Pathophysiological basis of haemodynamic alteration in high output heart failure
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Transcript of Pathophysiological basis of haemodynamic alteration in high output heart failure
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
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.
“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
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.
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
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