10 issues that big coffees should focus on in dealing with cardiogenic acute pulmonary edema

"Acute pulmonary edema (APE)" is one of the common causes of unplanned hospitalization in elderly patients, of which about 50% are critically ill, with high mortality and readmission rates

"Acute pulmonary edema (APE)" is one of the common causes of unplanned hospitalization in elderly patients, of which about 50% are critically ill, with high mortality and readmission rates

According to the different pathogenesis, APE can be divided into two types: "cardiogenic acute pulmonary edema (CPE)" and "non-cardiogenic acute pulmonary edema (NCPE)".

Cardiogenic acute pulmonary edema is defined as a sudden increase in pulmonary capillary wedge pressure (PCWP) caused by acute left ventricular systolic/diastolic dysfunction or acute severe mitral regurgitation

Acute heart failure (AHF) can be divided into four clinical phenotypes: acute pulmonary edema, cardiogenic shock, isolated right heart failure, and acute decompensated heart failure.

Clinical manifestations of acute pulmonary edema include dyspnea with orthopnea, respiratory rate >25 breaths/min, increased work of breathing, and respiratory failure

Hypoxia is an important feature of CPE, and CPE is differentiated from ARDS as follows:

0 2 0 2 Pathophysiological Mechanisms

The pathological mechanism of CPE cannot be explained purely by the principle of hydrostatic pressure or permeability dichotomy

The pathological mechanism of CPE cannot be explained purely by the principle of hydrostatic pressure or permeability dichotomy

Alveolar edema is caused by a rapid increase in pulmonary capillary hydrostatic pressure, and the protein content of the edema fluid is lower than that of plasma

 

Persistent lung injury may lead to destruction of alveolar capillaries, causing acute inflammation

Persistent lung injury may lead to destruction of alveolar capillaries, causing acute inflammation

CPE can cause congestive damage to the lung, kidney, liver, intestine, brain, neuroendocrine and circulatory systems, and cardiogenic shock can also occur due to hypoperfusion

The neuroendocrine and inflammatory responses of hyperemia and/or peripheral hypoperfusion may further induce organ damage, but the pathophysiological mechanisms are not fully understood

The early diagnosis of CPE relies on medical history (such as history of heart failure, angina pectoris, atrial fibrillation, etc.

"Brain natriuretic peptide" is produced and released by ventricular cardiomyocytes under the condition of ventricular volume expansion and pressure overload.

When CPE is suspected, a comprehensive approach including assessment of cardiorespiratory function, assessment of congestion, and identification of underlying etiologies/precipitates is recommended

  05 05Management by Objectives Management by Objectives

The goals of CPE management are to improve oxygenation, maintain adequate blood pressure and reduce excess extracellular fluid, and correct the etiology
.

The goals of CPE management are to improve oxygenation, maintain adequate blood pressure and reduce excess extracellular fluid, and correct the etiology
.
The goals of CPE management are to improve oxygenation, maintain adequate blood pressure and reduce excess extracellular fluid, and correct the etiology
.

Due to the lack of high-quality research conducted in this area and the lack of relevant clinical evidence, many recommendations for management decisions are mainly based on expert consensus
.
 

Due to the lack of high-quality research conducted in this area and the lack of relevant clinical evidence, many recommendations for management decisions are mainly based on expert consensus
.
How does consensus 06 06 ensure oxygenation? How to ensure oxygenation? 

The work of breathing and oxygen consumption increase by 20 times in pulmonary edema, which can partially relieve cardiac stress and improve oxygenation by non-invasive ventilation, positive end-expiratory pressure ventilation or continuous positive pressure ventilation
.

The work of breathing and oxygen consumption increase by 20 times in pulmonary edema, which can partially relieve cardiac stress and improve oxygenation by non-invasive ventilation, positive end-expiratory pressure ventilation or continuous positive pressure ventilation
.

"Non-invasive ventilation" reduces cardiac preload and left ventricular afterload, increases right ventricular afterload, and ultimately improves cardiac function to a certain extent
.
The use of non-invasive ventilation in patients with pulmonary edema can improve respiratory failure faster, avoid endotracheal intubation, and may even reduce mortality in high-risk patients
.
However, 15% of CPE patients still require invasive ventilation
.

"Non-invasive ventilation" reduces cardiac preload and left ventricular afterload, increases right ventricular afterload, and ultimately improves cardiac function to a certain extent
.
The use of non-invasive ventilation in patients with pulmonary edema can improve respiratory failure faster, avoid endotracheal intubation, and may even reduce mortality in high-risk patients
.
However, 15% of CPE patients still require invasive ventilation
.

"High-flow oxygenation (HFO)" can improve oxygenation and respiratory rate in patients with APE, potentially replacing non-invasive ventilation
.
However, when HFO fails to improve oxygenation, invasive ventilation should be performed as soon as possible
.

"High-flow oxygenation (HFO)" can improve oxygenation and respiratory rate in patients with APE, potentially replacing non-invasive ventilation
.
However, when HFO fails to improve oxygenation, invasive ventilation should be performed as soon as possible
.
07 07 Use of diuretics Use of diuretics

Decongestion with intravenous diuretics is the cornerstone of the treatment of pulmonary edema
.
Diuretics, which dilate the veins and act as diuretics, usually relieve symptoms quickly
.

Decongestion with intravenous diuretics is the cornerstone of the treatment of pulmonary edema
.
Diuretics, which dilate the veins and act as diuretics, usually relieve symptoms quickly
.
Decongestion with intravenous diuretics is the cornerstone of the treatment of pulmonary edema
.

High-dose diuretics rapidly improve dyspnea and reduce volume overload, but induce neuroendocrine responses, electrolyte disturbances, and are associated with poorer outcomes
.

High-dose diuretics rapidly improve dyspnea and reduce volume overload, but induce neuroendocrine responses, electrolyte disturbances, and are associated with poorer outcomes
.

It is more suitable to start with low-dose diuretics and evaluate the "diuretic response", that is, the urine volume in the first 6 hours is >100-150ml/h, and the 2-hour urine sodium content is >50-70mEq/L
.
If the diuretic response to the initial dose is insufficient, the dose should be increased, concomitantly with a thiazide
.
Patients who develop diuretic resistance have increased readmission rates and mortality
.

It is more suitable to start with low-dose diuretics and evaluate the "diuretic response", that is, the urine volume in the first 6 hours is >100-150ml/h, and the 2-hour urine sodium content is >50-70mEq/L
.
If the diuretic response to the initial dose is insufficient, the dose should be increased, concomitantly with a thiazide
.
Patients who develop diuretic resistance have increased readmission rates and mortality
.
0 8 0 8 Vasodilator use Vasodilator use

Vasodilators (nitrates or sodium nitroprusside) dilate venous and arterial vessels to varying degrees, reducing venous return, reducing congestion, and reducing afterload, thereby relieving symptoms
.

Vasodilators (nitrates or sodium nitroprusside) dilate venous and arterial vessels to varying degrees, reducing venous return, reducing congestion, and reducing afterload, thereby relieving symptoms
.
Vasodilators (nitrates or sodium nitroprusside) dilate venous and arterial vessels to varying degrees, reducing venous return, reducing congestion, and reducing afterload, thereby relieving symptoms
.

In cases of CPE caused by sudden hypertension , blood pressure is lowered primarily by the use of vasodilators rather than diuretics
.
In other settings, two recent randomized trials have failed to show a benefit of intravenous vasodilators over high-dose diuretics
.

In cases of CPE caused by sudden hypertension , blood pressure is lowered primarily by the use of vasodilators rather than diuretics
.
In other settings, two recent randomized trials have failed to show a benefit of intravenous vasodilators over high-dose diuretics
.
In cases of CPE caused by sudden hypertension , blood pressure is lowered primarily by the use of vasodilators rather than diuretics

No vasodilator-based regimen is recommended in the guidelines
.
Vasodilators may be considered in patients with APE, but should be used with caution in normotensive patients at risk for hypotension because vasodilator-induced hypotension may be associated with increased morbidity and mortality
.

No vasodilator-based regimen is recommended in the guidelines
.
Vasodilators may be considered in patients with APE, but should be used with caution in normotensive patients at risk for hypotension because vasodilator-induced hypotension may be associated with increased morbidity and mortality
.
Guidelines Vasodilator-induced hypotension may be associated with increased morbidity and mortality
.
0 9 0 9How to avoid readmissionsHow to avoid readmissions

Patients with persistent congestion prior to discharge were associated with increased risk of readmission and mortality
.
Once breathing and circulation are stabilized, optimal treatment should be performed prior to discharge, including: decongestion, treatment of complications, and resumption of oral medications
.
Thus, for CPE patients with LV systolic or diastolic dysfunction, the problem of early use of ACE inhibitors should be addressed
.

Patients with persistent congestion prior to discharge were associated with increased risk of readmission and mortality
.
Once breathing and circulation are stabilized, optimal treatment should be performed prior to discharge, including: decongestion, treatment of complications, and resumption of oral medications
.
Thus, for CPE patients with LV systolic or diastolic dysfunction, the problem of early use of ACE inhibitors should be addressed
.
Once breathing and circulation are stabilized, optimal treatment should be performed before discharge,

Beta-blockers are potentially dangerous when the patient is unstable, but should be reintroduced in patients already taking beta-blockers
.
Specialists should follow up these patients regularly
.

Beta-blockers are potentially dangerous when the patient is unstable, but should be reintroduced in patients already taking beta-blockers
.
Specialists should follow up these patients regularly
.
Does 10 10 need a multidisciplinary team? Need a multidisciplinary team?

Multidisciplinary teams facilitate better decision-making, standardized management, and prognosis
.
Due to the different specialties and years of practice of the physicians responsible for CPE patients (intensive care, emergency, cardiology, geriatrics), involving multiple organs such as the heart, lungs, kidneys, etc.
, there is a lack of strong evidence for CPE treatment and high mortality and high mortality.
readmission rates, so building a multidisciplinary team is necessary
.

Multidisciplinary teams facilitate better decision-making, standardized management, and prognosis
.
Due to the different specialties and years of practice of the physicians responsible for CPE patients (intensive care, emergency, cardiology, geriatrics), involving multiple organs such as the heart, lungs, kidneys, etc.
, there is a lack of strong evidence for CPE treatment and high mortality and high mortality.
readmission rates, so building a multidisciplinary team is necessary
.

 

 

references

references

[1]Aissaoui N, Hamzaoui O, Price S.
Ten questions ICU specialists should address when managing cardiogenic acute pulmonary oedema [J].
Intensive Care Med, 2022, 48(4): 482-5.

[1]Aissaoui N, Hamzaoui O, Price S.
Ten questions ICU specialists should address when managing cardiogenic acute pulmonary oedema [J].
Intensive Care Med, 2022, 48(4): 482-5.

[2] He Fangkai, Guan Xiaojun, Zhu Yehan.
Clinical research and diagnosis and treatment strategy of acute pulmonary edema [J].
International Journal of Respiratory Medicine, 2021, 41(15): 1190-1194.
DOI: 10.
3760/cma.
j.
cn131368- 20200814-00728.

[2] He Fangkai, Guan Xiaojun, Zhu Yehan.
Clinical research and diagnosis and treatment strategy of acute pulmonary edema [J].
International Journal of Respiratory Medicine, 2021, 41(15): 1190-1194.
DOI: 10.
3760/cma.
j.
cn131368- 20200814-00728.
Diagnosis and treatment

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