heart failure - case 1
Presented by: Huda Firdouse
Roll no. 105
I have been given this case to solve and interpret to enhance my competency and as an attempt to understand the topic of “patient clinical data analysis”.
You can find the entire clinical problem of the patient in this
link:
This is my understanding of the case:
35 year old male presented with
Chief complaints of:
1.
Shortness of breath [since 2 weeks]
2.
B/l Pedal edema [since 2 weeks]
h/o high grade fever with chills 1 months back which
relieved on taking anti malarial treatment
SHORTNESS OF BREATH:
Initially NYHA class 3 after treatment class 2 [at present]
h/o paroxysmal nocturnal dyspnea
and generalized weakness from 2 weeks.
B/L PEDAL EDEMA:
Extending upto knee
Pitting type
Progressive in nature
EXAMINATION FINDINGS:[positive
findings]
Edema upto knees
[grade 2]
Respiratory system:
right ISA early inspiratory crepts+
Raised JVP
INVESTIGATION
FINDINGS:
Hb:15.2
Tlc: 9600
Platelet count: 2.39
FBS: 102
PLBS: 205
Total cholesterol: 150
Triglycerides: 87
Hal:33
LDL: 72
Vldl:17.4
Urea: 24
Creatinine: 0.8
Uric acid: 6
USG abdomen:
·
right moderate pleural effusion,
·
grade 1
fatty liver,
·
mild
ascites
2D ECHO:
· EF – 27%,
·
IVC dilated[2.3cm] not collapsing,
·
mild TR +,
·
trivial AR +,
·
dilated all chambers,
·
global
hypokinesia, mild PAHT
MY THOUGHTS:
Symptoms like:
Grade 2 Dyspnea,
Paroxysmal nocturnal dyspnea
b/l pedal edema
Are most likely to be due to a cardiac origin
[ above findings are suggestive of heart failure- dyspnea on exertion and edema are characteristic
features of heart failure]
There is h/o fever with chills prior to the onset of
symptoms
This is suggestive of some infective cause of heart failure.
Most probably I suspect
a viral cause------>viral myocarditis--------->heart failure
On examination there is:
1.
raised JVP [supports probable diagnosis of heart
failure
2.
Right ISA early inspiratory crepts+
On further investigation:
FBS: 102
[ suggestive of DM type 2, not a known case of DM hence denovo]
USG:
• right moderate pleural effusion,
•
grade 1 fatty liver,
•
mild ascites
2D ECHO:
• EF
– 27%,
• IVC
dilated[2.3cm] not collapsing,
• mild TR +,
• trivial AR +,
• dilated
all chambers,
•
global hypokinesia, mild PAHT
SHOWS reduced ejection fraction- suggestive of heart failure with reduced ejection
fraction
Dilated cardiomyopathy
Pulmonary artery
hypertension
Probable diagnosis : heart failure with reduced
ejection fraction secondary to viral myocarditis with denovo type 2 DM.
what made me think of this is:
from the symptoms and signs in the patient-
>" The current American College of Cardiology Foundation (ACCF)/American Heart Association (AHA) guidelines define HF as a complex clinical syndrome that results from structural or functional impairment of ventricular filling or ejection of blood, which in turn leads to the cardinal clinical symptoms of dyspnea and fatigue and signs of HF, namely edema and rales."
source: harrison’s principles of internal medicine 20th edition
from above statement i suspect probable diagnosis of case as heart failure.
then the question is what could be the cause:
from the h/o high grade fever with chills 15 days prior to onset of symptoms and no h/o of similar complaints in the past- this makes me think of a acute onset of disease and infectious cause, examination and investigation findings direct me that the underlying cause could be myocarditis.
"Clinical Presentation of Viral Myocarditis Acute viral
myocarditis often presents with symptoms and signs of heart failure"
"The typical patient with presumed viral myocarditis is a young to middle-aged adult who develops progressive dyspnea and weakness within a few days to weeks after a viral syndrome that was accompanied by fever and myalgias"
>"In 20–30% of the cases of HF with a depressed EF, the exact etiologic basis is not known. These patients are referred to as having nonischemic, dilated, or idiopathic cardiomyopathy if the cause is unknown . Prior viral infection or toxin exposure (e.g., alcoholic or chemotherapeutic) also may lead to a dilated cardiomyopathy"
source: harrison’s principles of internal medicine 20th edition
the above statement are in support of probable cause as viral myocarditis
Anatomical site involved: myocardiumPathology involved:
Potential effects of viral infection of the heart:
Source: http://www.pjmonline.org/viral-infection-of-the-heart-pathogenesis-and-diagnosis/
Dilated cardiomyopathy
secondary to viral myocarditis:
Source: harrison’s principles of internal medicine 20th
edition
Dilated cardiomyopathy:
In dilated
cardiomyopathy- Mitral regurgitation
commonly develops as the valvular apparatus is distorted and is usually
substantial by the time heart failure is severe. Many cases that present
“acutely” have progressed silently through these stages over months to years.
Dilation and decreased function of the right ventricle may result directly from
the initial injury, but more often develops later in response to elevated
afterload presented by secondary
pulmonary hypertension and in relation to mechanical interactions with the
failing left ventricle.
Source: harrison’s principles of internal medicine 20th edition
Pathology behind pleural effusion , rales, ascites, fatty liver :
The lungs of chronic heart failure patients undergo adaptive
changes and have robust lymphatic drainage to compensate for elevated filling pressures.
However, a subset of patients may develop alveolar fluid accumulation, which is
appreciated as rales . These findings are more common in patients with acute
pulmonary edema due to sudden decompensation from an inciting event.
Fluid may also accumulate in the pleural space related to
the increased
transudation of fluid and impaired lymphatic drainage in the
setting of elevated
systemic venous pressures .The clinician should listen and
percuss
for the possible presence of pleural effusions , which tend
to
lateralize to the right side owing to the greater surface
area of the lungs and
the position of the diaphragm. The diagnosis of a moderate
or large pleural
effusion is critical because draining the effusion may
improve dyspnea.
Source: (26th edition) Lee Goldman, MD and Andrew I.
Schafer, MD - Goldman-Cecil Medicine, 2-Volume Set, 26th Edition-Elsevier
(2020). Chapter 52, page no. 279
In patients with heart failure:on-
Pulmonary Examination:
Pulmonary crackles (rales or crepitations) result from the transudation of fluid from the intravascular space into the alveoli. In patients with pulmonary edema, rales may be heard widely over both lung fields and may be accompanied by expiratory wheezing (cardiac asthma). When present in patients without concomitant lung disease, rales are specific for HF. Importantly, rales are frequently absent in patients with chronic HF, even when LV filling pressures are elevated, because of increased lymphatic drainage of alveolar fluid. Pleural effusions result from the elevation of pleural capillary pressure and the resulting transudation of fluid into the pleural cavities. Since the pleural veins drain into both the systemic and the pulmonary veins, pleural effusions occur most commonly with biventricular failure. Although pleural effusions are often bilateral in HF, when they are unilateral, they occur more frequently in the right pleural space.
Abdomen and Extremities:
Hepatomegaly is an important sign in patients with HF. When it is present, the enlarged liver is frequently tender and may pulsate during systole if tricuspid regurgitation is present. Ascites, a late sign, occurs as a consequence of increased pressure in the hepatic veins and the veins draining the peritoneum. Jaundice, also a late finding in HF, results from impairment of hepatic function secondary to hepatic congestion and hepatocellular hypoxemia and is associated with elevations of both direct and indirect bilirubin. Peripheral edema is a cardinal manifestation of HF, but it is nonspecific and usually is absent in patients who have been treated adequately with diuretics. Peripheral edema is usually symmetric and dependent in HF and occurs predominantly in the ankles and the pretibial region in ambulatory patients. In bedridden patients, edema may be found in the sacral area (presacral edema) and the scrotum. Long-standing edema may be associated with indurated and pigmented skin.
Source: harrison’s principles of internal medicine 20th edition
Clinical manifestations seen in
dilated cardiomyopathy:
The symptoms and signs associated with dilated
cardiomyopathy depend on the age of the patient and the degree of left
ventricular dysfunction. Although the first presentation may be with sudden
death or a thromboembolic event, most patients present with symptoms of high
pulmonary venous pressure or low cardiac output , which can be acute, sometimes
precipitated by intercurrent illness or arrhythmia, or chronic. Increasingly,
dilated cardiomyopathy is diagnosed incidentally in asymptomatic individuals
during family screening. Adults initially present with reduced exercise tolerance and dyspnea on exertion. With worsening left
ventricular function, patients may develop dyspnea at rest, orthopnea,
paroxysmal nocturnal dyspnea, peripheral edema, and ascites. Symptoms
related to mesenteric ischemia, such as abdominal pain after meals, nausea,
vomiting, and anorexia, may dominate, especially in children. Arrhythmia
symptoms, such as palpitations, presyncope, and syncope, can occur at any age.
In advanced disease, features of low cardiac output include sinus tachycardia,
weak peripheral pulses, and hypotension. The
jugular venous pressure may be elevated, and the apical impulse is displaced.
Peripheral edema, hepatomegaly, and ascites are common in patients with heart
failure. Auscultation of the chest typically reveals basal crackles. Auscultation of the heart may reveal the presence
of a third (and sometimes also a fourth) heart sound. In patients with
functional mitral regurgitation, a pansystolic murmur may be heard at the apex
and radiate to the axilla, but frequently no murmurs are heard, even in the
presence of mitral incompetence, especially if cardiac output is very low.
Source: : (26th edition) Lee Goldman, MD and Andrew I.
Schafer, MD - Goldman-Cecil Medicine, 2-Volume Set, 26th Edition-Elsevier
(2020). Chapter 54, page no. 304
Echo findings in dilated cardiomyopathy:
On echocardiography,
the presence of ventricular
end-diastolic dimensions greater than 2 standard deviations above body surface
area–corrected means (or greater than 112% of predicted dimension) and
fractional shortening less than 25% are sufficient to make the diagnosis. Other
common features include functional
mitral and tricuspid regurgitation and abnormalities of diastolic left
ventricular function. Cardiac magnetic resonance imaging may show areas of
myocardial fibrosis
Source: : (26th edition) Lee Goldman, MD and Andrew I.
Schafer, MD - Goldman-Cecil Medicine, 2-Volume Set, 26th Edition-Elsevier
(2020). Chapter 54, page no. 304
cardiology fact sheet stateing the reason for ascites and pleural effusion in patients with dilated cardiomyopathy:
If pressures on the left side of the heart become significantly high as a result of increased blood volume, left-sided congestive heart failure or pulmonary edema (fluid within the lungs) can result. Although less common, myocardial failure of the right side of the heart can also occur. Similar volume overload of the right heart may result in right-sided congestive heart failure, often resulting in excessive free-fluid in the abdomen (ascites) and/or chest (pleural effusion).
Pathophysiology
of pulmonary hypertension and right heart failure in left heart disease:
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348356/
Heart failure with reduced ejection fraction secondary to viral myocarditis with denovo DM type 2
TREATMENT:
PHARMACOLOGICAL:
Tab.lasix 80mg...40mg...40mg --Diuretic to treat edema
Tab.isosorbide mononitrate10mg bd
Tab.hydralazine 25mg --for Hypertension and heart failure
Tab. Telma20mg --for hypertension and heart failure
Tab.metformin 500mg po od -- for treating Diabetes type 2
NON-PHARMACOLOGICAL:
Fluid restriction <1litre/day
Salt restriction <2gms/day
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