Case Report

Hemodynamic effects of Key physiological insight/learning points:

acute tension The RV easily handles varying amounts of preload,

but it rapidly decompensates with an acute rise in
pneumothorax. afterload.
At first assessment, our patient presents with
Carolina Michel-Macías1, Eunice Valeria Serpa
evolving right ventricular failure and elevation of PVR
Maldonado2, José Guadalupe Mantilla Uresti3
as seen in tension physiology, that resolved quickly
Daniel Ibarra-Ríos2
after tension pneumothorax drainage.
1.Neonatology Department, Instituto Nacional de
Perinatología. 2. Neonatology Department, Hospital Infantil Ultrasound driven protocols for crashing infant in the
de México Federico Gómez. 3. Neonatology Department, NICU allows timely and efficient response and
Hospital Central “Dr. Ignacio Morones Prieto”. invasive procedures can be guided.
Background: Pneumothorax occurs more
frequently in the neonatal period than in any Medical History: At admission the newborn was
other period of life and is associated with found febrile and tachycardic. On chest
increased mortality and morbidity. Symptomatic radiography patchy bilateral infiltrates were
noted so evidence of early onset sepsis was
pneumothorax occurs in about 0.05% to 0.1% of
considered for which antibiotic coverage with
all live births, and in very low birthweight infants
ampicillin and amikacin was given. The fellow on
this rate can achieve 3.8% to 9%1, 2, 3. Among call found lung ultrasound at admission with
preterm neonates born at less than 32 weeks GA, pleural sliding, dense B-Line pattern, and
pneumothorax is significantly associated with collapse bronchogram. Cardiac POCUS with
mortality, BPD and IVH3,4. Birth trauma, neonatal adequate contractility and a left to right patent
resuscitation, meconium aspiration, underlying foramen ovale.
lung diseases or positive pressure ventilation are
Hemodynamic Consultation: On day 2 of
the main causes of pneumothorax in
admission sudden desaturation (70%) with
newborns3,5.
tachycardia and hypotension occurred so the
Birth History: Term male neonate, born at 38 hemodynamics team was paged.
weeks of gestation to a 35-year-old mother Vital signs: Heart rate 180, blood pressure right
(Gravida 4, para 3) mother with history of
arm 50/32 mmHg, respiratory rate 68, Saturation
repetitive urinary tract infections, treatment not
70%.
specified without cultures. Born by caesarean
section was found non vigorous at birth requiring Ultrasound assessment: With evidence of
aggressive resuscitation with positive pressure sudden respiratory deterioration, a modified
ventilation, chest compressions and one dose of SAFE protocol (Sonographic Algorithm for liFe
adrenaline. Apgar score was reported as 3, 5, 8 threatening Emergencies) was preformed
at 1, 5 and 10 minutes respectively. Birth weight encountering absence of pleural sliding with A-
was 3050 g. Tachypnea, grunting and jittery line pattern, no B lines and under M-mode the
progressed requiring CPAP of 6 cmH2O with an stratosphere sign was presented. No lung point
FiO2 of 30% and was transferred to third level was present and with evidence of previous
care. existence of dense B line pattern tension
pneumothorax (tPTX) was diagnosed. While

" Copyright. All rights reserved. This is an educational activity undertaken to facilitate sharing of opinions, provoke critical thinking and discussions.
The accuracy of data, steps to ensure and protect patient confidentiality such as obtaining informed consent, institutional approvals and waiver
of consent are wholesome responsibility of the reporting authors and not the Neonatal Hemodynamic Research Center (NHRC). The potentially
identifying demographic details have been modified. The case presented and ensuing discussion is author's opinion, has not been peer-reviewed
and does not represent an official statement or recommendation from the NHRC or its members."
 Case Report
material for chest drainage was prepared a quick Figure 1. Hemodynamics before and after
assessment of hemodynamics was undertaken tension pneumothorax drainage.
finding pulmonary hypertension with right
ventricle (RV) evolving dysfunction and low
cardiac output. On the left ventricle (LV) low
pulmonary venous return, an hyperdynamic
pattern with low cardiac output was found.
Hemodynamic effects resolved after tPTX was
drained. Table 1 shows hemodynamic variables
before and after chest drainage. See Figure 1 and
Video 1.
Vitals after drainage: heart rate 136, blood
pressure 72/45 mmHg, respiratory rate 50,
saturation 93%.
Table 1. Hemodynamic variables before and
after tension pneumothorax drainage.
Parameter Before After(1h)
RV
TAPSE mm 7 9
FAC % 23 39
S' cm/s 4.2 8.2
RVO 124 274
RV 14% 18.3%
longitudinal
strain
VRi 0.17 0.34
(PAAT/RVET)
A. Radiography with corresponding M mode comparing
IVS Paradoxical Round tPTX and normal pleural sliding (Stratosphere sign vs
LV Seashore sign). B. Paradoxical vs round shaped
S/D cm/s 21/22 41/38 interventricular septum. C. Pulsed doppler of the
E/A cm/s 40/68 48/64 pulmonary artery showing low output with short PAAT that
improves after drainage. D. RV free wall tissue doppler
E/A ratio 0.59 0.75 showing improvement of the systolic (S) wave. E. RV
LVO 142 180 longitudinal strain showing improvement. F. MCA showing
Simpson’s 79% 60% compensatory vasodilation and then normal pattern.
biplane Follow up: Chest tube was maintained for 6 days,
PFO Right to left Left to right and the patient was extubated at day 10.
MCA RI 0.64 0.71 Antibiotics were administered for 7 days with
MCA PI 1.04 1.44 negative blood culture. Newborn was discharged
RV: right ventricle, TAPSE tricuspid annular plane systolic
at day 16 enrolled in high risk follow up clinic.
excursion, FAC: fractional area change, RVO: right
ventricular output, VRi: vascular resistance index, PAAT:
pulmonary artery acceleration time, RVET: right ventricular
ejection time, IVS: interventricular septum, PFO: patent
foramen ovale, MCA: medium cerebral artery, RI: resistance
index, PI: pulsatility index.

" Copyright. All rights reserved. This is an educational activity undertaken to facilitate sharing of opinions, provoke critical thinking and discussions.
The accuracy of data, steps to ensure and protect patient confidentiality such as obtaining informed consent, institutional approvals and waiver
of consent are wholesome responsibility of the reporting authors and not the Neonatal Hemodynamic Research Center (NHRC). The potentially
identifying demographic details have been modified. The case presented and ensuing discussion is author's opinion, has not been peer-reviewed
and does not represent an official statement or recommendation from the NHRC or its members."
 Case Report
represents a collection of related but
Discussion significantly varying pathophysiologic
7
processes . Therefore, alveolar collapse with
Pneumothorax begins with the rupture of an normal pulmonary perfusion establishes that the
over-distended alveoli. The air escapes along the main mechanism of hypoxemia is shunt. In case
perivascular connective tissue sheath into the of hypoxic vasoconstriction, dead space
pleural space6. The classic description of tPTX mechanism could be also associated6,14,7.
involves mechanical shifting of the mediastinum
with equalization of cardiac filling pressures and Hypoxic pulmonary vasoconstriction leads to a
cardiogenic shock, as it was evolving in our redirection of the blood to the alveoli with higher
case7,8. oxygen tension, increasing pulmonary vascular
resistance by 50-300%, and pulmonary blood
In experimental studies, tPTX has been defined flow in a lung affected by a pneumothorax can
to cause a decrease of > 50% of ventricular decrease to 25-35% of the total blood flow14. The
output (VO) or cardiac index from baseline redirection of blood to the unaffected lung by
value7, as the point at which ipsilateral pleural increasing pulmonary vascular resistance in the
pressures became positive throughout the affected lung may prevent a decrease in blood
respiratory cycle9, “cardiovascular collapse” or oxygenation14.
injection of > 120% of total lung capacity to
induce pneumothorax10. In another animal Although the RV easily handles varying amounts
model, tPTX was defined as a positive of preload, it rapidly decompensates with an
intrapleural pressure > 1 mmHg and a significant acute rise in afterload5. Coronary perfusion to
deviation of hemodynamic parameters, the RV occurs in systole and diastole, compared
including a decline in VO > 20%11. with primarily diastolic flow in the LV, making the
RV dependent on systolic blood pressure15.
With regards to tension physiology, early models At first assessment, our patient presents with
of tPTX supported a theory of progressive evolving RV failure and elevation of PVR as seen
mechanical compression that resulted in
in tension physiology12,14,15. Hypotension is also
“kinking” of mediastinal structures and right
present, which causes further deterioration of
heart compression, culminating in cardiogenic
shock12,7. Later studies, however, have provided acute RV failure due to reduced transseptal
evidence to suggest that central hypoxia actually gradient and coronary perfusion (the double hit
represents the primary physiologic insult, with phenomenon), the RV diameter can be
preservation of VO by compensatory significantly reduced preceding arrest 15,16.
mechanisms, including tachycardia and
Rapid diagnosis of tPTX in the NICU is essential to
increased negative intrathoracic pressure on the
contralateral hemithorax until late in physiologic prompt life-saving management in the
process when sudden cardiovascular collapse newborn17,18. The SAFE protocol for the suddenly
occurs12,7,8,13. Our patient showed tachycardia, decompensating infant is a tool for rapid
hyperdynamic LV pattern and cerebral screening for the most common life-threatening
compensatory vasodilation that improved after complications needing immediate attention2,18.
drainage. The average time to perform diagnostic tests in
these studies was 5.3±5.6 min for LUS versus
It appears that both of these models of tension 19±11.7 min for a chest X-ray5.
physiology are actually correct and that tPTX

" Copyright. All rights reserved. This is an educational activity undertaken to facilitate sharing of opinions, provoke critical thinking and discussions.
The accuracy of data, steps to ensure and protect patient confidentiality such as obtaining informed consent, institutional approvals and waiver
of consent are wholesome responsibility of the reporting authors and not the Neonatal Hemodynamic Research Center (NHRC). The potentially
identifying demographic details have been modified. The case presented and ensuing discussion is author's opinion, has not been peer-reviewed
and does not represent an official statement or recommendation from the NHRC or its members."
 Case Report
In our institution we use a modified SAFE 4. Migliaro F, Sodano A, Capasso L, Raimondi F.
protocol that integrates the approach suggested Lung ultrasound-guided emergency
by Kharrat et al, and patients are categorized as pneumothorax needle aspiration in a very
cardiac arrest, hemodynamic decompensation, preterm infant. BMJ Case Rep 2014; doi:
respiratory decompensation 18,19. 10.1136/bcr-2014-206803
5. Liu J, Kurepa D, Feletti F, Alonso-Ojembarrena
Bedside ultrasound evaluation shows that basic A, Lovrenski J, Copetti R et al. International
training is sufficient to allow operators, Expert Consensus and Recommendations for
regardless of prior ultrasound experience, to Neonatal Pneumothorax Ultrasound
quickly screen for cardiac tamponade, Diagnosis and Ultrasound-guided
pneumothorax, and pleural effusion, in our Thoracocentesis procedure. J. Vis. Exp. 2020.
experience basically trained fellows have been Doi. 10.3791/603791/60836.
6. Connolly JP, Hemodynamic measurements
able to recognize and treat tension
during a tension pneumothorax. Critical Care
pneumothorax and tamponade20.
Medicine 1993; 21;2.
Importantly, lung ultrasound cannot 7. Nelson D, Porta C, Satterly S, Blair K, Johnson
differentiate PTX from tPTX . Cardiac 16 E, Inaba K et al., Physiology and
ultrasound, however, is capable of discerning cardiovascular effect of severe tension
pneumothorax in a porcine model. Journal of
between the two (small hyperkinetic cardiac
Surgical Research 2013; March,
chambers or hypokinetic right ventricle, dilated
doi:10.1016/j.jss.2013.05.057.
IVC, mediastinal shift)12,13. 8. Pavéz P. N. Interacción cardiopulmonar en el
In our patient, as soon as PTX was identified, a neumotórax durante la ventilación mecánica.
cardiac ultrasound was performed, and tension Caso clínico. Rev Chil Med Intensiv 2021;
36(1):38-45.
physiology was described.
9. Rutherford RB, Hurt HH Jr, Brickman RD, Tubb
JM. The pathophysiology of progressive
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" Copyright. All rights reserved. This is an educational activity undertaken to facilitate sharing of opinions, provoke critical thinking and discussions.
The accuracy of data, steps to ensure and protect patient confidentiality such as obtaining informed consent, institutional approvals and waiver
of consent are wholesome responsibility of the reporting authors and not the Neonatal Hemodynamic Research Center (NHRC). The potentially
identifying demographic details have been modified. The case presented and ensuing discussion is author's opinion, has not been peer-reviewed
and does not represent an official statement or recommendation from the NHRC or its members."
 Case Report
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04183-z.

" Copyright. All rights reserved. This is an educational activity undertaken to facilitate sharing of opinions, provoke critical thinking and discussions.
The accuracy of data, steps to ensure and protect patient confidentiality such as obtaining informed consent, institutional approvals and waiver
of consent are wholesome responsibility of the reporting authors and not the Neonatal Hemodynamic Research Center (NHRC). The potentially
identifying demographic details have been modified. The case presented and ensuing discussion is author's opinion, has not been peer-reviewed
and does not represent an official statement or recommendation from the NHRC or its members."