Heart-Lung Interactions*

M.R.Pinsky

Introduction

The primary goal of cardiovascular and respiratory systems is to supply adequate

amounts of O2 to the tissues to meet their metabolic demand. Since a primary
role of critical care resuscitative efforts is to insure the adequacy of O2 delivery in
stress states, an understanding of cardio-pulmonary physiology and the effects of
disease and therapeutic interventions on cardio-pulmonary status is central to
the management of the critically ill patient.
The majority of problems associated with heart-lung interactions center on
the effects of ventilation on the circulation. Ventilation can be spontaneous, par-
tially assisted or totally supported by mechanical devices. Spontaneous inspira-
tion decreases intrathoracic pressure (ITP), whereas positive-pressure inspira-
tion increases ITP. Assisted ventilation has a variable effect on ITP, sometimes de-
creasing ITP (especially during early inspiration when triggered by spontaneous
inspiratory efforts) and sometimes increasing ITP (especially at end-inspira-
tion). All forms of ventilation cyclically increase lung volume in a tidal fashion
above some end-expiratory value. Thus, changes in ITP and lung volume can oc-
cur in the same or opposite directions during ventilation depending on both ven-
tilatory effort and mode of ventilation. Since changes in lung volume reflect a
common aspect of all forms of ventilation, any hemodynamic differences that oc-
cur between spontaneous and positive-pressure breaths reflect effects of chang-
ing ITP and the energy necessary to create these changes.

Heart-lung interactions can be broadly grouped into interactions which involve

four basic concepts (Table l). Although addressed separately, these processes
often co-exist. The four basic concepts are:
a} inspiration increases lung volume above end-expiratory volume;
b} spontaneous inspiration decreases ITP;
c} positive-pressure ventilation increases ITP; and
d} ventilation is exercise, it consumes O2 and produces CO 2 and thus may stress
normal adaptive circulatory mechanisms.

* This work was supported in part by the Veterans Administration.

M. R. Pinsky (ed.), Applied Cardiovascular Physiology

© Springer-Verlag Berlin Heidelberg 1997
52 M.R.Pinsky

Table 1. Hemodynamic effects of ventilation

Mechanical
A) Increasing lung volume
1. autonomic tone
- Vt < 12 mllkg vagal withdrawal: cardiac acceleration
- Vt> 15 mllkg sympathetic withdrawal: cardiovascular depression
2. end-expiratory lung volume
- recruit to FRC: decrease pulmonary vascular resistance
- hyperinflation above FRC: increase pulmonary vascular resistance
3. compression of the heart in the cardiac fossa
B) Intrathoracic pressure (ITP)
1. decreasing lIP
- increase venous return (flow limited)
- increase LV afterload
2. increasing lIP
- decrease venous return (primary effect)
- decrease LV afterload (secondary effect, except in heart failure)
Metabolic
A) Increase oxygen consumption (V0 2 ), work cost of breathing
1. limit blood flow to non-respiratory muscles
2. limited ventilatory reserve in heart failure
B) Increase CO2 production (VC02 )
1. increase ventilatory load on respiratory muscles

Hemodynamic Effects of Changes in Lung Volume

Lung inflation alters autonomic tone and pulmonary vascular resistance and, at
high lung volumes interacts mechanically with the heart in the cardiac fossa to
limit absolute cardiac volumes. Each of these processes is important in determin-
ing the hemodynamic response to mechanical ventilation.

Autonomic Tone

The lungs are richly enervated with autonomic fibers that mediate multiple ho-
meostatic processes. Numerous cardiovascular reflexes are centered within this
network. Inflation-induced chronotropic responses act through vagally-mediat-
ed reflex arcs [1, 2]. Lung inflation at small tidal volumes ( < 10 ml!kg) increases
heart rate, via Vagal withdrawal. Larger tidal volumes (> 15 ml!kg) decrease
heart rate via sympathetic withdrawal.1nspiration-associated cardio-acce1era-
tion is referred to as respiratory sinus arrhythmia [3] and denotes normal auto-
nomic tone [4]. Loss of respiratory sinus arrhythmia commonly occurs in dys-
autonomic states, such as diabetic peripheral neuropathy, and the reappearance
of respiratory sinus arrhythmia precedes return of peripheral autonomic control
[5]. However, some degree of respiratory-associated heart rate change is intrinsic
to the heart itself and persists even following cardiac denervation, as occurs fo1-