Cardiogenic Shock - Critical Care Nursing

Vocabulary practice flashcards covering the aetiology, pathophysiology, clinical presentation, SCAI classification, hemodynamic profiling, and pharmacotherapy of cardiogenic shock based on critical care lecture notes.

Cardiogenic Shock

A state of decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume.

Epidemiology of Cardiogenic Shock

A critical condition associated with an approximate $70\%$ mortality rate (which is lowering with early revascularisation), occurring in $5-10\%$ of all patients presenting with myocardial infarction, with a mean presentation age of $71\text{ yo}$ and approximately $60\%$ occurring in males.

Ischaemic Aetiology of Cardiogenic Shock

The predominant underlying cause of cardiogenic shock, accounting for approximately $81\%$ of all cases.

Cardiomyopathic Causes of Cardiogenic Shock

Primary intrinsic muscle disorders capable of causing cardiogenic shock, specifically categorized into dilated, hypertrophic, restrictive, and Takotsubo cardiomyopathies.

Mechanical Causes of Cardiogenic Shock

Structural cardiac defects that disrupt forward flow, primarily valvulopathies such as acute aortic stenosis and mitral regurgitation (e.g., secondary to acute endocarditis).

Arrhythmic Causes of Cardiogenic Shock

Severe rate and rhythm disturbances, including tachycardias and bradycardias (such as rapid atrial fibrillation), that impair ventricular filling and abruptly decrease cardiac output and blood pressure.

Cardiogenic Shock Pathophysiologic Cycle

A downward spiral where primary pump failure reduces cardiac output and forward flow, triggering compensatory renin-aldosterone, ADH, and catecholamine release; this elevates systemic vascular resistance (SVR) and preload, which increases myocardial oxygen requirements, worsens ischaemia, and exacerbates myocardial dysfunction and tissue hypoperfusion.

Hemodynamic Profile of Cardiogenic Shock

The clinical picture characterized by decreased cardiac output ($\downarrow$), compensatory increased heart rate ($\uparrow$), elevated preload/CVP/JVP ($\uparrow$), decreased contractility ($\downarrow$), increased afterload/SVR ($\uparrow$), decreased blood pressure ($\downarrow$), and decreased skin temperature ($\downarrow$).

SCAI Stage A (At Risk)

A patient possessing risk factors for cardiogenic shock (such as large acute MI, prior infarction, or acute/acute-on-chronic heart failure) who is not currently experiencing signs or symptoms, demonstrating neither hypotension, tachycardia, nor hypoperfusion.

SCAI Stage B (Beginning)

A patient exhibiting clinical evidence of relative hypotension or tachycardia without clinical or biochemical signs of hypoperfusion.

SCAI Stage C (Classic)

A patient presenting with hypoperfusion requiring intervention beyond volume resuscitation (such as inotropes, vasopressors, or mechanical circulatory support including ECMO), typically presenting with relative hypotension.

SCAI Stage D (Deteriorating)

A patient in cardiogenic shock who fails to respond to initial therapeutic interventions and continues to worsen despite Stage C therapies.

SCAI Stage E (Extremis)

A patient experiencing refractory circulatory collapse supported by multiple simultaneous interventions, frequently in cardiac arrest with ongoing CPR and/or ECMO.

SCAI Arrest (A) Modifier

A clinical modifier appended to any SCAI stage designating the occurrence of cardiac arrest requiring cardiopulmonary resuscitation, including defibrillation.

Classical Cardiogenic Shock (Hemodynamic Classification)

A 'cold and wet' presentation characterized by decreased cardiac index ($\downarrow\text{CI}$), increased systemic vascular resistance index ($\uparrow\text{SVRI}$), and elevated pulmonary capillary wedge pressure ($\uparrow\text{PCWP}$).

Euvolemic Cardiogenic Shock (Hemodynamic Classification)

A 'cold and dry' presentation characterized by decreased cardiac index ($\downarrow\text{CI}$), increased systemic vascular resistance index ($\uparrow\text{SVRI}$), and normal or unchanged pulmonary capillary wedge pressure ($\leftrightarrow\text{PCWP}$).

Vasodilatory Cardiogenic Shock (Mixed Shock)

A 'warm and wet' presentation characterized by decreased cardiac index ($\downarrow\text{CI}$), decreased or normal systemic vascular resistance index ($\downarrow/\leftrightarrow\text{SVRI}$), and elevated pulmonary capillary wedge pressure ($\uparrow\text{PCWP}$).

Inotropes

Pharmacological agents that increase myocardial contractility to improve stroke volume and cardiac output; they are considered the therapeutic mainstay for the 'cold', poorly perfused patient.

Vasopressors

Pharmacological agents that elevate systemic vascular resistance to restore mean arterial pressure and coronary perfusion when severe hypotension threatens end-organ perfusion.

Noradrenaline

The first-line vasopressor in cardiogenic shock targeting $\alpha 1 > \beta 1$ receptors; it maintains or slightly increases cardiac output ($\leftrightarrow / \uparrow$), substantially elevates SVR ($\uparrow\uparrow$), and restores MAP with comparatively fewer arrhythmias than dopamine. It should be titrated to target MAP and administered via central access.

Adrenaline

A potent combined inotrope and vasopressor targeting $\alpha 1, \beta 1, \beta 2$ receptors that increases cardiac output ($\uparrow$) with variable effects on SVR; reserved for refractory shock due to high arrhythmogenic potential and transient rises in lactate and glucose.

Vasopressin

A non-catecholamine $V_1$ receptor agonist that markedly elevates SVR ($\uparrow\uparrow$) with a neutral effect on cardiac output ($\leftrightarrow$); used as a catecholamine-sparing adjunct in fixed low-dose infusions while monitoring for limb ischaemia.

Dobutamine

A $\beta 1$-predominant agonist ($\beta 1 > \beta 2$) that substantially increases contractility and heart rate ($\uparrow\uparrow\text{CO}$) with mild vasodilation ($\downarrow\text{SVR}$); cautioned due to risks of hypotension and tachyarrhythmias, and blunted in patients on chronic beta-blockade.

Milrinone

A phosphodiesterase-3 (PDE-3) inhibitor ('inodilator') that enhances contractility independent of beta-receptors ($\uparrow\uparrow\text{CO}$) and reduces afterload ($\downarrow\downarrow\text{SVR}$); requires avoiding loading doses in shock and necessitates dose adjustment in renal impairment due to renal clearance and a long half-life.

Levosimendan

A calcium sensitiser ($Ca^{2+}\text{ sensitiser}$) and inodilator that increases cardiac output ($\uparrow\uparrow$) and lowers SVR ($\downarrow$) without increasing myocardial oxygen consumption as much as catecholamines; features a long duration of action and is reserved for specialist use.

PEEP (Positive End-Expiratory Pressure)

A ventilatory modality delivered via CPAP, BiPAP, or invasive mechanical ventilation that maximises oxygenation, provides relief from pulmonary congestion, and reduces cardiac preload and afterload.

Preload Management Positioning

A physical supportive strategy for managing fluid overload in cardiogenic pulmonary oedema that involves sitting the patient upright with their legs hanging down in a dependent position.

Indications for NIV in Cardiogenic Pulmonary Oedema

Clinical scenarios warranting non-invasive ventilation: acute cardiogenic pulmonary oedema accompanied by respiratory distress, persistent hypoxaemia despite standard oxygen therapy, and increased work of breathing without immediate need for airway protection.

Contraindications to NIV in Cardiogenic Shock

Clinical factors precluding the safe use of non-invasive ventilation: ongoing haemodynamic instability or worsening hypotension, reduced GCS or inability to protect airway, copious secretions or high vomiting risk, untreated pneumothorax, and facial trauma.