a 45-year-old man is brought to the emergency department
following a minor traffic accident.
At the scene of the accident, the police noted that he
smelled of alcohol and was confused.
He has consumed one liter of vodka per day for 20 years.
On physical exam, the blood pressure's elevated at 155/90
mmHg as is the heart rate at a 102/min,
jugular venous pulse is also elevated 15 cm of water
demonstrating that right atrial pressure is elevated.
The respiratory sounds on the lung exam showed diffused
wheezes and crackles
and there's a prominent third heart sound.
That's the sound of heart failure marked decrease compliance
or elasticity in the left ventricle
and let's have a demonstration.
Here's a normal heart, lub-dub, lub-dub, lub-dub.
Here's the third heart sound, lub-dubd, lub-dubd, lub-dubd,
and the abdomen is distended, the liver's not palpable,
probably shrunken by cirrhosis, the distended abdomen is
that is fluid in the abdomen in end-stage liver disease.
And he has 3+ pitting edema again, a sign of heart failure.
On laboratory he's anemic with a low white blood cell count
and low platelet count quite common in end-stage liver
Fortunately, his kidneys are still working well. His
creatinine is normal.
And the liver function test demonstrates, of course marked
His bilirubin is 12 mg/dL. His brain natriuretic peptide or
BNP is elevated
at 2000 pg/mL implying significant volume overload.
Just to go through the critical points in the story,
he's an alcoholic with a huge alcohol consumption for many
His blood pressure's elevated, not uncommon in alcoholics.
Heart rate also along with the jugular venous pulse and the
crackles in the lung
and the third heart sound tell you that there's left
His abdomen is distended implying that he has ascites that
is fluid in the abdomen a sign of end-stage liver disease
and of course, his extremities head edema also part of the
He's anemic, has a low white blood cell count and a low
platelet count all of which go with end-stage liver disease
and of course, his liver function tests are very abnormal
and his brain natriuretic peptide
or BNP test is telling us that there's heart failure.
Here's his chest X-ray. It' clear he's in pulmonary edema.
There's lots of excess fluid in the lung and the heart
although on a PNS X-ray you can't be a hundred percent
The first diagnostic test is an echocardiogram which
confirms that this man has severe damage to his left
The left ventricular ejection fraction is only 15%, normal
would be above 50%
and he has a variety of blood tests and ultrasound showing
that he has advanced cirrhosis of the liver
and his physical exam suggests also ascites secondary to
So, the diagnosis: pulmonary edema secondary to alcohol
Alcohol intake in large amounts is a toxin to the myocardium
and taken over many years results in very severe myocardial
damage to the left ventricle.
If the patient stops drinking soon enough, there can be
but if it's been going on for a very long time, there may be
Well, to make the patient more comfortable,
we give intravenous diuretics to induce a diuresis to get
rid of some of the excess alcohol.
We have to have alcohol withdrawal monitoring to make sure
the patient doesn't go into delirium tremens
and there's a whole protocol for that, the so-called 'CIWA
And then he needs a heart failure evaluation and management
probably since his creatinine is normal,
we would use ACE inhibitors that is angiotensin converting
or angiotensin receptor blockers as well as a trial for beta
blockers such as carvedilol.
And it would be important for him absolutely not to drink
I tell patients like this, 'for you alcohol is poison'.
So in follow up, he diuresis, he loses 32 lbs over a couple
He starts on low doses of carvedilol, lisinopril as an
angiotensin converting enzyme inhibitor,
spironolactone blocks aldosterone also part of the renin
and we start with low doses in his medicines and gradually
For patients such as this one with heart failure with
reduced ejection fraction,
of course referred to as HfRef, as we talk about.
If patients have contraindications to any of the renin
angiotensin system antagonists,
an alternative is hydralazine plus a long-acting nitrate.
In patients who still have symptomatic heart failure,
secondary therapies may be added in addition to the initial
These include mineralocorticoid receptor antagonists such as
spironolactone that I just mentioned, or SGLT2 Inhibitors.
If further secondary therapies are needed, newer medications
include verciquat or ivabradine.
and as we talkt about befor Vericiguat
is indicated for people with New York heart association
class 2 to 4 heart failure
with an ejection fraction less than 45%
who were either hospitalized in the last 6 months or
required outpatient IV diuretics.
Ivabradine is a newer class of medication
called a hyperpolarization-activated cyclic nucleotide-gated
(HCN) channel blocker
It is indicated for patients with an ejection fraction 35%
who are in sinus rhythm with a resting heart rate at least
70 beats a minute or more
despite beta blockers or with contraindications to beta
blockers or contra indications to beta blockers.
Ivabradine works by slowing the sinus node
by slowing the spontaneous ingress of sodium through the
so-called funny channel into the sinus node cells.
He has a coronary angiogram to make sure he doesn't have
It's normal which is quite common in alcoholics since
cholesterol is produced in the liver.
And when you have a liver that's not working, usually the
cholesterol's quite low.
The abdominal ultrasound confirms liver cirrhosis and
and of course, we recommend that he never drink alcohol