Residency · Residency · Cardiothoracic Surgery
Pulmonary Vascular Physiology and Right Heart Function
Overview
The pulmonary circulation is a low-pressure, high-compliance system whose primary purpose is gas exchange. Right ventricular function and pulmonary vascular resistance profoundly influence perioperative outcomes across the spectrum of cardiothoracic surgery, from valve operations to transplantation and mechanical circulatory support.
Pulmonary Vascular Physiology
Normal Pulmonary Hemodynamics
The pulmonary circulation receives the entire cardiac output at roughly one-fifth the systemic pressure. Normal mean pulmonary artery pressure (mPAP) is 10 to 20 mmHg, and pulmonary vascular resistance (PVR) ranges from 0.25 to 1.6 Wood units. PVR is calculated as (mPAP - PCWP) / CO. Two additional metrics help characterize pulmonary hemodynamics: the transpulmonary gradient (TPG = mPAP - PCWP, normally less than 12 mmHg) and the diastolic pressure gradient (DPG = diastolic PAP - PCWP, normally less than 7 mmHg).
Regulation of Pulmonary Vascular Tone
Several mechanisms regulate pulmonary vascular tone. Hypoxic pulmonary vasoconstriction (HPV) is unique to the pulmonary circulation: when alveolar oxygen is low, local vasoconstriction diverts blood away from poorly ventilated lung segments toward better-ventilated areas. The mechanism involves inhibition of voltage-gated potassium channels in pulmonary artery smooth muscle cells. Surgically, one-lung ventilation exploits HPV to reduce shunt in the non-ventilated lung. HPV is inhibited by inhalational anesthetics, vasodilators, and systemic hypoxia.
Nitric oxide (NO), produced by the endothelium, is a vasodilator that activates guanylyl cyclase and increases cGMP. Prostacyclin (PGI2) is another endothelium-derived vasodilator that increases cAMP. Endothelin-1, by contrast, is a potent vasoconstrictor elevated in pulmonary hypertension. Finally, acidosis and hypercarbia increase PVR, while alkalosis and hypocarbia decrease it.
Zones of the Lung (West Zones)
The three West zones describe the relationship between alveolar, arterial, and venous pressures at different levels of the lung in an upright patient. In Zone 1 (apex), alveolar pressure exceeds both arterial and venous pressures, resulting in minimal perfusion and dead space. In Zone 2 (middle), arterial pressure exceeds alveolar pressure, and flow is determined by the arterial-alveolar gradient (the Starling resistor model). In Zone 3 (base), both arterial and venous pressures exceed alveolar pressure, producing continuous flow determined by the arterial-venous gradient. Positive pressure ventilation expands Zone 1, and accurate PCWP measurement requires the PA catheter tip to be in Zone 3.
Pulmonary Hypertension
Classification (Updated WHO Groups)
| WHO Group | Category | Examples | Key Feature |
|---|---|---|---|
| 1 | Pulmonary arterial hypertension (PAH) | Idiopathic, heritable, drug-induced, connective tissue disease | Pre-capillary PH |
| 2 | PH due to left heart disease | Mitral valve disease, LV dysfunction | Most common cause; PCWP > 15 mmHg |
| 3 | PH due to lung disease/hypoxia | COPD, interstitial lung disease | Hypoxia-driven vasoconstriction |
| 4 | Chronic thromboembolic PH (CTEPH) | Organized thrombus in pulmonary arteries | Potentially curable with pulmonary thromboendarterectomy |
| 5 | Multifactorial/unclear mechanisms | Sarcoidosis, metabolic disorders | Heterogeneous group |
Hemodynamic Definitions
| PH Type | mPAP | PCWP | PVR | Clinical Significance |
|---|---|---|---|---|
| Pre-capillary | > 20 mmHg | ≤ 15 mmHg | > 2 Wood units | Intrinsic pulmonary vascular disease |
| Isolated post-capillary (IpcPH) | > 20 mmHg | > 15 mmHg | ≤ 2 Wood units | Left heart disease without pulmonary remodeling |
| Combined pre- and post-capillary (CpcPH) | > 20 mmHg | > 15 mmHg | > 2 Wood units | Left heart disease with pulmonary vascular remodeling |
Distinguishing between pre- and post-capillary PH is critical for surgical planning, especially when evaluating transplant and LVAD candidacy.
Reactivity Testing
Vasoreactivity testing uses inhaled NO, prostacyclin, or adenosine. A positive response is defined as a decrease in mPAP of at least 10 mmHg to an absolute value of 40 mmHg or less, with stable or increased cardiac output. This testing is particularly relevant for heart transplant candidacy: PVR above 5 Wood units or TPG above 15 mmHg that does not respond to vasodilators is a relative contraindication to transplant due to the risk of post-transplant RV failure.
Right Ventricular Anatomy and Physiology
RV Anatomy
The right ventricle is a thin-walled (3–5 mm) crescent-shaped chamber that wraps around the left ventricle. It has three components: the inlet (containing the tricuspid apparatus), the trabeculated apical body, and the infundibulum (the smooth-walled outflow tract, also called the conus). The moderator band, which carries the right bundle branch from the septum to the anterior papillary muscle, is a distinctive feature. The RV's blood supply comes predominantly from the RCA, with contributions from the LAD via septal perforators.
RV Physiology
The RV functions as a volume pump in a low-impedance circuit. Its stroke work is approximately one-sixth that of the LV. Contraction follows a sequential, peristaltic-like pattern from the inlet to the infundibulum. The RV is more dependent on preload than the LV and tolerates volume loading well, but it is poorly tolerant of acute afterload increases (such as acute pulmonary embolism or acute pulmonary hypertension). While RV coronary perfusion normally occurs during both systole and diastole (unlike the predominantly diastolic perfusion of the LV), this pattern shifts in RV pressure overload states.
RV-Pulmonary Artery Coupling
Ventriculoarterial coupling is expressed as the ratio of end-systolic elastance (Ees) to arterial elastance (Ea), with an optimal ratio of 1.5 to 2.0. In pulmonary hypertension, increased Ea (afterload) is initially compensated by increased Ees (contractility), maintaining a coupled state. Decompensation occurs when the RV can no longer increase its contractility to match the rising afterload — an uncoupled state that manifests as RV dilatation, worsening tricuspid regurgitation, falling cardiac output, and systemic venous congestion.
RV Failure in Cardiothoracic Surgery
Risk Factors for Perioperative RV Failure
Several factors predispose to perioperative RV failure: pre-existing pulmonary hypertension, prolonged cardiopulmonary bypass time, inadequate myocardial protection (the RV is vulnerable to distension on bypass), air embolism to the RCA (the RV is anterior and first to receive air), post-LVAD implantation (occurring in 20–40% of cases), and protamine reactions causing acute pulmonary vasoconstriction.
After LVAD Implantation
RV failure after LVAD implantation is the most common early complication and the leading cause of early mortality. Several mechanisms contribute: leftward septal shift with LV unloading reduces the RV's septal contribution to ejection; increased venous return to the RV from improved LV output overwhelms a compromised RV; pre-existing RV dysfunction becomes unmasked; and perioperative myocardial injury from CPB and ischemia adds further insult. Multiple prediction scores exist (RVFRS, EUROMACS-RHF, Michigan score). Prevention strategies include optimizing PVR preoperatively, conducting a cautious LVAD speed ramp, and considering a temporary RVAD.
Management of Acute RV Failure
Managing acute RV failure requires attention to several domains simultaneously. Preload should be optimized with careful volume administration targeting a CVP of 8 to 12 mmHg, while avoiding volume overload, which dilates the RV and worsens tricuspid regurgitation. Afterload should be reduced using inhaled NO (20–40 ppm) as a selective pulmonary vasodilator that avoids systemic hypotension, inhaled epoprostenol (prostacyclin), or IV milrinone (which serves as both an inotrope and pulmonary vasodilator). Hypoxia, hypercarbia, and acidosis must be avoided, as all three increase PVR. Contractility should be augmented with dobutamine, epinephrine, or milrinone. Systemic perfusion pressure must be maintained with norepinephrine or vasopressin to ensure coronary perfusion of the RV. For refractory cases, mechanical support with VA-ECMO, Impella RP, or a temporary RVAD may be required. Finally, AV synchrony must be maintained — loss of the atrial kick is poorly tolerated — and arrhythmias should be treated aggressively.
<image>Diagram showing the three West zones of the lung in an upright patient, with the relationship between alveolar pressure (PA), arterial pressure (Pa), and venous pressure (Pv) illustrated in each zone. Blood flow arrows indicate perfusion pattern from minimal at the apex (Zone 1) to continuous at the base (Zone 3). The effect of positive pressure ventilation on expanding Zone 1 is shown with a dashed line overlay.</image>
<image>Anatomical illustration of the right ventricle opened to show its three components: the inlet with the tricuspid valve and chordal apparatus, the trabeculated apical body with the moderator band highlighted, and the smooth-walled infundibulum leading to the pulmonary valve. The crescent-shaped cross-section of the RV wrapping around the LV is shown in an inset. RCA and septal perforator blood supply is indicated.</image>
<image>Two-panel illustration showing RV-PA coupling. Left panel: normal coupling with matched end-systolic elastance (Ees) and arterial elastance (Ea), represented as balanced pressure-volume relationships. Right panel: uncoupled state in pulmonary hypertension showing increased Ea with failing Ees, RV dilatation, increased end-systolic volume, and reduced stroke volume. Clinical manifestations (TR, systemic congestion, low output) are annotated.</image>
Clinical Pearls
The RV is a volume pump that tolerates volume loading well but fails rapidly with acute afterload increases — the first principle in managing RV dysfunction is always to think about reducing PVR. Inhaled NO is the first-line pulmonary vasodilator in the perioperative setting because it acts selectively on ventilated lung segments without causing systemic hypotension. In heart transplant evaluation, fixed elevated PVR (above 5 Wood units, not responsive to vasodilators) is a contraindication due to the risk of donor RV failure. The triad that worsens PVR — hypoxia, hypercarbia, and acidosis — must be avoided aggressively. After LVAD implantation, RV failure is the most common early complication and the leading cause of early mortality, making pre-operative RV assessment essential. CVP is a poor surrogate for RV preload; echocardiographic assessment of RV size and function is superior. Protamine reactions can cause acute pulmonary hypertension and RV failure, so protamine should be administered slowly with readiness to treat.
References
- Vonk-Noordegraaf A, Haddad F, Chin KM, et al. Right heart adaptation to pulmonary arterial hypertension: physiology and pathobiology. J Am Coll Cardiol. 2013;62(25 Suppl):D22-D33.
- Humbert M, Kovacs G, Hoeper MM, et al. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J. 2022;43(38):3618-3731.
- Haddad F, Hunt SA, Rosenthal DN, Murphy DJ. Right ventricular function in cardiovascular disease, part I: anatomy, physiology, aging, and functional assessment. Circulation. 2008;117(11):1436-1448.
- Kormos RL, Teuteberg JJ, Pagani FD, et al. Right ventricular failure in patients with the HeartMate II continuous-flow LVAD. J Thorac Cardiovasc Surg. 2010;139(5):1316-1324.
