- systolic blood pressure fluctuates with spontaneously breathing, normally by 5-10 mmHg
- aka ‘respiratory swing’
- Pulsus paradoxus is a phenomenon in which the difference in systolic blood pressure (BP) between inspiration and expiration is more than 10 mmHg.
- Reverse pulsus paradoxus — occurs during controlled mechanical ventilation when arterial pressure rises during inspiration and falls during expiration due to changes in intra-thoracic pressure secondary to positive pressure ventilation.
- Other names for reverse pulsus paradoxus are paradoxical pulsus, respiratory paradox, systolic pressure variation and pulse pressure variation.
- Stroke volume variation (SVV) is calculated by taking the( SVmax – SVmin) / SVmean over a respiratory cycle or other period of time
- pulse pressure variation (PPV) = (PPmax – PPmin) / PPmean over a respiratory cycle or other period of time
- SVV or PPV >10% suggests that the patient is fluid responsiveness as indicates that stroke volume is sensitive to fluctuations in preload caused by the respiratory cycle
Pulse pressure = stroke volume / arterial compliance
- increase in negative intrathoracic pressure during inspiration
-> blood pools in pulmonary circulation
-> left heart filling reduced and lower stroke volume
The reverse occurs during mechanical ventilation, LV SV is lower during expiration
- left ventricular stroke volume increases during inspiration because left ventricular preload increases while left ventricular afterload decreases
- right ventricular stroke volume decreases during inspiration because right ventricular preload decreases while right ventricular afterload increases
- Because of the long (approximately 2 s) pulmonary transit time of blood, the inspiratory decrease in right ventricular output causes a decrease in left ventricular filling and output only a few heartbeats later, i.e., usually during the expiratory period
CAUSES OF INCREASED SYSTOLIC PRESSURE VARIATION
- Constrictive pericarditis
- LV dysfunction
- Massive PE
- Dynamic hyperinflation
- Raised intrathoracic pressure
- Raised intra-abdominal pressure
SVV and PPV are not indicators of actual preload but of relative preload responsiveness.
- Also, just because a patient is fluid responsive does not mean they actually need fluid.
- SVV has a very high sensitivity and specificity when compared to traditional indicators of volume status (HR, MAP, CVP, PAD, PAOP), and their ability to determine fluid responsiveness.
The utility of SVV is limited in the following settings:
- small tidal volumes (tidal volume must be at least 8 mL/kg)
- spontaneous breathing (patient must have 100% controlled mechanical ventilations at a fixed rate)
- ARDS and low lung compliance (false negatives more likely)
- PEEP (may increase SVV)
- arrhythmia (R-R interval must be regular on ECG)
- low heart rate/respiratory rate ratio
- open chest
- right ventricular systolic dysfunction
- norepinephrine (may decrease SVV)
- vasodilators (may increase SVV)
- b-blocker medication
References and Links
- CCC – Fluid responsiveness
- CCC – Fluid bolus therapy
- CCC – Fluid challenge
- Cardiovascular Curveball 006 — The Paradoxical Alternative
- DDX — Pulsus Paradoxus
- Marik PE, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Crit Care Med. 2009 Sep;37(9):2642-7. PMID: 19602972.
- Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology. 2005 Aug;103(2):419-28; quiz 449-5.PMID: 16052125. [Free Full Text]
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of three amazing children.
On Twitter, he is @precordialthump.