Wondershare EdrawMind
EdrawMindPathophysiology - Heart failure
MindMap Gallery Pathophysiology - Heart failure
- 43
Pathophysiology - Heart failure
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
Edited at 2025-03-10 15:40:22- Rumi 10 spiritual high-dimensional awakenings
Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
- Pathophysiology - Heart failure
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
- Pathophysiology - ischemia - reperfusion injury
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
Pathophysiology - Heart failure
- Rumi 10 spiritual high-dimensional awakenings
Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
- Pathophysiology - Heart failure
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
- Pathophysiology - ischemia - reperfusion injury
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
- Recommended to you
- Outline
Chapter 10 Heart failure
Refers to the pathophysiological process of heart contraction and diastolic function under the action of various pathogenic factors, resulting in absolute or relative cardiac output, that is, the function of the heart pump is weakened and cannot meet the body's metabolic needs.
Absolutely ↓
Below normal level
Relatively ↓
Usually higher than normal level, in abnormal situations, but still higher than normal level
Heart failure
concept
Refers to the pathophysiological process of heart contraction and diastolic function under the action of various pathogenic factors, resulting in absolute or relative cardiac output, that is, the function of the heart pump is weakened and cannot meet the body's metabolic needs.
Absolutely ↓
Below normal level
Relatively ↓
Usually higher than normal level, in abnormal situations, but still higher than normal level
Section 1 Causes, Inducements and Classification
Causes
Primary myocardial comfort dysfunction
Poisoning, ischemia
Coronary heart disease, cardiomyopathy, myocarditis, etc.
Myocardial hyperload
Pressure (post) compound
Valve stenosis
Hypertension (left ventricle)
Pulmonary hypertension (right ventricle)
Capacity (foreload)
Incomplete closure of the valve
Repay the effort↑
High power cycle state
e.g. Circulating blood ↑
Induce
Not the root cause, heart failure caused by the cause
main
Systemic infection
fever
Basal metabolic rate↑
Induce heart rate acceleration
Endotoxin
G- can generally be released
Various ways to inhibit cardiac function
Acid-base balance and electrolyte metabolism disorders
Acidosis
H blocks Ca2
Entering from extracellular
Release from sarcoplasmic reticulum into cells
Compete with Ca2 to bind troponin
Causes cardiomyocyte energy metabolism disorder
ATP↓
Inhibiting myocardial excitation-contraction coupling
Hyperkalemia
Hyperkalemia
Severe arrhythmia
Arrhythmia
Mainly rapid arrhythmia
The heart rate is too fast →
Myocardial oxygen consumption is significant↑
After the heart rate is output ↓, the heart rate will generally be compensated, and the meaning of compensation will disappear in this era.
The diastolic period is relatively shortened
Repay the effort↓
Appropriate heart rate increase will not be
Reduced coronary perfusion
Heart perfusion usually occurs during diastolic period
Pregnancy and childbirth
Blood volume during pregnancy↑
The heart is under a large load
Normal production process
Stress (tension, pain)
Sympathetic nerve-adrenaline medulla system, catecholamine, etc.
Mainly peripheral resistance vasoconstriction → increase afterload
Abdominal pressure is high → return to heart and blood↑→ increase preload
Pregnant women with heart problems choose to have caesarean section
Illegal accidents caused by overwork, cardiac enhancement and other treatments
Classification
By severity of the condition
Mild
Moderate
Heavy
Developing at the speed of the disease course
acute
e.g. Myocardial infarction, severe myocarditis, large amounts of infusion, etc.
Chronic
e.g. caused by lung diseases, hypertension, etc.
According to the output of the heart
Low cardiac output
Most clinical cases
High cardiac output
Comparing with the average level of normal people
But lower than normal
e.g. Hyperthyroidism, severe anemia, vitamin B/E deficiency, arteriovenous fistula, etc.
Normally, the output of the heart is higher than the average
According to the location of heart failure
Left heart failure
Mainly refer to the right heart ventricular
e.g.Hypertension
Right heart failure
Mainly refer to the right heart ventricular
e.g.Pulmonary hypertension
Total heart failure
e.g.Rheumatoid heart disease
By dysfunction
Systolic dysfunction
Diastolic dysfunction
It will generally affect, but it has a focus
Section 2 The mechanism of heart failure
Myocardial contractility weakens
Destruction of cardiomyocytes and contractile-related proteins
Cardiac myocardial cell necrosis
Ischemia and hypoxia
Bacterial virus infection, poisoning, etc.
Cardiac myocardial cell apoptosis
The role of oxidative stress and cytokines
Calcium homeostasis imbalance, mitochondrial abnormality, etc.
Myocardial energy metabolism disorder
Energy generation barrier
Ischemia and hypoxia
VitB1 lack
As a coenzyme, it affects oxidative phosphorylation
Energy utilization barriers
(Mainly seen in) Myocardial hypertrophy → "Myosin ATPase" activity decreased
Isozyme
V1
The most active
↓
V2
V3
The weakest activity
↑
Myocardial excitation-contraction coupling disorder
Abnormal treatment of Ca2 in the sarcoplasmic reticulum
Intake ability↓
Calcium pumps on sarcoplasma require energy
Storage amount↓
Release amount↓
Situation 1: Intake ↓→Storage ↓→Release ↓
Situation 2: It may not be stored, and it may be in the effect of H such as acidosis → Calcium-binding protein in Ca2 and sarcoplasmic reticulum ↑→ Release ↓
Case 3: Channel activity that releases Ca2↓
Myocardial contraction coupling disorder
Extracellular Ca2 influenza barrier
Calcium channel blocked
Receptor manipulated Ca2 channel blocked
Heart failure (especially the imbalanced growth of myocardial hypertrophy) → Sympathetic nerve density ↓ → Catecholamine (NE) ↓ → Not effective on β receptor → Ca2 is difficult to open
Voltage dependent Ca2 channel impeded
Not affected generally
Na —Ca2 Exchange
Not affected generally
Ca2 and troponin binding disorder
Acidosis
H competes with Ca2 to bind troponin
Hyperkalemia
K competes with Ca2 to bind troponin
Imbalanced growth of myocardial hypertrophy
Normally, it is a stronger way of compensation
Unbalanced growth
Organ level
Myocardial sympathetic nerve distribution density decreases
Reason: The increase in sympathetic N is smaller
Consequence: Excitement contraction coupling disorder
Organizational level
The number of capillaries is relatively insufficient
"oppression"
Poor myocardial microcirculation perfusion
Cell level
Myocardial mitochondria
The quantity cannot be increased proportionally
The ratio of mitochondrial membrane surface area to the weight of myocardial fibers is significantly reduced
Myocardial energy supply per unit weight↓
The ratio of surface area to weight of hypertrophic myocardium is significantly reduced → (especially Ca2) ion transport efficiency is relative↓
Molecular level
Myosin ATPase activity decreased
V1 relative ↓→Energy utilization obstacles
Sarcoplasmic reticulum Ca2 treatment dysfunction
The overall heart output is ↑, but the unit myocardial function is ↓ and burden↑
Dissatisfaction of ventricular diastolic function
Calcium ion reset delay
Way
Back to the sarcoplasmic network
Flow out of the cell
Calcium pump → ATP is required
Dissociation disorder of myosome-actin complex
ATP is also required
Non-dissociation → Continuous contraction
Reduced ventricular diastolic potential energy
Insufficient filling
Ventricular compliance↓
Ventricular compliance: refers to the change in the volume of the ventricle under unit pressure
Uncoordinated comfort activities in various parts of the heart
The coordination of activities between the left and right hearts, between the atrioventricular and the ventricle itself is destroyed
The most common clinical causes are various types of arrhythmias
Section 3 Compensational reaction of the body
Basic concepts
Complete compensation
No clinical symptoms
Incomplete compensation
No clinical symptoms in a quiet state
Decompensated
There are obvious symptoms in a quiet state
Compensation
Cardiac Compensation Response
Accelerate heart rate
The heart rate of patients with chronic heart failure may not be accelerated
mechanism
Pressure sensor
Aortic arch
Carotid sinus
Cardiac output ↓→pressure ↓→sympathetic N excitation → positive effect on the heart
Capacity sensor
Heart atrium
Vein cava
Capacity ↑→Sympathetic N excitation→Positive effect on the heart
significance
It can increase cardiac output and maintain arterial blood pressure within a certain range to ensure cerebrovascular and coronary perfusion
limitation
Increased oxygen consumption of myocardial
Possible damage caused by oxygen consumption > its compensatory effect
Shorten diastolic period
→Insufficient ventricular filling →Cardous output ↓
→Insufficient coronary perfusion →Mynaecology and hypoxia
Heart dilation
Frank-Starling Law
Myocardial contraction force and cardiac output increase within a certain range with the increase of myocardial fiber sarcoma length (≤2.2μm)
This kind of expansion is called "tension-induced expansion"
Exceeding the optimal length of the sarcoma (2.2μm), the expansion of myocardial elongation without the enhancement of contraction is called "myosinogenic dilation"
limitation
Excessive elongation of the sarcoma and increased oxygen consumption of myocardium are important factors leading to decompensation
Myocardial hypertrophy
concept
Increased volume and weight of cardiomyocytes
It is often a compensation mechanism for chronic heart failure
Economical, better
Morphological classification
Centripetal hypertrophy
It refers to the parallel hyperplasia of myocardial fibers under the action of long-term pressure load (ejaculation resistance↑), that is, the muscle fibers become thicker, the ventricular wall thickness increases, and no significant enlargement of the heart cavity.
Centrifugal hypertrophy
Refers to the tandem hyperplasia of myocardial fibers under the action of long-term capacity load (return to heart blood volume↑), that is, muscle fibers become longer and the heart cavity is significantly enlarged.
significance
Increases myocardial contraction and helps maintain cardiac output
Unit myocardial contraction force↓ but overall contraction force↑
Reduce chamber wall tension → reduce myocardial oxygen consumption
limitation
Imbalance of hypertrophy myocardium → even lead to heart failure
Extracardial Compensation Reaction
Blood volume↑
Main ways
Reimbursement for the kidney
Blood pressure ↓→sympathetic nerve excitation, etc. → renal vasoconstriction → glomerular filtration rate ↓
ADH and aldosterone → tubular reabsorption ↑
Water and sodium retention
effect
Increase cardiac output
Maintain arterial blood pressure
limitation
May increase the anterior and afterload of the heart and cause cardiac edema
Blood flow redistribution
Catecholamine↑→No effect on cardiovascular and cerebrovascular, but arterioles are contracted → Increase cardiac afterload
RBC increase
For chronic heart failure
damage
Increase blood viscosity → blood flow resistance ↑→ resistance to heart ejaculation ↑
Enhanced tissue capacity of oxygen
For chronic heart failure
Good, no obvious harmful effects on the body
Section 4 Clinical manifestations of heart failure
Pulmonary circulatory congestion
Mainly due to left heart failure
The left heart cannot pump out the blood transmitted from the pulmonary vein in time
Clinical Symptoms
Difficulty in breathing
Expression form
Exercise dyspnea
mechanism
Physical activity requires aerobic life↑
Normally, the cardiac output is mainly increased
But left heart failure cannot provide appropriate cardiac output
Exacerbation of hypoxia and CO2 retention
Physical activity → heart rate increases, so the diastolic period becomes shorter and return to left heart blood↓→
Physical activity → whole body venous blood returns to the right heart↑ → right heart ejaculation ↑ →
Pulmonary circulating blood volume↑→ Lung cap. Pressure↑→ Severe lung congestion→Alveolar compliance↓→Alveolar dilation is limited → Hypoxia
Sit upright and breathe
mechanism
When sitting upright, part of the blood is transferred to the lower half of the body due to gravity.
When sitting upright, the edema fluid in the lower part of the body enters the blood less
Reduced pulmonary congestion
When sitting upright, the position of the diaphragm moves downward relative to → the volume of the chest cavity increases, and the lung capacity is ↑
Paroxysmal dyspnea at night
Concept: Usually there is no difficulty in falling asleep, but after sleeping soundly at night, you are suddenly forced to sit up due to chest tightness and irritability.
mechanism
Flat lying
Edema fluid enters blood more frequently than when sitting upright
The effort to return is higher than when sitting upright
Pulmonary congestion↑
Reduced chest volume
After falling asleep
Relative excitement of the vagus nerve → bronchial contraction → airway resistance ↑
CNS reaction sensitivity↓, patients can only wake up when hypoxia reaches a certain level and feel short of breath
Explain "parallel"
Pulmonary edema
mechanism
Lung cap. Pressure increase
Lung cap.permeability↑
Thrombin, histamine and other substances
Systemic circulation blood stasis
Mainly due to right heart failure
Clinical Symptoms
Venous congestion/increased venous pressure
reason
Water and sodium retention
Right heart failure → Return to heart blood ↓ → Cardiac output ↓ → Kidney blood flow ↓ → Filtration ↓
Right atrial pressure increases and venous return is blocked
Edema—"cardiac edema"
Main mechanism
Water and sodium retention
cap.press↑
Transfer of blood to tissue space
Hepatomegaly and tenderness and abnormal liver function
It is mainly caused by liver congestion
Insufficient cardiac output
Pale or cyanotic skin
CNS lack of energy → inhibition: fatigue, insomnia, sleepiness
Urine volume↓
Cardiac shock
Section 5: The basics of preventing and treating heart failure
Prevent and treat basic causes and eliminate inducement
Improve heart comfort
Shrink function
Heart-boosting medicine, etc.
Diastolic function
Calcium antagonists, beta blockers, etc.
Reduce the front and afterload of the heart
Drugs that selectively dilate small veins → reduce backtrack blood → reduce preload
Drugs that selectively dilate arterioles → reduce perivascular resistance → reduce afterload
Control edema
Diuretics
Section 1 Causes, Inducements and Classification
Causes
Primary myocardial comfort dysfunction
Poisoning, ischemia
Coronary heart disease, cardiomyopathy, myocarditis, etc.
Myocardial hyperload
Pressure (post) compound
Valve stenosis
Hypertension (left ventricle)
Pulmonary hypertension (right ventricle)
Capacity (foreload)
Incomplete closure of the valve
Repay the effort↑
High power cycle state
e.g. Circulating blood ↑
Induce
Not the root cause, heart failure caused by the cause
main
Systemic infection
fever
Basal metabolic rate↑
Induce heart rate acceleration
Endotoxin
G- can generally be released
Various ways to inhibit cardiac function
Acid-base balance and electrolyte metabolism disorders
Acidosis
H blocks Ca2
Entering from extracellular
Release from sarcoplasmic reticulum into cells
Compete with Ca2 to bind troponin
Causes cardiomyocyte energy metabolism disorder
ATP↓
Inhibiting myocardial excitation-contraction coupling
Hyperkalemia
Hyperkalemia
Severe arrhythmia
Arrhythmia
Mainly rapid arrhythmia
The heart rate is too fast →
Myocardial oxygen consumption is significant↑
After the heart rate is output ↓, the heart rate will generally be compensated, and the meaning of compensation will disappear in this era.
The diastolic period is relatively shortened
Repay the effort↓
Appropriate heart rate increase will not be
Reduced coronary perfusion
Heart perfusion usually occurs during diastolic period
Pregnancy and childbirth
Blood volume during pregnancy↑
The heart is under a large load
Normal production process
Stress (tension, pain)
Sympathetic nerve-adrenaline medulla system, catecholamine, etc.
Mainly peripheral resistance vasoconstriction → increase afterload
Abdominal pressure is high → return to heart and blood↑→ increase preload
Pregnant women with heart problems choose to have caesarean section
Illegal accidents caused by overwork, cardiac enhancement and other treatments
Classification
By severity of the condition
Mild
Moderate
Heavy
Developing at the speed of the disease course
acute
e.g. Myocardial infarction, severe myocarditis, large amounts of infusion, etc.
Chronic
e.g. caused by lung diseases, hypertension, etc.
According to the output of the heart
Low cardiac output
Most clinical cases
High cardiac output
Comparing with the average level of normal people
But lower than normal
e.g. Hyperthyroidism, severe anemia, vitamin B/E deficiency, arteriovenous fistula, etc.
Normally, the output of the heart is higher than the average
According to the location of heart failure
Left heart failure
Mainly refer to the right heart ventricular
e.g.Hypertension
Right heart failure
Mainly refer to the right heart ventricular
e.g.Pulmonary hypertension
Total heart failure
e.g.Rheumatoid heart disease
By dysfunction
Systolic dysfunction
Diastolic dysfunction
It will generally affect, but it has a focus
Section 2 The mechanism of heart failure
Myocardial contractility weakens
Destruction of cardiomyocytes and contractile-related proteins
Cardiac myocardial cell necrosis
Ischemia and hypoxia
Bacterial virus infection, poisoning, etc.
Cardiac myocardial cell apoptosis
The role of oxidative stress and cytokines
Calcium homeostasis imbalance, mitochondrial abnormality, etc.
Myocardial energy metabolism disorder
Energy generation barrier
Ischemia and hypoxia
VitB1 lack
As a coenzyme, it affects oxidative phosphorylation
Energy utilization barriers
(Mainly seen in) Myocardial hypertrophy → "Myosin ATPase" activity decreased
Isozyme
V1
The most active
↓
V2
V3
The weakest activity
↑
Myocardial excitation-contraction coupling disorder
Abnormal treatment of Ca2 in the sarcoplasmic reticulum
Intake ability↓
Calcium pumps on sarcoplasma require energy
Storage amount↓
Release amount↓
Situation 1: Intake ↓→Storage ↓→Release ↓
Situation 2: It may not be stored, and it may be in the effect of H such as acidosis → Calcium-binding protein in Ca2 and sarcoplasmic reticulum ↑→ Release ↓
Case 3: Channel activity that releases Ca2↓
Myocardial contraction coupling disorder
Extracellular Ca2 influenza barrier
Calcium channel blocked
Receptor manipulated Ca2 channel blocked
Heart failure (especially the imbalanced growth of myocardial hypertrophy) → Sympathetic nerve density ↓ → Catecholamine (NE) ↓ → Not effective on β receptor → Ca2 is difficult to open
Voltage dependent Ca2 channel impeded
Not affected generally
Na —Ca2 Exchange
Not affected generally
Ca2 and troponin binding disorder
Acidosis
H competes with Ca2 to bind troponin
Hyperkalemia
K competes with Ca2 to bind troponin
Imbalanced growth of myocardial hypertrophy
Normally, it is a stronger way of compensation
Unbalanced growth
Organ level
Myocardial sympathetic nerve distribution density decreases
Reason: The increase in sympathetic N is smaller
Consequence: Excitement contraction coupling disorder
Organizational level
The number of capillaries is relatively insufficient
"oppression"
Poor myocardial microcirculation perfusion
Cell level
Myocardial mitochondria
The quantity cannot be increased proportionally
The ratio of mitochondrial membrane surface area to the weight of myocardial fibers is significantly reduced
Myocardial energy supply per unit weight↓
The ratio of surface area to weight of hypertrophic myocardium is significantly reduced → (especially Ca2) ion transport efficiency is relative↓
Molecular level
Myosin ATPase activity decreased
V1 relative ↓→Energy utilization obstacles
Sarcoplasmic reticulum Ca2 treatment dysfunction
The overall heart output is ↑, but the unit myocardial function is ↓ and burden↑
Dissatisfaction of ventricular diastolic function
Calcium ion reset delay
Way
Back to the sarcoplasmic network
Flow out of the cell
Calcium pump → ATP is required
Dissociation disorder of myosome-actin complex
ATP is also required
Non-dissociation → Continuous contraction
Reduced ventricular diastolic potential energy
Insufficient filling
Ventricular compliance↓
Ventricular compliance: refers to the change in the volume of the ventricle under unit pressure
Uncoordinated comfort activities in various parts of the heart
The coordination of activities between the left and right hearts, between the atrioventricular and the ventricle itself is destroyed
The most common clinical causes are various types of arrhythmias
Section 3 Compensational reaction of the body
Basic concepts
Complete compensation
No clinical symptoms
Incomplete compensation
No clinical symptoms in a quiet state
Decompensated
There are obvious symptoms in a quiet state
Compensation
Cardiac Compensation Response
Accelerate heart rate
The heart rate of patients with chronic heart failure may not be accelerated
mechanism
Pressure sensor
Aortic arch
Carotid sinus
Cardiac output ↓→pressure ↓→sympathetic N excitation → positive effect on the heart
Capacity sensor
Heart atrium
Vein cava
Capacity ↑→Sympathetic N excitation→Positive effect on the heart
significance
It can increase cardiac output and maintain arterial blood pressure within a certain range to ensure cerebrovascular and coronary perfusion
limitation
Increased oxygen consumption of myocardial
Possible damage caused by oxygen consumption > its compensatory effect
Shorten diastolic period
→Insufficient ventricular filling →Cardous output ↓
→Insufficient coronary perfusion →Mynaecology and hypoxia
Heart dilation
Frank-Starling Law
Myocardial contraction force and cardiac output increase within a certain range with the increase of myocardial fiber sarcoma length (≤2.2μm)
This kind of expansion is called "tension-induced expansion"
Exceeding the optimal length of the sarcoma (2.2μm), the expansion of myocardial elongation without the enhancement of contraction is called "myosinogenic dilation"
limitation
Excessive elongation of the sarcoma and increased oxygen consumption of myocardium are important factors leading to decompensation
Myocardial hypertrophy
concept
Increased volume and weight of cardiomyocytes
It is often a compensation mechanism for chronic heart failure
Economical, better
Morphological classification
Centripetal hypertrophy
It refers to the parallel hyperplasia of myocardial fibers under the action of long-term pressure load (ejaculation resistance↑), that is, the muscle fibers become thicker, the ventricular wall thickness increases, and no significant enlargement of the heart cavity.
Centrifugal hypertrophy
Refers to the tandem hyperplasia of myocardial fibers under the action of long-term capacity load (return to heart blood volume↑), that is, muscle fibers become longer and the heart cavity is significantly enlarged.
significance
Increases myocardial contraction and helps maintain cardiac output
Unit myocardial contraction force↓ but overall contraction force↑
Reduce chamber wall tension → reduce myocardial oxygen consumption
limitation
Imbalance of hypertrophy myocardium → even lead to heart failure
Extracardial Compensation Reaction
Blood volume↑
Main ways
Reimbursement for the kidney
Blood pressure ↓→sympathetic nerve excitation, etc. → renal vasoconstriction → glomerular filtration rate ↓
ADH and aldosterone → tubular reabsorption ↑
Water and sodium retention
effect
Increase cardiac output
Maintain arterial blood pressure
limitation
May increase the anterior and afterload of the heart and cause cardiac edema
Blood flow redistribution
Catecholamine↑→No effect on cardiovascular and cerebrovascular, but arterioles are contracted → Increase cardiac afterload
RBC increase
For chronic heart failure
damage
Increase blood viscosity → blood flow resistance ↑→ resistance to heart ejaculation ↑
Enhanced tissue capacity of oxygen
For chronic heart failure
Good, no obvious harmful effects on the body
Section 4 Clinical manifestations of heart failure
Pulmonary circulatory congestion
Mainly due to left heart failure
The left heart cannot pump out the blood transmitted from the pulmonary vein in time
Clinical Symptoms
Difficulty in breathing
Expression form
Exercise dyspnea
mechanism
Physical activity requires aerobic life↑
Normally, the cardiac output is mainly increased
But left heart failure cannot provide appropriate cardiac output
Exacerbation of hypoxia and CO2 retention
Physical activity → heart rate increases, so the diastolic period becomes shorter and return to left heart blood↓→
Physical activity → whole body venous blood returns to the right heart↑ → right heart ejaculation ↑ →
Pulmonary circulating blood volume↑→ Lung cap. Pressure↑→ Severe lung congestion→Alveolar compliance↓→Alveolar dilation is limited → Hypoxia
Sit upright and breathe
mechanism
When sitting upright, part of the blood is transferred to the lower half of the body due to gravity.
When sitting upright, the edema fluid in the lower part of the body enters the blood less
Reduced pulmonary congestion
When sitting upright, the position of the diaphragm moves downward relative to → the volume of the chest cavity increases, and the lung capacity is ↑
Paroxysmal dyspnea at night
Concept: Usually there is no difficulty in falling asleep, but after sleeping soundly at night, you are suddenly forced to sit up due to chest tightness and irritability.
mechanism
Flat lying
Edema fluid enters blood more frequently than when sitting upright
The effort to return is higher than when sitting upright
Pulmonary congestion↑
Reduced chest volume
After falling asleep
Relative excitement of the vagus nerve → bronchial contraction → airway resistance ↑
CNS reaction sensitivity↓, patients can only wake up when hypoxia reaches a certain level and feel short of breath
Explain "parallel"
Pulmonary edema
mechanism
Lung cap. Pressure increase
Lung cap.permeability↑
Thrombin, histamine and other substances
Systemic circulation blood stasis
Mainly due to right heart failure
Clinical Symptoms
Venous congestion/increased venous pressure
reason
Water and sodium retention
Right heart failure → Return to heart blood ↓ → Cardiac output ↓ → Kidney blood flow ↓ → Filtration ↓
Right atrial pressure increases and venous return is blocked
Edema—"cardiac edema"
Main mechanism
Water and sodium retention
cap.press↑
Transfer of blood to tissue space
Hepatomegaly and tenderness and abnormal liver function
It is mainly caused by liver congestion
Insufficient cardiac output
Pale or cyanotic skin
CNS lack of energy → inhibition: fatigue, insomnia, sleepiness
Urine volume↓
Cardiac shock
Section 5: The basics of preventing and treating heart failure
Prevent and treat basic causes and eliminate inducement
Improve heart comfort
Shrink function
Heart-boosting medicine, etc.
Diastolic function
Calcium antagonists, beta blockers, etc.
Reduce the front and afterload of the heart
Drugs that selectively dilate small veins → reduce backtrack blood → reduce preload
Drugs that selectively dilate arterioles → reduce perivascular resistance → reduce afterload
Control edema
Diuretics