A 49-year-old man presented with shortness of breath and orthopnea for 3 months. Examination found tachycardia, elevated blood pressure, basal crackles, and leg swelling. His history included spine surgery 2 years prior. Imaging found an ilio-caval fistula. Fistulas can be congenital or acquired, and the increase in cardiac output depends on fistula size and flow. Management of high-output cardiac failure depends on treating the underlying cause.

1. Dr. Somedeb Ball
Chairperson : Prof. Dr. Soura Mookherjee

2. Case 1…
49 years old male,non smoker and non alcoholic,
neither diabetic nor hypertensive , presented with c/o progressively
increasing shortness of breath with features of Orthopnoea for last
3 months ; occasional h/o PND; no h/o prior heart disease
O/E pulse 120/min ,BP- 200/110 mmHg ; S3 + , Basal rales +,pedal
oedema present
He has a history of undergoing Lumber spine surgery 2 yrs
back

3. MR Angio
Abdomen
Ilio-caval
fistula

4. SYSTEMIC A-V FISTULA
 Types - A. Congenital
e.g. Osler-Weber-Rendu disease
Parks Weber syndrome
Klippel Trenauay syndrome
B. Acquired
Trauma
Iatrogenic – Dialysis
Spine surgery
 Extent of increase in CO depends on Physical size and
Flow magnitude of the Fistula

6. The circulation is a
consumer-led economy!
Just like electricity, it is
the consumer not the
producer that determines
current flow.
It is the tissues not the heart
that determine cardiac output.

8. CO = SV × HR
(70 ml)
CO = BP ÷ SVR
(5 lit/min)
CI = CO ÷ BSA
( 3 lit/min/sqm)

9. “Normal BP” = High SVR x Low CO
(e.g. Hemorrhagic or
cardiogenic shock)
“Normal BP” =
“Normal BP” =
Normal SVR x Normal CO
(e.g. Healthy person)
Low SVR x High CO
(e.g. Sepsis)
Blood pressure, while important, does not tell the whole story
about health of the circulation. CO and SVR are important too!!

11. HIGH OUTPUT STATE
 A high Cardiac Output state has been described as being
> 8 lit/min or a Cardiac Index of > 3.9l/min/sqm
 Some authors suggest that the term “High output heart
failure” is a misnomer as the heart is intrinsically normal
and is capable of generating a high CO
 Others stated that in High output states, Heart failure
occurs only when there is underlying heart disease

12.  It is likely that in chronic High Output states, heart failure
occurs due to deterioration of already present heart disease
or in most cases development of it
 A persistent High output state gives rise to
Ventricular dilatation and/or,Hypertrophy
Persistent Tachycardia
Functional Valvular abnormalities
- all of which may culminate in Heart Failure

13. COMMON CAUSES..
 Chronic Anaemia
 Beri beri (wet)
 A-V fistula ( shunt)
 Hyperthyroidism
 Pregnancy
 Paget’s disease

15. NODAL REGULATOR OF
HEMODYNAMICS - SVR
• The underlying primary hemodynamic alteration in
HOCF is - Fall in SVR
• Reduction in SVR occurs due to
Systemic arterio-venous shunting
or, Peripheral Vasodilatation
• Secondary to fall in SVR –there occurs Neurohormonal
Activation (SNS, RAS and Vasopressin)

17. ACUTE LOCAL BLOOD FLOW
REGULATION
 Decrease in O2 saturation to 25% of normal
- causes increase in tissue blood flow by 3 fold !!!
 O2 saturation can decline due to- either reduced supply
or, increased consumption because of metabolic demand
 Two theories are put forward
1. Vasodilator theory ( critical role of Adenosine)
2. Oxygen lack theory / Nutrient lack theory

18. Vasodilator theory…
 Due to less availability of O2 or increased rate of
metabolism – there occurs Rate of formation of
Vasodilator substances
e.g. Adenosine or its Phosphate compounds
Carbon di-oxide
Histamine
Potassium or Hydrogen ions
 These substances diffuse through the tissues to precapillary
sphincters, metarterioles and arterioles to cause their
Dilatation

20. O2 Lack theory..
 Oxygen is one of the most important metabolic nutrients
needed for vascular smooth muscle contraction
 So, Lack of O2 or increased utilization of it by tissues
would theoreticaly decrease the availability of O2 for
smooth muscle cells of local blood vessels
Relaxation of those smooth muscle cells causing Local
Vasodilatation

22. Concept of Vasomotion
 At the origin of capillary, there is a Precapillary Sphincter
which is either completely open or completely closed
 Their cyclical opening and closing is called Vasomotion
 No of open Precapillary Sphincters at any given time is
roughly proportonal to the nutrition requirements of the
tissue

24. Case 2…
35 years old female presented with SOB & swelling of
both feet for last 2 wks ; no h/o sore throat, PND,chest
pain,oliguria or hematuria; no h/o cardiac ailments in the
past; non smoker non alcoholic ,no significant drug history.
O/E – Afebrile, pulse 112/min irregularly irregular , BP
140/70 mmHg, RR 22/min , Pallor-mild, JVP raised , b/l
pitting pedal oedema +, postural tremor + ,Thyroid gland
uniformly enlarged both lobes, Tender hepatomegaly ;
Apex – lt 5th ICS just outside MCL, hyperdynamic , Grade 3
pansystolic flow murmur over mitral area

25. INVESTIGATIONS

26. INVESTIGATIONS
 Hb 11.5 gm/dl
 Free T3 7.75 ng/dl
 Free T4 4.48 ng/dl
 TSH 0.035 micIU/ml
 US Thyroid – Diffuse enlargement of both lobes

27. Effect of Thyroid Hormones on
Heart..
Thyroid hormones act on heart by two modes of action
1. Direct Genomic effect on Transcription of
specific and non specific cardiac genes.
2. Non genomic action on Plasma membrane,
Mitochondria and Sarcoplasmic Reticulum.

28. GENOMIC EFFECT

29. NON GENOMIC ACTION
 Probably explains the rapid hemodynamic changes following systemic
administration of Thyroid hormones (e.g. increase in CO following i.v.
injection of T3)
 It causes acute increase in inotropic activity by-
Prolongs Na channel opening in the inactivation phase
Increase the intracellular uptake of Na.
Increase intracellular Ca by modulation of Na- Ca exchanger
 Directly acting on L-type Ca channel- increases the Ca entry into the
cardiac myocytes

31. Case 3..
50 yrs old man with type 2 DM, Hypertension,
diabetic neuropathy and Alcohol dependence and tobacco
abuse presented with a 25 lb weight gain over last 2.5 months
,abdominal distension and lower extremity oedema
O/E – lungs clear, pulse regular, no murmur,rub,
gallop or S3; Abdomen distended; 1 + peripheral as well as
sacral oedema

32. Case 3 continues..
He was investigated for Alcoholic Cirrhosis and
discharged on Frusemide 40 mg BD and Spironolactone 25
mg OD
3 wks later …
he again returned with worsening oedema and
abdominal distension and a new onset Dyspnoea at rest ;
on enquiry it was found that he was taking the prescribed
medications but was still drinking alcohol regularly

33. on examination..
His blood alcohol level was 266 mg/dl on admission
pulse 110 / min ,regular ; BP 130/44 mmHg, RR 20/min
2 + peripheral and sacral oedema
Bibasal rales + , S3 + , 4/6 Ejection systolic murmur
Cognition and Cerebellar function intact

34. Lab..
MCV 104.7 Folate level -
CXR – Cardiomegaly with lung congestion
ECG - Sinus tachycardia
On 3rd day of hospital admission, emergent Thiamine
replacement trial was given..
Dramatic improvement within next 24 hrs!!

38. Pathophysiology of HOCF in
Thiamine deficiency..
 Thiamine is needed for the generation of very important co-
factor of enzymes of TCA cycle / Oxidative Phosphorylation
 So due to its deficiency , there is ATP synthesis
 Lack of ATP hampers vascular smooth muscle contraction –
leading to Vasodilatation and subsequent reduction in SVR
 Additionally Thiamine deficiency is thought to cause direct
myocardial injury also

40. CHRONIC ANAEMIA
 Chronic Anaemia causes low SVR by
- 1. Increased renal and vascular NOS activity
2. Low blood Viscosity
3. Vasodilatation due to Hypoxia
 Treatment directed to correction of cause
 Cautious blood transfusion is critical as rapid volume expansion
may aggrevate pulmonary oedema

42. HOCF IN PAGET’S DISEASE
 CVS complications are noted in patients with involvement of
large (15-35%) skeleton and a high degree of disease activity
( ALP – 4 times above normal)
 High output state occurs due to Extensive A-V shunting
and markedly increased blood flow through vascular
Pagetic bone
 Failure is relatively rare except in patients with concomitant
cardiac pathology

43. HEMODYNAMICS IN PREGNANACY

45. During Labour and Delivery..
 Abrupt Hemodynamic changes
 Due to each uterine contraction,approx 500 ml of blood is
released into circulation – causing rapid increase in CO
and BP
 CO reaches 50% above baseline in 2nd stage of labour
and even higher during Delivery

46. Following Delivery..
 Following delivery, there occurs increase in Venous return
because of-
a. Auto transfusion of blood from uterus (24-72 hrs post
delivery)
b. Baby no longer compresses IVC

48. THANK
YOU