Cardiogenic Shock - Management
Cardiogenic Shock - Management
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Introduction
Introduction
Identifying and managing patients with CS requires an understanding of hemodynamics.
Every patient must be carefully assessed - There is no one-size-fits-all approach with regard to treatment.
Patients presenting with CS clinically behave very differently than other forms of shock, and are treated differently.
To review:
Abbreviations
Abbreviations
CS - Cardiogenic Shock
Items in pink are key learning points that are often the subject of questions on the quiz.
Approach to Management
Approach to Management
The general approach to managing patients with CS involves concurrently addressing the following areas:
Identify & Correct Reversible Causes
Optimize Hemodynamics
Medical Therapy for Cardiac Output
Advanced Therapies / Palliation
1. Correct the underlying cause
1. Correct the underlying cause
Patient's survival depends on identification and correction of potential causes of CS. Delaying the diagnosis carries significant risks to the patient.
Pulmonary Embolism must be ruled out (can mimic cardiogenic shock)
Acute Myocardial Infarction
Patients presenting with CS and STEMI must be revascularized as soon as possible.
See "Revascularization" Section
Acute Myocarditis
Consider empiric immunosupression
Acute Valve Dysfunction
Urgent cardiac surgery consultation.
Pericardial Effusion
Perform pericardiocentesis as soon as possible.
Arrhythmia / Bradycardia
Electrical cardioversion
Urgent transvenous pacing.
2. Optimize Hemodynamics
2. Optimize Hemodynamics
Frank-starling relationship. Note that increasing preload (i.e. volume expansion) leads to minimal changes in stroke volume in patients with high preload (heart failure congestion. However, aggressive fluid removal can reduce preload and cause hypotension.
NOTE: Cardiac output is dependent on the MAP (mean arterial pressure), CVP (central venous pressure), and SVR (systemic vascular resistance). Patients with CS can have a normal blood pressure but have very low cardiac output due to very high SVR.
Preload Optimization (the dilemma)
On one hand preload improves ventricular filling resulting in increased stroke volume - being mindful of diminishing returns based on Frank-Starling Law (see diagram).
On the other hand, excess preload leads to pulmonary edema, and results in hypoxemia. High venous pressures can also reduce tissue perfusion pressure.
A careful balance of preload must be achieved.
The vast majority of patients with CS have very high filling pressures (i.e. LVEDP of 25-40 mmHg) - the "cold & wet" phenotype. Further volume expansion with IV fluids is unlikely to improve stroke volume, and will result in:
Worsening of hypoxemia due to pulmonary edema
Reduction in tissue perfusion pressure by raising CVP.
Small boluses of fluid can be considered for rare patients with CS who are "cold and dry" - especially if they do not require supplemental oxygen.
Keep in mind that fluid is easy to give, but very challenging to remove. Patients in CS are resistant to diuretics and require extreme doses and/or ultrafiltration.
Decongestion can be achieved by:
Diuresis
IV furosemide (5-20 mg/h) - infusion preferred by many Cardiologists
IV bumetanide - if patients are furosemide resistant.
Oral metolazone (2.5-5mg) - can be added to furosemide for synergistic effect.
NOTE: diuretics are often not effective in CS due to reduced renal perfusion and strong fluid-retention mechanisms (i.e. RAAS). Ultrafiltration is often required.
Ultrafiltration (dialysis)
Allows controlled removal of fluid.
Must be done gently to minimize large changes in preload causing hypotension.
Afterload Reduction
Reduction of afterload has the following beneficial effects:
Improves stroke volume / cardiac output (see diagram for ventricular hemodynamics).
Reduces cardiac work
Reduces myocardial oxygen requirements
Improves myocardial perfusion (by reducing wall tension)
However, a very low MAP can result in poor tissue/coronary perfusion pressure, and can contribute to ischemia. A careful balance must be achieved.
A lower MAP should be targeted in patients with CS compared to patients with other types of shock. The exact number is not well established and must be tailored to the patient. Many clinicians use ~ 60-65mmHg as a general target.
NOTE: Many patients with CS are hypotensive, and afterload reduction is not possible. If hypotension is significant, a vasopressor must be used to raise perfusion pressure.
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