Pt's ECG: Sinus Tachycardia, Left Axis Deviation, Anterolateral Wall Ischemia

2020-2021 IM2
DIAGNOSIS:
PWI: Atherosclerosis, Coronary Artery Disease s/p MI, s/p CABG (1997), dilated LV, MR, sinus rhythm, in HFREF,
NYHA Functional Class III
Secondary Dx: Hypertension, Diabetes mellitus Type 2
Worsening dyspnea is a cardinal symptom of HF and typically is related to increases in cardiac filling pressures but
also may represent restricted cardiac output. PND is one of the highly reliable indicators of HF, nocturnal cough is a
frequently overlooked symptom. These symptoms all typically reflect pulmonary congestion whereas a history of weight
gain, increasing abdominal girth, early satiety and onset of edema in dependent organs indicate right heart congestion.
The presence of hypertension, CAD and diabetes is particularly helpful because these conditions account for 90% of the
population attributable risk for HF.
The physical findings complement information from the medical history in defining the presence and severity of HF. The
examiner should assess a patient’s body habitus and state of alertness, as well as whether the patient is comfortable,
short of breath, coughing or in pain. The skin may show pallor or cyanosis due to underperfusion.
A characteristic MR murmur is heard in many patients in HF due to either ischemia of the papillary muscle itself or
noncoaptation of the valves due to dilated ventricle. The presence of an S3 suggests an increased ventricular filling
volume. It is highly specific for HF and carries a substantial prognostic meaning.
A key objective of the examination of patients is to detect and quantify the presence of volume retention with or without
pulmonary congestion and/or systemic congestion. The most definitive method for assessing a patient’s volume
status by PE is by measuring JVP. An elevated JVP has a good sensitivity and sensitivity for elevated left sided filling
pressures and may be improved by doing the hepatojugular reflux (sustained rise of more than 3 cm in JVP for at
least 15 seconds after release of pressure on RUQ).
Leakage of fluid from the pulmonary capillaries into the alveoli can manifest as rales or rhonchi and wheezing may
occur with reactive bronchoscontriction. Rales due to heart failure are usually fine. However, rales are not often heard in
patients with background of chronic heart failure and pulmonary venous hypertension because of increased lymphatic
drainage reinforcing the clinical pearl that absence of rales DOES NOT necessarily mean normal LV filling
pressures.
Peripheral edema is present in up to 65% of patients hospitalized for AHF and less common in low output states. It has a
reasonable predictive value for AHF but its absence also does not exclude the diagnsosi. Usually it is dependent,
symmetric and pitting. Ascites occurs in response to elevated CVP by retarding emptying of the peritoneal veins and
hepatic veins.
Diagnosis of CHF is a clinical one, using the Framingham criteria.

D. Differentials: MUST primarily rule out Acute Coronary Syndromes (diabetic patients may have atypical
presentation or angina equivalents), infection (ie CAP which may be a differential or an aggravating comorbidity in this
patient).
TESTS:
ECG - is a standard part of the initial evaluation of a patient with HF because it may present clues about the incident HF
while also assisting in episodes of decompensation. (Pt’s ECG: sinus tachycardia, left axis deviation, anterolateral
wall ischemia)
CXR - should be a routine part of the early evaluation. In many cases, particularly in those with advanced heart failure
may be entirely clear despite significant symptoms of dyspnea. The classic findings are the “butterfly” pattern of interstitial
or alveolar edema. Many patients will have subtle findings of which are increased interstitial markings including Kerley B
lines.
(Pt’s CXR: cardiomegaly – LV form, LA enlargement (loss of cardiac waistline), pulmonary edema – (+)
cephalization, Kerley B lines, poss pleural effusion, right)
CBC and Blood chemistry

Patients with HF should undergo testing with a laboratory panel that includes electrolytes, BUN, serum crea, hepatic
enzymes, lipid profile, TSH, uric acid, CBC and urinalysis. HBa1c is also needed in this patient. Look for treatable causes
of decompensation.
Labs for this patient: Hypokalemia may be due to diuretic use. Ace-I, ARB’s and spironolactone may also increase
creatinine. Uric acid levels are also prognostic and may increase due to use of diuretics. Liver enzymes may increase due
to hepatic congestion and due to medications. Anemia may be present due to chronic disease and is associated with
more severe symptoms and decreased exercise capacity.
2020-2021 IM2
Biomarkers (Natriuretic peptides)

Now being used to distinguish HF from other disease states and as an adjunct to the initial and subsequent evaluation
to provide important prognostic information.
BNP and NT pro BNP are released form cardiomyocytes in response to stretch. It may also increase in other conditons
like renal failure and sepsis. Hence, their results should be interpreted in the context of sound clinical judgment. Serial
follow up measurements add incrementally important prognostic information. A BNP or NT pro BNP decrease of 30% or
more by hospital discharge is desirable.
Cardiac enzymes
Need to rule out possibility of acute coronary syndrome in this patient (may be atypical presentation since diabetic) which
may have triggered acute decompensation.
2D-echo
Imaging helps confirm diagnosis of HF by assessing presence and severity of structural and functional changes in the
heart, provide clues about the etiology of cardiac dysfunction, risk stratify patients and probably guide treatment
strategies. Which data is important? Wall motion abnormalities, ejection fraction, chamber sizes, degree of regurgitation,
pulmonary pressures.
MANAGEMENT:
Since the patient is acutely decompensated, hospitalization is warranted.
Acute Heart Failure:

1) Diuretics – Loop diuretics are the primary agents for treatment of volume overload
Potassium sparing diuretics in hypokalemic patients
2) Vasodilators
In the absence of hypotension, may be used as 1st line in combination with diuretics.
- Nitrates are potent venodilators producing rapid decreases in pulmonary venous and ventricular filling pressure.
-Nitroprusside produces balanced reduction in afterload and preload, particularly effective in those with increased
afterload (hypertensive heart disease).
3) Inotropes
Associated with significant side effects such as hypertension and arrhythmia. Reserved for selected cases of
hypoperfusion
Prevention of Disease progression:

1) Ace inhibitors/ARB or ARNIs
ACEi/ARBs are the cornerstone of CHF management which have been proven to stabilize LV remodeling, relieve patient
symptoms, prevent hospitalization and prolong it. The doses should be titrated up to the levels of the clinical trials.
Higher doses are more effective in preventing rehospitalization. BP, renal function and potassium should be
evaluated within 1 to 2 weeks of initiation. Abrupt withdrawal may lead to clinical deterioration. ACEi reduce mortality in
direct relation to the degree of severity of HF.
ARNIs (sacubitril-valsartan) quickly became Class 1 recommendation for HFrEF due to its proven benefit in decreasing
morbidity and mortality over enalapril alone.
2) Beta blockers
Interfere with the harmful effects of sustained activation of the SNS by competitively antagonizing one or two adrenergic
receptors (alpha1, B1 and B2). Most of the deleterious effects are mediated by the beta1 receptor. When given in concert
with ACE-inhibitors, they reverse the process of LV remodeling, ameliorate symptoms, reduce hospitalization and
prolong life. Only three beta blockers have been shown to reduce mortality: Carvedilol, long-acting metoprolol
(succinate NOT tartrate) and bisoprolol. DO NOT GIVE during ACUTE HEART FAILURE. Dose titration must be done
every two weeks.
3) Aldosterone Antagonists
Have beneficial effects independent to their effect in Na homeostasis. Administration is recommended in patiens with
NYHA Class II or IV who have a depressed EF < 35% and who are receiving standard therapy including ACEi, diuretic
and beta blockers. Not recommended if crea > 2.5 or K > 5.5.
Others:
2020-2021 IM2
Digoxin
Inhibition of Na-K-ATPase pump in cell membranes leading to increase in intracellular Ca and hence increase in cardiac
contractility. More likely mechanism is to sensitize Na-K-ATPase activity in vagal afferent nerves leading to an increase in
vagal tone that counterbalances the increased activation of the adrenergic system in advanced HF.
Useful in patients with systolic dysfunction. Decreases symptoms and hospitalization but NO EFFECT on
morbidity/mortality. Side effects: Arrhythmias, neurologic complaints of visual disturbances, disorientation and confusion.

Pt's ECG: Sinus Tachycardia, Left Axis Deviation, Anterolateral Wall Ischemia

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Pt's ECG: Sinus Tachycardia, Left Axis Deviation, Anterolateral Wall Ischemia

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2020-2021 IM2

Diagnosis of CHF is a clinical one, using the Framingham criteria.

CBC and Blood chemistry

Biomarkers (Natriuretic peptides)

Acute Heart Failure:

Prevention of Disease progression:

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