Clinical presentations - 2021 ESC Guidelines for the Diagnosis and Treatment of Acute and Chron

Four major clinical presentations can be described with possible overlaps between them (Table 21).

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Clinical presentations are mainly based on the presence of signs of congestion and/or periph- eral hypoperfusion and require different treatments (Table 21).

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11.2.1 Acute decompensated heart failure

Acute decompensated heart failure (ADHF) is the most common form of AHF, accounting for 5070% of presentations.

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It Table 20 Diagnostic tests in patients with acute heart failure

Exam Time of measurement Possible findings Diagnostic value for AHF

Indication

ECG Admission, during hospitali-

zation,^a,bpre-discharge

Arrhythmias, myocardial ischaemia

Exclusion of ACS or arrhythmias

Recommended

Chest-X ray Admission, during hospitalization^a

Congestion, lung infection Confirmatory May be considered

LUS Admission, during hospitali-

zation,^apre-discharge

Congestion Confirmatory May be considered

Echocardiography Admission, during hospitalization,^apre-discharge

Congestion, cardiac dysfunction, mechanical causes

Major Recommended

Natriuretic peptides (BNP, NT-proBNP, MR-proANP)

Admission, pre-discharge Congestion High negative predictive value

Recommended

Serum troponin Admission Myocardial injury Exclusion of ACS Recommended

Serum creatinine Admission, during hospitalization,^apre-discharge

Renal dysfunction None Recommended for prognos-

tic assessment Serum electrolytes

(sodium, potassium, chloride)

Admission, during hospitalization,^apre-discharge

Electrolyte disorders None Recommended for prognos-

tic assessment and treatment Iron status (transferrin,

ferritin)

Pre-discharge Iron depletion None Recommended for prognos-

tic assessment and treatment

TSH Admission Hypo- hyperthyroidism None Recommended when hypo-

hyperthyroidism is suspected

D-dimer Admission Pulmonary embolism Useful to exclude pulmo-

nary embolism

Recommended when pulmonary embolism is suspected

Procalcitonin Admission Pneumonia Useful for diagnosis of

pneumonia

May be done when pneumonia is suspected

Lactate Admission, during

hospitalization^a

Lactic acidosis Useful to assess perfusion status

Recommended when peripheral hypoperfusion is suspected

Pulse oximetry and arterial blood gas analysis

Admission, during hospitalization^a

Respiratory failure Useful to assess respiratory function

Recommended when respiratory failure is suspected

ACS = acute coronary syndrome; AHF = acute heart failure; BNP = B-type natriuretic peptide; ECG = electrocardiogram; LUS = lung ultrasound; MR-proANP = mid-regional pro-atrial natriuretic peptide; NT-proBNP = N-terminal pro-B-type natriuretic peptide; TSH = thyroid-stimulating hormone.

aBased on clinical conditions.

bContinuous ECG monitoring can be considered based on clinical conditions.

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usually occurs in patients with history of HF and previous cardiac ..

dysfunction across the spectrum of LVEF and may include RV dys- function. Distinct from the acute pulmonary oedema phenotype, it has a more gradual onset, and the main alteration is progressive fluid retention responsible for systemic congestion. Sometimes, congestion is associated with hypoperfusion.

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The objectives of treatment are identification of precipitants, decongestion, and in rare instances, correction of hypoperfusion (Figure 7).

11.2.2 Acute pulmonary oedema

Acute pulmonary oedema is related to lung congestion. Clinical crite- ria for acute pulmonary oedema diagnosis include dyspnoea with orthopnoea, respiratory failure (hypoxaemia-hypercapnia), tachyp- noea, >25 breaths/min, and increased work of breathing.

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Three therapies should be commenced, if indicated. First, oxygen, given as continuous positive airway pressure, non-invasive positive- pressure-ventilation and/or high-flow nasal cannula, should be started. Second, i.v. diuretics should be administered, and third, i.v.

vasodilators may be given if systolic BP (SBP) is high, to reduce LV afterload (Figure 8). In a few cases of advanced HF, acute pulmonary oedema may be associated with low cardiac output and, in this case, inotropes, vasopressors, and/or MCS are indicated to restore organ perfusion.

11.2.3 Isolated right ventricular failure

RV failure is associated with increased RV and atrial pressure and systemic congestion. RV failure may also impair LV filling, and

ultimately reduce systemic cardiac output, through ventricular interdependence.

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Diuretics are often the first option of therapy for venous conges- tion. Noradrenaline and/or inotropes are indicated for low cardiac output and haemodynamic instability. Inotropes reducing cardiac fill- ing pressures may be preferred (i.e. levosimendan, phosphodiester- ase type III inhibitors). Since inotropic agents may aggravate arterial hypotension, they may be combined with norepinephrine if needed (Figure 9).

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11.2.4 Cardiogenic shock

Cardiogenic shock is a syndrome due to primary cardiac dysfunction resulting in an inadequate cardiac output, comprising a life- threatening state of tissue hypoperfusion, which can result in multi- organ failure and death.

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Cardiac insult causing severe impair- ment of cardiac performance may be acute, as a result of the acute loss of myocardial tissue (acute MI, myocarditis) or may be progres- sive as seen in patients with chronic decompensated HF who may experience a decline in disease stability as a result of the natural pro- gression of advanced HF and/or specific precipitants.

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Diagnosis of cardiogenic shock mandates the presence of clini- cal signs of hypoperfusion, such as cold sweated extremities, oli- guria, mental confusion, dizziness, narrow pulse pressure. In addition, biochemical manifestations of hypoperfusion, elevated serum creatinine, metabolic acidosis and elevated serum lactate are present and reflect tissue hypoxia and alterations of cellular Table 21 Clinical presentations of acute heart failure

Acute decompensated heart failure

Acute pulmonary oedema

Isolated right ventricular failure

Cardiogenic shock Main mechanisms LV dysfunction

Sodium and water renal retention

Increased afterload and/or predominant LV diastolic dysfunction

Valvular heart disease

RV dysfunction and/or pre-capillary pulmonary hypertension

Severe cardiac dysfunction

Main cause of symptoms

Fluid accumulation, increased intraventricular pressure

Fluid redistribution to the lungs and acute respiratory failure

Increased central venous pressure and often systemic hypoperfusion

Systemic hypoperfusion

Onset Gradual (days) Rapid (hours) Gradual or rapid Gradual or rapid

Main haemodynamic abnormalities

Increased LVEDP and PCWP^a Low or normal cardiac output Normal to low SBP

Increased LVEDP and PCWP^a

Normal cardiac output Normal to high SBP

Increased RVEDP Low cardiac output Low SBP

Increased LVEDP and PCWP^a

Low cardiac output Low SBP

Main clinical presentations^1,446

Wet and warm OR Dry and cold

Wet and warm^b Dry and cold OR Wet and cold

Wet and cold

Main treatment Diuretics

Inotropic agents/vasopressors (if peripheral hypoperfusion/hypotension) Short-term MCS or RRT if

needed

Diuretics Vasodilators^b

Diuretics for peripheral congestion

Inotropic agents/vasopressors (if peripheral hypoperfusion/hypotension) Short-term MCS or RRT if

needed

Inotropic agents/

vasopressors Short-term MCS RRT

LV = left ventricular; LVEDP = left ventricular end-diastolic pressure; MCS = mechanical circulatory support; PCWP = pulmonary capillary wedge pressure; RV = right ventricular;

RVEDP = right ventricular end-diastolic pressure; RRT = renal replacement therapy; SBP = systolic blood pressure.

aMay be normal with low cardiac output.

bWet and cold profile with need of inotropes and/or vasopressors may rarely occur.

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metabolism leading to organ dysfunction.

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Of note, hypoper- .

fusion is not always accompanied by hypotension, as BP may be preserved by compensatory vasoconstriction (with/without pressor agents), albeit at the cost of impaired tissue perfusion and oxygenation.

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Management of cardiogenic shock should start as early as pos- sible. Early identification and treatment of the underlying cause, concomitant with haemodynamic stabilization and management of organ dysfunction, are key components of its management (Figure 10, Supplementary text 11.1; Supplementary Figure 2).

N Management of patients with acute decompensated heart failure

Congestion/Fluid overload

Hypoperfusion

Medical therapy optimization (Class I)

Loop diuretics^a (Class I)

Loop diuretics^a (Class I) and consider inotropes (Class IIb)

Congestion relief Hypoperfusion and

congestion relief N

Increase diuretic doses (Class I) and/or combine

diuretics (Class IIa)

Consider vasopressors (Class IIb) (i.e. norepinephrine)

Diuretic resistance or end-stage renal failure

Persistent hypoperfusion Organ damage

N N

Renal replacement therapy (Class IIa)

OR Consider palliative care

MCS (Class IIa)

AND/OR Renal replacement

therapy (Class IIa)

OR Consider palliative care

N Y

Y Y

Figure 7 Management of acute decompensated heart failure. MCS = mechanical circulatory support.

Adequate diuretic doses to relieve congestion and close monitoring of diuresis is recommended (see

Figure13) regardless of perfusion status.

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Dalam dokumen 2021 ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure (Halaman 48-51)