FINAL Thesis To Upload

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LIST OF CONTENTS
S.NO. LIST OF CONTENTS PAGE
NO.
1 INTRODUCTION
2 AIMS AND OBJECTIVES
3 REVIEW OF LITERATURE
4 MATERIALS AND METHODS
5 RESULTS AND OBSERVATION
6 DISCUSSION
7 CONCLUSION
8. SUMMARY
9 LIMITATIONS
10 CLINICAL PROFORMA
11 REFERENCES
12 MASTER CHART
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LIST OF FIGURES
S.NO. LIST OF FIGURES PAGE
NO.
1 Figure 1: The development of acute decompensated heart failure
(ADHF)
2 Figure 2 : The Framingham criteria
3 Figure 3 : The American College of Cardiology/ American Heart
Association Grading
4 Figure 4 : Classification of Acute decompensated heart failure.
5 Figure 5 : According to their initial clinical presentation
6 Figure 6: Management protocol
7 Figure : 7: schematic diagram of clinical profile
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LIST OF TABLES
S.NO. LIST OF TABLES PAGE

NO.
1 TABLE 1 : Bar diagram showing SEX DISTRIBUTION
2 TABLE 2 : Bar diagram showing distribution of ANAEMIA
3 TABLE 3 : Bar diagram showing distribution of CYANOSIS
4 TABLE 4 : Pie diagram showing distribution of JAUNDICE
5 TABLE 5 : Bar diagram showing distribution of EDEMA
6 TABLE 6 : Pie diagram showing distribution of JVP
7 TABLE 7 : Pie diagram showing distribution of STEVENSON
8 TABLE 8 : Bar diagram showing distribution of S3 Heart sound
9 TABLE 9 : Pie diagram showing distribution of CREPTS
10 TABLE 10 : Pie diagram showing distribution of HEPATOMEGALY
11 TABLE 11 : Pie diagram showing distribution of MENTAL STATUS
12 TABLE 12 : BAR diagram showing distribution of BIOMARKERS
13 TABLE 13 : BAR diagram showing distribution of CHEST X RAY
14 TABLE 14 : BAR diagram showing distribution of CONGESTION
15 TABLE 15 : BAR diagram showing distribution of EFFUSSION
16 TABLE 16 : BAR diagram showing distribution of RSIK FACTORS
17 TABLE 17 : STATISTICAL ANALYSIS
18 Graph 17 : BAR diagram showing distribution of NHYA
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CLASSIFICATION
19 TABLE 18 : BAR diagram showing distribution of STATISTICAL
ANALYSIS OF RHC PCWP
ANALYSIS OF CI
ANALYSIS OF CO
22 TABLE 21: BAR diagram showing distribution of STATISTICAL
ANALYSIS OF PVR
ANALYSIS OF SVR
ANALYSIS OF PA PRESSURE
CORRELATION BETWEEN EDEMA AND CO
ANALYSIS OF S3
CORRELATION OF PA PRESUURE WITH HEPATOMEGALY
CORRELATION OF MENTAL STATUS
CORRELATION OF PA PRESSURE WITH EFFUSION
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31 TABLE 30: BAR diagram showing distribution of PEARSON
STATISTICAL CORRELATION OF STEVENSON
32 TABLE 31: Histogram diagram showing distribution of PEARSON
STATISTICAL CORRELATION OF QRS COMPLEX
33 TABLE 32: Histogram diagram showing distribution of PEARSON
STATISTICAL CORRELATION OF RHC PCWP
34 TABLE 33: Histogram diagram showing PROBNP
35 TABLE 34: COMPARATIVE STUDIES OF PCWP, mm Hg
36 TABLE 35 :DISTRIBUTION OF NUMBER OF SUBJECTS WITH
DESIGNATED H&P EXAMINATION .
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LIST OF GRAPHS
S.NO. LIST OF GRAPHS PAGE NO.
1 Graph 1 : Bar diagram showing SEX DISTRIBUTION
2 Graph 2 : Bar diagram showing distribution of ANAEMIA
3 Graph 3 : Bar diagram showing distribution of CYANOSIS
4 Graph 4 : Pie diagram showing distribution of JAUNDICE
5 Graph 5 : Bar diagram showing distribution of EDEMA
6 Graph 6 : Pie diagram showing distribution of JVP
7 Graph 7 : Pie diagram showing distribution of STEVENSON
8 Graph 8 : Bar diagram showing distribution of S3 Heart sound
9 Graph 9 : Pie diagram showing distribution of CREPTS
10 Graph 10 : Pie diagram showing distribution of HEPATOMEGALY
11 Graph 11 : Pie diagram showing distribution of MENTAL STATUS
12 Graph 12 : BAR diagram showing distribution of BIOMARKERS
13 Graph 13 : BAR diagram showing distribution of CHEST X RAY
14 Graph 14 : BAR diagram showing distribution of CONGESTION
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15 Graph 15 : BAR diagram showing distribution of EFFUSSION
16 Graph 16 : BAR diagram showing distribution of RSIK FACTORS
17 TABLE 17 : STATISTICAL ANALYSIS
18 Graph 17 : BAR diagram showing distribution of NHYA
CLASSIFICATION
19 Graph 18 : BAR diagram showing distribution of STATISTICAL
ANALYSIS OF CI
ANALYSIS OF CO
22 Graph 21: BAR diagram showing distribution of STATISTICAL
ANALYSIS OF PVR
ANALYSIS OF SVR
ANALYSIS OF PA PRESSURE
CORRELATION BETWEEN EDEMA AND CO
ANALYSIS OF S3
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CORRELATION OF PA PRESUURE WITH HEPATOMEGALY
CORRELATION OF MENTAL STATUS
CORRELATION OF PA PRESSURE WITH EFFUSION
31 Graph 30: BAR diagram showing distribution of PEARSON
STATISTICAL CORRELATION OF STEVENSON
32 Graph 31: Histogram diagram showing distribution of PEARSON
STATISTICAL CORRELATION OF QRS COMPLEX
33 Graph 32: Histogram diagram showing distribution of PEARSON
STATISTICAL CORRELATION OF RHC PCWP
34 Graph 33: Histogram diagram showing PROBNP
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LIST OF ABBRVATIONS
ACC- American College of Cardiology
AHA-American Heart Association
ACE -Angiotensin converting
enzyme ADHF-Acute decompensated
HF
ANP -Atrial natriuretic
peptide BMI-Body mass index
BNP- Brain natriuretic
peptide CHD- coronary heart
disease CHF- Congestive
heart failure CI -Cardiac index
CO -Cardiac output
HF -Heart failure
HTX-Heart transplantation
HOT-Hypertension Optimal Treatment
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ICD-International Classification of Diseases
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IL -interleukins
JVP- Jugular venous pressure
LV -Left ventricle
LVEF- Left ventricle ejection fraction
NPR-A-Natriuretic peptide receptor A
NT-proBNP -N-terminal pro-brain natriuretic peptide ,
PA Pressure -Pulmonary artery pressure
PCWP-Pulmonary capillary wedge
pressure PVR-Peripheral vascular
resistance
SBP- Systolic blood pressure SVR
—Systemic vascular resistance
SPO2-Oxygen saturation
RHC-Right heart
catheterization RHD-Rheumatic
heart disease TNF -tumour
necrosis factor
TGF- Ttransforming growth factor
UKPDS-United Kingdom Prospective Diabetes
Study WHO-World health organization
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ABSTRACT
Background: Patients with ADHF may persist for prolonged times with hemodynamic
abnormalities. Patients with heart failure may remain in a hemodynamic state consistent with
cardiogenic shock and congestion for prolonged periods of time. However, data on the
impact of persistent hemodynamic abnormalities are limited.
Aim of the study : To study “Correlation between clinical status in ADHF and
hemodynamic assessment by Right Heart Catheterization”
Materials and Methods : Prospective study done in the Department of cardiology , KIMS
hospital ,Secunderabad for duration of 3 years ie, from December 1st 2021 to January 31st
2023 .
Results: Mean age was 46.2 years .Males (63.4%) were predominant compared to females (
36.6% ).M:F ratio – 1.7:1.Raised JVP noted in 95.1% cases.Wet ,cold noted in 36.6% cases.
And wet ,warm noted in 63.4% cases. Majority were class III constituting 46.3% , class II
occupied 36.6% and class IV were 17.1%,. There is no statistical correlation of RHC PCWP
with NYHA classification with p value 0.28.There is no statistical correlation of cardiac index
with NYHA classification with p value 0.58.There is no statistical correlation of cardiac output
with NYHA classification with p value 0.37
Conclusion: Clinical assessment can be used to define profiles in patients admitted with
ADHF. These profiles predict outcomes and may be used to guide therapy and identify
populations for future investigations. However in this study ,there is inconsistent correlation of
clinical parameters with intrinsic haemodynamic measurement. However, a significant number
of patients were on additional therapy like vasopressors and IABP supports . Furthermore
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studies are needed to answer this question thoroughly .
INTRODUCTION
Heart failure (HF) is the end stage of all diseases of the heart and is a major cause of
morbidity and mortality. According to American College of Cardiology (ACC), Heart failure
is a complex clinical syndrome that results from any structural or functional impairment of
ventricular filling or ejection of blood. Acute decompensated heart failure (ADHF) has
emerged as a major public health problem over the past 2 decades.1,2
Heart Failure is the leading cause of hospitalization in patients older than 65 years of age3.
Acute decompensated HF (ADHF) is defined as the acute or gradual onset of clinical
progression of HF necessitating urgent medical care. In- hospital published mortality rates of
ADHF in the US and Europe range from 4% to 7%. Similar data are not available for HF
from India.
The major symptoms of Acute decompensated heart failure (ADHF)—shortness of breath,
congestion, and fatigue—are not specific for cardiac and circulatory failure. They may be
caused by other conditions which mimic Heart Failure, complicating the identification of
patients with this syndrome. Various forms of pulmonary disease, including pneumonia,
reactive airway disease and pulmonary embolus, may be especially difficult to differentiate
clinically from HF.
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EPIDEMIOLOGY HF IN INDIA:
In 2001, Mendez and Cowie4 found that population-based Heart failure (HF) studies in all
developing countries including India not properly done because of lack of proper
surveillance system and making is difficult to estimate global prevalence.
In 1949 Vakil5 reported The epidemiology of Heart failure (HF) in India, in his study
report, hypertension-coronary (31%), RHD (29%), syphilis (12%), and pulmonary (9%) as
the primary causes in hospitalized due to Heart failure (HF).
Reddy et al.6 estimated the prevalence of obesity (BMI >30 kg/m2) in 10 970 participants
from urban Delhi and rural Haryana in 2002 to be 6.8%.
Based his study upon prevalence for obesity estimated was 5%, so the total number of heart
failure (HF) patients accrued could range from 900 000–1.5 million; with an estimated 50%
mortality at 5 years, the prevalence of HF due to obesity alone could be estimated to range
from 450 000 to 750 000.
Recent study also provided only limited data on in India, since these have focused on
specific aetiologies of HF (such as HF caused by endomyocardial fibrosis and ST-segment
elevation myocardial infarction), and these performed in tertiary care hospitals,7 rather than
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community-based surveillance.
In 2000, 30 million people with coronary heart disease (CHD) alone in India, or a nearly
3% prevalence. The annual incidence of Heart failure (HF) for patients with CHD
ranges from 0.4% to 2.3% per year,
According to a study conducted by Seth S et al8 the proportion deaths from ADHF in Indian
population was found 10%,
The prevalence of other risk factors of Heart failure (HF) is also rising in India. It is projected
that to increase prevalence of hypertension from 118 million (2000) to 214 million (2025).
And as demonstrated in the Hypertension Optimal Treatment (HOT) and United Kingdom
Prospective Diabetes Study (UKPDS) trials Incidence of HF in patients with a systolic blood
pressure (SBP) of is 0.1% to 0.6%, so it is predicted that, then the number of new Heart
failure (HF) cases due to hypertension may increase from 118 000–708 000 per year in 2000
to 2021 1.3 million per year in 2025, After 5 years of HF incidence based upon year 2000
estimates for hypertension, the total number of HF patients occurred could range from 590
000 to 3.5 million; with an estimated 50% mortality at 5 years, the prevalence of HF due to
hypertension alone could be estimated to range from 295 000 to 1.8 million.,9,10
Obesity is also proven risk factor for heart failure (HF)11. In the Framingham Heart Study,
the annual incidence of HF due to obesity (body mass index [BMI] >30 kg/m2) has been
estimated to increase by 0.3% in women and 0.5% in men,
2
Few studies in India have used a BMI threshold of 30 kg/m2, which makes it difficult
to accurately estimate the prevalence of obesity.
AIM OF THE STUDY
AIM OF THE STUDY : To study “Correlation between clinical status in ADHF and
hemodynamic assessment by Right Heart Catheterization”
Its objectives:
To evaluate clinical status in ADHF.
To obtain hemodynamic parameters by Right Heart Catheterization.
To study Correlation between clinical status in ADHF and hemodynamic assessment by
Right heart catheterization.( PCWP,CI , MPA , CO , PVR , SVR )
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REVIEW OF LITERATURE
Acute decompensated heart failure (ADHF) is one of the most common hospital diagnoses
globally, although its pathogenesis is unknown and treatment options are limited. In-hospital
morbidity and mortality are significant in ADHF patients, as are frequent rehospitalizations and
consequent cardiovascular death. This heinous clinical trajectory is owing in part to inefficient
medical management of ADHF, with persisting congestion after hospital release and insufficient
pre discharge commencement of life-saving guideline-directed medications. While new
medications for the treatment of chronic heart failure continue to be licensed, no new therapies
for ADHF have been approved in decades.12
Epidemiology
ADHF has remained an entity with an incomplete aetiology and limited treatment choices.
Although medications for the treatment of chronic heart failure continue to be developed, and
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the
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arsenal of guideline-directed medical interventions is extensive, the same cannot be said for the
treatment of ADHF. This is clinically significant since acute heart failure (AHF) occurrences
and repeat hospitalizations are linked to a worse prognosis and progressive multi organ failure1.
In the United States and Europe, over 1 million people are hospitalized for heart failure each
year, with a staggering 24% readmission rate within 30 days and 50% within 6 months. Patients
who are readmitted for cardiovascular disease within 90 days of being discharged from a
hospital for heart failure have a greater chance of death, regardless of the exact period from
discharge13,14,15
One in every six individuals brought to the hospital for heart failure dies within 30 days 16. The
disparity between the bleak statistics for ADHF and the optimistic future of chronic HF therapy
highlights the need for a deeper understanding of the separate entity of ADHF. Furthermore,
poor medical therapy of ADHF frequently results in chronic congestion after hospital discharge,
as well as an increased risk of recurrent hospitalization, morbidity, and mortality 17.In response to
the stagnant clinical outcomes associated with ADHF, the American College of Cardiology
published an expert consensus decision route in 2019 to aid in risk assessment, management, and
evaluation of the clinical trajectory of ADHF patients18.
There are various reasons why global AHF data is so scarce. The syndrome's differential coding,
combined with complex variances in case definitions, makes straightforward regional
comparison impossible. AHF and chronic HF are classified as intermediate conditions rather
than underlying causes of death by the International Classification of Diseases (ICD) system.
The ICD also does not differentiate between de novo and ADHF as reasons for hospitalization.
There is no global data on the proportion of HFrEF and HFpEF as underlying causes of AHF.
Annual HF hospitalizations in the United States and Europe approach one million in both
regions8. More than 90% of these hospitalizations were caused by symptoms and signs of fluid
buildup (indicating AHF). Furthermore, one in every four patients (24%) is re-admitted within
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30 days, and readmission rates for AHF in the first three months following hospitalization may
approach 30%
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in the United States and other countries. Within 6 months, one in every four patients (50%) is
19,20
readmitted Recurrent fluid buildup in patients with HF has been consistently linked to
poorer outcomes, regardless of age or renal function9. Multiple studies of the 30-day to 90-day
post- discharge period have found that 25-30% of AHF patients are readmitted over this time
frame 21- 25
However, a significant proportion of these patients are readmitted for reasons other than heart
failure. Medical comorbidities cause rehospitalization and, when untreated, lead to the
26,27
progression of HF. Anxiety, depression, cognitive impairment, and social isolation are also
associated with a higher risk of unplanned recurrent readmission or death in individuals who
have been hospitalized with AHF28.
National data on the prevalence of AHF or chronic HF in low- and middle-income countries are
lacking. All HF registries for these locations are based on hospital registries that included only
individuals admitted for AHF, with no distinction made between de novo HF and ADHF. Data
from several of the important registries have recently been summarized 29, but the focus is on
aetiology, risk factors, sociodemographic profile, and mortality. One of the largest registries, the
INTER-CHF project, reported on 5,823 patients with HF from 108 center's throughout six
geographical regions25. The total 1-year mortality rate was 16.5%, with Africa (34%) and India
(23%), around average mortality in Southeast Asia (15%), and the lowest mortality in China
(7%), South America (9%), and the Middle East (9%)30
SCENARIO IN INDIA
Mendez and Cowie4 discovered in 2001 that population-based heart failure (HF) studies in all
poor nations, including India, were not carried out correctly due to a lack of a proper monitoring
system, making it difficult to determine global prevalence. In 1949, Vakil published The
Epidemiology of Heart Failure (HF) in India, citing hypertension-coronary (31%), RHD (29%),
syphilis (12%), and pulmonary (9%) as the leading reasons of hospitalisation for HF. Recent
2
studies have also offered only limited data on HF in India, because these have concentrated on
specific aetiologies of HF(such as HF caused by endomyocardial fibrosis and ST-segment
elevation myocardial infarction), and these have been undertaken in tertiary care hospitals7
rather than community-based surveillance.
In 2000, 30 million persons in India had coronary heart disease (CHD), representing a nearly 3%
prevalence. The annual incidence of heart failure (HF) in CHD patients ranges from 0.4% to
2.3%. Other risk factors for heart failure (HF) are also becoming more prevalent in India. The
prevalence of hypertension is expected to rise from 118 million in 2000 to 214 million by 2025.
As demonstrated in the Hypertension Optimal Treatment (HOT) and United Kingdom
Prospective Diabetes Study (UKPDS) trials, the incidence of HF in patients with a systolic blood
pressure (SBP) of is 0.1% to 0.6%, so the number of new Heart failure (HF) cases due to
hypertension may increase from 118 000-708 000 per year in 2000 to 2021 1.3 million per year
in 2025. Based on year 2000 hypertension estimates, the total number of HF patients could
range from 590 000 to
3.5 million after 5 years; with an estimated 50% mortality at 5 years, the prevalence of HF due
to hypertension alone could range from 295 000 to 1.8 million.32-35
Obesity has also been linked to an increased risk of heart failure (HF). According to the
Framingham Heart Study, the annual incidence of HF owing to obesity (BMI >30 kg/m2)
increases by 0.3% in women and 0.5% in men. Few research in India have utilized a BMI
criterion of 30 kg/m2, making it difficult to assess the prevalence of obesity accurately. Obesity
(BMI >30 kg/m2) was assessed to be 6.8% in 10 970 participants from urban Delhi and rural
Haryana in 2002 by Reddy et al.6. Based on his study's estimated 5% obesity prevalence, the
overall number of heart failure (HF) patients might range from 900 000 to 1.5 million; with an
estimated 50% mortality at 5 years, the prevalence of HF owing to obesity alone could range
from 450 000 to 750.
2
Acute decompensated heart failure (ADHF) is described as the sudden or gradual beginning of
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clinical progression of HF requiring immediate medical attention. ADHF in-hospital mortality
rates in the United States and Europe range from 4% to 7%. Similar data for HF from India are
not available. The control arm of published Indian studies in HF therapeutic trials shows a 6-
month death rate of roughly 10%. Unlike in Western populations, rheumatic heart disease
(RHD) is a major source of illness and mortality in India. According to a study conducted by
Seth S et al8 10% of deaths in the Indian population are caused by ADHF.
DEFINITION & PATHOPHYSIOLOGY
Patients with ADHF are more likely to present with signs and symptoms of congestion and fluid
retention (weight gain, exertional dyspnoea, orthopnoea, dependent edema) than with pulmonary
oedema or cardiogenic shock, which are hallmarks of acute LV systolic failure. This is due to
chronic, frequently dysregulated, neuro-humoral compensatory processes that act to maintain a
stable haemodynamic condition despite deteriorating LV performance. Decompensation occurs
when the balance shifts towards fluid overload because the compensatory mechanisms are
insufficient or fail entirely. This is supported by data from the IMPACT-HF registry, which
demonstrates that acute decompensated heart disease takes a more insidious course, with patients
presenting to hospital in extremis following reported symptoms of congestion days or even
weeks before their admission32
The degree of systolic and diastolic cardiac dysfunction, the relative involvement of the right
and left ventricles, the arterial and venous vascular tone, the neurohormonal and inflammatory
activation state, and comorbid contributing influences are just a few of the variables that affect
the pathophysiology of ADHF. The distinction between the underlying substrate and
pathophysiology of chronic (Heart failure with reduced ejection fraction) HFrEF and HFpEF
further complicates the standardisation of ADHF therapy. The central defect in HFrEF is easily
understood as being reduced systolic function with ensuing increases in left ventricular filling
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pressures and diastolic
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dysfunction producing increased pulmonary venous pressures and congestion, frequently leading
to right HF and peripheral signs of congestion, coupled with decreased cardiac output leading to
end-organ hypoperfusion and dysfunction.
The pathophysiology of HFpEF, however, is more complex and poorly understood. It is thought
to be connected, in part, to peripheral arterial stiffness and vasoconstriction affecting afterload,
cardiomyocyte hypertrophy and fibrosis, impaired compliance and diastolic filling of the left
ventricle, microvascular inflammation, and altered adrenergic-adipokine signalling. 37,38,39 There
are few chronic treatment options available for patients with HFpEF, most of which concentrate
on the management of comorbidities. Additionally, because of severe logistical constraints
associated with the acuity and frequently clinical severity of patients admitted with ADHF, the
vast majority of landmark studies and current guideline-directed medical therapy have only been
shown to have a significant clinical benefit in the chronic HF patient population.
This background pathophysiologic environment, in which compensated HF has established a
complex balance between preload, afterload, intrinsic inotropy, and neurohormonal signalling, is
the setting in which ADHF develops (Figure). There is a strong interdependence that, if changed,
can lead to elevated intracardiac filling pressures, venous and arterial congestion and
vasoconstriction, as well as reduced inotropy, which in turn leads to ADHF. End-organ injury
and feedback signaling, pulmonary insults, and certain comorbidities are additional important
contributors.
Figure 01: The development of acute decompensated heart failure (ADHF) and available
medicinal treatments are complicated by the interdependence of cardiac and multi-organ
involvement. NIV stands for non-invasive ventilation, BNP/ANP stands for B-type/atrial
natriuretic peptide, and RAAS stands for renin-angiotensin-aldosterone system.
2
Figure 01: The development of acute decompensated heart failure (ADHF)
Intravascular Congestion40,41
The most prevalent ADHF symptoms and signs are directly related to intravascular
congestion18, which can be brought on by a variety of interrelated factors, such as sodium
retention due to renal dysfunction, dietary indiscretion, or noncompliance with prescribed
medication, increased left ventricular filling pressures that result in increased pulmonary and
central venous congestion, or rapid central redistribution of intravascular volume from
peripheral or splanchnic sources. Multiple positive feedback interactions caused by progressive
intravascular fluid volume expansion or redistribution32 aggravate the onset of ADHF. For
instance, neurohormonal-induced vascular redistribution into the central venous system may
result in elevated central venous pressures, which may impair renal function and increase salt
and fluid retention, which in turn increases intravascular volume and cardiac preload. Given that
both HFpEF and HFrEF frequently have diastolic dysfunction, the extra preload will raise end-
diastolic pressures, causing more ventricular wall stress and myocardial oxygen consumption,
further deteriorating diastolic function. Expanded ventricular volumes can cause or worsen
functional mitral or tricuspid regurgitation, raising venous pressures and potentially impairing
renal function.
2
This example makes it clear that there are various potential triggers for this cycle, as well as
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numerous potential points at which to intervene. Concurrent or subsequent valve illness,
particularly mitral regurgitation, is an additional contributing element to consider when
considering congestion reasons, as was mentioned in the example above. Retrograde blood flow
brought on by mitral regurgitation immediately raises pulmonary pressures and congestion. It
can be classified as primary dysfunction brought on by structural abnormalities or secondary
dysfunction brought on by effects of the mitral apparatus, left ventricular dysfunction, or left
ventricular or atrial dilatation.33 It is generally recognized that patients with HFrEF who have
moderate or severe mitral regurgitation experience worse clinical outcomes.33,34,35
Initiating diuresis and using vasodilators to treat these pathophysiologic mechanisms can help
the clinical signs of intravascular congestion. To focus on treatment options, it can be
challenging to identify the main causative component. In patients admitted with ADHF,
invasive examination with right cardiac catheterization may be helpful to direct aggressive
diuresis and determine whether to begin vasodilator treatments. Once euvoluemia is
reached in patients who have moderate to severe mitral regurgitation during ADHF, the
degree of the regurgitation should be re-evaluated to determine whether additional transcatheter
or surgical intervention is necessary. Importantly, even when clinical congestion has subsided,
considerable hemodynamic congestion frequently persists. Patients admitted with AHF and
treated insufficiently with diuretics are more likely to relapse to a clinically congested state
with repeated hospital stays if the issue is not resolved prior to release. With a relative lack of
symptoms, hemodynamic congestion can arrive before clinical congestion by up to weeks.
Continuous pulmonary artery pressure monitoring has made it possible to analyze data and-
confirm a link between high filling pressures and the risk of cardiovascular events.37
Inotropy
Myocardial contractility, which is created by the thick and thin filament cross-bridges of myosin
and actin, is necessary for inotropy.38,39Calcium availability boosts the binding strength by
3
activating the thin filament, boosting cross-bridge production, and enhancing contractility.
Ischemia, myocarditis, valvular disease, pericardial illness, arrhythmias, toxic cardiomyopathies,
and aberrant metabolic processes are clinical conditions that alter inotropy. One mechanism of
advanced diastolic dysfunction is decreased compliance and end-diastolic volume, resulting in
lower stroke volume. Systolic dysfunction is characterised by a direct inotropic derangement.
Cardiogenic shock is typically described as hypotension 90 mm Hg, a cardiac index 2.2 L/min
perm2, and symptoms of end-organ hypoperfusion such as decreased urine output, chilly
extremities, altered mental status, and elevated serum lactate. The severity and acuity of
inotropic dysfunction can cause this condition. 40 Decreased systolic function can play a
significant part in the aetiology of ADHF, and in carefully chosen patients, it offers an important
therapeutic target even in the absence of shock. Fortunately, cardiogenic shock only accounts for
a small fraction of cases with ADHF. Acute coronary syndromes must also be identified and
treated as a potential underlying or aggravating cause of the systolic dysfunction.
Venous and Arterial Vasoconstriction
Another significant factor in the development of ADHF is dynamic changes in vascular tone. As
mentioned above, splanchnic and peripheral venous vasoconstriction increases can cause a
significant volume redistribution to the central venous system. Significant and sudden rises in
central venous pressure are brought on by this redistribution and direct central venous
vasoconstriction, which can impair renal and right ventricular function. In ADHF, increasing left
ventricular filling pressures, preexisting pulmonary hypertension, and hypoventilation-related
pulmonary artery vasoconstriction are typically detected as increased pulmonary arterial
pressures. Systemic vascular resistance increases are primarily mediated by arteriolar
vasoconstriction, which causes increased left ventricular pressures that exacerbate myocardial
ischemia, increase ventricular wall stress, and cause myocardial damage.
Particularly when there is underlying systemic hypertension and endothelial impairment, the
3
substantial sympathetic activation linked to ADHF can worsen arterial vasoconstriction.
Importantly, as part of a loop mechanism, decreased baroreceptor
activation causes signalling to paradoxically enhance peripheral artery vasoconstriction, which
negatively affects afterload in ADHF with lower cardiac output. Particularly in the presence of
diastolic dysfunction and HFpEF, abrupt and frequently dramatic increases in afterload brought
on by sympathetic system activation in ADHF can lead to the rapid development of pulmonary
congestion or flash pulmonary edoema.
Neurohormonal Signalling
Renin-angiotensin-aldosterone system imbalance and feedback signalling can lead to harmful
hemodynamic alterations and the release of circulating proteins that act as clinical indicators in
ADHF.An enzyme called renin, which the kidneys secrete, alerts angiotensin I to the activation
of angiotensinogen. Vascular endothelium releases ACE (angiotensin-converting enzyme) to
cleave angiotensin I into active angiotensin II. Increased systemic vascular resistance is the
result of angiotensin II signalling vasoconstriction both directly on vascular endothelium and via
release of vasopressin and norepinephrine. Additionally, it triggers the production of aldosterone
from the adrenal glands and activates renal sodium transporters to promote glomerular sodium
reabsorption. Aldosterone increases glomerular salt and water reabsorption by directly impacting
the kidneys. When there are indicators of reduced renal perfusion or elevated sympathetic
nervous system activation, the renin-angiotensin-aldosterone system is triggered. The
paradoxical worsening of ADHF is caused by increased vasoconstriction and volume retention
as a result of the overall activity. The production of endothelin-1, one of the most potent
vasoconstrictors, by vascular endothelial cells, which causes the peripheral vascular smooth
muscle to contract, is stimulated in ADHF. Endothelin-1 expression is elevated in chronic HF
and systemic hypertension.42,43
Myocardial cells release BNP (B-type natriuretic peptides), which signal for vasodilation,
3
decreased renin activity, and eventual diuresis, when the ventricular chamber dilates due to an
increase in volume or pressure. PreproBNP, an inactive form of BNP produced by the ventricles,
is cleaved by enzymes into proBNP, which is then further broken down into active BNP and
inactive N-terminal-proBNP. The active form, known as BNP, indicates suppression of the
sympathetic nervous system, endothelin activity, and the renin-angiotensin-aldosterone system.
Due to its longer half-life and inability to be altered by sacubitril's neprilysin inhibition, NT-
proBNP is a more stable indicator of intravascular congestion and left ventricular failure than
BNP.
Atrial myocardial cells release ANP (Atrial natriuretic peptide) in response to atrial dilatation,
but sympathetic activity can also signal through -adrenergic activation. Natriuretic peptide
receptor A (NPR-A), which is extensively expressed in the kidney and vascular endothelium, is
the binding site for both ANP and BNP. When NPR-A and, to a lesser extent, NPR-B are bound,
guanylyl cyclase is activated, indicating the formation of cyclic guanosine monophosphate. The
main signalling molecule used by natriuretic peptides to promote vasodilation and diuresis while
suppressing mitogenesis, inflammation, and tissue hypertrophy is cyclic guanosine
monophosphate. Neprilysin, a circulating endopeptidase, and insulin-degrading enzymes both
cleave and inactivate natriuretic peptides. Neprilysin has also been demonstrated to degrade and
inactivate angiotensin II.
Natriuretic peptides and other proteins specific to the cardiovascular system have been employed
often as biomarkers because of their direct roles in ADHF, and many of them are being
investigated as potential treatment targets. Major guideline committees have included explicit
recommendations for widely used biomarkers including BNP, NT-proBNP, and troponin,
including the American College of Cardiology Foundation/American Heart Association and
European Society of Cardiology.44,45
Circulating biomarkers have played two functions in clinical trials in relation to one another. First
3
off, natriuretic peptides are a sign of increased risk for rehospitalization and cardiovascular death
in patients admitted for ADHF and can therefore be used to enrich the patient group that has
been enrolled for clinical events that may be subject to modifiable risk factors.It is widely
known that some subgroups of HF patients may not exhibit the normal BNP or NT-proBNP
elevation during episodes of HF, which has a negative impact on participation in studies that call
for increased levels to be included.46,47
Numerous studies have shown that troponin, a measure of myocardial damage in patients
hospitalised for ADHF, has prognostic value.46-50
In studies of ADHF treatments, baseline troponin levels could be employed, similar to how
natriuretic peptides are, to enhance the patient population for possibly modifiable events.
Indicating the prospect that medicines may be able to target the immediate myocardial injury in
ADHF and potentially enhance intermediate-term clinical outcomes is the shift
in troponin during the early stage of admission, which has also been demonstrated to be
predictive.50,51
ST2 and galectin-3 are novel myocardial damage and stretch indicators with predictive value in
ADHF that are being verified in ongoing investigations. ST2 is a member of the IL-1 family of
inflammatory signalling molecules. Elevated ST2 levels are also a sign of fibrosis and
unfavourable cardiac remodelling.51,52,53
In ADHF, it has consistently connected with vascular obstruction and in particular with New
York Heart Association class, with greater serum levels being associated with higher 1-year
cardiovascular mortality in patients.53,54 Galectin-3, a lectin molecule with antiapoptotic activity
discovered to enhance cardiac fibroblast activity leading to left ventricular failure, is another
developing biomarker.55-57 By tracking blood levels in patients, ST2 and Galectin-3 in
combination with BNP during hospitalization provide a better prognostic assessment even
though their molecular roles are still unclear.
3
Inflammation
TNF (tumour necrosis factor), TGF- (transforming growth factor), IL (interleukins)-6, and IL-1
are among the cytokines recognized to play a role in the pathogenesis of HF.58-60 These cytokine
cascades, which individually have the ability to cause endothelial dysfunction, pulmonary
edema, and left ventricular failure, are thought to play a role in some of the clinical
manifestations of HF. A more precise use of treatment strategies may be made possible by a
better comprehension of the role played by inflammatory mediators in the pathophysiology
of ADHF. While the neurohormonal activation and oxidative stress that are associated with
ADHF may be the primary causes of these inflammatory cytokine cascades, there is
evidence of increased bacterial or endotoxin translocation in ADHF, which may be linked to
gut edoema or relative hypoperfusion.61 High-sensitivity C-reactive protein levels have also
been found to be elevated in ADHF, supporting an elevated inflammatory state.62 In a study that
evaluated the biomarkers of patients admitted for ADHF across a range of EFs, inflammatory
biomarkers were elevated in patients with reduced, mid-range, and preserved EFs, and markers
of inflammation had predictive value for cardiovascular outcomes in patients with HF with
mid-range EF and HFpEF.63 These results imply that medicines that target decreasing
inflammatory signaling may be useful in treating ADHF. Comorbidities
When talking about ADHF, comorbidities are important to take into account because they act as
risk factors as well as complications that affect prognosis both during and after hospitalisations
for ADHF.64-66
Data from numerous significant AHF trials were compiled by the European Society of
Cardiology. Cardiovascular comorbidities were noted in HF patients hospitalised for treatment,
including hypertension (present in 70% of patients), coronary artery disease (50%–60%), and
atrial fibrillation (30%–40%).65 Diabetes (40%) renal dysfunction (20%-30%) chronic
obstructive pulmonary disease (20%-30%), and anaemia (15%-30%) were among the
3
noncardiac
3
comorbidities. Cardiac comorbidities in ADHF, such as acute coronary syndromes, hypertensive
urgency/emergency, and clinically severe atrial or ventricular arrhythmias, may require rapid
management.
The function of noncardiac comorbidities and the ideal moment for their therapies is less clear-
cut. Acute hyperglycemia and glycemic variability during cardiac
hospitalisations are associated with worse outcomes; however, data are still inconclusive as to
whether tight glycemic control is beneficial or associated with an increased risk of
rehospitalizations and cardiovascular morbidity and mortality. 66-68 Although a comprehensive
underlying mechanism is not completely understood, hyperglycemia increases endothelial
dysfunction, oxidative stress, the resulting myocardial fibrosis, decreased sarcolemmal calcium
transport, and myocardial metabolism, all of which may affect cardiac function during ADHF
hospitalisations.69
In addition to its effects on treatment restrictions, renal impairment has a high connection with
poor clinical outcomes.70,71 The use of ACE inhibitors, ARBs, and MRAs as well as diuretics is
consistently underdosed or undertreated in these patients when they are treated for heart failure
(HF), regardless of the degree of renal injury relative to baseline. This is either due to concern
for worsening renal function or being constrained by loop diuretic resistance.72-74
It is difficult to distinguish the aetiology of common symptoms, such as dyspnea, palpitations,
and occasionally chest tightness, due to the frequent confounding presence of chronic
obstructive pulmonary disease.75Due to widespread medical myths, patients with established
chronic obstructive pulmonary disease who are admitted with ADHF are also less likely to
receive -blocker therapy and underutilize ACE inhibitors and mineralocorticoid receptor
antagonists.76,77,78
In addition to the endothelial consequences of acute vasoconstriction and hypoxia, the link
between ADHF and chronic obstructive pulmonary disease can be seen in the acute ventilatory
3
and hemodynamic changes superimposed on both chronic pulmonary and cardiac fibrosis and
3
dysfunction.79
Compared to 10% in the general population, anaemia can be seen in up to 50% of patients
hospitalised with ADHF and 30% of patients with CHF. 80,81,82 Anaemia can have a variety of
causes, but iron deficiency anaemia is the most important one in ADHF because it reduces the
ability of red blood cells to carry oxygen, which in turn causes mitochondrial dysfunction,
aberrant sarcomere formation, and eventually left ventricular systolic failure.83,84,85 Importantly,
the existence of iron deficiency, with or without anaemia, is regarded as clinically relevant, and
intravenous iron therapy should be investigated throughout the patient's current hospitalisation. 86
Organ Damage
End-organ damage from ADHF can happen via two basic hemodynamic pathways, including
increased venous and ventricular filling pressures that cause congestion and hypoperfusion
because of either decreased cardiac output or local hemodynamic control. These hemodynamic
consequences can be made worse by elevated inflammation and oxidative stress. The lungs,
kidneys, liver, and intestines are among the commonly impacted organs by congestion. Increased
hydrostatic stresses across leaky pulmonary capillaries brought on by pulmonary congestion
result in pulmonary edoema and, frequently, pleural effusions.87 Alveolar stiffness and
pulmonary fibrosis are brought on by repeated cardiac trauma, which worsens alveolar gas
diffusion and ultimately leads to pulmonary hypertension (WHO Group II) and restrictive
ventilation88,89 The aetiology and treatment of ADHF depend heavily on the interaction of the
heart and kidneys. The renin-angiotensin-aldosterone system, which controls neurohormonal
pathways that further regulate autonomic nervous system activation and vascular endothelium as
previously mentioned, is one of the complex pathways that the renal system uses to signal for
increased or decreased urine output in order to manage preload. Acute renal damage, which can
develop as a result of ADHF or as a triggering cause, affects this system. The five subtypes of
the cardiorenal syndrome have been formally identified, with the combination of inadequate
3
cardiac output, poor renal
3
perfusion, central venous congestion, and increased afterload on the kidneys being the most
important pathophysiology.90,91
The majority of research have indicated that elevated central venous pressure is a considerably
more important component than decreased cardiac output, and some studies have shown that
deteriorating renal function is only a predictor of poor cardiovascular outcomes in the presence
of chronic congestion.92-96
Hepatic congestion is a typical aftereffect of severe cardiac failure and can result in catastrophic
hepatic dysfunction when ADHF is present. Elevated liver enzymes are poor prognostic
indicators on their own, despite being relatively common during admissions for
ADHF.97Furthermore, coagulopathies and biliary cholestasis are examples of separate
consequences that can result from severe hepatic failure. Due to the liver's dual circulatory
system, hypoperfusion as a cause of hepatic dysfunction in ADHF is less frequent. However, as
the name shock implies, it can be observed in cases of severe cardiac malfunction. Splanchnic
arterioles and veins are signalled to constrict during ADHF with increased sympathetic activity
to direct blood flow to vital organs like the heart and brain, which results in hypoperfusion of the
splanchnic system98,99 While it has already been mentioned that changes in gut permeability may
play a role in the elevated inflammatory state in ADHF, the gastrointestinal system also suffers
from increased vascular congestion, which is typically more relevant in the chronic period and
results in gut oedema and decreased absorption. When determining the aetiology of acute
decompensations in patients admitted with ADHF, this is a crucial factor to take into account.100
All of the body's organs can suffer from hypoperfusion brought on by low cardiac output and
increased vascular congestion. Increased sympathetic inotropic and chronotropic stimulation,
elevated ventricular pressures and wall stress, increased afterload as a result of vasoconstriction,
and elevated sympathetic stimulation are all potential causes of supply demand mismatch and
myocardial ischemia or injury in ADHF, particularly in patients with pre-existing coronary
3
disease. The higher troponin levels in patients with ADHF, who do not have an acute coronary
syndrome, clinically reflect this myocardial damage. A crucial indicator of serious cardiac
malfunction, altered mental status, sleepiness, and obtundation are all signs of cerebral
hypoperfusion. To validate transcranial doppler sonography during episodes of ADHF,
noninvasive methods to assess central hypoperfusion have been researched.101,102 Early
identification of cerebral hypoperfusion can help decision-makers determine when inotrope
support is necessary. Repeated trauma is likely to cause chronic brain malfunction and may even
cause early dementia.103
CLINICAL FEATURES34
The most common symptoms include dyspnoea during exercise or at rest, orthopnoea, fatigue,
and reduced exercise tolerance; symptoms are often accompanied by clinical signs such as
peripheral oedema, jugular vein distension, the presence of a third heart sound (known as “S3
gallop”, an early diastolic low-frequency sound that may be present under different
haemodynamic conditions and might represent termination of the rapid filling of the left
ventricle), and pulmonary rales In patients presenting with chest discomfort, the differentiation
between AHF and acute coronary syndrome may be challenging. Symptoms and signs related to
peripheral hypoperfusion, such as cold and clammy skin, altered mental status and oliguria,
characterize cardiogenic shock. Cardiogenic shock, as well as respiratory failure, myocardial
infarction and arrhythmia, should be rapidly excluded during the initial triage of patients
admitted for suspected AHF because these conditions require an appropriate level of monitoring
and specific treatments
The most typical symptoms are dyspnoea, either while exercising or at rest, orthopnoea,
exhaustion, and decreased exercise tolerance. Symptoms are frequently accompanied by clinical
signs like peripheral oedema, jugular vein distension, the presence of a third heart sound (also
known as a "S3 gallop," an early diastolic low-frequency sound that may be present under
3
different haemodynamic conditions and may indicate termination of the rapid filling of the
left. The
3
distinction between AHF and acute coronary syndrome may be difficult in patients who report
with chest discomfort. Cardiogenic shock is characterised by oliguria, impaired mental status,
and skin that is chilly and clammy due to peripheral hypoperfusion. The GWTG-HF score,
which allows stratification into nine categories with in-hospital mortality risks ranging from 1%
to >50%, is calculated by adding the points derived from seven variables (age, systolic blood
pressure, heart rate, blood urea nitrogen, plasma sodium, history of chronic obstructive
pulmonary disease, and black ethnicity) The 30-day mortality in patients with AHF can be
estimated using the MEESSI- AHF score, which contains 13 independent risk variables36
DIAGNOSTIC INVESTIGATIONS
Additional testing is necessary since the clinical picture of AHF is not sensitive or specific
enough to confirm or rule out the diagnosis94. Cardiovascular biomarkers are extremely
important for the diagnosis of AHF. Plasma natriuretic peptides, such as brain natriuretic peptide
(BNP), N-terminal pro-brain natriuretic peptide (NT-proBNP), or mid-regional pro-atrial
natriuretic peptide (MR- proANP), should be measured in patients who have suspected AHF.
Since all cardiovascular indicators are impaired in both patient groups, no diagnostic test can
effectively distinguish between acute heart failure (AHF) and chronic heart failure (CHF).
However, natriuretic peptides have a high sensitivity for diagnosing underlying cardiac disease
in patients who come with acute dyspnoea.Interestingly, dyspnoea in patients whose levels of
circulating natriuretic peptides are normal (or unchanged) is very likely to have a non-cardiac
cause. When a patient has suspected AHF, the detection of natriuretic peptides is advised 98. A
significant rise in circulating natriuretic peptides may signal AHF in patients with persistently
increased natriuretic peptides caused by chronic HF. For patients with increased natriuretic
peptides, additional testing, such as echocardiography or other imaging techniques, are
necessary to confirm the diagnosis of AHF. For diagnostic or predictive reasons, a number of
novel biomarkers reflecting various pathophysiological elements of AHF (such as cardiac
4
damage, systemic congestion, inflammation,
4
and fibrosis) may be helpful, although their place in standard clinical practice is still not clear.
The initial diagnostic procedure ought to involve a thorough assessment of the clinical
phenotype as well as the underlying cardiac diseases, contributing variables, and coexisting
conditions. A "7- P" protocol has been proposed by our M.A. group to direct evaluation and
treatment customization. Phenotype, pathophysiology, precipitants, pathology, polymorbidity,

component104AHF
possible iatrogenic effects, and patient preferences are the seven is frequently
diagnosed clinically using the patient's medical history, clinical symptoms, and circulating
natriuretic peptide measurements. For the initial assessment of AHF, imaging is only useful in
patients with unclear underlying heart conditions (for instance, patients with de novo HF, who
need a more thorough diagnostic procedure than those with ADHF) or uncertain congestion
detection. Echocardiography and lung ultrasonography in these patients may provide useful
information. To assess LV and RV function and rule out serious valve
disease or pericardial tamponade, transthoracic echocardiography should
be done on all patients with de novo HF or in patients with ADHF when a relevant change in
cardiac pathology is detected. Lung ultrasonography has become a useful tool for identifying
and tracking pulmonary congestion in AHF patients. This bedside method makes it possible to
identify interstitial fluid quickly, affordably, and accurately in the pulmonary
parenchyma105,106.
Electrocardiography and (serial) measurement of cardiac troponins should be used to rule out an
ischaemic cause of AHF, such as acute coronary syndromes. Arrhythmias can be assessed using
electrocardiography, continuous electrocardiographic monitoring, or interrogation of implantable
cardioverter-defibrillators in certain patients. Infections can be determined by measuring
inflammatory markers (such as C-reactive protein and procalcitonin) and conducting additional
research. Although they are rarely necessary during the first work-up, additional imaging
modalities (like MRI) may be beneficial during follow-up studies. Additionally, a fundamental
4
review of the operation of other organ systems, such as the kidney, liver, and blood, should be
4
done as part of the initial laboratory evaluation.
DIAGNOSTIC CRITERIA
To diagnose HF, several criteria have been put forth. These include the European Society of
Cardiology criteria, the Framingham criteria, the Boston criteria, the Gothenburg criteria, and so
on. All of them combine information from the medical history, physical exam, and chest
radiograph and rely on similar symptoms and increased filling pressures as their primary
markers. 1] The New York Heart Association (NYHA)13 classification system categorizes heart
failure on a scale of I to IV, as follows:
● Class I: No limitation of physical activity
● Class II: Slight limitation of physical activity
● Class III: Marked limitation of physical activity
● Class IV: Symptoms occur even at rest; discomfort with any physical activity.
FIG 2] : The Framingham criteria
The simultaneous presence of either two main criteria or one major and two minor criteria
constitutes the Framingham criteria for the diagnosis of heart failure.
4
Major criteria comprise the following:
● Paroxysmal nocturnal dyspnoea
● Weight loss of 4.5 kg in 5 days in response to treatment
● Neck vein distention
● Rales
● Acute pulmonary oedema
● Hepatojugular reflux
● S 3 gallop
● Central venous pressure greater than 16 cm water
● Circulation time of 25 seconds or longer
● Radiographic cardiomegaly
● Pulmonary oedema, visceral congestion, or cardiomegaly at autopsy
Minor criteria (accepted only if they cannot be attributed to another medical condition) are as
follows:
● Nocturnal cough
● Dyspnoea on ordinary exertion
● A decrease in vital capacity by one third the maximal value recorded
● Pleural effusion
● Tachycardia (rate of 120 bpm)
● Hepatomegaly
● Bilateral ankle oedema
3] The American College of Cardiology/ American Heart Association Grading
The American College of Cardiology/American Heart Association (ACC/AHA)3 staging system
is defined by the following four stages:
Stage A: High risk of heart failure but no structural heart disease or symptoms of heart failure
4
Stage B: Structural heart disease but no symptoms of heart failure
Stage C: Structural heart disease and symptoms of heart failure
Stage D: Refractory heart failure requiring specialized interventions
FIG 3 : The American College of Cardiology/ American Heart Association Grading
CLASSIFICATION OF ACUTE HEART FAILURE
The definition of AHF described is wide, and numerous attempts to further stratify it have been
made37. A fundamental obstacle to categorizing AHF as a unique entity is that the patient
population is not homogenous, despite the fact that it is distinguished by a particular collection
of signs and symptoms. A wide variety of illness symptoms are present in patients with HF who
are admitted, from severe LV systolic dysfunction and inadequate cardiac output to severe
hypertension and normal or almost normal LV systolic function. Since most AHF patients fall
somewhere in the middle of these two extremes, they also exhibit a distribution of underlying
pathology and precipitants, which results in the common endpoint of fluid overload.
Older European Society of Cardiology recommendations26 divided patients into six groups (I–
VI) based on their clinical and hemodynamic features. More than 90% of hospital admissions
fall into one of the first three categories: ADHF (I), hypertensive AHF (II), or AHF with
pulmonary
4
oedema (III). Patients with AHF and pulmonary
4
oedema (III) have a clinical presentation dominated by respiratory distress and hypoxaemia and
display a continuum of severity from low-output states (IVa) to outright cardiogenic shock
(IVb). Patients with ADHF typically present with mild-moderate symptoms. AHF is
occasionally caused by high-output failure (V), which is linked to diseases such anaemia,
thyrotoxicosis, and Paget's disease. Warm extremities and lung congestion are typical symptoms,
and hypotension may be present in cases of systemic sepsis. Acute myocardial
ischaemia/infarction affecting the right ventricle is also included in the right-sided heart failure
category (VI) of the classification system, which is predominated by individuals with pre-
existing lung illness and cor pulmonale.
fig 4 : Classification of Acute decompensated heart failure
This is a simple classification system that directs the treating doctor's attention to treating the
AHF's underlying causes. The causes of decompensation, however, might not be obvious at first
presentation because patients frequently have a variety of co-morbidities, or there might be
several contributory variables. Therefore, stratifying patients with AHF based on their first
clinical presentation may be more judicious practically. This enables the attending physician to
4
pinpoint
4
people who are most vulnerable and then implement targeted measures such implementing
ionotropic drugs and/or mechanical circulatory support.
Systolic blood pressure (SBP) at admission is one of these markers used to categorize patients.
Patients with AHF typically present with either preserved (90-140 mmHg) or raised (>140
mmHg) SBP, with the latter indicating a better prognosis. This might be because vasodilator
therapy is permitted, which inherently has a hypotensive impact, or it might be because greater
SBP is more frequently observed in conjunction with intact LV function. Systolic hypotension,
which has a bad prognosis and is present in less than 10% of patients, allows for the
categorization of these individuals into higher dependence areas and more severe therapy27.
Stevenson and colleagues28 created a more thorough classification system for individuals who
present with AHF, and it is recommended by the most recent European Society of Cardiology
[1••] guidelines. This method is based on the initial clinical assessment of the patient to take into
account signs and symptoms of peripheral perfusion (cold extremities, oliguria, and narrow pulse
pressure) and congestion (orthopnoea, dependent oedema, elevated jugular venous pulsation),
rather than the underlying aetiology. According to their fluid status, patients are classified as
either "wet" or "dry," and according to the assessment of their perfusion status, as either "cold"
or "warm." The four patient groups identified by this combined clinical
assessment—warm and wet, warm and dry, cold and dry, and cold and wet—allow for initial
stratification as a guide for therapy (Fig.02) and also provide prognosis information [1••]. those
who are warm and dry had an 11% 6-month death rate, compared to 40% for those who are cold
and wet28. This strategy of categorization and risk stratification is a sensible step in the
management of AHF from a practical standpoint.
4
Figure 5 : According to their initial clinical presentation,
MANAGEMENT
Early Management:
A growing body of research shows that delayed therapy administration in AHF107 is linked to
poor outcomes. AHF patients should start receiving therapy as soon as possible, ideally before
being admitted to the hospital. Current guidelines support a "time-to-treatment" approach,
similar to those for acute myocardial infarctions or cerebrovascular accidents. Patients with AHF
should receive adequate non-invasive monitoring in the pre-hospital setting, including
continuous electrocardiography, blood pressure monitoring, and measurements of peripheral
oxygen saturation (SpO2), oxygen supplementation in cases of hypoxia (SpO2 90%), and non-
invasive ventilation in cases of respiratory distress. Patients with cardiogenic pulmonary oedema
may benefit from preclinical non-invasive ventilation therapy since it lowers intubation rates and
improves short-term outcomes. When the clinical diagnosis of AHF is simple, intravenous
4
therapy
4
(often vasodilators and/or diuretics) should be started right once depending on the clinical
phenotype and involved pathophysiology. Diuretics are typically used when there is fluid
retention, whereas vasodilators are used when there is fluid redistribution and preserved systolic
blood pressure (>110 mmHg; caution should be used if the systolic blood pressure is 90-110
mmHg) to lower filling pressures and modulate ventricular-vascular coupling. The usage of
vasodilators is advised by current recommendations. These suggestions may alter, however, in
light of recent findings from randomised clinical trials (such as RELAX-AHF-2, TRUE-AHF,
and GALACTIC) demonstrating no predictive benefit of vasodilatory drugs in AHF. Since
incorrect use of inotropes is linked to arrhythmias, elevated morbidity, and higher mortality108, its
use should be confined to patients in cardiogenic shock due to reduced cardiac contractility.
Notably, pre- hospital care shouldn't prevent a quick hospital transfer, particularly to a facility
with an intensive care unit and/or a cardiology and cardiac care unit. Patients should be
evaluated thoroughly upon admission to the hospital in order to rule out cardiopulmonary
instability (that is, cardiogenic shock and respiratory failure).
In Hospital Management
It is crucial that the treatment plan address both of these problems since people with AHF run
the danger of dying not just from cardiovascular failure but also from the effects of organ
dysfunction brought on by congestion and hypoperfusion. The impact of diuretics on symptoms
and organ congestion is obvious, even though there is limited evidence from randomized
controlled trials that treating congestion improves survival. Initial treatment objectives in
patients with AHF include achieving decongestion without residual fluid retention, optimising
perfusion pressures to preserve organ perfusion, and maintaining or starting disease-modifying
oral therapies directed towards neurohumoral activation because these medications also increase
diuretic response and impotence. Once oxygen saturation has been restored (with oxygen
supplementation, non-invasive ventilation, or mechanical ventilation), these treatments are
4
administered which proves beneficial
4
in long term survival.
Figure 6: Management protocol
The existence of compatible clinical symptoms (such as pulmonary rales, dilated jugular veins,
and peripheral edoema), indications of organ congestion on chest X-ray radiography or lung
ultrasonography, and high filling pressures on invasive monitoring are used to determine the
presence of congestion. The presence of compatible clinical symptoms, such as clammy, cold
skin, oliguria, and altered mental status, as well as additional indicators of abnormal oxygen
transport, such as elevated blood lactate and low central venous or mixed venous oxygen
saturation, are used to diagnose abnormal peripheral perfusion. The effect of positive inotropic
agents (intravenous drugs that increase cardiac contractility), fluid challenge (change in cardiac
output after administration of 250–500 ml of fluids), and vasopressors (intravenous drugs that
increase arterial blood pressure by inducing peripheral vasoconstriction) should be carefully
evaluated by measuring changes in stroke volume, either by echocardiography or by other
4
invasive monitoring
4
systems. SBP is for systolic blood pressure; HFpEF stands for heart failure with preserved
ejection fraction; HFrEF stands for heart failure with reduced ejection fraction.
Decongestive Therapy
Decongestive treatment is similar in patients with HFrEF or HFpEF1 because individuals with
AHF present with a similar congestion profile regardless of their LVEF96 To increase the
efficacy of the decongestive treatment, it should be customised to the haemodynamic
phenotype and underlying pathophysiology and delivered (intravenously, to overcome
restricted enteral absorption caused by gastrointestinal congestion). A thorough description of
the practical application of diuretic therapy may be found in a consensus statement by the Heart
Failure Association of the European Society of Cardiology. Since loop diuretics must be
secreted into the proximal convoluted tubule through a number of organic anion transporters and
are >90% protein- bound by albumin in the blood, diuretic dosage must be altered when renal
blood flow is decreased (as it is in AHF) in order to reach a plasma concentration high
enough to produce the desired effect. However, to maintain the decongestive effect, the
administration of diuretics should continue until euvolaemia is achieved, with three or four
daily doses or continuous infusion. Furthermore, the peak effect of intravenous loop
diuretics occurs within the first hours, with sodium excretion returning to baseline by 6-8
hours.
Within the first few hours following loop diuretic administration, the urine volume output and
spot urinary salt content can be measured to assess the diuretic response75. Spot urinary salt
content measurements are very helpful for patients with low to moderate urine flow. Recent
studies show that in individuals with a low to medium urine output, spot urinary salt
concentration offers independent predictive information in addition to urinary volume
5
output110, but natriuresis is virtually uniformly high in patients producing high urinary
volumes. An hourly urine output of
5
between 100 and 150 ml over the first six hours and/or a spot urinary salt concentration of
between 50 and 70 mmol two hours after loop diuretic treatment in patients with congestion
often suggest an insufficient response to diuretics84
To swiftly intensify the loop diuretic dose (such as by doubling it), identify patients with diuretic
resistance, and reach the ceiling (maximum) dose, early evaluation of the diuretic response is
advised. The addition of another diuretic drug with a different mode of action (sequential
nephron blockage) should be taken into consideration as raising the loop diuretic dose past the
ceiling dose does not result in incremental diuresis and/or natriuresis. Renal replacement
treatment may be used for refractory forms, but studies have not demonstrated that it improves
outcomes109-111 despite the fact that these technologies are quite effective at removing volume.
Diuretic resistance mechanisms and therapeutic strategies have been studied in-depth
elsewhere.112. Until euvolaemia has been reached and the drugs are converted to an oral form,
decongestive therapy should be continued. The lowest dose of loop diuretic therapy required to
used113
maintain euvolemia should then be In clinical practice, quantifying fluid surplus and
identifying euvolaemia may be difficult, necessitating a multimodal strategy that includes
symptoms, clinical indicators, imaging (such as echocardiography, chest X-ray radiography, and
lung ultrasonography), and biomarkers. Other methods, such as data from implanted cardiac
devices, pulmonary artery pressure sensors, bioelectrical impedance analysis, and indicator
dilution techniques, may offer additional insightful data, but their general application is
constrained by technological issues and cost.
Tolvaptan blocks the release of vasopressin, which is generally activated in response to
physiological events such as hypotension, reduced atrial filling, renal hyperosmolarity,
sympathetic activation, or angiotensin II activity and has been demonstrated to be considerably
enhanced in ADHF. Vasopressin signals fluid reabsorption in the kidney directly, and it signals
vasoconstriction in vascular endothelial cells, which raises arterial pressure. Tolvaptan has
5
undergone extensive testing in the hopes of preventing loop diuretic resistance, and in numerous
5
trials in patients with ADHF, it has shown promise in accelerating weight loss and diuresis in
addition to diuretic therapy, but not in significantly improving renal function or overall mortality
Comprehensive Therapy
During the hospital stay, specific therapies for the underlying heart illness and the contributing
causes should be carried out. When cardiac ischemia or infection are the causes of AHF, for
instance, adequate antimicrobial treatment and myocardial revascularization should not be
postponed. Clinicians should be able to predict the need for specific medications for some
specific forms of HF (for example, HF associated with amyloidosis), surgical procedures (for
example, for valvular heart disease), mechanical circulatory support (such as an LV assist
device), or cardiac transplantation based on the comorbidities discovered during the initial
evaluation and treatment. Last but not least, enrolling patients in a thorough multidisciplinary
HF care management programme, encouraging medication compliance, increasing the dosage of
disease-modifying therapy, cardiac rehabilitation, treating underlying comorbidities, and timely
follow-up with the medical staff, is essential.
Long Term Management23
People who survive the initial episode of AHF are more likely to experience subsequent
episodes. Therefore, increasing survival and lowering the likelihood of hospital readmission
owing to further AHF episodes are therapeutic objectives. The main goal of pre-discharge
management is to make sure that the patient's condition has stabilised enough for a secure
hospital discharge. After receiving enough decongestion and stable renal function while
receiving oral medication based on recommended guidelines, patients with AHF are deemed
ready for discharge. The most frequent reason for AHF readmission is congestion, and
continuing congestion and renal failure are recognised indicators of a poor post-discharge
prognosis
Numerous clinical and biochemical markers, such as natriuretic peptides, are used as proxies for
5
congestion, but they cannot be applied consistently to all AHF patients because HF
5
decompensation can occur due to both fluid accumulation and redistribution. Natriuretic
peptides and cardiac troponins have been shown to be helpful in predicting the likelihood of
114,115,116
death and readmission for HF in a number of studies . Pre-discharge natriuretic peptide
levels in AHF patients with considerably increased levels are associated with worse clinical
outcomes, including all-cause and cardiovascular mortality and morbidity, compared to
individuals with lower levels.
The advantages of obtaining particular natriuretic peptide target values before discharge,
however, have not been proven. Even in the absence of obvious myocardial ischaemia,
abnormally high cardiac troponins are frequently found in patients with AHF and are similarly
linked to poor outcomes. IL-1 receptor-like 1, a protein implicated in the process of myocardial
fibrosis and hypertrophy, is another biomarker of myocardial fibrosis that has been linked to
117
disease severity and a poor prognosis in patients with AHF ST2, along with other oxidative
stress, inflammation, and remodeling biomarkers, needs more research and is still in the
preclinical stages. Overall, the main challenge in AHF management continues to be defining and
attaining sufficient decongestion.To improve post-discharge outcomes, implementation of the
medical treatment of triggering causes is advised in addition to ensuring adequate decongestion.
A-adrenergic receptor blockers, angiotensin-converting enzyme inhibitors or angiotensin
receptor-neprilysin inhibitors, and mineralocorticoid receptor antagonists should be continued or
started during hospitalization and gradually titrated thereafter1 in patients with HFrEF because
they are linked to better outcomes. It is advised that comorbidities and precipitating factors be
managed as best as possible in individuals with HFpEF1. During hospitalization, additional
treatments, such as appropriate medications for some particular types of HF or surgical
procedures, should be assessed.
Finally, ensuring a purposeful transition to outpatient care and developing a plan to evaluate and
enhance post-discharge prognosis are key components of pre-discharge management. Since
5
clinicians, patients, carers, and ancillary services must work together to titrate pharmaceutical
5
therapy, monitor fluid volume status and electrolytes, treat comorbidities, start lifestyle changes,
and establish plans for adherence to treatment and emergency care, care coordination for patients
with HF is extremely complex. Prior to release, discussions on the seriousness of the illness,
obstacles to self-care, and advance care planning should start.
The European Society of Cardiology guidelines recommend the first follow-up outpatient visit
within 7 days of discharge, while the American College of Cardiology Foundation-American
Heart Association guidelines for the management of HF recommend the first post-discharge
telephone contact within 3 days and a follow-up visit 7-14 days after discharge. The readmission
rate is a common statistic used to clarify patient characteristics (as indicated above) and health-
care system factors that contribute to HF-related morbidity and mortality, despite the complexity
of factors linked with rehospitalization for HF. These aspects of the health care system include,
for instance, the standard of care delivered, patient education, transitional support, and
medication reconciliation (maintaining an accurate and current list of all the medications a
patient is taking in order to facilitate therapy adjustments whenever the patient is admitted to,
transferred to, or discharged from, a hospital). The costs associated with HF readmissions are
continuing to rise, and there is mounting
evidence that some national health policies, such as the Hospital Readmissions Reduction
Programme in the USA, which were designed to lower these readmissions, may have increased
post-discharge mortality . Actually without admission mortality increased because hospital were
reluctant for admission.
RIGHT HEART CATHETERIZATION
It is an invasive hemodynamic procedure known as right heart catheterization allows for the
precise measurement of right-sided cardiac pressures and the estimation of cardiac output. This
exercise outlines right cardiac catheterization, including its indications, contraindications,
clinical significance, and the role of the interprofessional team for patients who have the
5
procedure done.
5
Historical Background
In 1929, Werner Forssmann, a surgical resident in Germany, inserted a 65 cm urethral catheter
on himself through his left antecubital vein to accomplish the first right heart catheterization on a
human. Afterward, he moved it into the right atrium and injected medication right into the right
heart chambers. Prior to that, in the 1700s, an English vicar named Reverend Stephen Hale
performed equine venous cannulation. In 1844, the physiologist Claude Bernard used glass tubes
to cannulate the jugular veins and carotid arteries of horses in order to determine the
temperatures of both ventricles. Even though it had previously been done on animals, this was
the first time it had been done on a person. This led to the development of the idea of
catheterization operations, which employ catheters inserted through arteries or veins to scan,
diagnose, and treat problems without requiring open surgery. Right cardiac catheterization
methods and the catheters were improved by health professionals. In New York, Andre Frederic
Cournand and Dickinson W. Richards. Their efforts helped to establish the central and
peripheral catheterization techniques that are used today. The three doctors shared the 1956
Nobel Prize in Medicine for their contributions. After that, the right heart catheter was
extensively employed to examine the cardiac and pulmonary hemodynamics in patients with
congenital heart disease and chronic pulmonary disease. Since mixed venous blood from the
pulmonary artery was necessary to calculate cardiac output, the catheter was known as the
pulmonary artery catheter44
A normal pulmonary catheter was modified by Dr. Swan to include a balloon at the catheter's
tip. This enabled for bedside implantation using floatation and allowed for continuous pressure
monitoring of the right atrium and pulmonary arteries. The thermistor at the tip was an invention
by Dr. Ganz that enabled thermodilution to measure cardiac output directly. The pulmonary
artery catheter later came to be known as the "Swan-Ganz" catheter as a result of its widespread
use44,45 Procedure
5
There are numerous pulmonary artery catheters on the market. Some can be utilized for pressure
5
measurements as well as the thermodilution evaluation of cardiac output. Thermodilution
cardiac output evaluation can be done with catheters that have a specific thermistor. The French
sizes of catheters range from 5F to 8F, depending on the manufacturer, and the pulmonary artery
catheter is 110 cm long. Every catheter has a proximal blue port and a distal yellow port. The
third port on the catheter is added by the thermistor45
At the access site, a local anaesthetic is applied subcutaneously. It is possible to gain venous
access with or without ultrasound assistance. In the femoral and jugular sites, access can be
gained with a typical 18-gauge needle or a smaller 21-gauge needle.
Using a 21-gauge needle in the antecubital vein may lessen the possibility of damaging nearby
artery systems. To prevent contamination of the surrounding sterile environment during
ultrasound guidance, an ultrasonic probe sleeve must be sterile. After gaining venous access, a
sheath of the right size is inserted into the vein and fastened. The vein is reached after the
pulmonary artery catheter has been inserted through the sheath. To avoid inflating the balloon
inside the access sheath, the balloon is inflated after the catheter has advanced around 15 cm.
The catheter can then be advanced to the right atrium much more quickly after balloon inflation.
Wire cannulation is not required if the catheter advances readily. When the catheter is pushed
from the internal jugular vein to around 20 cm, the right atrium will be reached. When it is
progressed to about 45 cm from the femoral venous access site, it will reach the right atrium.
However, fluoroscopy can also be used to see the catheter movement.
A pulsatile right atrial waveform can be seen as the catheter enters the right atrium. The system
is zeroed before establishing a reference for pressure measurements. To reach zero, the air-fluid
transducer must be exposed to air for it to equalize with atmospheric pressure. The air-fluid
transducer needs to be at the heart's level when this is being done. Holding the air-fluid
transducer in an imaginary plane between the anterior and posterior chest walls at the level of the
fourth intercostal gap is roughly how this is accomplished. The pressures that are being
5
detected could
5
be artificially high if they are lower than the heart level. The pressures that are being detected
could be unnecessarily low if the transducer is placed higher than the heart level.
After obtaining the right atrial pressure waveform, the catheter is moved to point at the right
ventricle, where the right ventricular pressure is measured. The catheter is then typically moved
to a wedge position to assess the pressure in the pulmonary capillary wedge. After that, the
balloon can be deflated and reinserted a few centimeters into the pulmonary artery to measure
the pressure there. It is crucial to be aware that optimal end-expiration pressure measurements
should be taken at all pressures. Using the distal yellow port, a sample of blood from the
pulmonary artery is taken, and mixed venous oxygen saturation is measured. The Fick method
must be used to obtain arterial saturation independently in order to calculate cardiac output. The
right atrium's proximal blue port can be used to do thermodilution by injecting cold saline there,
where it mixes with blood and the temperature difference is measured by a thermistor. To
determine an average cardiac output and cardiac index, thermodilution has to be performed a
minimum of three times. For the purpose of taking blood samples and calculating oxygen
saturations, the pulmonary artery catheter can be moved and positioned in either the superior or
inferior vena cava. The right atrium or ventricle can be treated in the same way 44,45.
Clinical Significance – as Tool of Hemodynamic Studies
Right heart catheterization can be used to collect a variety of pressure readings and
hemodynamic characteristics. The next sections include a description of the typical parameters
that are assessed as well as the hemodynamic profiles of typical scenarios. 1 to 5 mm Hg is the
range of the normal mean right atrial pressure. The normal range for the systolic and diastolic
pressures of the right ventricle is 15 to 30 mm Hg and 1 to 7 mm Hg, respectively. The normal
systolic and diastolic pressures in the pulmonary arteries are 15 to 30 mm Hg and 4 to 12 mm
Hg, respectively. The average pulmonary artery pressure is around 15 mm Hg. The pulmonary
capillary wedge pressure ranges between 4 and 12 mm Hg46. Calculations of cardiac output,
5
cardiac index, pulmonary
5
vascular resistance, systemic vascular resistance, right ventricle stroke work, pulmonary artery
pulsatility index (PAPi), mitral and aortic valve
areas using the Gorlin equation, and aortic valve area using the Hakki equation can all be done
using the measured pressures48.
Pulmonary or Right Atrial Capillary Pressure Wedge Waveforms
Three positive upstrokes and two positive descents make up the waveform of the right atrial
pressure. Associated with atrial systole, the "a" wave is the first positive upstroke. Atrial
relaxation is indicated by the "x" descent that follows. The "c" wave, which denotes closure of
the tricuspid valve, is the next wave. The subsequent wave is an upstroke "V" wave with a
positive component that shows passive atrial filling during right ventricular contraction. After
the tricuspid valve opens in ventricular diastole, the "v" wave is followed by the "y" descent,
which denotes atrial emptying. The pulmonary capillary wedge waveform has three positive
upstrokes and two negative downstrokes, comparable to the right atrial pressure waveform36.
Due to the loss of the atrial contribution to the waveform in the context of atrial fibrillation, the
"a" wave is lost. An increase in atrial pressure that can happen in tricuspid or mitral stenosis can
cause tall "a" waves. Any condition that might lead to atrioventricular dissociation, such as total
heart block, ventricular tachycardia, or AV nodal reentrant tachycardia, can result in cannon "a"
waves, which are very big "a" waves. Large "V" waves are caused by conditions such tricuspid
or mitral regurgitation, right or left ventricular failure, severe right or left ventricle non-
compliance, and ventricular septal defect that increase the volume of the ventricles during right
ventricular contraction. Large atrial "V" waves can also be caused by mitral stenosis, post-
operative complications, or rheumatic alterations of the atrium38.Rapid diastolic filling of the
ventricle, which can happen in constrictive pericarditis, causes a very rapid "y" descent. Similar
to that, constrictive pericarditis causes a rapid "x" fall51. Since the diastolic pressures are
equalised and the ventricular diastolic pressure does not fall far enough to allow for full diastolic
5
filling, the "y" descent is absent in cardiac tamponade
5
Right Ventricle Systolic and Diastolic Pressure
In pulmonary embolism and pulmonary hypertension, the systolic pressures of the right ventricle
51,52
and the pulmonary arteries are increased In constrictive pericarditis, restrictive
cardiomyopathy, and cardiac tamponade, end-diastolic pressures rise and pulmonary capillary
wedge pressures equalize. The best way to detect ventricular interdependence in constrictive
pericarditis, however, is through simultaneous right and left cardiac catheterization. When there
is an increase in the left ventricle pressure trace when there is a decrease in the right ventricle
systolic pressure trace, and vice versa with respiration, there is an interdependence that causes
the right and left ventricular pressures to be out of sync.Because there is no interdependence in
restricted cardiomyopathy, simultaneous measurements of the pressures in the right and left
ventricles agree. Concordant right ventricular and left ventricle systolic pressure tracings with
respiration serve as a sign of concordance. The ratio of the area of the right and left ventricles
between inspiration and expiration is known as the systolic area index, and it may be computed
numerically. A systolic area index greater than 1.1 can detect constrictive pericarditis with
greater than 95% sensitivity. The systolic area index appears to have the best predictive accuracy
among the several criteria that have been created in the past to differentiate between constrictive
pericarditis and restrictive cardiomyopathy. Cardiovascular tamponade physiology is typically
transient, in contrast to the predominantly chronic clinical manifestation of constrictive
pericarditis and restrictive cardiomyopathy
Cardiac Output55,56
The indirect Fick principle and the thermodilution method are typically used to calculate cardiac
output by right heart catheterization. The Fick principle was developed in 1870 by Adolf Fick,
5
who noticed that the blood volume needed to carry a given amount of oxygen could be
calculated based on the amount of oxygen carried in the systemic and pulmonary circulation.
Haemoglobin levels, central arterial and venous oxygen saturation levels, and maximum oxygen
consumption values are needed for this approach. The maximum oxygen intake is estimated to
be 125 ml per minute, or 250 ml per minute using the direct measurement approach. This is
laborious and calls for specialized tools. As a result, the indirect Fick approach, which relies on
the maximal oxygen consumption value assumed, is frequently used. However, it has been
demonstrated that in up to 25% of people, the cardiac output calculated using the indirect Fick
approach differs from the direct Fick method by about 25%. These variations seem to be
noticeable in people with a body mass index of over 40 kg/m43,
The proximal blue port of the pulmonary artery catheter is used to administer 10 cc of saline for
the thermodilution procedure. The thermistor at the catheter tip detects the temperature reduction
that results from the mixture with the right atrial blood. The thermodilution method has
drawbacks, though. When cardiac output is low, the Thermodilution technique is not thought to
be accurate. In this situation, the area under the curve is tiny, and anything that makes the area
under the curve smaller can inflate cardiac output. Similar to this, there is a recirculation of
blood in severe tricuspid or
pulmonic valve regurgitation, which can lead to an incorrect estimation of cardiac output. It may
have the reverse effect and erroneously exaggerate cardiac output in the presence of intracardiac
shunts. It is crucial to be aware of the potential difficulties with these measurements and the fact
that the Fick and thermodilution procedures might result in inconsistent results even within the
same patient.
Cardiac Index
By adjusting the cardiac output for body surface area, the cardiac index is determined.
Depending on body size and mass, the normal cardiac output may vary. However, a healthy
6
heart index is
6
more than 2.5 liters per minute per square meter. A pulmonary capillary wedge pressure greater
than 15 mm Hg and an index of less than 2.2 litres per minute per square meter are considered to
be signs of cardiogenic shock
Pulmonary and Systemic Vascular Resistance
Systemic vascular resistance is calculated by the equation,
[(Mean arterial pressure – right atrial pressure) x 80 / cardiac output]
It is expressed as dynes per second per square centimeter or Wood units. The typical range is 10
to 20 Wood units, or 700 to 1600 dynes per second per cm. Similarly, the equation, which
calculates pulmonary vascular resistance,
[(Mean pulmonary artery pressure – pulmonary capillary wedge pressure) x 80/ cardiac output]
It is expressed as dynes per second per square centimeter or Wood units. 20–120 dynes per
second per cm, or less than 2 Wood units, constitute the typical range.
Pulmonary Artery Pulsatility Index
PAPi, also known as the pulmonary artery pulsatility index, is the ratio of right atrial pressure to
pulmonary artery pressure. [(Systolic pulmonary artery pressure - Diastolic pulmonary artery
pressure)/right atrial pressure] is the formula for calculating it.
In acute inferior wall myocardial infarction, PAPi of less than 0.9 has extremely high sensitivity
and specificity in predicting right ventricular failure and in-hospital mortality. When left
ventricular assist devices have been implanted, PAPi less than 1.85 is utilized to determine
whether or not patients may have right ventricle failure and need help from right ventricular
hemodynamic devices. When a patient has persistent right heart failure, it is also utilized to
predict poor outcomes.
Cardiac Power Index
The product of mean arterial pressure and cardiac output in litres per minute is divided by 451 to
get cardiac power output in Watts. The output of the heart measured in terms of the surface area
6
of the body is called the cardiac power index. In-hospital mortality in shock patients is
substantially correlated with cardiac power output less than 0.6 Watts. Cardiogenic shock causes
poor outcomes to be more closely correlated with cardiac power output than with cardiac index,
ejection fraction, pulmonary artery systolic pressure, or mean arterial pressure62
INDICATIONS
In doubt of cardiogenic shock
Diagnosis or exclusion of restrictive cardiomyopathy, pulmonary hypertension, constrictive
pericardial disease, and heart failure with a preserved ejection fraction in a patient with dyspnoea
Analyse the effectiveness of vasodilator treatment for pulmonary hypertension.
Heart tamponade
Quantification of the intracardiac left-to-right shunt
directing the management of patients' fluid intake and hemodynamic monitoring following
surgery or serious myocardial infarction, heart failure, or shock
Congenital heart disease in adults
A cardiac transplantation evaluation
monitoring condition following a heart transplant
post-cardiac transplant with new or worsening graft rejection-suggestive symptoms
Assessment of left ventricular assist devices prior to insertion
optimisation following implantation of the left ventricular assist device
When there are differences between the clinical presentation and non-invasive diagnostic
testing in valve disease 63,64
Right-sided endocarditis, a tumor on the right side, or a thrombus are absolute contraindications.
Severe bleeding disorders or coagulopathy are relative contraindications. To prevent inducing
dysrhythmias, appropriate caution should be used when there are arrhythmias or a left bundle
branch block.
6
MATERIALS AND METHODS
Type of study : Prospective study
Duration of study : 3 years ie, from December 1st 2021 to January 31st 2023
Place of study: Department of cardiology , KIMS hospital ,Secunderabad
Sampling technique: Convenience sampling
Sample size calculation:
According to a study conducted by Seth S et al [8.] the proportion deaths from ADHF
in Indian population was found 10% in hospital mortality ( as well in our institution)
So, p = 10%
Using Cochran’s formula for sample size (n) calculation, n = 4 x p x q

e2
Where, p = 10% = 0.1
q = 1 - p = 0.9
Taking e, absolute error of 10%, e = 0.1 So, n = 4 x

0.1 x 0.9
0.1 x 0.1
n = 36
A minimum of 36 patients will be included in the study, rounding it up to
40 patients.
So, Sample size calculated (approx) = n = 40
6
INCLUSION CRITERIA:-
 Acute decompensated heart failure patients of all class from I to V admitted
in hospital.(IPD)
 Both genders.
 Patients Between the age group of 18 to 75 years.
EXCLUSION CRITERIA
 Patients less than 18 yrs. of age
 Patients more than 75 years of age
 Patients with severe pulmonary stenosis.
 Patients with malignancy
 Patients with Infective endocarditis
 Pregnant females.
 Patients with severe renal dysfunction
 Patients with Poor GCS patients
 Patients who had recent acute myocardial infarction.
 Patients with febrile illness.
6
METHODOLOGY
Right Heart Catheterization
RHCs of Acute decompensated HF (n=41 patients) patients enrolled was done .
Supine RHC was performed, with the most common access for indwelling pulmonary artery
catheter (PAC) placement occurring in the right internal jugular vein.
Hemodynamics collected included
RAP,
Right ventricular pressure,
Pulmonary artery
pressure, PCWP,
Estimated Fick cardiac output and index,
Systemic and pulmonary vascular resistances.
Thermodilution cardiac output and index measurements were collected at the discretion of
primary operator performing the procedure.
Measurements were obtained at end-expiration.
Formula for estimated oxygen uptake was: VO2 (ml/min) = 125 (ml/min/m2 ) x body surface
area (m2 )(7).
6
Body surface area was calculated according to the formula of mostellar
Estimated Fick cardiac index was then calculated by the following equation: [125 (ml/min/m2
) x body surface area]/[(13.6 hemoglobin (g/L)* (ambient oxygen saturation – mixed venous
saturation)]/body surface area.
Post-procedure, the PAC was kept in place with subsequent transfer to the cardiac care unit.
Clinical Assessment for Estimation of Hemodynamics
History and physical examination was done and recorded their findings on a proforma at
randomization.
Signs and symptoms were categorized as follows:
 Rales (none, <1/3, 1/3 to 2/3); Hepatomegaly (absent, 2 to 4 finger breadths, <4 finger
breadths); ascites (none, trace, moderate, massive);
 Peripheral pedal edema (0, 1+, 2+, 3+, 4+); ( LEGS SCALE )
 Orthopnea (needs only 1 pillow, occasional orthopnea with 1 pillow, needs 2
pillows most of time, needs 3 pillows most of time, needs 4 pillows most of time);
 Gastrointestinal distress (none, occasional, constant); fatigue (at rest, any activity,
routine daily activity);
 Dyspnea (at rest, walking in room, walking <1 block).
 Supine blood pressure was measured.
 Hepatojugular reflux and S3 were recorded as present or absent.
 Elevated filling pressures were assessed by symptoms (dyspnea, abdominal
discomfort, nausea, or vomiting attributable to hepato splanchnic congestion) or signs
(RAP >8 cm
6
above right atrium, rales, peripheral edema, ascites, or hepatomegaly).
6
 peripheral perfusion with emphasis on warmth of extremities and proportional
pulse pressure >25%.
The clinical profiles were defined by:
1) the absence or presence of signs of congestion, and
2) evidence suggesting adequate or inadequate perfusion
Indications of congestion included a recent history of orthopnea and/or physical exam
evidence of jugular venous distention, rales, hepatojugular reflux, ascites, peripheral
edema, leftward radiation of the pulmonic heart sound, or a square wave blood pressure
response to the Valsalva maneuver.
Compromised perfusion was assessed by the presence of a narrow proportional pulse
pressure ([systolic - diastolic blood pressure]/systolic blood pressure <25%), pulsus
alternans, symptomatic hypotension (without orthostasis), cool extremities, and/or
impaired mentation.
Estimated hemodynamics were categorized:
RAP <8, 8 to 12, 13 to 16, >16 mmHg;
PCWP <12, 12 to 22, 23 to 30, >30 mmHg; and
Cardiac index: <1.8, 1.8 to 2.2, 2.3 to 2.5, >2.5 L/(minm2 ).
we classified subjects into 1 of 4 previously described profiles based on adequacy of cardiac
output (“warm” or “cold”) and increase in left-sided filling pressures (“wet” or “dry”). Specific
6
criteria for when to classify the patient as “wet” or “cold” (ie, at what estimated PCWP or
cardiac output) were left to the investigator’s discretion.
Statistical Analysis:
A predesigned pretested questionnaire will be used to collect the data. Data Collected will be
entered in Microsoft Excel. Data will be represented in frequencies and percentages, charts,
and graphs. Mean and standard deviation of quantitative variables will be shown. Appropriate
statistical tests will be applied using EpiInfo version 7.2 and SPSS software version 20 for
analysis. Chi square test will be used for association between nominal variables, Wilcoxon
signed rank test will be used to compare ordinal data and student’s t test will be used for
correlation between the continuous data wherever applicable. Statistical significance will be
considered at p<0.05.
RESULTS AND OBSERVATION
TABLE 1 : SEX DISTRIBUTION
Sex distribution Frequency Percent
Male 26 63.4
Female 15 36.6
6
Total 41 100.0
In the present study males (63.4%) were predominant compared to females ( 36.6% ).
M:F ratio – 1.7:1
36.60%, 37% Male

Female
63.40%, 63%
Graph 1 : Bar diagram showing sex distribution
TABLE 2: DISTRIBUTION OF ANAEMIA
DISTRIBUTION OF ANAEMIA Frequency Percent
Present 6 14.6
6
Absent 35 85.4
Total 41 100.0
In the present study Anaemia was noted in 0nly 14.6% cases.
90.00% 85.40%
80.00%
70.00%
60.00%
50.00%
40.00%
30.00%
20.00%
14.60%
10.00%
0.00%
Present Absent
Graph 2 : Bar diagram showing distribution of Anaemia
TABLE 3 : DISTRIBUTION OF CYANOSIS
7
DISTRIBUTION OF
CYANOSIS Frequency Percent
Present 2 4.9
Absent 39 95.1
Total 41 100.0
In the present study Cyanosis was noted in 4.9% cases .
100.00% 95.10%
90.00%
80.00%
70.00%
60.00%
50.00%
40.00%
30.00%
20.00%
10.00%
0.00%
4.90%
Present Absent
Graph 3 : Bar diagram showing distribution of Cyanosis
TABLE 4 : DISTRIBUTION OF JAUNDICE
DISTRIBUTION OF JAUNDICE
Frequency Percent
7
Present 7 17.1
Absent 34 82.9
Total 41 100.0
In the present study jaundice noted in 17.1% cases.
17.10%, 17%
Present
Absent
82.90%, 83%
Graph 4 : Pie diagram showing distribution of Jaundice
TABLE 5: DISTRIBUTION OF PEDAL EDEMA
7
DISTRIBUTION OF EDEMA
Frequency Percent
Present 25 61.0
Absent 16 39.0
Total 41 100.0
In the present study Edema noted in 61.0% cases.
70% 61%
60%
50%
39%
40%
30%
20%
10%
0%
Present Absent
Graph 5 : Bar diagram showing distribution of edema
7
TABLE 6 : DISTRIBUTION OF JVP
DISTRIBUTION OF JVP
Frequency Percent
Raised 39 95.1
Normal 2 4.9
Total 41 100.0
In the present study Raised JVP noted in 95.1% cases.
4.90%
Raised Normal
95.10%
Graph 6 : Pie diagram showing distribution of JVP
7
TABLE 7 : DISTRIBUTION OF STEVENSON ( Clinical findings)
DISTRIBUTION OF STEVENSON
Frequency Percent
Wet, Cold 15 36.6
Wet, Warm 26 63.4
Total 41 100.0
In the present study wet ,cold noted in 36.6% cases. And wet ,warm noted in 63.4% cases.
Graph 7 : Pie diagram showing distribution of STEVENSON
36.60%
63.40%
Wet, ColdWet, Warm
7
TABLE 8 : DISTRIBUTION OF S3
DISTRIBUTION OF S3
Frequency Percent
Present 19 46.3
Absent 22 53.7
Total 41 100.0
In the present study S3 noted in 46.3% cases
56.00%
53.70%
54.00%
52.00%
50.00%
46.30%
48.00%
46.00%
44.00%
42.00%
Present Absent
Graph 8: Bar diagram showing distribution of S3 Heart sound
7
TABLE 9 : DISTRIBUTION OF BASAL LUNG CREPITATIONS .
DISTRIBUTION OF CREPTS
Frequency Percent
Present 40 97.6
Absent 1 2.4
Total 41 100.0
In the present study Crepts noted in 97.6% cases
2.40%
97.60%
PresentAbsent
Graph 9 : Pie diagram showing distribution of CREPTS.
7
TABLE 10 :DISTRIBUTION OF HEPATOMEGALY
DISTRIBUTION OF HEPATOMEGALY Frequency Percent
Present 18 43.9
Absent 23 56.1
Total 41 100.0
In the present study Hepatomegaly noted in 43.9% cases
43.90%
56.10%
PresentAbsent
Graph 10 : Pie diagram showing distribution of HEPATOMEGALY
7
TABLE 11: DISTRIBUTION OF MENTAL STATUS
DISTRIBUTION OF MENTAL STATUS
Frequency Percent
Conscious, orientated 31 75.6
Irritable confused 3 7.3
Drowsy 7 17.1
Total 41 100.0
In the present study Conscious, orientated noted in 75.6% cases, Irritable confused in 7.3% cases
and drowsy in 17.1% cases.
17.10%
7.30%
75.60%
Conscious, orientated Irritable confused Drowsy
Graph 11 : Pie diagram showing distribution of MENTAL STATUS
7
TABLE 12 : DISTRIBUTION OF BIOMARKER ( TROPONINS)
DISTRIBUTION OF BIOMARKER Frequency Percent
Positive 13 31.7
Negative 28 68.3
Total 41 100.0
In the present study Biomarkers were positive in 31.7% cases.
80.00%
70.00% 68.30%
60.00%
50.00%
31.70%
40.00%
30.00%
20.00%
10.00%
0.00%
Positive Negative
Graph 12 : BAR diagram showing distribution of BIOMARKERS
8
TABLE 13 : DISTRIBUTION OF CHEST X RAY AND CARDIOMEGALY
DISTRIBUTION OF CHEST X RAY
CARDIOMEGALY Frequency Percent
Yes 31 75.6
No 10 24.4
Total 41 100.0
In the present study On chest x ray cardiomegaly note din 75.6% cases.
distributionof CHEST X RAY

80
70
60
50
40
30
20
10
0
Yes No
Graph 13 : BAR diagram showing distribution of CHEST X RAY
8
TABLE 14 : DISTRIBUTION OF CONGESTION ( CREPTS + HEPATOMEGALY )
DISTRIBUTION OF CONGESTION
Frequency Percent
Yes 38 92.7
No 3 7.3
Total 41 100.0
In the present study Congestion noted in 92.7% cases.
DISTRIBUTION OF CONGESTION
100
90
80
70
60
50
40
30
20
10
0
Yes No
Graph 14 : BAR diagram showing distribution of CONGESTION
8
TABLE 15 : DISTRIBUTION OF PLEURAL EFFUSION ON CXR
DISTRIBUTION OF EFFUSION
Frequency Percent
Yes 25 61.0
No 16 39.0
Total 41 100.0
In the present study Effusion noted in 61.0% cases. (CXR - CARDIOMEGALY.)
100% 92.70%
90%
75.60%
80%
70% 61%
60%
50%
40%
30%
20%
10%
Effusion CXR Congestion
0%
Graph 15 : BAR diagram showing distribution of PLEURAL EFFUSSION
8
ABLE 16 : DISTRIBUTION OF RISK FACTORS
DISTRIBUTION OF RISK FACTORS
N Percent
DM 17 38.6%
Smoker 7 15.9%
CAD 3 6.8%
HTN 11 25.0%
ILD 1 2.3%
CKD 1 2.3%
TVD S/P PTCA 1 2.3%
HODKINS LYMPHOMA 1 2.3%
Old PTB 1 2.3%
BA 1 2.3%
Total 44 100.0%
In the present study DM noted in 38.6% cases, Next common was HTN in 25% cases and CAD
in 6.8% cases.
8
45.00% 38.60%
40.00%
35.00%
30.00% 25.00%
25.00%
15.90%
20.00%
15.00% 6.80%
10.00% 2.30%2.30%2.30%2.30%2.30%2.30%
5.00%
0.00%
Graph 16 : BAR diagram showing distribution of RISK FACTORS
TABLE 17 : STATISTICAL ANALYSIS
PARAMETER N Mean Std. Deviation
AGE 41 48.20 17.73
BMI 41 25.2 3.52
Saturation 41 96.28% 3.06%
HR 41 103.46 18.07
HB 41 12.91 2.18
PROBNP 41 14511.46 7845.001
TAPSE 41 1.43 0.27
EDD 41 5.46 0.47
ESD 41 4.4 0.52
EF 41 30.75% 8.99%
LAP 41 19 3.24
8
RATE 41 102.76 16.77
QRS 41 116.22 15.7
RHC PCWP 41 22.29 3.8
CI 41 2.35 0.97
CO 41 4.11 1.74
PVR 41 4.63 6.18
SVR 41 23.73 17.01
PA PRESSURE 41 35.78 13.49
TABLE 18 : DISTRIBUTION OF NYHA CLASS
CLASS Frequency Percent
Class II 15 36.6
Class III 19 46.3
Class IV 7 17.1
Total 41 100.0
In our study majority were class III constituting 46.3% , class II occupied 36.6% and class IV
were 17.1%
8
50.00% 46.30%
45.00%36.60%
40.00%
35.00%
30.00%
25.00%
17.10%
20.00%
15.00%
10.00%
5.00%
0.00%
Class II Class III Class IV
Graph 17 : BAR diagram showing distribution of NHYA CLASSIFICATION
TABLE 19 : STATISTICAL ANALYSIS OF RHC PCWP WITH NYHA CLASS
PARAMETER N Mean Std. Deviation P value
RHC PCWP Class II 15 21 3.14 0.28
Class III 19 23 4.55
Class IV 7 23.14 3.02
Total 41 22.29 3.89
There is no statistical correlation of RHC PCWP with NYHA classification with p value 0.28.
8
30
25 23±4.5 23.14±3.02
21±3.14
20
15
10
Graph 18 : BAR diagram showing distribution of STATISTICAL ANALYSIS OF RHC PCWP
WITH NYHA CLASS
TABLE 20 : STATISTICAL ANALYSIS OF CIWITH NYHA CLASS
PARAMETER CLASS N Mean Std. Deviation P value
CI Class II 15 2.3 0.95
Class III 19 2.5 1.1 0.58
Class IV 7 2.05 0.62
8
Total 41 2.35 0.97
There is no statistical correlation of cardiac index with NYHA classification with p value 0.58
3.5
3
2.5±1.1
2.5 2.3±0.95
2.05±0.62
2
1.5
0.5
0
Graph 19 : BAR diagram showing distribution of STATISTICAL ANALYSIS OF CI
TABLE 21 : STATISTICAL ANALYSIS OF CO WITH NYHA CLASS
CO Class II 15 4.08 1.75 0.37
8
Class III 19 4.41 1.91
Class IV 7 3.32 1.02
Total 41 4.11 1.74
There is no statistical correlation of CARDIAC OUTPUT with NYHA classification with p
value 0.37.
5
4.41±1.91
4.08±1.75
4
3.32±1.02
Graph 20 : BAR diagram showing distribution of STATISTICAL ANALYSIS OF CO
TABLE 22 : STATISTICAL ANALYSIS OF PVR WITH NYHA CLASS
PAPRAMETER CLASS N Mean Std. Deviation P value
PVR Class II 15 4.29 3.28
Class III 19 3.92 1.81

0.46
Class IV 7 7.3 14.4
Total 41 4.63 6.18
9
There is no statistical correlation of PVR with NYHA classification with p value 0.46
8
7.3
7
5
4.29
3.925
4
Graph 21: BAR diagram showing distribution of STATISTICAL ANALYSIS OF PVR
TABLE 23 : STATISTICAL ANALYSIS OF SVR WITH NYHA CLASS
PAPRAMETER CLASS N Mean Std. Deviation P value
SVR Class II 15 30.39 25.62 0.16
9
Class III 19 19.57 7.9
Class IV 7 20.76 5.81
Total 41 23.73 17.01
There is no statistical correlation of SVR with NYHA classification with p value 0.16
60
50
40
30.39±25.6
30
19.57±7.9 20.76±5.8
20
10
0
Graph 22: BAR diagram showing distribution of STATISTICAL ANALYSIS OF SVR
TABLE 24: STATISTICAL ANALYSIS OF MEAN PA PRESSURE WITH NYHA CLAS
PA PRESSURE Class II 15 39.47 14.63 0.07
9
Class III 19 36.63 12.1
Class IV 7 25.57 10.81
Total 41 35.78 13.49
There is no significant statistical correlation of PA with NYHA classification with p value 0.07
60
50
39.47±14.63
40 36.63±12.1
30 25.57±10.81
20
10
0
Graph 23: BAR diagram showing distribution of STATISTICAL ANALYSIS OF PA PRESSURE
TABLE 25 : STATISTICAL ANALYSIS OF PERIPHERAL EDEMA WITH CO
9
Std.
Edema N Mean Deviation P value
CO Present 25 4.38 1.79 0.19
Absent 16 3.67 1.61
In our study there is no significant statistical correlation between edema and Cardiac output.
5
4.38±1.79
4 3.67±1.61
0
Present Absent
CO
Graph 24: BAR diagram showing distribution of STATISTICAL CORRELATION BETWEEN
EDEMA AND CO .
TABLE 26 : STATISTICAL ANALYSIS OF PRESENCE OF S3 WITH CO
S3 N Mean Std. Deviation P value
9
CO Present 19 4.53 1.84 0.15
Absent 22 3.74 1.61
In our study there is no significant statistical correlation between s3 and CO .
5
4.53±1.84
4 3.74±1.61
0
Present Absent
CO
Graph 25: BAR diagram showing distribution of STATISTICAL ANALYSIS OF S3
9
TABLE 27 : STATISTICAL ANALYSIS OF RHC PCWP WITH PLEURAL EFFUSION
STATISTICAL ANALYSIS N Mean Std. Deviation P value
RHC PCWP Present 19 21.63 3.13 0.30
Absent 22 22.86 4.44
In our study there is no significant statistical analysis of RHC PCWP with p value 0.30 .
30
25 22.86±4.44
21.63±3.13
20
15
10
0
Present Absent
RHC PCWP
Graph 26: BAR diagram showing distribution of STATISTICAL ANALYSIS OF RHC PCWP
TABLE 28 : STATISTICAL CORRELATION OF PA PRESUURE WITH HEPATOMEGALY
HEPATOMEGALY N Mean Std. P value
9
Deviation
PA PRESSURE Present 18 36.28 16.71 0.880
Absent 23 35.39 10.71
In our study there is no significant statistical correlation between PA pressure and
Hepatomegaly with p value 0.880
60
50
40 36.28±16.17 35.39±10.71
30
20
10
0
Present Absent
PA PRESSURE
Graph 27: BAR diagram showing distribution of STATISTICAL CORRELATION OF PA
PRESUURE WITH HEPATOMEGALY
9
TABLE 29 : STATISTICAL CORRELATION MENTAL STATUS WITH CI
Std.
Mental status N Mean Deviation P value
Conscious, orientated 31 2.5 1.03 0.2
Irritable confused 3 2.04 0.74
Drowsy 7 1.81 0.58
Total 41 2.35 0.97
In our study there is no significant statistical correlation of mental status with p value 0.2
3.5
2.5±1.03
2.5
2.04±0.74
2 1.81±0.58
1.5
0.5
0
Conscious, orientated Irritable confused Drowsy
Graph 28: BAR diagram showing distribution of STATISTICAL CORRELATION OF MENTAL
STATUS
TABLE 30 : STATISTICAL CORRELATION OF MEAN PA PRESSURE WITH
9
PLEURAL EFFUSION
Std.
EFFUSION N Mean Deviation P value
PA PRESSURE Yes 25 36.88 13.55 0.52
No 16 34.06 13.65
In our study there is no significant statistical correlation between PA pressure and Effusion
with p value 0.52.
60
50
40 36.88±13.55
34.06±13.65
30
20
10
0
Yes No
PA PRESSURE
Graph 29: BAR diagram showing distribution of STATISTICAL CORRELATION OF PA
PRESSURE WITH EFFUSION
9
TABLE 31 : PEARSON CORRELATION OF STEVENSON WITH CI
PEARSON CORRELATION OF Std.
STEVENSON N Mean Deviation P value
CI Wet, Cold 15 2.34 1.042 0.96
Wet, Warm 26 2.36 0.95
In our study there is no significant statistical correlation between Stevenson with p value 0.96.
3.5
3
2.34±1.04 2.36±0.95
2.5
1.5
0.5
Wet, Cold Wet, Warm
0 CI
Graph 30: BAR diagram showing distribution of PEARSON STATISTICAL CORRELATION OF
STEVENSON
1
TABLE 32 : PEARSON CORRELATION OF QRS DURATION WITH CO
PEARSON CORRELATION OF QRS COMPLEX
DURATION
CO
QRS Pearson Correlation -0.556
Sig. (2-tailed) 0.0001
N 41
In our study pearson correlation of QRS complex showed significant correlation with p value
0.0001.
160
140
120
100
Q
80
60
40
20
0 0 1 2 3 4 5 6 7 8 9
CO
Graph 31: Histogram diagram showing distribution of PEARSON STATISTICAL
CORRELATION OF QRS COMPLEX DURATION
1
TABLE 33 : PEARSON CORRELATION OF RHC PCWP
PEARSON CORRELATION OF RHC PCWP LAP (ECHOWISE )
RHC PCWP Pearson Correlation 0.198
N 41
In our study No significant correlation with RHC PCWP and LAP(ECHOWISE)
30
25
20
15
L
10
0 5 10 15 20 25 30 35
PCWP
Graph 32: Histogram diagram showing distribution of PEARSON STATISTICAL
CORRELATION OF RHC PCWP
1
TABLE 34 : PEARSON CORRELATION OF PROBNP WITH CO
STATISTICAL CORRELATION OF PROBNP CO
PROBNP Pearson Correlation 0.096
N 41
In our study No significant correlation with PROBNP and CO
9
8
7
6
5
4
3
2
C
1
0
0 5000 10000 15000 20000 25000 30000 35000 40000

PRO BNP
Graph 33: Histogram diagram showing PROBNP
1
DISCUSSION
In 1976, Forrester et al119 demonstrated that among patients who had heart failure the physical
examination identified four hemodynamic profiles defined by Swan-Ganz catheterization.
These profiles were based on the presence or absence of congestion (pulmonary capillary wedge
pressure [PCWP] > or <18 mm Hg) and adequacy of perfusion (cardiac index [CI] >2.2
l/min/m2 ).
Profile I represented no congestion or hypoperfusion;
Profile II, congestion without hypoperfusion;
Profile III, hypoperfusion without congestion; and
Profile IV, both congestion and hypoperfusion.
Furthermore, both the clinical and invasive hemodynamic profiles predicted short-term survival,
with increased mortality when congestion was present and even worse outcomes when both
congestion and hypo perfusion were evident 119
Several studies have shown that hemodynamics predict outcomes in patients with ADHF 120-121
The small subset of patients who underwent right heart catheterization in their study suggests
that clinical profiles may derive prognostic value because they reflect invasive hemodynamic
measurements.
Several clinical features reliably predict hemodynamic derangements in ADHF. Orthopnea
accurately predicts increased PCWP in 91% of patients with ADHF HF 122
Positive hepatojugular reflux also correlates well with elevated PCWP in ADHF (123,124,125) An
abnormal arterial blood pressure response to the Valsalva maneuver predicts elevated PCWP
with a sensitivity of 92% to 100% and a specificity of 83% to 91% 126
Additionally, a proportional pulse pressure <25% strongly parallels hemodynamic evidence of
hypoperfusion (CI <2.2 l/min/ m2 ) 127. Because the determination of clinical profiles involves
1
integration of multiple physical findings, clinical profiles may provide a more reliable estimate
of invasive hemodynamics than any one sign alone.
A previous study 127 comparing retrospectively assigned clinical profiles to invasive
hemodynamics showed that patients with a “wet” profile tended to have higher PCWP than
those with a “dry” profile. Similarly, patients with a “cold” profile tended to have lower CI than
patients with a “warm” profile. Although outcomes did not differ significantly between the
various clinical profiles the trend for survival was similar to that seen in the present analysis.
Our study provides correlation of Clinical and hemodynamic assessment of patients with acute
decompensated HF. First, we estimated the RAP and PCWP by the History and physical
examination. In particular, the estimates of RAP from JVP were relatively useful as compared
with measured values (AUC 0.74). Because the RAP is usually concordant with the PCWP in
patients with acute decompensated HF.
The JVP is a useful surrogate of left-sided filling pressures in many patients. In fact, once
estimated RAP was considered, no other History and physical examination parameter provided
additional information to detect a PCWP >22 mmHg, thus endorsing assessment of JVP as a
critical component of the History and physical in patients with HF.
A recent report demonstrated that the presence of an elevated jugular venous pressure and S3
was associated with an increased risk of hospitalization and death among patients enrolled in the
Studies Of Left Ventricular Dysfunction (SOLVD) treatment trial 128
Another study evaluating patients four to six weeks after treatment for NYHA class IV
symptoms also showed that persistent evidence of congestion predicted worse outcomes in
patients with chronic HF 129 Furthermore, objective exercise limitation, which predicts outcomes
in patients with chronic HF 130, has also been shown to correlate with physical findings of
congestion 131. These results reinforce the value of evaluating disease severity by means of a
simple bedside clinical evaluation.
1
In addition to estimated RAP, Orthopnea was also a marker of increased PCWP, albeit only
for higher levels of PCWP.
The second important finding was that a simple classification as to whether a patient was poorly
perfused (“cold”) or well perfused (“warm”) had utility in stratifying patients based on their
true cardiac index (1.75 versus 2 L/(minm2 ); P<0.004).
Clinical profiling may also help guide titration of beta blocker therapy. Patients with profile A
may tolerate initiation and up-titration of beta-blockers with the success observed in major trials,
whereas profile B might represent a population where chronic beta-blocker therapy could be
maintained but initiation or up-titration deferred until restoration of profile A. Conversely,
determination of profile C might lead to a decrease or withdrawal of recently initiated beta-
blockers until better compensation is achieved. The greater use of beta-blockers on admission in
patients with profile A relative to those with profiles B and C is consistent with this management
strategy.
Estimation of PCWP by the H&P Examination
Previous data have questioned the ability of the H&P examination to yield accurate estimates
of RAP.132,133,134
In a study of 25 patients, H&P examination estimates were accurate when RAP was normal but
systematically underestimated RAP when increased.134
In an earlier study of critically ill patients, H&P examination estimates of RAP overall were
inaccurate, though were said to be more frequently correct in those with low cardiac index with
or without increased PCWP (>18 mmHg).132
In contrast, others have reported that assessment of low central venous pressure had a likelihood
ratio of 3.4 for a low central venous pressure and an assessment of high central venous pressure
had a likelihood ratio of 4.1 for a high central venous pressure.134
1
Recent evidence suggests that using the external jugular veins allows accurate estimation of the
central venous pressure.135Nevertheless, the inconsistent ability to demonstrate accurate
assessments of RAP has led to the suggestion that clinicians should decide only whether the
venous pressure is increased or not and forsake attempts to determine actual RAP values.
In the present study, we categorized the JVP and RAP into 3 categories, and these H&P
examination guided estimates were associated with measured RAP .The role of the
H&P examination in detecting increased left-sided filling pressures has also been
assessed .
A recent study suggested echocardiography was more accurate than the H&P
examination,136though the H&P examination parameters may have been suboptimal as JVP was
not used to estimate the PCWP.
A systematic review of 12 studies suggested that increased JVP was a “very helpful” finding for
detecting increased filling pressure.137
In mark et al study is consistent with and extends this conclusion by demonstrating that
increased JVP and orthopnea >2 pillows were the only H&P examination parameters that
provided incremental value in detecting an increased PCWP in patients with acute
decompensated HF. 138
Estimation of Cardiac Index by H&P Examination
There are few data regarding the reliability of the H&P examination to detect a low cardiac
index.139
A decreased proportional pulse pressure was associated with low cardiac index in a study of 50
patients with advanced HF.8 The toe temperature measured by a thermistor placed on the digital
pad of the first toe has been correlated with cardiac output.140
In ESCAPE, both a low proportional pulse pressure and cool extremities had no significant
1
association with measured CI <2.3 L/(minm2 ) in univariable analysis .In contrast, a global
1
assessment of inadequate perfusion (“cold” profile) was associated with a reduced cardiac index,
whether defined as <2.3 or <1.8 L/(minm2 ). Even when the cardiac index was estimated to be
<2.3 L/(minm2 ), a “cold” profile detected by the same assessor was associated with a
significantly lower cardiac index. In total, these data suggest that physicians should focus on a
global assessment leading to a dichotomous classification (“warm” or “cold”) to stratify patients
into those with adequate or inadequate perfusion/
H&P Examination and Prognosis
A number of H&P examination findings have been shown to be risk markers for poor prognosis
in patients with systolic HF including increased JVP.141
Previously, in a single-center observational study, the admission H&P-based hemodynamic
profile of “wet” with either “warm” or “cold” was shown to be an independent risk factor for the
composite end point of mortality or urgent transplant at one year.142
However, similar hemodynamic profiles ascertained by right heart catheterization were not
associated with outcomes in the Flolan International Randomized Survival Trial.143
We now demonstrate that the H&P-based hemodynamic profile at discharge appears more
important than on admission and that subjects assessed as being “wet” or “cold” at discharge
were at 50% increased risk of rehospitalization or death independently of other markers of
disease severity. In addition to suggesting potential targets for therapy, these data may prove
useful in the management of patients with advanced HF in guiding intensity of follow-up in the
outpatient setting..
We analyzed the clinical assessments of hemodynamic profiles compared with invasive
measurements in consecutive advanced HF patients presenting with ADHF. Our main findings
are:
(1) The “Cold and Wet” subgroup is identified at an alarmingly low rate by clinical assessment;
(2) Overall clinical assessments of RAP, PCWP, and CI are inaccurate regardless of clinical
1
experience, with clinical assessments by interns the least accurate;
(3) Interobserver agreement in clinical assessment was low
(4) RHCguided therapy altered clinical decision-making in a majority of patients.
Filling pressures are assessed by examination of jugular venous pressure, lower extremity
edema, auscultation of rales, presence of ascites, and a positive hepatojugular reflux.
Assessment of N-terminal pro-B type natriuretic peptide, mitral valve annular tissue .
COMPARATIVE STUDIES
Present study mean age 46. years ……Mean and SD of LAP was 19+3.24,Mean PCWP was
22.29+3.8 and estimated CI 2.35 (0.97) L/min/m2. In Nikhil Narang et al143 study median
patient age was 60 (51, 67.5) years, 80.4% were male. Median RAP was 15 (9.5, 21) mmHg,
PCWP 26 (21, 30.5) mmHg and estimated Fick CI 1.9 (1.6, 2.5) L/min/m2.
Overall diagnostic accuracy of hemodynamic classification
In a study done by Nikhil Narang et al 143 , patients defined as “Cold and Wet” by RHC were
most prevalent (59.6%, n=130). PPV for this category was 74.7% and NPV was 50.4%. “Warm
and Wet” profiles were the next most prevalent hemodynamic classifications (20.2%, n=44),
followed by “Warm and Dry” (13.8%, n=30) and “Cold and Dry” (6.4%, n=14). PPV’s and
NPV’s were comparable for “Warm and Wet” and “Warm and Dry”, with lower PPV and higher
NPV seen in patients identified as “Cold and Dry”. 73 patients (75.3%) had thermodilution-
derived cardiac outputs measured, which did not significantly change accuracy of hemodynamic
classification .
1
Mark et al 138Of the 194 subjects who underwent PAC placement, 73% were male, 61% were
white, and half had ischemic cardiomyopathy. Most patients had PCWP >22 mm Hg (64%)
and cardiac index <2.3 L/(min/m2) (73%). Atrial fibrillation or flutter was present in 14% of
subjects, whereas a paced rhythm was present in 21% of subjects on the baseline ECG.
TABLE 34: COMPARATIVE STUDIES OF PCWP, mm Hg
Measured PCWP, mm Hg Mark et al 138 Present study
<12 5 15
12–22 32 9
23–30 38 7
>30 26 -
11
TABLE 35 :DISTRIBUTION OF NUMBER OF SUBJECTS WITH DESIGNATED H&P
EXAMINATION .
Mark et al138 Present study
Finding on H&P Examination
DISTRIBUTION OF JVP
Raised 168 39
Normal 18 2
DISTRIBUTION OF S3
Present 123 19
Absent 69 22
DISTRIBUTION OF HEPATOMEGALY
Present 105 18
Absent 86 23
DISTRIBUTION OF EDEMA
Present 128 25
Absent 64 16
We compared with mark et al study and assessed which components of the H&P examination
were associated with an increased PCWP defined as 22 mmHg. The number of subjects who
exhibited the various signs and symptoms of HF, and the percentage of those who had a
measured PCWP >22 mmHg,
When assessing the operating characteristics of components of the H&P examination as a
diagnostic tool for assessing PCWP 22 mmHg (Table 3), estimated JVP >12 mmHg had nearly
equal sensitivity and specificity and yielded likelihood ratios (positive and negative) of 1.8.
11
The majority of other H&P examination components, including symptoms (orthopnea,
gastrointestinal distress, fatigue, and dyspnea) and signs (rales, ascites, edema, and
hepatomegaly) were insensitive markers of PCWP >22 mmHg, limiting their use in this setting.
Once JVP >12 mmHg was entered in a multivariable model with PCWP >22 mmHg as the
dependent variable, no other component of the H&P examination remained associated with
PCWP >22 mmHg (JVP odds ratio, 3.3; 95% CI, 1.8, 6.1).
In a sensitivity analysis, we determined if other H&P findings were associated with higher
threshold values of PCWP. In addition to JVP >2 mmHg, only orthopnea was associated with
increased.
Association of the H&P Examination With Reduced Cardiac Index
In contrast to the relationship of estimated and measured PCWP (above), there was not a
strong relationship between estimated and measured cardiac index .Similar findings were
observed by study done by Mark et al . 138
138
Mark et al study A proportional pulse pressure <25% and cool extremities had good
positive predictive value but were relatively infrequent findings and were not
significantly associated with reduced cardiac index.
In contrast, the integrated assessment of a “cold” profile was significantly associated with CI
2.3 L/(minm2 ) (P<0.015). A “cold” profile was also significantly associated with measured
cardiac index 1.8 L/(minm2 ) (odds ratio, 2.7; 95% CI, 1.4, 5.2; P<0.004). The median
invasively
measured CI in those classified as “cold” versus “warm” was 1.75 (1.5, 2.05) versus 2.0 (1.7,
2.3) L/(minm2 ), respectively (P<0.004). The finding that a “cold” versus “warm” designation
was associated with a significantly lower invasively measured CI, whereas estimated cardiac
index was not, suggests that there is utility in a binary classification of adequacy of perfusion.
This hypothesis is supported by the finding that among those with an estimated cardiac index 2.3
11
L/(minm2 ), the invasively measured cardiac index in those who were classified as “cold” [1.7
11
(1.5, 2.0) L/(min/m2 )] was lower than in those classified as “warm” [1.9 (1.7, 2.3) L/(min/m2 ),
P<0.006]. There were no differences between the comparator groups in blood pressure, heart
rate, ejection fraction, sodium, creatinine, and BNP (data not shown), suggesting that underlying
differences in perfusion were indeed the basis for the “cold” classification.
11
CONCLUSION
In ADHF, the presence of increased jugular venous pressure,edema , hepatomegaly and S3 is
useful to detect increased pulmonary capillary wedge pressure, and a global assessment of
inadequate perfusion is useful to detect reduced cardiac index. Clinical profiles are easy to
define, predict prognosis, and appear to do so better than traditional markers of disease severity.
These profiles may be useful to guide therapy and to select appropriate patients for clinical trials,
particularly those designed for patients with a poor prognosis on current medical therapy.
11
SUMMARY
 In the present study Mean age was 46.2 years
 Males (63.4%) were predominant compared to females ( 36.6% ).M:F ratio – 1.7:1
 Cyanosis was noted in 4.9% cases .
 Edema noted in 61.0% cases.
 Raised JVP noted in 95.1% cases.
 Wet ,cold noted in 36.6% cases. And wet ,warm noted in 63.4% cases.
 S3 noted in 46.3% cases
 CREPITATIONS noted in 97.6% cases
 Hepatomegaly noted in 43.9% cases
 Conscious, orientated noted in 75.6% cases, Irritable confused in 7.3% cases and
drowsy in 17.1% cases.
 According to NYHA classification , Majority were class III constituting 46.3%
, class II occupied 36.6% and class IV were 17.1%
 Biomarkers were positive in 31.7% cases
 On chest x ray cardiomegaly noted in 75.6% cases.
 Congestion noted in 92.7% cases
 Effusion noted in 61.0% cases.
 DM noted in 38.6% cases, Next common was HTN in 25% cases and CAD in 6.8%
cases
 There is no statistical correlation of RHC PCWP with NYHA classification with
p value 0.28
11
 There is no statistical correlation of CARDIAC INDEX with NYHA classification
with p value 0.58
 There is no statistical correlation of CARDIAC OUTPUT with NYHA
classification with p value 0.37
 There is no statistical correlation of PVR with NYHA classification with p value 0.46
 There is no statistical correlation of SVR with NYHA classification with p value 0.16
 There is no significant statistical correlation of PA with NYHA classification with
p value 0.07
 There is no significant statistical correlation between edema and CO
 There is no significant statistical correlation between s3 and CO .
 There is no significant statistical correlation between PA pressure and Hepatomegaly .
 There is no significant statistical correlation between PA pressure and Hepatomegaly
with p value 0.880
 There is no significant statistical correlation of mental status with p value 0.2
 There is no significant statistical correlation between PA pressure and Effusion with p

value 0.52
 There is no significant statistical correlation between Stevenson with p value 0.96.
 In our study Pearson correlation of QRS complex showed significant correlation with
p value 0.0001.
 No significant correlation with RHC PCWP and LAP.
 No significant correlation with PROBNP and CO
11
LIMITATIONS
In our study limitations includes:
1. Limited sample size, Furthermore, due to the small sample size and few
number of events, a multivariable analysis could not be done.
2. Patients had known HF in which increased filling pressures were likely;
accuracy of increased RAP in other patient populations may be lower.
Additionally, the patient population was younger (median age 46.2 years)
3. Severity of tricuspid regurgitation was not routinely assessed and thus we
cannot assess its impact on RAP and thermodilution cardiac index.
4. Likewise, the relationship between RAP and PCWP would be expected to be
different in patients with primary right ventricular failure and may be affected
in the presence of severe TR or MR.
5. It is not known whether accurate estimation of the hemodynamics improves
clinical outcomes. Indeed, detection of a low output state by a “cold” assessment
could lead to initiation of intravenous inotropic agents which can worsen
outcomes.
6. Most of the NYHA CLASS IV patients were critically ill and was on multiple
inotropic supports and L V assist devices support for circulatory supports ,which
may cause some alterations in invasive RHC parameters.
11
CLINICAL PRO-FORMA
A. PARTICULARS OF THE PATIENTS
Name : SL. No
Age : Dept :
Sex : M/F . :
Religion : War
Occupation:
Address :
B. HISTORY OF PATIENT
RELATED TO CARDIOVASCULAR MEDICINE
11
C. GENERAL EXAMINATION
12
1. Anaemia / cyanosis/ jaundice/ clubbing/ oedema.
2. Body weight = kgs, Height = CMS.
3. Pulse = / min, regular/ irregular/ inequality/ arterial wall
thickened, PERIPHERAL PULSES
4. BP = mmHg. ALL FOUR LIMBS IN SITTING
AND STANDING
5. Temperature =
6. Lymph nodes = not enlarged/ enlarged – site:
7. Neck vein = not engorged/ engorged (pulsatile / not pulsatile)
8. Xanthoma/ Xanthelasma / locomotor brachialis.
9. Peripheral signs of IE
D. SYSTEMIC EXAMINATION:
A. Cardiovascular system.
INSPECTION: - PALPATION: ASCULTATION:

JUGULAR VENOUS PRESSURE: NYHA
CLASS OF HF:
LOW OUTPUT STATE: YES/NO
CONGESTION: YES/NO HEMODYNAMIC
PROFILE: A/B/C/D
a. Respiratory system
b. Examination of abdomen
12
c. Nervous system:
E. INVESTIGATIONS:
1. Hemogram:
ii. Hb= g/dl ESR= mm/hr
iii. TLC = /cu mm
iv. DC N L E M B
v. Platelet= L/cu mm.
12
2. Serum Sugar (R) = mg/dl.
3. Serum lipid profile:
i. Total cholesterol = mg/dl
ii. HDL-C = mg/dl.
iii. LDL-C = mg/dl.
iv. VLDL-C = mg/dl.
v. Triglycerides = mg/ dl.
4. NT PRO BNP
5. Cardiac biomarkers
6. D dimer
7. Chest X-ray (PA view) :
8. ECG :
9. 2D ECHO :
10. RVC -
CVP= PCWP= CARDIAC
INDEX= STROKE VOLUME INDEX=
LVSWI= RVSWI = RVEF= RVEDV
= SVRI = PVRI=
12
Clinical status to be judged by following criteria and signs and symptoms:
severely decompensated HF, including:
1 Hypotension 2 Worsening renal function 3 Altered mentation
4 Dyspnoea at rest 5 Resting tachypnoea 6 oxygen saturation<90%
7. Hemodynamically significant arrhythmia as new onset of rapid AF
8. 8.Acute coronary syndromes
Signs and Symptoms of Congestion in HF
Pulmonary Systemic
Symptoms Dyspnea Edema
Abdominal (or
Orthopnea hepatic) swelling
and pain
Paroxysmal nocturnal
dyspnea (PND)
Signs Rales Edema
12
Pulmonary Systemic
Wheezing Elevated JVP
Pleural effusion Hepatic enlargement

and tenderness
Hypoxemia Ascites
Third heart sound Third heart

(left-sided) ∗ sound (right-
sided) ∗
Worsening mitral Worsening

regurgitation tricuspid
regurgitation
Hepatojugular reflux
* May occur without congestion.

With clinical status patients will be categorised according to AHA/AAC/ NYHA CLASS
guidelines Heart failure grading and corelated with findings of RHC.
12
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1

S.NO. LIST OF CONTENTS PAGE

2 AIMS AND OBJECTIVES

4 MATERIALS AND METHODS

5 RESULTS AND OBSERVATION

S.NO. LIST OF FIGURES PAGE

1 Figure 1: The development of acute decompensated heart failure

2 Figure 2 : The Framingham criteria

3 Figure 3 : The American College of Cardiology/ American Heart

4 Figure 4 : Classification of Acute decompensated heart failure.

5 Figure 5 : According to their initial clinical presentation

6 Figure 6: Management protocol

7 Figure : 7: schematic diagram of clinical profile

S.NO. LIST OF TABLES PAGE

2 TABLE 2 : Bar diagram showing distribution of ANAEMIA

3 TABLE 3 : Bar diagram showing distribution of CYANOSIS

4 TABLE 4 : Pie diagram showing distribution of JAUNDICE

5 TABLE 5 : Bar diagram showing distribution of EDEMA

6 TABLE 6 : Pie diagram showing distribution of JVP

7 TABLE 7 : Pie diagram showing distribution of STEVENSON

8 TABLE 8 : Bar diagram showing distribution of S3 Heart sound

9 TABLE 9 : Pie diagram showing distribution of CREPTS

10 TABLE 10 : Pie diagram showing distribution of HEPATOMEGALY

11 TABLE 11 : Pie diagram showing distribution of MENTAL STATUS

12 TABLE 12 : BAR diagram showing distribution of BIOMARKERS

13 TABLE 13 : BAR diagram showing distribution of CHEST X RAY

14 TABLE 14 : BAR diagram showing distribution of CONGESTION

15 TABLE 15 : BAR diagram showing distribution of EFFUSSION

16 TABLE 16 : BAR diagram showing distribution of RSIK FACTORS

17 TABLE 17 : STATISTICAL ANALYSIS

18 Graph 17 : BAR diagram showing distribution of NHYA

19 TABLE 18 : BAR diagram showing distribution of STATISTICAL

ANALYSIS OF RHC PCWP

20 TABLE 19 : BAR diagram showing distribution of STATISTICAL

21 TABLE 20 : BAR diagram showing distribution of STATISTICAL

22 TABLE 21: BAR diagram showing distribution of STATISTICAL

23 TABLE 22: BAR diagram showing distribution of STATISTICAL

24 TABLE 23: BAR diagram showing distribution of STATISTICAL

25 TABLE 24: BAR diagram showing distribution of STATISTICAL

CORRELATION BETWEEN EDEMA AND CO

26 TABLE 25: BAR diagram showing distribution of STATISTICAL

27 TABLE 26: BAR diagram showing distribution of STATISTICAL

ANALYSIS OF RHC PCWP

28 TABLE 27: BAR diagram showing distribution of STATISTICAL

CORRELATION OF PA PRESUURE WITH HEPATOMEGALY

29 TABLE 28: BAR diagram showing distribution of STATISTICAL

CORRELATION OF MENTAL STATUS

30 TABLE 29: BAR diagram showing distribution of STATISTICAL

CORRELATION OF PA PRESSURE WITH EFFUSION

STATISTICAL CORRELATION OF STEVENSON

32 TABLE 31: Histogram diagram showing distribution of PEARSON

STATISTICAL CORRELATION OF QRS COMPLEX

33 TABLE 32: Histogram diagram showing distribution of PEARSON

STATISTICAL CORRELATION OF RHC PCWP

34 TABLE 33: Histogram diagram showing PROBNP

35 TABLE 34: COMPARATIVE STUDIES OF PCWP, mm Hg

36 TABLE 35 :DISTRIBUTION OF NUMBER OF SUBJECTS WITH

DESIGNATED H&P EXAMINATION .