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\begin{document}

\title{Cardiorenal syndrome type I recovery post heart rate correction -
Cardiac Output is not only stroke volume.}



\author[1]{Ossama Maadarani}%
\author[1]{zouheir Bitar}%
\author[2]{Tamer Zaalouk}%
\author[1]{Boutros Hana}%
\author[1]{Mohamed Elhabibi}%
\author[1]{Moataz Aldaher}%
\author[1]{Adnan Hajjia}%
\affil[1]{Ahmadi Hospital}%
\affil[2]{Borg Alarab central hospital}%


\vspace{-1em}



  
  \date{May 25, 2024}


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\selectlanguage{english}
\begin{abstract}
Bradyarrhhtmias can cause low cardiac output (CO) state despite normal
left ventricular ejection fraction and normal stroke volume. CO defined
as product of the heart rate (HR) and SV. Cardiorenal syndrome (CRS)
type I can be a consequences of Low CO state secondary to slow HR%
\end{abstract}%



\sloppy


\textbf{Cardiorenal syndrome type I recovery post heart rate correction
- Cardiac Output is not only stroke volume.}

Ossama Maadarani 1, Zouheir Bitar 1, Tamer Zaalouk 2, Boutros Hanna 1,
Mohamad Elhabibi 1, Moataz Aldaher 1, Adnan Hajjia 3

1-- Internal Medicine Department/Critical care department, Ahmadi
Hospital -- Kuwait Oil Company, Al Ahmadi, Kuwait

2- Critical care department, Borg Alarab central hospital- Alexandria,
Egypt

3- Clinical Pharmacy Department, Ahmadi Hospital -- Kuwait Oil Company,
Al Ahmadi, Kuwait

Abstract

Bradyarrhhtmias can cause low cardiac output (CO) state despite normal
left ventricular ejection fraction and normal stroke volume. CO defined
as product of the heart rate (HR) and SV. Cardiorenal syndrome (CRS)
type I can be a consequences of Low CO state secondary to slow HR

Keywords:

Heart rate, Cardiac output, Cardio-renal syndrome, pacemaker

Cardiorenal syndrome is an umbrella of disorders of heart and kidney in
either an acute or chronic fashion where the determinant factors in
pathophysiology are the hemodynamic cross-talk between these organs and
the neurohormonal mechanisms. Cardiac output is the product of the heart
rate and the stroke volume which implies that the reduction of any these
components can cause low cardiac output state. Cardiac output can be
calculated non-invasively using Transthoracic Echocardiography which has
high levels of reliability and reproducibility in experienced hand. We
describe a case of a patient where bradarrhythmia was responsible for
low cardiac output state, despite normal ejection fraction, that
manifested clinically in cardiorenal syndrome type I and resolved
completely after pacemaker insertion.

1 \textbar{}CASE REPORT

An 78-year-old female patient with history of hypertension and
dyslipidemia presented to emergency department with acute dizziness and
severe general fatigue of few hours duration. She denied chest pain or
shortness of breath and she did not experience similar symptoms before.
She had no history of kidney disease previously and her kidney function
reported normal one month back on routine check-up. Her chronic
medication included amlodipine 5 mg once daily and atorvastatin 40 mg
once daily. Physical examination was remarkable for overweight (body
mass index 29 kg/m2), severe bradycardia of 30 beat per minute of
regular rate, blood pressure of 150/80 mmHg, normal respiratory rate and
oxygen saturation. Neurological, chest and abdominal examination were
unremarkable. Cardiovascular examination was remarkable for severe
bradycardia with no additional heart sounds or murmurs. Her
electrocardiogram revealed high grade Atrioventricular (AV) block in
form of Second degree heart block with P: QRS ratio of 3:1 or higher,
causing extremely slow ventricular rate (Figure 1).Patient admitted to
critical care unit for continuous monitoring of vital signs. Her
Laboratory results showed Haemoglobin of 12 g/dl, normal coagulation
profile and normal liver function test. Serum electrolytes were also
normal apart from mildly elevated serum potassium and elevated serum
lactate of 3 mmol/L. Her kidney function revealed creatinine of 203
\selectlanguage{greek}μ\selectlanguage{english}mol/L, blood urea nitrogen (BUN) of 28.5 mmol/L and albumin of 3.5 g/dL
which are new findings for her as compared with her baseline level one
month back. Urine analysis showed no evidence of urinary tract infection
and no other abnormality .Computed tomography of brain revealed no
neurological insult. Her Echocardiography study revealed normal left
ventricular size and systolic function with estimated ejection fraction
of 65\% and grade I diastolic dysfunction. No significant valvular
pathology and normal function of right ventricle. Stroke volume (SV) was
calculated using echocardiographic measurement of velocity time integral
(VTI) at the left ventricular outflow tract (LVOT) (Figure 2) and
cross-sectional area ( CSA) of LVOT at aortic annulus and was of 65 ml
per beat which is within the normal range, however due to low
ventricular rate, the cardiac output was only of 1.9 Liter per minute
and cardiac index of 1.1 liter per minute per meter2 (L/M/M2) and these
value can explain the low cardiac output state.

To improve ventricular rate the patient was give atropine of 1 mg twice
with no significant response and then dopamine infusion started. During
stay in critical care patient remained dizzy with normal blood pressure
recording with no improvement of heart rate despite dopamine infusion of
15 mic/kg/min. Follow up of renal function after 12 hours showed more
raising of creatinine and BUN and she was anuric and remained
bradycardic

Patient was diagnosed as an acute kidney injury and cardiorenal syndrome
type I due to low cardiac output state related to low ventricular rate
that most probably due to progressive atherosclerotic changes in the
atrioventricular node. The decision was to insert temporary Transvenous
single lead pacemaker with target heart rate of 60 beat per minute
(B/min) (Figure 3) and higher to improve cardiac output. With heart rate
of 60 B/min her cardiac output increased from 1.9 to 3.9 liter per
minute. 2 hours post insertion of pacemaker the patient symptoms
disappeared and urine output improved with gradual recovery of the
kidney function. Permanent pacemaker inserted later on and patient
discharged from hospital with normal kidney function.

In our case it was a key to recognize early the state of low cardia
output state secondary to bradyarrhythmia with subsequent manifestation
of acute kidney injury and cardiorenal syndrome type I. This early
recognition lead to successful treatment with Transvenous pacemaker.

DISCUSSION

Cardiac output measurement is an important parameter in cardiac function
assessment. The two components that defined CO are HR and SV and the
product of these 2 components will determine the amount of blood pumped
by the heart per each minute. The amount of blood that pushed out of the
ventricles with every beat called stroke volume. The 3 variables that
determine the SV are preload, contractility, and afterload of each
ventricle. Depending on the metabolic needs of the body the range of
cardiac output can widely vary. Cardiac index is defined as the cardiac
output divided by the body surface area.

Transthoracic echocardiography (TTE) is a non-invasive tool that can be
used to calculate the stroke volume of the left ventricle by measuring
the following variables: 1- the velocity-time integral (VTI) at LVOT and
2- the cross-sectional area of the LVOT (1'). VTI is the distance that
blood travels with each beat. Using pulse wave (PW) Doppler at LVOT site
from Apical 5-Chamber View, the operator can trace the LVOT signal and
get the value of LVOT VTI in centimeter (Figure2) (2'). On the other
hand cross-sectional area of LVOT at aortic annulus can be calculated by
measuring LVOT dimeter at aortic annulus in centimeter from Parasternal
Long Axis View (2'). Assuming a circular geometry of the LVOT, CSA of
LVOT can be calculated through the following formula: \selectlanguage{greek}π \selectlanguage{english}(D/2)2 where D
is LVOT diameter and \selectlanguage{greek}π \selectlanguage{english}value is approximately 3.14. Having the above
mentioned parameters, the SV can be calculated from the following
formula: SV at LVOT (cm3) = CSA (cm2) x VTI (cm). Once Stroke volume
value calculated then cardiac output is the product of SV by heart rate.
The CO calculation using TTE has shown very good correlation with
thermodilution-derived cardiac output measurements (3') that considered
gold standard of CO measurement.

CRS is an umbrella of pathologies of heart and kidney in which
dysfunction of one organ may lead to similar dysfunction of the other
organ and can be either in an acute or chronic condition (4').Based on
which organ failing first, in 2008 two major categories had been
identified as cardiorenal and renocardiac syndromes(5'). The sequential
involvement of organs and the acuity of disease can distinguish 5 types
of CRS according to the Consensus Conference of the Acute Dialysis
Quality Initiative. CRS type I and II consistent of acute and chronic
cardiorenal syndrome respectively, whereas CRS type III and IV imply
acute and chronic renocardiac syndrome respectively. CRS type 5 is a
secondary CRS where a systemic process resulting in heart failure and
kidney failure. The determinant factors in pathophysiology of CRS are
the hemodynamic cross-talk between organs and the activation of
neurohormonal systems (Renin Angiotensin Aldosterone axis, sympathetic
nervous system, and arginine vasopressin secretion), which will take
place as a response to hemodynamic factors (6). The venous congestion or
reduction in the cardiac output as a result of cardiac dysfunction will
lead to reduction in glomeral filtration rate (GFR) in CRS Type I and II
(7'). Type I CRS is a common condition in 25\% to 33\% of patients
admitted with acute decompensated heart failure (8'). Ronco et al
described in the literature 4 subtypes of type I CRS (9'). Subtype 1 of
CRS type I consistent of new cardiac injury with subsequent new kidney
injury whereas subtype 2 is a new cardiac injury that result in
acute-on-chronic kidney injury. Subtype 3 happens when an
acute-on-chronic cardiac decompensation leads to new kidney injury and
whenever acute-on-chronic cardiac decompensation leads to
acute-on-chronic kidney injury, subtype 4 considered (9'). Aoun et al
reported a case of severe bradycardia as a reversible cause of
cardio-renal --cerebral syndrome (10).

Our case demonstrated a subtype 1 of CRS type I when a bradyarrhythmia
resulted in denovo cardiac injury and low cardiac output state that
subsequently led to acute kidney injury. Early recognition of the role
of severe bradyarrhythmia in the low cardiac output state using TTE
resulted in early correction of a reversible cause with subsequent
recovery of kidney function.

CONCLUSION

Cardiac output is not only stroke volume. Severe bradyarrhythmia can be
a cause of low cardiac output state and lead to cardiorenal syndrome
type I.

CONFLICT OF INTEREST

The author(s) declare no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article

AUTHOR CONTRIBUTIONS

OM: wrote the article, ZB and TZ shared in the discussion and, with
MA,BH,MA and AH, in collecting the data and revision of the manuscript.
Our working website is www.kockw.com (Kuwait Oil Company, Ahamdi
Hospital).

CONSENT

Informed consent was obtained from the patient for the publication of
this case report.

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available from the
corresponding author upon reasonable request.

Reference

1- Quinones MA, Otto CM, Stoddard M, Wagonner A, Zoqhbi WA, et al.
Recommendations for Quantification of Doppler echocardiography: a report
from the Doppler quantification task force of the nomenclature and
standards committee of the American society of echocardiography. J Am
Soc Echocardiogr 2002;15:167-84.

2- McLean AS, Needham A, Stewart D, Parkin R. Estimation of cardiac
output by noninvasive echocardiographic techniques in the critically ill
subject. Anaesth Intensive Care. 1997;25:250--4.

3- Mercado P, Maizel J,Beyls C, et al. Transthoracic echocardiography:
an accurate and precise method for estimating cardiac output in the
critically ill patient. Mercado et al. Critical Care (2017) 21:136 DOI
10.1186/s13054-017-1737-7

4- Rangaswami J , Bhalla V ,Blair J, et al . Cardiorenal Syndrome:
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5- Ronco C, Haapio M, House AA, Anavekar N, Bellomo R. Cardiorenal
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6- Schrier RW, Abraham WT. Hormones and hemodynamics in heart failure. N
Engl J Med. 1999;341:577--585. doi: 10.1056/NEJM199908193410806.

7- Gnanaraj J and Radhakrishnan J. Cardio-renal syndrome {[}version 1;
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(doi: 10.12688/f1000research.8004.1).

8- Ronco C, McCullough PA, Anker SD, et al., Acute Dialysis Quality
Initiative (ADQI) Consensus Group. Cardiorenal syndromes: an executive
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9 - Ronco C, Cicoira M, McCullough P. Cardiorenal Syndrome Type 1:
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Dysfunction in the Setting of Acutely Decompensated Heart Failure. J Am
Coll Cardiol. 2012;60(12):1031--42.

10-Aoun M, Tabbah R. Case report: severe bradycardia, a reversible cause
of ''Cardio-Renal-Cerebral Syndrome''. BMC Nephrol. 2016 Oct
26;17(1):162. doi: 10.1186/s12882-016-0375-7. PMID: 27784284; PMCID:
PMC5081674.

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