Arrhythmia as a

Hypovolemic Shock
Manifestation in
Daily Practice
Ricko Ciady, Nurwahyudi
Department of Cardiology and
Vascular Medicine,
Dr. Haji Koesnadi General Hospital,
Bondowoso, Indonesia

Introduction Discussion Conclusion

As a primary care physician with limited resources we often
facing a hard decision either to give an aggressive fluid
resuscitation or combining between fluid resuscitation
and inotropic agent in a shock with hypovolemic
mimicking cardiogenic shock. More over in remote and
limited resources to make a diagnosis
Sinus tachycardia as a secondary respond from the
body to maintain hemodynamic imbalance due the
bleeding, by increase the rate to maintain cardiac
output and peripheral perfusion. Usually after
adequate resuscitation given, sinus tachycardia
will be diminished into sinus rhythm as the volume
depletion resolved. But in some circumstance when
Based on this case, we conclude that the principles
cause from this inappropriate sinus tachycardia (IST) is
stunned myocardium which is occurred by ischemia in
myocardium due to hypovolemic shock. [1-7]
Early aggressive therapy on fluid and blood
replacement are proven as main modality to treat

01
Case Description
A 21-year-old woman was admitted with altered mental
status after having profuse bleeding due to labor,
vitals sign blood pressure is 70/30, heart rate 170 beat
per minute, respiration rate is 32 per minute, body
temperature is 35.9 Celsius.
On systemic examination inferior palpebral
conjunctiva was anemic, there was rhonchi on bilateral
thorax and murmur was found along with retraction
on suprasternal and intercostal, decrease tissue turgor,
delayed capillary refill time (CRT) and profuse bleeding
from vagina. Laboratory finding showed anemia with
hemoglobin level 5,7 g/dl. Electrocardiogram (ECG)
showed inappropriate sinus tachycardia (IST) before
and after adequate fluid resuscitation was given. In ED
patient also given a prescription of tranexamic acid
intravenously to treat the bleeding and vasoactive
agents such as norepinephrine to treat low blood
pressure.
After anemia being corrected with blood
transfusion, the patient was underwent emergency
curettage for suspected restrained placenta. At time
when PPH solved, hemodynamic status become stable
and ECG is back to sinus rhythm again. The patient
was discharged on third day after having intensive care
and being monitored for her ECG, which shown no
abnormalities.
the biochemical intervene on cellular level can cause hemorrhagic shock. At the end we recommended fluid
prolonged arrhythmia. challenge as a therapy and basic modality test to every
physician to treat the hypovolemic shock and also
Hypovolemic shock results from depletion of differentiate it from cardiogenic shock.
intravascular volume, whether extracellular fluid
loss or blood loss. The body will compensate with
increased sympathetic tone resulting in increased heart
rate, increased cardiac contractility, and peripheral fin.
vasoconstriction. First there will be change in vital sign
include an increased in diastolic blood pressure with
narrowed pulse pressure as we found in this patient.
If left untreated, the systolic blood pressure drops as
the volume continues to decrease. As a result, oxygen
Figures
delivery to vital organs is unable to meet oxygen
demand. Cells switch from aerobic metabolism to
anaerobic metabolism, resulting in lactic acidosis. As
sympathetic drive increases, blood flow is diverted
from other organs to preserve blood flow to the heart
and brain. This propagates tissue ischemia and worsen
lactic acidosis.
Furthermore, this condition affected heart
myocardium. It is undergo what we called stunned
myocardium, a condition when heart has dysfunction
after having transient ischemia which trigger a
catecholamine-mediated factor which contribute
to autonomic dysfunction and potentially induced
tachycardia and hypotension. All these factors
contribute to inappropriate sinus tachycardia in this
Figure 1 Monitor ECG when patient was admitted showing IST
patient. Other mechanism which can explain this
condition is an act from pro-anti-inflammatory agent
induced by severe bleeding. It could be resulting
in oxidative stress and cardiac dysfunction like
hypokinetic of left ventricle (LV). And why in this
patient, after having a correction in fluid and blood
loss, all the abnormalities was found in physical
examination related to cardiomyopathy diminished?.
The answer is role of innervation of cardiac adrenergic
and alpha-lipoid-acid (ALA), helps recovery LV in
Figure 2 ECG during resuscitation
stunned myocardium.

02 03 Figure 3 ECG normal sinus rhythm after resuscitation

[1] Taghavi S, Askari R. Shock, Hypovolemic. StatPearls. 2018

[2] O.N. K, J.D. R, J.E. W, D.T. P, A. C, E.B. V, et al. Shock - Classification and Pathophysiological Principles of Therapeutics. Curr Cardiol Rev. 2019
[3] Rhee JW, Sabatine MS, Lilly LS. “Ischemic heart disease”, in Pathophysiology of heart disease. Baltimore:Lippincott Williams& Wilkins. 2011. pp.144,170
[4] HS L, C H. Stunned Myocardium due to Decompensation from Hypovolemic Shock in a Pregnant Woman with Uterine Atony Following Cesarean Section. J Clin Exp Cardiolog. 2016;07(05):5–9
[5] Depre C, Vatner SF. Cardioprotection in stunned and hibernating myocardium. Heart Fail Rev. 2007
[6] Shavelle DM, Gersh BJ, Bax JJ, Saperia GM. Pathophysiology of stunned or hibernating myocardium. 2017
[7] Camici PG, Prasad SK, Rimoldi OE. Stunning, Hibernation, and Assessment of Myocardial Viability. Circulation [Internet]. 2008;117(1):103–14 [accessed: June 2019]
Available from: https://www.ahajournals.org/ doi/10.1161CIRCULATIONAHA.107.702993
[8] Binz S, McCollester J, Thomas S, Miller J, Pohlman T, Waxman D, et al. CRASH-2 Study of Tranexamic Acid to Treat Bleeding in Trauma Patients: A Controversy Fueled by Science and Social Media.
J Blood Transfus. 2015;2015(2):1–12
[9] Roberts I, Shakur H, Coats T, Hunt B, Balogun E, Barnetson L, et al. The CRASH-2 trial: A randomised controlled trial and economic evaluation of the effects of tranexamic acid on death, vascular occlusive
events and transfusion requirement in bleeding trauma patients. Health Technol Assess (Rockv).2013
[10] Herget-Rosenthal S, Saner F, Chawla LS. Approach to Hemodynamic Shock and Vasopressors. Clin J Am Soc Nephrol. 2008;3(2):546–53.
[11] He B, Kong L, Ge J. Viewpoint Cardiogenic Shock : Dopamine or Norepinepherine ? It ’ s a question. Cardiol Plus Mar. 2017;2(1):2–5
[12] Hollenberg SM. Vasoactive drugs in circulatory shock. Am J Respir Crit Care Med. 2011;183(7):847–55.
[13] VanValkinburgh D, McGuigan JJ. Inotropes And Vasopressors. [Updated 2019 Mar 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. [accessed: June 2019] Available from:
https://www.ncbi.nlm.nih.gov/books NBK482411/