RespiratoryTier 2Topic

Effects of interactions between pulmonary and systemic circulation and cardiac function

The framework

The heart and lungs share a rigid thoracic cavity, a common circulation and a shared pericardial space
- -> intrathoracic pressure is a determinant of cardiac loading, and cardiac filling pressure is a determinant of lung mechanics
The single most useful framework: transmural pressure, not intracavitary pressure, is the true load on the ventricle

```

LV transmural pressure = LV intracavitary pressure - intrathoracic pressure

```

Raising intrathoracic pressure (positive pressure ventilation) dec preload AND dec LV afterload
Lowering intrathoracic pressure (forceful spontaneous inspiration, obstructive apnoea) inc preload AND inc LV afterload
- -> a patient in respiratory distress is doing the opposite of what their failing LV needs

Epidemiology

COPD and heart failure coexist in ~20-30% of each population - and each is under-diagnosed in the presence of the other
Cor pulmonale complicates advanced COPD, ILD and OSA
Acute cardiogenic pulmonary oedema: a major cause of emergency NIV use; ~1 in 6 acute breathless presentations
OSA in ~50-80% of resistant hypertension and in ~50% of heart failure

1. Ventricular interdependence

The ventricles share the septum and the pericardium - a fixed total volume
RV dilatation -> septal shift to the left -> impaired LV filling -> dec cardiac output (the "D-shaped septum")
-> why a massive PE causes systemic hypotension despite a normal LV

2. Intrathoracic pressure and the respiratory cycle

Spontaneous inspiration: intrathoracic pressure falls
- inc venous return -> inc RV preload; RV dilates -> septal shift
- inc LV transmural pressure -> inc LV afterload
- -> the physiological basis of pulsus paradoxus (exaggerated in tamponade, severe asthma, COPD)
Positive pressure ventilation: intrathoracic pressure rises
- dec venous return -> dec preload (harmful in hypovolaemia, RV infarction, tamponade)
- dec LV transmural pressure -> dec afterload (beneficial in a failing LV)

3. Lung volume and pulmonary vascular resistance

PVR is minimal at FRC, and rises at both extremes
- Low volume (atelectasis) -> alveolar hypoxia -> hypoxic pulmonary vasoconstriction -> inc PVR (extra-alveolar vessel collapse)
- High volume (hyperinflation, high PEEP) -> alveolar vessel compression -> inc PVR
-> both under- and over-inflation increase RV afterload

4. Cardiogenic pulmonary oedema and CPAP

inc LV filling pressure -> pulmonary interstitial and alveolar oedema
- -> dec FRC, dec compliance, alveolar flooding -> intrapulmonary shunt -> hypoxaemia
- -> inc work of breathing -> inc respiratory muscle O2 demand (up to 20-30% of cardiac output) - steals output from vital organs
CPAP reverses each step
- Alveolar recruitment -> restores FRC -> dec shunt -> inc oxygenation and compliance
- inc intrathoracic pressure -> dec venous return -> dec LVEDV -> dec preload
- dec LV transmural pressure -> dec afterload -> inc stroke volume and cardiac output
- dec work of breathing -> reduced respiratory muscle oxygen consumption

5. Hypoxia, hypercapnia and the pulmonary circulation

Chronic alveolar hypoxia -> sustained hypoxic pulmonary vasoconstriction + vascular remodelling -> pulmonary hypertension -> RV hypertrophy -> cor pulmonale
Hypercapnia -> pulmonary vasoconstriction, systemic vasodilation, inc sympathetic drive
OSA: repetitive large negative intrathoracic pressure swings against a closed airway (Mueller manoeuvre) + surges of sympathetic activity + hypoxia
- -> inc LV afterload, atrial stretch -> AF, nocturnal hypertension, RV strain

Separating cardiac from respiratory dyspnoea

	Favours cardiac	Favours respiratory
NT-proBNP	High (dec by obesity; inc by age, AF, renal impairment)	Low/normal
Orthopnoea/PND	Yes	Also in COPD, OSA, diaphragm palsy
Spirometry after treatment	Restrictive/normal	Persistent obstruction
Echo	Impaired LV, raised filling pressure, RV dilatation	Often normal LV, may show RV changes
CPET	Cardiac limitation, early anaerobic threshold	Ventilatory limitation, exhausted breathing reserve

Echocardiography is the pivot - LV and RV size and function, TR jet velocity for pulmonary pressures, septal flattening, IVC size and collapsibility
Right heart catheterisation where pulmonary hypertension classification matters
Beware: a raised BNP in cor pulmonale reflects RV strain, not LV failure

Pulsus paradoxus

Inspiratory fall in systolic BP >10 mmHg
Tamponade, severe asthma/COPD, massive PE, constrictive pericarditis, tension pneumothorax
Reverse pulsus paradoxus: positive pressure ventilation, HOCM

Acute cardiogenic pulmonary oedema

Sit upright, high-flow oxygen
CPAP (or bilevel NIV) early - improves oxygenation, reduces work of breathing and reduces intubation rate and mortality
- Typical CPAP 5-10 cmH2O, titrated
- Bilevel is preferred if hypercapnic or exhausted; earlier concerns about excess MI have not been substantiated
GTN infusion (vasodilation, dec preload and afterload) if BP adequate
IV loop diuretic; treat the precipitant (ischaemia, AF, hypertension, non-adherence, sepsis)
Beware: CPAP in a preload-dependent patient (RV infarct, hypovolaemia, tamponade) drops cardiac output

COPD with heart failure

Cardioselective beta-blockers (bisoprolol, metoprolol succinate, nebivolol) are safe and indicated in COPD - withholding them is a common and costly error
Inhaled therapy per COPD guidelines; long-acting beta-agonists are not contraindicated in heart failure
Treat coexisting OSA with CPAP - improves BP, LV function and AF recurrence

Ventilating the cardiovascular patient

RV failure/pulmonary hypertension: avoid hypoxia, hypercapnia and acidosis (all raise PVR); ventilate near FRC with modest tidal volumes and the lowest effective PEEP; avoid excessive PEEP
Severe asthma/COPD: dynamic hyperinflation and auto-PEEP -> dec venous return -> shock
- -> disconnect the circuit and compress the chest as a diagnostic and therapeutic manoeuvre
- -> low respiratory rate, long expiratory time, permissive hypercapnia
Intubation of a shocked patient: the transition from negative to positive intrathoracic pressure plus induction-agent vasodilation causes peri-intubation arrest - optimise volume and start a vasopressor first

Chronic management

Chronic

Pulmonary rehabilitation, exercise training, vaccination, smoking cessation
Long-term oxygen therapy where criteria are met - reduces hypoxic pulmonary vasoconstriction and mortality in COPD

Associations

Cor pulmonale - COPD, ILD, OSA, obesity hypoventilation, kyphoscoliosis, chronic thromboembolic disease
Obstructive sleep apnoea - hypertension, AF, heart failure, stroke
Massive pulmonary embolism - acute cor pulmonale, ventricular interdependence
Cardiac tamponade, constrictive pericarditis - pulsus paradoxus, Kussmaul sign
Hepatopulmonary syndrome and portopulmonary hypertension
Eisenmenger syndrome and congenital shunts
ARDS - RV failure from inc PVR and ventilation strategy
Obesity - restrictive physiology + inc preload + OSA

Prognosis

The presence of both cardiac and respiratory disease is worse than the sum of the parts - each limits the treatment of the other, and each accelerates deconditioning
Cor pulmonale marks advanced lung disease: once right heart failure is established in COPD, prognosis is poor (historically ~50% 5-year survival)
Untreated OSA -> incident hypertension, AF, heart failure and stroke; CPAP improves BP and symptoms, but randomised trials have not shown a clear reduction in cardiovascular events (SAVE, RICCADSA) - adherence is the limiting factor
Pulmonary hypertension due to lung disease (WHO group 3) responds poorly to pulmonary vasodilators - treat the lung disease and the hypoxia; targeted PAH therapy can worsen V/Q matching
Peri-operative and peri-intubation deterioration is predictable from these interactions and largely preventable
The recurring teaching point: treat the shared physiology, not the two organs separately**

14 more sections, plus exam facts

Premium unlocks every note across every specialty, and the full exam fact library behind it.

Get premium access