Dr. Somedeb Ball

Chairperson : Prof. Dr. Soura Mookherjee

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

MR Angio

Abdomen

Ilio-caval

fistula

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

The circulation is a consumer-led economy!

Just like electricity, it isthe consumer not the

producer that determinescurrent flow.

It is the tissues not the heartthat determine cardiac output.

CO = SV × HR(70 ml)

CO = BP ÷ SVR(5 lit/min)

CI = CO ÷ BSA

( 3 lit/min/sqm)

“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!!

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

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

COMMON CAUSES.. Chronic Anaemia

Beri beri (wet)

A-V fistula ( shunt)

Hyperthyroidism

Pregnancy

Paget’s disease

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 NeurohormonalActivation (SNS, RAS and Vasopressin)

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 supplyor, increased consumption because of metabolic demand

Two theories are put forward1. Vasodilator theory ( critical role of Adenosine)2. Oxygen lack theory / Nutrient lack theory

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 precapillarysphincters, metarterioles and arterioles to cause their Dilatation

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

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

Case 2…

35 years old female presented with SOB & swelling of both feet for last 2 wks ; no h/o sore throat, PND,chestpain,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/lpitting 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

INVESTIGATIONS

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

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.

GENOMIC EFFECT

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

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

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

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

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!!

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

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

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 shuntingand markedly increased blood flow through vascular Pagetic bone

Failure is relatively rare except in patients with concomitant cardiac pathology

HEMODYNAMICS IN PREGNANACY

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

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

THANK

YOU