with nitrates and
some drugs with an oxidizing capacity.
•Hereditary anomalies of hemoglobin (thalassemia,
sickle-cell anemia).
107. Histotoxic (tissue) hypoxia that due to
impaired use of oxygen by tissues.
Poisoning with cyanides (they inactivate
cytochrome oxidase)
Alcohol, narcotics, some drugs inhibit
dehydrogenase of the Krebs cycle.
Deficite Vit B2, nicotinic asid –decreases syntesis
respiratory enzyme.
Circulatory hypoxia that due to failure to
transport sufficient oxygen because of inadequate
blood flow.
