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Heart failure mind map
This is a mind map about cardiac dysfunction, including causes, incentives, classification, pathogenesis, changes in metabolism and function, etc. Hope this helps!
Edited at 2023-11-05 20:40:46- bacteria
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Heart failure mind map
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- Outline
Heart failure (heart failure)
Cause
Cardiac insufficiency (aurtine inuficicenoy) refers to a pathophysiological process that causes changes in the structure and function of the heart due to various reasons, causing the ventricular pumping volume and/or filling function to decrease, so that it cannot meet the needs of tissue metabolism. Clinically, it manifests as respiratory failure. The syndrome of venous congestion and reduced cardiac output such as difficulty, scuba, and elevated venous pressure is also known as heart failure, which refers to the decompensated stage of cardiac insufficiency. Due to water and sodium retention and increased blood volume, some patients develop symptoms of cardiac chamber enlargement, venous congestion and tissue edema, which is called congestive heart failure.
心功能不全——是指各种病因导致心脏舒缩功能受损或心室血液充盈受限，在有足够循环血量的情况下，使心排出量减少，以致不能满足机体代谢需要，出现全身组织器官灌流不足，肺循环和体循环静脉淤血的病理过程。
心力衰竭——是指心功能不全的失代偿阶段，两者在本质上是相同的，可以通用。
充血性心衰——慢性心衰时，常伴有血容量及组织间液代偿性增多及体循环和（或）肺循环静脉系统淤血、水肿。
1 Decreased myocardial contractility
myocardial infarction
myocarditis
Cardiomyopathy
Myocardial poisoning (doxorubicin, alcohol)
2. Ventricular overload
Pressure overload (afterload) The resistance the heart overcomes when contracting
Left heart: hypertension, aortic stenosis
Right heart: cor pulmonale, pulmonary stenosis
Volume overload (preload) Filling volume during diastole
Left heart: mitral valve, aortic valve regurgitation
Right heart: tricuspid valve, pulmonary valve insufficiency
atrial septum, ventricular septal defect
Whole heart: inflammation anemia, hyperthyroidism, vitamin B1 deficiency, arteriovenous fistula, etc.
3. Restricted ventricular relaxation and filling
Atrioventricular valve (mitral valve, tricuspid valve) stenosis
restrictive cardiomyopathy
Cardiac tamponade, constrictive pericarditis
inducement
1.Infection
Especially for respiratory infections, fever leads to an increase in metabolic rate, which in turn leads to an increase in myocardial oxygen consumption. Pathogenic microorganisms and their products can also directly damage myocardial cells
2.Arrhythmia
Cardiac output⬇️, myocardial oxygen consumption⬆️, coronary blood flow⬇️
3. Electrolyte disorders and acid-base balance disorders
Both hydrogen ions and potassium ions can competitively antagonize calcium ions. thereby reducing myocardial contractility
4. Pregnancy, childbirth
Increase heart load
5. Other factors
Too much infusion too quickly
Increased cardiac preload
emotional
Sympathetic nerve excitement increases myocardial contractility and increases the burden on the heart.
excessive exercise
climate change
Classification
According to the location of occurrence
left heart failure
Coronary heart disease, hypertension ---> Pulmonary circulation congestion --> Pulmonary edema, dyspnea
Right heart failure
COPD, pulmonary embolism ---> systemic circulation congestion --> edema, jugular venous distension, hepatomegaly
total heart failure
Lesions invade both left and right ventricles simultaneously
myocarditis, cardiomyopathy
Left heart failure leads to increased pulmonary circulatory resistance
According to the location of occurrence
acute heart failure
Acute heart failure refers to a clinical syndrome in which sudden onset or acute exacerbation of original chronic heart failure results in reduced myocardial contractility and increased cardiac load, resulting in an acute sudden drop in cardiac output and tissue congestion. Clinically, acute left heart failure is the most common, most manifesting as systolic heart failure, but may also manifest as diastolic heart failure, which is often life-threatening.
chronic heart failure
Press diastolic and systolic dysfunction
systolic heart failure
Give inotropes
diastolic heart failure
Give CCB drugs
mixed heart failure
Classification according to degree of disease
Class I - unrestricted physical activity, no symptoms of heart failure
mild heart failure
Level II - Asymptomatic at rest, limited physical activity and movement
moderate heart failure
III-Asymptomatic at rest, but limited sensation during mild activities
severe heart failure
IV-resting also has symptoms
Classification by cardiac output
low cardiac output heart failure
Commonly seen in heart failure caused by coronary heart disease, hypertension, heart valve disease and myocarditis
high cardiac output heart failure
Mainly seen in severe anemia, pregnancy, hyperthyroidism, arteriovenous fistula and vitamin B1 deficiency, etc.
Even if cardiac insufficiency develops, the patient's cardiac output is still higher or not lower than the average level of the normal population
body's compensatory response
Short time: the advantages outweigh the disadvantages; long time: the disadvantages outweigh the advantages
First activate neuro-humoral regulatory mechanisms
1. The sympathetic nervous system is activated
Benefits: Improve heart pumping function; redistribute blood in systemic circulation. (Mainly vasoconstriction of the skin, skeletal muscles, kidneys and abdominal organs, and vasodilation of the heart, brain and other important organs) Disadvantages: Increase myocardial oxygen consumption, increase before and after load, induce arrhythmia, and promote myocardial cell remodeling
Decreased cardiac output activates baroreceptors in the jugular sinus and aortic arch, which in turn activates the sympathoadrenal medullary system
Improve heart pumping function
Visceral resistance vasoconstriction Venous vasoconstriction Increases blood flow to the heart
2.RAAS system is activated
Benefits: Directly constrict blood vessels, increase renal perfusion, and maintain circulating blood volume
Disadvantages: Increased myocardial preload and postload, water and sodium retention, increased ventricular filling pressure, resulting in myocardial cell remodeling
3. Activation of natriuretic peptide system
Natriuretic and potassium excretion, dilation of blood vessels, inhibition of renin and aldosterone systems
The heart's own compensatory response
acute heart failure
increased heart rate
Benefits: Increase myocardial blood output Disadvantages: Myocardial oxygen consumption increases, and excessive heart rate reduces coronary perfusion and filling volume. When the adult heart rate is greater than 180 beats/min - cardiac output is further reduced
1. Baroreceptor-aortic arch and carotid sinus stimulation is weakened
2. Volume receptor regulation
3. Chemoreceptor regulation - combined with hypoxia - stimulation of aortic body and carotid body chemoreceptors - increased heart rate
myocardial tensogenic dilation
According to Frank-Stariing's law: the stroke volume decreases, the cardiac chambers expand, and the initial length of the myocardium increases. Sarcomere length increases in the range of 1.7-2.2 μm Increased myocardial contractility, called cardiogenic dilation, helps pump out excess blood in the ventricle If the sarcomere length is >2.2μm, myocardial contractility will decrease and cardiac output will decrease.
Pros: Increased end-diastolic filling volume-->lengthened sarcomere length-->increased myocardial contractility-->increased stroke volume
Disadvantages: excessive preload (sarcomere length>2.2μm)-->decreased myocardial contractility (myogenic dilation)
Increased myocardial contractility
Pros: Maintain cardiac output and hemodynamic homeostasis (short-term)
Disadvantages: Myocardial beta-adrenergic receptor desensitization (chronic)
chronic heart failure
cardiomyocyte remodeling
cardiac hypertrophy
reactive hypertrophy
overload hypertrophy
eccentric hypertrophy
Sarcomeres grow in tandem
Sarcomeres can also grow in parallel
Seen in mitral and aortic regurgitation
concentric hypertrophy
Sarcomeres grow side by side
Hypertensive heart disease aortic stenosis
When myocardial hypertrophy occurs, the myocardial contractility per unit weight decreases, but as the weight of the entire heart increases, the total contraction of the heart increases, helping to maintain cardiac output.
Ventricular wall thickening can reduce ventricular wall tension and reduce myocardial oxygen consumption
Cardiomyocyte phenotypic changes
myocardial interstitial remodeling
Abnormal ratio of type 1 to type 3 collagen - affects myocardial compliance and increases stiffness
Fibrous proliferation and wall thickening around the coronary arteries – affecting coronary blood flow
Affects information transmission between cardiomyocytes
extracardiac compensation
increase blood volume
Benefits: Increase cardiac output and tissue perfusion Disadvantages: Increased cardiac load leading to ventricular remodeling
Sympathetic nervous excitement
RAAS system activation
Increased ADH release
Decreased synthesis of PEG2 and ANP, promoting water and sodium excretion
blood flow redistribution
Benefits: Guaranteed blood supply to important organs such as the heart and brain Disadvantages: decreased organ function, increased cardiac afterload, and decreased cardiac output.
Sympathetic nerve excitement leads to selective contraction of peripheral blood vessels, most notably in the kidneys
Increased red blood cells
Cardiac insufficiency-->Circulating hypoxia-->Increased bone hematopoietic function-->Increased bone marrow hematopoietic function and increased cellular compensation
Increased ability of tissues to utilize oxygen
Pathogenesis
Decrease in the number of cardiomyocytes and changes in myocardial structure
Myocardial energy metabolism disorder
Myocardial excitation-contraction coupling disorder
Decreased myocardial compliance
Uncoordinated ventricular wall diastolic and systolic activity
Metabolic and functional changes
Decreased cardiac output - congestion of the arterial system
1. The ability of cardiac output to increase with the metabolic needs of tissue cells is called cardiac reserve. 2. Systolic cardiac dysfunction caused by reduced myocardial contractility and ventricular overload is clinically manifested as a syndrome of reduced cardiac output, which is called forward failure.
Reduced heart pump function
1. Cardiac output ⬇️, heart index ⬇️
2. Ejection fraction (EF) ⬇️
3. Ventricular end-diastolic pressure ⬆️
Pulmonary capillary wedge pressure (PCWP)⬆️——reflects left heart failure
Central venous pressure (CVP)⬆️——Reflects right heart failure
4. Increased heart rate: palpitations - often the earliest and most obvious symptom of patients with heart failure
Redistribution of blood flow to organs
Subtopic Changes in Arterial Blood Pressure
In acute heart failure (eg. acute myocardial infarction) -> stroke volume ⬇️⬇️; systolic blood pressure ⬇️⬇️; diastolic blood pressure ⬇️ -> arterial blood pressure drops -> even cardiogenic shock occurs
In chronic heart failure (eg. hypertensive heart disease) -> the body compensates, blood volume ⬆️, sodium and water retention -> arterial blood pressure can be maintained within the normal range -> cardiac function deteriorates sharply, and sympathetic nerves are excited ——>Elevated arterial blood pressure may also occur
Redistribution of blood flow to organs
Reduced renal blood flow: reduced urine output, sodium and water retention, and may also be accompanied by azotemia.
Reduced skeletal muscle blood flow: reduced ability to perform physical activities, fatigue and weakness, etc.
Reduced skin blood flow: manifested as pale skin and lowered skin temperature. If combined with hypoxia, cyanosis may occur.
Decreased blood flow to the brain: dizziness, headache, insomnia, memory loss, and restlessness.
When cardiac output is acutely reduced, it can lead to cerebral ischemia and transient loss of consciousness, which is called cardiogenic syncope.
In severe cases, syncope attacks can last for several seconds and are accompanied by clinical manifestations such as limb twitching, apnea, and cyanosis, which is called Aspen syndrome.
Venous congestion - congestion of the venous system
systemic congestion
Seen in: Right heart failure and total heart failure
Performance
1. Jugular vein filling or distention - abnormal filling of the jugular vein after pressing the liver is called a positive hepatic venous reflux sign
2. Liver congestion - hepatomegaly and liver function damage
3. Gastrointestinal congestion-digestive tract symptoms
4. Congestion of lower limbs - pitting edema from top to bottom, called "cardiogenic edema"
Pulmonary circulation congestion
Seen in: Patients with left heart failure
Performance
Difficulty breathing
1. Exertional dyspnea
2. Nocturnal formation dyspnea
3. Sit upright and breathe
4. Acute pulmonary edema: Patients may develop cyanosis, shortness of breath, orthopnea, cough, and pink foamy sputum.
Prevention and control principles
(1) Prevent and treat primary diseases and eliminate the causes
(2) Improve heart pumping function
1. Reduce heart load
rest
Reduce preload: diuretics, venodilators
Reduce afterload: hydralazine, CCB, ACEI
Sodium nitroprusside - reduces pre- and post-load
2. Improve myocardial structure
Metoprolol
growth hormone
3. Improve cardiac diastolic function
Digitalis
calcium sensitizer
CCB
(3) Intervention in myocardial remodeling
ACEI, AngII receptor blocker, β-blocker, anti-TNF-α, etc.
Decreased cardiac output
Activation of neurohumoral regulatory mechanisms
Intracardiac compensation: increased heart rate, increased contractility, ventricular remodeling
ventricular remodeling
Myocardium: ventricular hypertrophy, cardiomyocyte phenotypic changes
Non-cardiomyocyte and extracellular matrix changes
Early type III collagen increase
Late type I collagen increase
Extracardiac compensation: increased blood volume and redistribution of blood flow
Intracardiac Compensation: Tentogenic Dilation