• High cardiac output (HCO) is a hyperdynamic circulatory state marked by low mean arterial blood pressure (MAP) and tachycardia:
  • Cardiac output (CO) > 8 L/min or cardiac index (CI) > 4 L/min/m²
  • Systemic vascular resistance (SVR) <900 dynes × seconds/cm⁵ or SVR index (SVRI) <1680 dynes × seconds/cm⁵/m²

• Physiologic causes: Anxiety, exercise, pregnancy, fever
• Common pathologic causes: ESLD, SIRS/sepsis, hyperthyroidism, obesity
• Less common pathologic causes: Arteriovenous (AV) fistula, anemia (Hg <7 g/dL), carcinoid, beriberi, hereditary hemorrhagic telangiectasia, dermatologic diseases, Kaposi sarcoma, multiple myeloma, Paget's disease.

• Decreased SVR leading to a low MAP is often the primary circulatory derangement leading to HCO. Two principal causes of low SVR are as follows:
  • Vasodilated small and precapillary arterioles
  • AV shunting, including iatrogenic AV fistulas
• Compensatory mechanisms are triggered by a low SVR and MAP:
  • Chronic activation of the sympathetic nervous system (SNS) causes tachycardia and increases plasma catecholamines, vasomotor tone, myocardial contractility, and CO.
  • Activated renin-angiotensin-aldosterone system (RAAS) maintains systemic BP by vasoconstriction and sodium retention.
  • Nonosmotic hypersecretion of arginine vasopressin results in retention of free water in order to preserve the circulatory volume.
• Heart failure may occur regardless of the etiology of HCO; it is defined by clinical evidence of heart failure and a CI > 4 L/min/m² (3) [A]. Chronic SNS activation and an excess of catecholamines cause tachycardia, arrhythmogenesis, 1 receptor down-regulation, increased myocardial oxygen consumption VO₂, and tachycardia-mediated dilated cardiomyopathy.
• ESLD: Mesenteric vasodilators (nitric oxide [NO], carbon monoxide, cytokines, etc.) cause splanchnic arterial and venous vasodilatation (1) [A].
  • Splanchnic arterial dilatation is so profound that it lowers the overall systemic SVR.
  • Splanchnic venous dilatation causes pooling of venous blood and functional hypovolemia.
  • A dual circulation exists with a (1) [A]:
    • Primary derangement causing a low resistance-high capacitance splanchnic circulation
    • Compensatory response causing a high resistance-low capacitance extrasplanchnic circulation
• Cirrhotic cardiomyopathy: Describes systolic dysfunction in the setting of HCO and low SVR, diastolic dysfunction, and supportive criteria (e.g., long QTc and abnormal chronotropy due to 1 receptor down-regulation). Pharmacologic and physiologic stress can unmask an impaired LVEF and elevated LVEDV (1) [A].
• SIRS/sepsis: Adequately fluid-resuscitated patients have a hyperdynamic circulation and low SVR. The extent of SVR reduction appears to be related to mortality (2) [B].
  • Mechanisms of low SVR: A blunted rise of intracellular Ca²⁺ in vascular smooth muscle by activated K_ATP channels, increased expression of NO synthase, and depletion of vasopressin stores due to sustained baroreflex stimulation (2) [A].
  • Septic cardiomyopathy presents as an isolated or combined diastolic and systolic dysfunction. The etiology is unknown but appears to include NO, TNF-, and cytokines. Impaired LVEF is associated with poor prognosis in septic patients (2) [A].
  • Increased troponins (nonischemic "leak") predict LV dysfunction and mortality (2) [A].
• Hyperthyroidism: Decreased SVR combined with increased chronotropy and inotropy can result in a greater than 250%.

• Ensure adequate perioperative organ/tissue perfusion and oxygenation.
• The degree of circulatory derangement and type of surgery determine the invasiveness of monitoring and the acuity of postop care.

• Anxiety
• Palpitations, angina-like chest pain
• Dyspnea, orthopnea
• Fatigue, poor exercise tolerance
• Lower extremity swelling
• Symptoms related to primary disease

• Treatment of primary etiology
• Treatment of heart failure

• -1 Adrenergic agonist (phenylephrine, norepinephrine, midodrine) (3) [A]
• Dopamine (dosed as -1 agonist; lower doses act to lower the SVR) (3) [A]
• Vasopressin, terlipressin (4) [A]
• Catecholamine inotropes have decreased efficacy due to 1 receptor downregulation. Alternative inotropic agents include milrinone (phosphodiesterase inhibitor) and levosimendan (troponin C sensitizer to Ca²⁺) (4) [C].
• Diuretics, digoxin if in heart failure (1) [A]
• Drugs specific to underlying cause

• Poorly managed primary pathology (e.g., poorly controlled hyperthyroidism)
• Symptoms and signs of heart failure

No classification specific to HCO

Telemetry, intensive care unit (ICU) based on underlying condition, hemodynamic status, and extent of surgery

• Dependent on extent of surgery
• ECG, cardiac enzymes, BNP if in HCO failure

• Heart failure, ischemia/MI, arrhythmias
• Instability, dynamic LVOT obstruction
• Decreased organ perfusion, circulatory shock

• Cardiac Output
• Hyperthyroidism
• End-Stage Liver Disease

Rashmi R. Rathor , MD

Ivan M. Kangrga , MD, PhD