MindMap Gallery Pathophysiology-cardiac insufficiency
This is a mind map about pathophysiology - cardiac insufficiency, damage to the pumping function of the heart - the process from compensation to decompensation.
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This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
cardiac insufficiency
Note
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increase/expand/activate/promote
↓
reduce/shrink/suppress
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No change/little change
Overview
cardiac insufficiency
Impairment of heart pumping function-process from compensation to decompensation
heart failure
Causative factors - ventricular pumping/filling function ↓ - pathophysiological process that does not meet tissue metabolic needs (decompensation)
congestive heart failure
(Chronic) cardiac insufficiency - due to sodium and water retention - blood volume ↑ - cardiac chambers ↑, venous congestion, tissue edema
Cause
Myocardial contractility↓
Overloaded
Preload (volume load) – ventricular end-diastolic volume
Afterload (pressure load) - the resistance to ventricular ejection
Ventricular diastole, restricted filling
inducement
Increased metabolism
Increased load
Myocardial contractility↓
Classification
According to the location of occurrence
left heart failure
Right heart failure
total heart failure
left ventricular ejection fraction
Heart failure with reduced ejection fraction HFrEF
Left ventricular ejection fraction LVEF<40%
Normal 55%-70%
systolic heart failure
Heart failure with intermediate ejection fraction HFmeEF
LVEF40%-49%
Mild systolic function↓, diastolic function↓
Heart failure with preserved ejection fraction HFpEF
LVEF≥50%
diastolic heart failure
cardiac output
low output heart failure
high output heart failure
body compensatory response
neuro-humoral regulatory mechanisms
Sympatho-adrenomedullary system
Cardiac output ↓-↑baroreceptors-↑renal medullary system-catecholamines↑
positive effect
↓Peripheral blood vessels
↓Arteries-maintain blood pressure
↓Venous - blood return volume↑
renin-angiotensin-aldosterone system
Cardiac output↓-renal blood flow↓-↑renal aldehyde system
AngII↑
↓Vascular
blood pressure ↑
Left ventricular afterload↑
cardiac hypertrophy
Aldosterone↑
Retain sodium, water and eliminate potassium
Blood volume returned↑
Front load↑
myocardial fibrosis
Disadvantages>Advantages
natriuretic peptide system
Atrial-atrial natriuretic peptide ANP
Ventricular-B-type natriuretic peptide BNP
N-terminal B-type natriuretic peptide NT-proBNP (precursor) - reflects newly synthesized BNP - dynamically monitors blood BNP/NT-proBNP concentration - assesses left ventricular function
effect
natriuresis
↑Vascular
↓Renin, aldosterone
The heart itself compensates
intracardiac compensation
Heart rate↑
mechanism
baroreceptor
Cardiac Output↓—↓Baroreceptors-Inhibitory Sexual Impulse↓—↑Sympathetic N
volume receptor
End-diastolic volume↑—↑Volume receptor—↓vagal N, ↑sympathetic N
chemoreceptors
Hypoxia - ↑ Chemoreceptors - reflexes
effect
profit
Cardiac output↑
Disadvantages
Myocardial oxygen consumption↑
Too fast heart rate (>150) - diastole↓↓
Coronary perfusion↓-ischemia and hypoxia
Cardiac output↓
Myocardial Contractility↑
Cross-renal medullary system-catecholamine↑-↑β receptor-myocardial contractility↑
Cardiac tensogenic dilation—myocardial length↑-cardiac chamber↑with myocardial contractility↑
Decompensation - myogenic dilatation - myocardial overlongness (sarcomere >2.2μm) - cardiac chamber ↑ with myocardial contractility ↓
ventricular remodeling
Myocardial damage/load↑—chronic compensatory response—changes in ventricular structure and function
include
cardiomyocyte remodeling
cardiac hypertrophy
concentric hypertrophy
Hypertensive heart disease, aortic stenosis—long-term afterload↑—parallel sarcomeric hyperplasia
feature
Ventricular wall↑, cardiac chamber-/↓
eccentric hypertrophy
Mitral valve and aortic valve insufficiency—long-term preload↑—sarcomeric tandem hyperplasia
feature
Ventricular wall↑, cardiac chamber↑
significance
profit
Total cardiac contractility↑-maintain cardiac output
Ventricular wall thickness↑-ventricular wall tension↓-myocardial oxygen consumption↓
Disadvantages
Hypertrophic myocardium
Mitochondrial density↓, myofibril arrangement disorder-myocardial contractility↓
Ischemia and hypoxia-ATP↓-energy metabolism disorder
Conductive↓-cardiac rhythm disorder
Cardiomyocyte phenotypic changes
Non-cardiomyocyte and extracellular matrix changes
NE, AngII, aldosterone-nonmyocardial c-activated proliferation
extracardiac compensation
blood volume↑
mechanism
Sympathetic excitement-renal blood vessels↓-renal blood flow↓-proximal tubule reabsorption of sodium and water↑
Renal aldehyde system-distal and collecting duct reabsorption of sodium and water↑
ADH↑-distal tubule reabsorption of sodium and water↑
Hormone that inhibits sodium and water reabsorption↓-PGE2, atrial natriuretic peptide
significance
profit
Blood volume returned↑
Disadvantages
Front load↑
blood flow redistribution
1
Blood supply to important organs↑
2
Afterload↑
Red blood cells↑
1
Blood oxygen capacity↑
2
Blood viscosity↑
Tissue oxygen capacity↑
Mitochondria, myoglobin↑
The mechanism of cardiac insufficiency
Myocardial Contractile Function↓
Related protein changes
Number of myocardium↓
Necrosis
acute myocardial infarction
apoptosis
Aged myocardium
cardiac hypertrophy
Structural changes in myocardium
molecular level
Fetal period gene overexpression, calcium channel protein↓
cellular level
Disordered myofibril arrangement
organ level
Heart chamber ↑, ventricular wall ↓, valve regurgitation
energy metabolism disorder
energy production disorder
Ischemia - coronary heart disease, shock, anemia, myocardial hypertrophy, VitB1 deficiency
energy reserve disorder
Cardiac hypertrophy-phosphocreatine kinase activity↓-phosphocreatine↓
energy utilization disorder
Fetal isoform ↑ (such as TnT4)-ATPase activity ↓
excitation-contraction coupling disorder
Ca influx disorder
NE, beta receptor, receptor sensitivity↓-L calcium channel phosphorylation↓-opening↓-Ca influx↓
Heart-Chronic Load↑/Ischemia
Sarcoplasmic reticulum calcium transport dysfunction
Sarcoplasmic reticulum Ca release↓
Sarcoplasmic reticulum Ca uptake and storage↓
Myocardial ischemia-insufficient ATP supply
Ca-troponin binding disorder
Acidosis—H-troponin competitive binding (H affinity > Ca)
myocardial diastolic dysfunction
Active diastolic function↓
early diastole
Myocardial ischemia-ATP↓
Sarcoplasmic reticulum Ca uptake↓, Ca efflux↓-Intracellular high calcium-Ca-troponin dissociation↓
Ca reset delay
Myosin-actin dissociation↓
Arrhythmia - fast heart rate
Passive diastolic function↓
late diastole
Myocardial hypertrophy, restrictive cardiomyopathy, fibrosis - ventricular compliance ↓ (stiffness ↑)
Uncoordinated contraction and contraction of various parts of the heart
Mild lesions - diastole↓
Severe disease - loss of function
Not diseased - normal function
Pathophysiological basis of cardiac dysfunction
Cardiac output ↓ (forward failure)
Heart pump function↓
Cardiac output CO↓, cardiac index CI↓
CI—CO/body surface area
Left ventricular ejection fraction↓
Stroke volume/ventricular end-diastolic volume*100%—reflects left ventricular pumping function
Heart failure cannot be diagnosed based on ejection fraction alone
blood flow redistribution
Venous congestion (posterior failure)
systemic congestion
Right heart failure/total heart failure-CVP>16cmH2O
Venous congestion, venous pressure↑
Hepatomegaly, liver function ↓ (cardiogenic cirrhosis)
gastrointestinal dysfunction
Edema
Pulmonary circulation congestion
Left heart failure-pulmonary capillary wedge pressure PCWP>18mmHg
Difficulty breathing
exertional dyspnea
labor
Cardiac blood return↑-Pulmonary congestion↑
Heart rate↑
Myocardial oxygen consumption↑
orthopnea
Lower extremity reflux↓-Pulmonary congestion↓
Chest volume↑-vital capacity↑
Paroxysmal nocturnal dyspnea (cardiogenic asthma)
fall asleep
↑Vagus N-Bronchi↓
Central sensitivity↓
Lying supine - lower limb reflux ↑ - pulmonary congestion ↑
acute pulmonary edema