1. Acute circulatory failure. Cardiogenic shock. Flashcards
What is acute heart failure ?
Acute heart failure: rapid onset of new or worsening signs and symptoms of heart failure
Acute decompensated heart failure (ADHF): acute heart failure due to decompensation of preexisting disease/cardiomyopathy (most common) [1]
De novo heart failure: acute heart failure occurring for the first time in a patient without known cardiomyopathy
What are the types of Acute heart failures and their ethology?
- De novo heart failures: a. Acute myocardial dysfunction:
- Cardiac ischemia from ACS
- Myocarditis
- Drug-induced cardiomyopathy
- Peripartum cardiomyopathy
- Thyroid storm
- Tachycardia-induced cardiomyopathy
b. Acquired valvular pathology:
- Acute mitral regurgitation after ACS
- Bacterial endocarditis
- Nonbacterial thrombotic endocarditis
c. Extracardiac pathologies that affect left ventricular output:
- Pulmonary embolus
- Pericardial effusion causing tamponade
- Aortic dissection
what is the ADHF etiology?
- Uncontrolled and/or refractory hypertension
- New/worsening cardiac ischemia
- Arrhythmias (e.g., atrial fibrillation with RVR, complete heart block)
- Serious infection/sepsis (e.g., pneumonia)
- Drugs: NSAID use, Drugs with negative inotropic properties (e.g., nondihydropyridine CCBs), uptitrating beta blockers
- Anemia
- Renal failure
- Volume overload, e.g., due to inappropriate fluid/salt intake or IV fluid therapy
what is the classification of acute heart failure?
- warm and dry: adequate perfusion and no congestion
- warm and wet: adequate perfusion and congestion
- cool and dry: no adequate perfusion and no congestion
- cool and wet: no adequate perfusion and congestion
what are the clinical features of the acute HF?
mainly to do with perfusion and congestion at rest.
- congestion: a. Clinical features of left heart failure
- Acute dyspnea and orthopnea (i.e., worse when supine)
- Flash pulmonary edema: rapid, life-threatening accumulation of fluid associated with the risk of acute respiratory distress
- Signs of increased work of breathing (WOB)
- Cough (occasionally with frothy, blood-tinged sputum)
- Coarse crackles/rales (and occasionally wheezing) on auscultation
- Severe cases: central cyanosis
b. Clinical features of right heart failure: peripheral edema
- Hypoperfusion
- Weakness, fatigue, altered mental status
- Signs of poor peripheral perfusion (e.g., cold, clammy skin, peripheral cyanosis, skin mottling)
what are the diagnostics for AHF?
- Labs: ↑ BNP (or NT-proBNP): Measure in every patient suspected of having acute heart failure.
-To evaluate for underlying cause/severity
Troponin: to rule out ACS
BMP and serum electrolytes
CBC
Consider also: liver function tests, thyroid function tests - ECG: Acute ischemic changes due to ACS
-Atrial fibrillation
-Left ventricular hypertrophy
-Bundle branch block
-Non-specific ST-segment changes
-Low voltage QRS
-ECG findings may be normal. - Imaging: CXR: X-ray findings in pulmonary congestion
-Cardiomegaly
-Septal lines/Kerley B lines: visible horizontal interlobular septa caused by pulmonary edema
-Prominent pulmonary vessels and perihilar alveolar edema (the hilar shadow has a butterfly or “bat wing” appearance)
-Basilar interstitial edema
-Bilateral pleural effusions
-Cephalization: increased prominence of pulmonary vessels in the upper lobes of the lungs due to venous congestion
-Peribronchial cuffing: bronchial wall thickening, is a radiologic sign which occurs when excess fluid or mucus buildup in the small airway passages of the lung causes localized patches of atelectasis
ABCDE: Alveolar edema (bat wings), Kerley B lines (interstitial edema), Cardiomegaly, Dilated prominent pulmonary vessels, and Effusions.
3b. Echo: Reduced or normal LVEF
Diastolic dysfunction
Left atrial dilation, valvular disorders
Pericardial effusion
Right ventricular systolic dysfunction, increase in right ventricular systolic pressure
what is the differential diagnosis of AHF?
remeber DD of dyspnea: Acute coronary syndrome Pneumonia COPD, asthma Pulmonary embolus Noncardiogenic pulmonary edema (e.g., ARDS) Pulmonary embolism Transfusion-related acute lung injury High altitude
what is the management of AHF?
- Haemodynamically unstable pts (Treatment for cardigenic shock):
a. Dry and cold: Consider an initial small fluid bolus (250–500 mL)
Assess fluid responsiveness; consider additional bolus if fluid responsive.
Reassess for volume overload
If shock persists, start a vasopressor, ideally, norepinephrine.
Administer inotropic support if hypoperfusion persists despite fluids and vasopressors :Dobutamine, Dopamine, Milrinone
1b. Wet and cold: Administer inotropic support.
If shock persists, start a vasopressor (ideally, norepinephrine)
Once systolic BP is > 90 mm Hg, start diuretics
If symptoms persist, see the section on “Refractory acute heart failure.” Avoid inotropes in patients with left ventricular outflow tract obstruction (e.g., hypertrophic cardiomyopathy, aortic stenosis)
2.Heamodynamically stable: dry and warm= oral therapy is fine.
dry and wet/ cold and wet: start diuretic therpy of rvol overload and consider vasodilator - Resp support: orthopneic position
-Supplemental oxygen: indicated for patients with an SpO2 < 90% or PaO2 < 60 mm Hg
-NIPPV: for patients with respiratory distress despite supplemental oxygen
-Invasive mechanical ventilation: Indications: Hypoxemic respiratory failure unresponsive to NIPPV, Refractory hypoxemia (PaO2 < 60 mm Hg), Hypercapnia (PaCO2 > 50 mm Hg), Acidosis (pH < 7.35)
what is the diuretic and vasodilator therapy in AHF?
- Initial treatment: Diuretics should administered intravenously .
Diuretic-naive patients: IV furosemide or bumetanide
-Patients already taking diuretics: Administer 1–2.5 times the patient’s usual oral dose intravenously as a bolus or continuous infusion.
-Continuing treatment:
Assess the effect of diuretics (e.g., urine output, symptoms) every 6 hours. [34][35]
If urinary output is < 100 mL/hour : Consider doubling the diuretic dose.
If urinary output is > 100–150 mL/hour :
For patients with continued congestion (e.g., pulmonary edema): Continue scheduled duiretic at current dose.
For patients with no residual congestion: Consider less frequent dosing or transition to oral diuretic.
-Options for refractory congestion despite high doses of loop diuretics:
Combination therapy with a thiazide diuretic
Addition of a vasodilator
Low-dose dopamine infusion
Monitoring
Monitor and replete serum electrolytes (potassium, magnesium, sodium) every 12–24 hours
-Monitor urine function (creatinine) at least daily.
Consider continuous cardiac monitoring.
Transition to oral diuretic: Once the patient is euvolemic/at their baseline. - Vasodilator therapy :Acute heart failure caused by hypertensive emergency
Flash pulmonary edema
Adjuvant to diuretics for symptomatic relief of dyspnea
Treatment options:
IV nitroglycerin
Sodium nitroprusside
If there are contraindications to nitroglycerin, consider nesiritide. - start Beta blockers patients not previously on beta blockers: start beta blockers cautiously at a low dose after stabilization (e.g., after volume status has been optimized and IV diuretics, vasodilators, and inotropic agents have been discontinued)
what is Treatment of refractory acute heart failure?
Ultrafiltration (e.g., hemodialysis): indicated in congestion with no response to medical therapy
Mechanical circulatory support: indicated in reversible refractory acute heart failure
ECMO is the most widely used form of mechanical support in acute heart failure.
Intra-aortic balloon pump and left ventricular assist device may be useful in certain etiologies, e.g., mitral regurgitation.
Management of effusions: Consider therapeutic thoracentesis or pericardiocentesis as needed.
what is the pathophysiology of cardiogenic shock
underlying event causes dysfunction of the heart → heart failure → ↓ CO and blood pressure → ↑ catecholamines → vasoconstriction and ↑ myocardial oxygen demand → ↑ renin-angiotensin-aldosterone system → further ↑ vasoconstriction and retention of sodium and water → shunting of blood to brain and vital organs → insufficient perfusion of peripheral organs
what is the aetiology of cardiogenic shock?
- non obstructive (might not be obstructive and non obstructive): Myocardial infarction (MI) is the most common cause.
Arrhythmias
Heart failure - Obstructive: Cardiomyopathy
Myocarditis
Ventricular septal defect, ventricular rupture
Severe aortic or mitral regurgitation (Valvular defect)
Certain drugs (e.g., beta blockers, calcium channel blockers)
Blunt cardiac trauma
what are the clinical features of cardiogenic shock?
Weak pulse, tachycardia
Hypotension
Dyspnea
Mental status change
Other clinical features related to the underlying disease:
Chest pain in MI
Palpitations, syncope in arrhythmias
-Physical examination might show:
Cold, clammy extremities, poor capillary refill
Abnormal auscultatory findings (e.g., S3, S4)
Pulmonary edema, diffuse lung crackles (fine basal crepitations )
Elevated JVP and distended neck veins
how do you diagnose cardiogenic shock?
Identifying the cause
-ECG: myocardial infarction, cardiac arrhythmias
-Cardiac markers (e.g., ↑ troponin I, troponin T): to identify acute coronary syndrome
-Echocardiography: valvular lesions
Pulmonary artery catheterization: to monitor hemodynamic parameters as a guide to therapy
↑ PCWP (> 15 mmHg), can also be ↓
↓ CO
↑ SVR
what is the treatment for cardiogenic shock?
-Cardiopulmonary resuscitation if necessary
-Fluid bolus only in cases of decreased blood pressure and/or PCWP < 15 mmHg
-Inotropic therapy: to maintain perfusion
Dopamine in patients with low blood pressure
Dobutamine in patients with normal blood pressure
-Vasopressors: norepinephrine
-Intra-aortic balloon pump if medical therapy fails
-Diuresis
-Treat the underlying cause (e.g., revascularization in MI)
