Pharmacologic Treatment for Cardiac failure

Most people with heart failure are treated with medication. Often you'll need to take 2 or
3 different medicines.

Some of the main medicines for heart failure include:

 ACE inhibitors
 angiotensin-2 receptor blockers (ARBs)
 beta blockers
 mineralocorticoid receptor antagonists
 diuretics
 ivabradine
 sacubitril valsartan
 hydralazine with nitrate
 digoxin
You may need to try a few different medicines before you find a combination that
controls your symptoms but doesn't cause unpleasant side effects.

ACE inhibitors

Angiotensin-converting enzyme (ACE) inhibitors work by relaxing and opening up your

blood vessels, which makes it easier for your heart to pump blood around the body.

Examples of ACE inhibitors include ramipril,

captopril, enalapril, lisinopril and perindopril.

The most common side effect of ACE inhibitors is a dry, irritating cough.

If you have a troublesome cough, an ACE inhibitor may be switched to an ARB.

ACE inhibitors can also cause your blood pressure to fall too low, and they may cause
kidney problems. Your GP will monitor this.

Angiotensin-2 receptor blockers (ARBs)

Angiotensin-2 receptor blockers (ARBs) work in a similar way to ACE inhibitors by

relaxing blood vessels and reducing blood pressure.
 They tend to be used as an alternative to ACE inhibitors because they don't usually
cause a cough, although they may not be quite as effective as ACE inhibitors.

Examples of ARBs include candesartan, losartan, telmisartan and valsartan.

Side effects of ARBs can include low blood pressure and high levels of potassium in
your blood.

Your doctor will carry out regular blood tests to monitor your potassium level.

Coronavirus advice
If you have coronavirus (COVID-19), or think you might have it, keep taking your blood
pressure medicines as usual.

There is no clear evidence that taking angiotensin-converting enzyme (ACE) inhibitors

or angiotensin-2 receptor blockers (ARBs) will cause complications.
Beta blockers

Beta blockers work by slowing your heart down and protecting your heart from the
effects of adrenaline and noradrenaline, "fight or flight" chemicals produced by the body.

There are several different beta blockers, but the main ones used to treat heart failure in
the UK are bisoprolol, carvedilol and nebivolol.

Possible side effects include dizziness, tiredness and blurred vision.

But most people taking them have either no or very mild side effects that become less
troublesome with time.

Mineralocorticoid receptor antagonists (MRAs)

MRAs make you pass more urine, and help lower blood pressure and reduce fluid
around the heart, but they don't reduce potassium levels.

The most widely used MRAs are spironolactone and eplerenone.

Spironolactone may cause enlarged breasts in men (gynaecomastia) and breast

tenderness and increased hair growth in women.

Eplerenone can cause sleeping difficulties, dizziness and headaches.

The most serious side effect of these medicines is that they can cause the level of
potassium in your blood to become dangerously high.

Your doctor will carry out regular blood tests to check for this.

Diuretics

Diuretics (water pills) make you pass more urine and help relieve ankle swelling and
breathlessness caused by heart failure.

There are many different types of diuretic, but the most widely used for heart failure
are furosemide (also called frusemide) and bumetanide.

Possible side effects of diuretics include dehydration and reduced levels of sodium and
potassium in the blood.

Ivabradine

Ivabradine is a medicine that can help slow your heart down.

It's a useful alternative to beta blockers if you can't take them or they cause
troublesome side effects.

It can also be used alongside beta blockers if they don't slow the heart enough.

Possible side effects include headaches, dizziness and blurred vision.

Sacubitril valsartan

Sacubitril valsartan is a single tablet that combines an ARB and a medication called a
neprilysin inhibitor.

It's suitable for people with more severe heart failure, whose heart is only able to pump
a reduced amount of oxygenated blood around the body despite taking other
medication.

The most common side effects of sacubitril valsartan are low blood pressure, high
potassium levels and kidney problems.

Hydralazine with nitrate

Hydralazine in combination with nitrate can help relax and open up the blood vessels.

These medicines are sometimes prescribed by heart specialists (cardiologists) for

people who are unable to take an ACE inhibitor or ARB.

Side effects can include headaches, a fast heartbeat and a pounding, fluttering or
irregular heartbeat (palpitations).

Digoxin

Digoxin can improve your symptoms by strengthening your heart muscle contractions
and slowing down your heart rate.

It's normally only recommended for people who have symptoms despite treatment with
ACE inhibitors, ARBs, beta blockers and diuretics.

Possible side effects include dizziness, blurred vision, feeling and being
sick, diarrhoea and an irregular heartbeat.

Pharmacologic Treatment for Acute Myocardial Infection

Aspirin
All patients with a suspected myocardial infarction should be given aspirin. It is a
powerful antiplatelet drug, with a rapid effect, which reduces mortality by 20%. 2 Aspirin,
150-300 mg, should be swallowed as early as possible. General practitioners should
give aspirin or advise the patient to take an aspirin when they are called by a patient
who may be suffering a myocardial infarction. There is no need to wait for an
electrocardiograph (ECG). If the patient has not already taken aspirin, it should be given
in the ambulance or emergency room.

Fibrinolytic therapy
The mainstay of treatment is fibrinolytic therapy. This is given to dissolve the thrombus
in the artery and restore flow. There are two fibrinolytic drugs commonly used in
Australia - streptokinase and tissue plasminogen activator (tPA).

Fibrinolytic therapy should be given to all patients with appropriate indications and no
contraindications (Table 1).

The indications for fibrinolytic therapy are symptoms of myocardial ischaemia, of less
than 12 hours' duration, with ECG changes of ST elevation or left bundle branch block.
Patients without these ECG changes should not be given fibrinolytic therapy.3
 Table 1
Indications and contraindications for fibrinolytic therapy

Indications
 within 12 hours of onset of chest pain lasting for at least 30 minutes
 ECG changes of ST elevation of at least 1 mm in two or more contiguous leads, or left bundle
branch block
Contraindications
 cerebral event within 6 months
 major trauma including surgery within 1 month
 bleeding peptic ulcer within 2 months
 uncontrolled hypertension
 non-compressible vascular puncture

The concern with fibrinolytic therapy is bleeding. The most feared form of bleeding is
intracerebral bleeding which is usually fatal. Therefore, patients with contraindications
(Table 1) should be considered for acute PTCA. Uncontrolled hypertension is a relative
contraindication and attempts should be made to lower the blood pressure below 175
mmHg systolic and 100 mmHg diastolic. A history of an ulcer or recent cardio-
pulmonary resuscitation is not an absolute contraindication.

Streptokinase
Streptokinase produces generalised systemic fibrinolysis and is the drug most
commonly used in Australia. Despite reducing mortality by 25%1,2, only about 30% of
patients have their coronary flow restored to normal within 90 minutes of treatment. This
increases to over 50% by 3 hours and up to 80% by 5-7 days.4

An intravenous infusion of 1.5 million units is given over 30-60 minutes. Most patients
will develop hypotension if streptokinase is given quickly, but this is usually easily
overcome by slowing the infusion and giving fluid.

Streptokinase is derived from Streptococci and will produce an antibody reaction. These
antibodies appear after 2-3 days and persist for some years. The presence of
antibodies reduces the efficacy of subsequent doses of streptokinase and increases the
potential for anaphylaxis. The present consensus is that streptokinase should be used
only once per patient.5 All patients should be informed about being treated with
streptokinase and ideally given a card or other form of record so that this information is
available should they have another infarction.
Tissue plasminogen activator (tPA)
As tPA specifically binds to thrombus, it produces local fibrinolysis. It does not have the
same systemic effects as streptokinase.

Clot dissolution occurs more promptly with tPA than streptokinase restoring patency at
90 minutes in 55% of patients.4 However, by 3 hours and 5-7 days there is no major
difference in patency in patients treated with streptokinase or tPA. This improved early
patency results in slightly improved mortality (6.3% tPA versus 7.1% streptokinase). 6

Compared with streptokinase, tPA appears to cause more bleeding and, in particular,
produces a higher incidence of cerebral bleeding. There are 2-3 extra strokes per 1000
patients treated and one of these patients dies from their stroke. Therefore, care should
be taken with patients at risk of stroke, the elderly and those with high blood pressure.

Despite the increased risk of stroke, the net clinical benefit is greater with tPA in nearly
all subgroups of patients. For every 1000 patients treated with tPA, there will be 10
extra survivors at the cost of one patient surviving with disability from a stroke.

tPA is not used in all patients because of its cost - approximately $1900 compared with
$150 for streptokinase. The current consensus in Australia is that tPA should be utilised
in

 patients who have previously had streptokinase

 patients aged less than 75 years having large myocardial infarctions who arrive within 4
hours of the onset of symptoms.5

The treatment regimen is shown in Table 2.

Table 2
tPA regimen
Bolus Maintenance
15 0.75 mg/kg over 30 minutes (not to exceed 50 mg) then 0.5 mg/kg over 60 minutes (not
mg to exceed 35 mg)

Heparin
Heparin is an antithrombin agent. It has been utilised with both fibrinolytic drugs and
given subcutaneously and intravenously.

Heparin and streptokinase

There is contention about the routine use of heparin with streptokinase. There has been
no apparent benefit on mortality of subcutaneous versus no heparin7 and no benefit of
intravenous heparin versus subcutaneous heparin.6 Equally, the addition of routine
intravenous or subcutaneous heparin does not appear to do any harm. Not giving
routine heparin has the benefit that clotting studies are not necessary and this may be
particularly advantageous in smaller hospitals without 24-hour laboratory facilities.
However, heparin may be required for clinical reasons e.g. large infarcts, ongoing
ischaemia.

Intravenous heparin is given as a 5000 unit bolus followed by 1000 units per hour
intravenously, adjusted after 24 hours according to the activated partial thromboplastin
time (APTT). (APTT measurements are little use in the first 24 hours as streptokinase
also raises the APTT.)

Heparin and tPA

Currently, it is believed that heparin should be given with tPA. The standard regimen is
an initial bolus of 5000 units, followed by an infusion of 1000 units per hour adjusted
after 6 hours for APTT.

ACE inhibitors
ACE inhibitors reduce the mortality of myocardial infarction and this benefit is seen
within the first 30 days. Issues in relation to the use of ACE inhibitors are:

 whether they should be given to all patients or only those with large infarcts
 when they should be given

Most Australian cardiologists give ACE inhibitors only to patients with large infarcts and
those with clinical signs of left ventricular failure. Captopril 6.25 mg, or equivalent low
doses of another ACE inhibitor, should be used as a first dose and, if tolerated, the dose
increased to at least 25 mg twice daily of captopril or the equivalent dose of the
alternatives. Current consensus is that they should be given as early as feasible when
the patient is haemodynamically stable.

Beta blockers
Intravenous beta blockers such as atenolol, metoprolol and timolol reduce the incidence
of arrhythmias, infarct size and mortality. As the effect is relatively small, they are not
widely used.

Beta blockers can be given if the patient is haemodynamically stable with a heart rate
above 50 beats per minute and systolic blood pressure above 100 mmHg.

The standard regimen is atenolol 5 mg intravenously over 5 minutes followed 10

minutes later by a further 5 mg. Oral beta blockade is commenced 30 minutes later.
Many centres use only oral beta blockade (atenolol 50 mg, metoprolol 50 mg)
commenced as soon as possible after admission.

Much of the data on beta blockers was obtained before the widespread use of
thrombolytic therapy. It is likely that the relative improvement in outcome would be the
same in patients treated with thrombolysis, but it is possible that the absolute magnitude
of the benefit would be reduced.

Glyceryl trinitrate
Intravenous glyceryl trinitrate reduces preload and after load and may help to keep the
coronary vessels open. In small studies, intravenous glyceryl trinitrate for 24 hours
reduced mortality, but this has not been confirmed by large trials. Intravenous glyceryl
trinitrate can be used routinely or only for ongoing chest pain or left ventricular failure
(the standard dose is 5 microgram/minute and this can be titrated against the blood
pressure).

Oral nitrates should not be used routinely as they are of no benefit.

Other drugs
Treatment with a calcium channel blocker or magnesium should not be used routinely in
patients with acute myocardial infarction as trials have not shown them to be beneficial.

Pain relief is important and should not be forgotten while administering thrombolytic
therapy or other drugs. Intravenous morphine titrated slowly, starting at 2.5 mg until
adequate relief is obtained, is the most appropriate drug. Intramuscular injection should
be avoided. Oxygen therapy is thought to be beneficial, although there have been no
trials to confirm this.

Pharmacologic Treatment for Acute Respiratory Failure

 Diuretics. Doctors commonly prescribe diuretics, such as furosemide (Lasix), to

decrease the pressure caused by excess fluid in your heart and lungs.

 Morphine (MS Contin, Oramorph, others). This narcotic may be taken by mouth
or given through an IV to relieve shortness of breath and anxiety. But some doctors
believe that the risks of morphine may outweigh the benefits and are more likely to
use other drugs.

 Blood pressure drugs. If you have high or low blood pressure when you develop
pulmonary edema, you'll be given medications to help manage the condition. Your
doctor may also prescribe medications that lower the pressure going into or out of
your heart. Examples of such medicines are nitroglycerin (Nitromist, Nitrostat,
others) and nitroprusside (Nitropress).

 Inotropes. This type of medication is given through an IV if you are in the hospital
with severe heart failure. Inotropes improve heart pumping function and maintain
blood pressure.
Pharmacologic Treatment for acute renal failure (ARF) may involve vasopressor drugs to help
raise the blood pressure, intravenous fluids to aid in rehydration, diuretics to increase urine
output, and hemodialysis to help filter the blood while the kidneys are healing.

The course of treatment is directed by the underlying cause, which is broadly classified into one
of three groups:1

 Prerenal ARF, in which the blood flow to the kidneys is impeded.

 Intrinsic ARF, in which the kidneys themselves are impaired.
 Postrenal ARF, in which the flow of urine out of the body is obstructed.

Prerenal ARF Treatment

For prerenal ARF to occur, both kidneys would need to be affected. There are several common
reasons for this, including dehydration (low blood volume), low blood pressure, congestive heart
failure, and liver cirrhosis.

These conditions directly or indirectly reduce the volume of blood received by the kidneys and
facilitate the progressive (and sometimes rapid) build-up of toxins in the body.

The aim of the treatment would be to restore the blood flow. There are several ways a doctor
might do this.

Dehydration and Low Blood Pressure

Dehydration may be treated with intravenous fluids. 1 The infusion of fluids would be monitored
with a central venous catheter (CVC) to ensure that you are neither overhydrated nor
underhydrated. If your low blood pressure persists despite intravenous fluids, vasopressor drugs
may be used to raise the blood pressure.

Norepinephrine is a common option. Injected into the blood, the hormone causes blood vessels to
contract, increasing the relative pressure within the vein. Side effects include headache, slowed
heart rate, and anxiety.

Congestive Heart Failure

Congestive heart failure (CHF) occurs when the heart is unable to pump sufficiently to maintain
the blood flow needed by the body. When this happens, it can lead to a state known
as cardiorenal syndrome (CRS). CRS is actually a two-way street in which the lack of blood flow
from the heart can affect kidney function, while the failure of the kidneys can lead to the
impairment of the heart.2

In the former state, diuretics are commonly used to increase the output of urine and aid in the
excretion of toxins from the body. Lasix (furosemide) in the most commonly prescribed diuretic
but one that needs to be managed to prevent drug resistance.
In addition, the combined use of ACE inhibitors (commonly used to treat high blood pressure)
and statin drugs (used to reduce cholesterol) may help normalize kidney function.

While it may seem counterintuitive to use a drug that would further reduce blood pressure, the
aim of therapy is to normalize the equilibrium between the heart and kidneys.

While there may, in fact, be a slight deterioration in kidney function over the short-term, the
continued, combined use of an ACE inhibitor and statin will ultimately have a protective effect
on the kidneys.

Commonly prescribed ACE inhibitors include Capoten (captopril), Lotensin (benazepril), and
Vasotec (enalapril). Commonly prescribed statins include Crestor (rosuvastatin), Lipitor
(atorvastatin), Pravachol (pravastatin), and Zocor (simvastatin).

Liver Cirrhosis

Cirrhosis is the state in which the progressive scarring of the liver leads to liver damage.
Cirrhosis can either be compensated, meaning the liver is still functioning, or decompensated,
meaning that it is not.

ARF most commonly occurs in the latter context, resulting in another irrelated condition known
as hepatorenal syndrome (HRS).

Liver transplant is considered the only definitive form of treatment.

In the absence of a transplant, your doctor may recommend the other interim approaches. Among
them:

 Transjugular intrahepatic portosystemic shunt (TIPS) is a procedure in which an

artificial channel is created in the liver using a wire mesh stent. This reduces the vascular
pressure within the liver which, in turn, alleviates the burden on the kidneys.
 Hemodialysis (popularly referred to as dialysis) involves the mechanical filtering of
blood to effectively take over the function of the kidneys.
 Liver dialysis is a newer form of mechanical detoxification still in its infancy that, unlike
hemodialysis, cannot be used for an extended period of time.
 Vasopressor drugs like midodrine, ornipressin, and terlipressin may help normalize
vascular pressure in people with HRS but may also adversely restrict the blood flow to
the heart and other organs. The combined use of the vasopressor midodrine and the
hormone Sandostatin (octreotide) may increase survival times in persons awaiting a
donor liver.

Intrinsic ARF Treatment

There are myriad reasons why a kidney may not function as normal, including trauma, infection,
toxins, vascular diseases, cancer, autoimmune disorders, and even complications of surgery.
While the approach to treatment will vary by the cause, the outcome will typically result in one
of three conditions: glomerulonephritis (GN), acute tubular necrosis (ATN), and acute interstitial
nephritis (AIN).3

Glomerulonephritis

Glomerulonephritis (GN) is the acute secondary inflammation of the kidneys that develops in
response to a primary disease. The diseases may include chronic illnesses like diabetes,
autoimmune ones like lupus, or even an infection like strep throat.

Medications such as ACE inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), and

penicillin can trigger GN in people with underlying kidney dysfunction.

Treatment depends on the underlying cause and may include:

 Termination of the suspected drug if the cause is believed to be drug-related.1

 Corticosteroids, a man-made hormone that can suppress the overall immune response and
alleviate inflammation.
 Lasix to increase urine output taken with a calcium supplement to prevent excessive
calcium loss.
 Potassium-reducing drug like Kayexalate (sodium polystyrene sulfonate) to
prevent hyperkalemia (high potassium) common with GN.
 Plasmapheresis, a procedure in which your plasma (the fluid part of your blood) is
removed and replaced with fluids or donated plasma that do not contain inflammatory
proteins.
 The restriction of protein, salt, and potassium from your diet, especially if the GN is
chronic.

Acute Tubular Necrosis

Acute tubular necrosis (ATN) is a condition in which the tubules of the kidney begin to die from
the lack of oxygen. Common causes include low blood pressure and nephrotoxic drugs (drugs
toxic to the kidneys).

Many of the same approaches used for GN will be applied here, including:

 Termination of suspected nephrotoxic drug

 Lasix
 Vasopressor medications
 Potassium-reducing drugs
 Restriction of protein, salt, and potassium
 Hemodialysis in severe cases

Acute Interstitial Nephritis

Acute interstitial nephritis (AIN) is the swelling of the tissue in between the kidney tubules, often
caused by a drug allergy or autoimmune disease.

Over 100 medications are associated with allergy-triggered AIN.

Of the autoimmune causes, lupus (a disease in which the immune system may attack its own
kidney tissues) remains the prime suspect. Some infections can cause AIN, as well.

Treatment of AIN is primarily focused on the termination of the suspected drug and the
restriction of potassium, salt, and protein during recovery. Corticosteroids appear to provide little
relief but may be used if the termination of the drug is unable to restore normal kidney function.

Postrenal ARF Treatment

Postrenal ARF is caused by an obstruction of the urinary tract, which includes the kidneys,
bladder, prostate, and urethra. Common causes include an enlarged prostate, kidney
stones, bladder stones, or cancer of the kidneys, bladder, or prostate.4

The aim of treatment would be to normalize the urine flow while the underlying cause of the
impairment is investigated.

Postrenal ARF requires immediate treatment to either remove or bypass the obstruction before
any permanent damage to the kidneys can occur.

This may involve:

 A urinary catheter or stent to reroute the urinary flow around the obstruction whatever
the underlying cause
 Cystoscopy/ureteral stent (which is a small temporary straw) to remove hydronephrosis
(dilation of kidney/ureter) and relieve blockage
 Drainage of the kidneys using a type of catheter, known as percutaneous nephrostomy
tube, which is inserted through the skin if above is not effective or feasible
 Ureteroscopy/laser lithotripsy for renal or ureteral stones that are causing obstruction
 Cystolitholapaxy for bladder stones that are causing obstruction
 Extracorporeal shock wave lithotripsy (ESWL), which uses sound waves to break up
kidney or bladder stones

Most people will regain normal kidney function if the condition is promptly reversed. 5 If left
untreated, the excessive pressure exerted on the kidneys, as well as the build-up of waste, can
lead to kidney damage, sometimes permanent.
Stroke Pharmacologic treatment
tPA (tissue plasminogen activator)
Thrombolytic drugs such as tPA are often called clot busters. tPA is short for
tissue plasminogen activator and can only be given to patients who are
having a stroke caused by a blood clot (ischemic stroke). It can stop a
stroke by breaking up the blood clot. It must be given as soon as possible
and within 4½ hours after stroke symptoms start.* Receiving tPA can
reduce the severity of a stroke and reverse some of the effects, helping you
recover more quickly.

In some cases, tPA cannot be used and other treatments are required.

* In 1999, Health Canada approved the clot-busting drug called tPA to be

used within 3 hours from the time stroke symptoms begin. Since that time,
considerable evidence shows that tPA could be effective up to 4½ hours from
the time symptoms begin. As a result, the Heart and Stroke Foundation has
issued updated Canadian Stroke Best Practices Recommendations to includ e
this longer possible treatment time. It will be up to the attending doctors to
determine when tPA may be administered and if it is appropriate.

Blood thinners

There are two kinds of blood thinners: antiplatelet drugs and anticoagulants.
Antiplatelet drugs
When your skin is cut, platelets bind together to form a blood clot, which
stops the bleeding. Similarly, when a blood vessel is injured, platelets cause
blood clots to develop in the vessel. However, a clot located in an artery that
is already stressed can lead to a stroke. Antiplatelet drugs help prevent
platelets from sticking together and therefore prevent blood clots from
forming. The most commonly used antiplatelet drug is ASA (acetylsalicylic
acid, Aspirin). Your doctor can tell you if you should take ASA and how much
you need to take to reduce your risk of stroke. Some people are not able to
take ASA because of bleeding problems, allergies or other medical
conditions. You should always talk to your doctor before taking ASA regularly
to prevent stroke. Other antiplatelet drugs include clopidogrel, dipyridamole
and ticlopidine.

If you are taking a blood thinner, you are at risk of bleeding more than usual
if you injure yourself. Be sure to tell your doctor and dentist that you take a
blood thinner.
Learn more about antiplatelet drugs (acetylsalicylic acid (ASA),
clopidogrel, ticlopidine)
 Anticoagulants
Anticoagulants are blood thinners that prevent new blood clots from forming
and keep existing blood clots from getting larger. They work by interfering
with certain parts of the blood needed to form clots. They are usually
prescribed for people with an irregular heartbeat (atrial fibrillation), which
can cause blood clots to travel from the heart to the brain. They are
commonly used in people who have had a stroke to help prevent stroke from
recurring. Anticoagulant medications include:
 Heparin – given by needle at the hospital and often used after a stroke to prevent clotting. It can
only be taken for a few days.
 Warfarin – a pill that can be taken for a longer period of time. It must be taken for several days
before it takes effect. (While you are on Warfarin, you should be aware that some foods may
interfere with its absorption – grapefruit and grapefruit juice – and effectiveness – cruciferous
vegetables such as broccoli and cauliflower.) Visit Health Canada to learn more about The
Effects of Grapefruit and its Juice on Certain Drugs .
Generally, people who have high blood pressure, had a recent brain injury,
or are prone to falls or abuse alcohol are not prescribed an anticoagulant. If
you are prescribed an anticoagulant, follow your doctor's instructions
carefully. You may have to periodically have your blood tested to see how
long it takes for it to clot. Try to avoid injuries because the anticoagulant may
cause you to bleed more if you cut or bruise yourself. Tell all healthcare
providers including your dentist that you are on anticoagulants.
Learn more about anticoagulants.

Blood pressure lowering medications

Known as antihypertensives, these medications treat high blood pressure.
There are many different kinds of blood pressure-lowering drugs. Your doctor
will work with you to find the drug, or combination of drugs, that is best for
you. Some antihypertensives include:
 ACE (Angiotensin-Converting Enzyme) Inhibitors
 ARB’s (Angiotensin Receptor Antagonists)
 Beta-blockers
 Calcium channel blockers
 Diuretics

Cholesterol lowering medications

Your doctor may ask you to change your diet, lose weight or become more
active to lower your cholesterol. Your doctor may also prescribe medication.
Drugs that lower cholesterol include:
 Cholesterol absorption inhibitors (ezetimibe)
 Fibrates (Fibric Acid Derivatives)
 Niacin
 Resins
 Statins

Treatment of Elevated Intracranial Pressure

The use of sedatives to lower ICP is controversial – in the absence of

agitation or anxiety there is no clear evidence that paralysis or sedation are
beneficial. In fact, data from the Traumatic Coma Data Bank suggest that
general use of sedation did not improve outcomes but increased
complications and lengthened ICU stay. On the other hand, anxiety, agitation,
or spontaneous posturing can raise ICP and should be treated with morphine
at 2-5 mg/kg/hr and vecuronium at 10 mg/hr.

CSF Drainage

CSF drainage can be highly effective, even if only a small amount is removed.
Continuous drainage is NOT recommended as it precludes ICP monitoring
and has been shown to increase the risk of catheter malfunction (secondary to
closed ventricular walls).

Mannitol

Mannitol boluses at 0.25-1g/kg are preferred over continuous infusion as the

infusion increases uptake into brain tissue, reversing the osmotic gradient and
potentially causing harm. Mannitol works by both improved osmotic gradient
and rheology – studies have shown that mannitol increases CBF by as much
as 20% and decreases CBF after brain injury, although it was recently shown
not to affect brain tissue oxygenation. Note that there is some evidence that
Osm > 320 will impair renal function, and most people will hold mannitol of
[Na+] > 155-160, however the data supporting either of these is not strong.

A series of 8 patients who went into ARF s/p mannitol showed failure within
3.5 +/- 1.1 days after mannitol doses of 189 +/- 64 g daily (626 +/- 270 g total).
Peak osmolal gap was 74 +/- 39 mOsm/kg water. In patients with normal
baseline renal function ARF developed after receiving total mannitol doses of
1171 +/- 376 g. The peak osmolal gap was 107 +/- 17 (ie measured serum
osmolality 376). In those with underlying renal compromise, renal function
worsened after a total mannitol dose of 295 +/- 143 g. Limited data suggest
that prolonged Osm > 320 mOsm/L are associated with a higher mortality.

Much of this is refuted by a recent retrospective study of 98 patients on

mannitol at WUSTL, the multivariate analysis of which showed that APACHE
II and history of CHF were the only predictive factors leading to mannitol-
induced renal failure. Osmolality gap and mannitol dose had no correlation.
Furthermore, all cases of MI-RF reversed. Loop diuretics are helpful as well
but are also recommended only when Osm < 320 and [Na+] < 155.

Hyperventilation

Hyperventilation is known to lower ICP however CBF drops 3-4% for every 1
mm Hg decrease in PCO2 [Raichle et l, Arch Neurol 23: 394, 1970] – this is
dangerous as CBF may drop by as much as 50% following TBI.
Hyperventilation is highly controversial, with the 2007 Cochrane Database
Review concluding that there is inadequate data to assess whether benefit or
harm exists. The Brain Trauma Foundation recommends against chronic
hyperventilation – Andrews recommends 35 mm Hg.

Barbiturates

Barbiturates have been studied by in several prospective, randomized clinical

trials with none of them showing a clear benefit, however one suggested a
benefit in patients in whom barbiturates lowered ICP – a 2000 Cochrane
Database Review, however, concluded that “there is no evidence that
barbiturate therapy in patients with acute severe head injury improves
outcome. Barbiturate therapy results in a fall in blood pressure in 1 in 4
treated patients. The hypotensive effect of barbiturate therapy will offset any
ICP lowering effect on cerebral perfusion pressure.” If patients are tried on
barbiturates, wean them as soon as possible to avoid myocardial
complications as well as pneumonia, for which these patients are at a high
risk

Hypothermia

There is some data to suggest that moderate hypothermia (32-33°C) can

reduce ICP. One trial suggested a benefit in terms of early outcomes, but this
dissipated by 12 months.
Treatment for DKA
 IV 0.9% saline

 Correction of hypokalemia

 IV insulin (as long as serum potassium is ≥ 3.3 mEq/L [3.3 mmol/L])

 Rarely IV sodium bicarbonate (if pH < 7 after 1 hour of treatment)
 Fluid replacement. You'll receive fluids — either by mouth or through a vein —
until you're rehydrated. The fluids will replace those you've lost through excessive
urination, as well as help dilute the excess sugar in your blood.
 Electrolyte replacement. Electrolytes are minerals in your blood that carry an
electric charge, such as sodium, potassium and chloride. The absence of insulin
can lower the level of several electrolytes in your blood. You'll receive electrolytes
through a vein to help keep your heart, muscles and nerve cells functioning
normally.
 Insulin therapy. Insulin reverses the processes that cause diabetic ketoacidosis.
In addition to fluids and electrolytes, you'll receive insulin therapy — usually
through a vein. When your blood sugar level falls to about 200 mg/dL (11.1
mmol/L) and your blood is no longer acidic, you may be able to stop intravenous
insulin therapy and resume your normal subcutaneous insulin therapy.
The most urgent goals for treating diabetic ketoacidosis are rapid intravascular volume repletion,
correction of hyperglycemia and acidosis, and prevention of hypokalemia (1). Identification of
precipitating factors is also important. Treatment should occur in intensive care settings because
clinical and laboratory assessments are initially needed every hour or every other hour with
appropriate adjustments in treatment.

Treatment for HHNK

 IV 0.9% saline

 Correction of any hypokalemia

 IV insulin (as long as serum potassium is ≥3.3 mEq/L [≥ 3.3 mmol/L])

Treatment consists of IV saline, correction of hypokalemia, and IV insulin (1).
Treatment is 0.9% (isotonic) saline solution at a rate of 15 to 20 mL/kg/hour, for the first few hours.
After that, the corrected sodium should be calculated. If the corrected sodium is < 135 mEq/L
(< 135 mmol/L), then isotonic saline should be continued at a rate of 250 to 500 mL/hour. If the
corrected sodium is normal or elevated, then 0.45% saline (half normal) should be used.
Dextrose should be added once the glucose level reaches 250 to 300 mg/dL (13.9 to 16.7
mmol/L). The rate of infusion of IV fluids should be adjusted depending on blood pressure, cardiac
status, and the balance between fluid input and output.

Insulin is given at 0.1 unit/kg IV bolus followed by a 0.1 unit/kg/hour infusion after the first liter of
saline has been infused. Hydration alone can sometimes precipitously decrease plasma glucose,
so insulin dose may need to be reduced. A too-quick reduction in osmolality can lead to cerebral
edema. Occasional patients with insulin-resistant type 2 diabetes with hyperosmolar
hyperglycemic state require larger insulin doses. Once plasma glucose reaches 300 mg/dL (16.7
mmol/L), insulin infusion should be reduced to basal levels (1 to 2 units/hour) until rehydration is
complete and the patient is able to eat.
Target plasma glucose is between 250 and 300 mg/dL (13.9 to 16.7 mmol/L). After recovery from
the acute episode, patients are usually switched to adjusted doses of subcutaneous insulin.

Potassium replacement is similar to that in diabetic ketoacidosis: 40 mEq/hour for serum

potassium < 3.3 mEq/L (< 3.3 mmol/L); 20 to 30 mEq/hour for serum potassium between 3.3 and
4.9 mEq/L (3.3 and 4.9 mmol/L); and none for serum potassium ≥ 5 mEq/L (≥ 5 mmol/L).

Treatment for Massive Bleeding

Coagulopathy in massive hemorrhage
Dilution
The dilution of coagulation factors and platelets is an important cause of coagulopathy in
massively transfused trauma patients[10]. The Advanced Trauma Life Support guideline
recommends aggressive crystalloid resuscitation but the dilutional effects of such administration
on coagulation competence are well described[11, 12] and this strategy provokes acidosis,
formation of interstitial oedema with tissue swelling, impairment of the microcirculation and
hence compromised oxygenation[13, 14].

Furthermore, synthetic colloid resuscitation fluids influence coagulation competence more

profoundly than crystalloids. Hydroxyethyl starch (HES) causes efflux of plasma proteins from
blood to the interstitial space, reduction in plasma concentration of coagulation factor VIII and
von Willebrand factor (vWF), inhibition of platelet function and reduced interaction of activated
FXIII with fibrin polymers[11, 12, 15].. This was further corroborated by a recent meta-analysis
of 24 studies evaluating the safety of HES 130/0.4 administration in surgical, emergency and
intensive care patients, with results demonstrating that HES administration promotes a dose-
dependent coagulopathy[16]. Also, administration of blood products such as RBC, FFP and PLT
may cause significant dilution since these blood products are stored in anticoagulation solutions
reducing coagulation factor concentration to approximately 60% and platelet count to
approximately 80x109/l when a hematocrit of 30% is warranted[17].

Hypothermia
Hypothermia is associated with risk of uncontrolled bleeding and death in trauma patients.
Hypothermia induced coagulopathy is attributed to platelet dysfunction, reduced coagulation
factor activity (significant below 33°C)[14, 18], and induction of fibrinolysis[19] and these
effects are reversible with normalization of body temperature.

Acidosis
In trauma patients acidosis is often induced by hypoperfusion and excess administration of ionic
chloride, i.e. NaCl during resuscitation[20]. Acidosis impairs almost all essential parts of the
coagulation process: At pH < 7.4, platelets change their structure and shape[21]. The activity of
coagulation factor complexes on the cell surface is reduced and the resulting impaired thrombin
generation is a major cause of coagulopathic bleeding. Furthermore, acidosis leads to increased
degradation of fibrinogen[22] which further aggravates the coagulopathy.

Trauma
Brohi et al.[23–27] described an early “endogenous” coagulopathy in trauma patients not
attributed to dilution and hypothermia with shock and hypoperfusion as the key drivers of acute
traumatic coagulopathy through widespread activation of the anticoagulant and fibrinolytic
pathways.

We recently suggested that the coagulopathy observed in trauma patients, which reflects the state
of the fluid phase including its cellular elements i.e., circulating whole blood, is a consequence
of the degree of the tissue injury and the thereby generated sympathoadrenal activity and
importantly, critically related to the degree of endothelial damage, with a progressively more
procoagulant endothelium (solid phase) inducing a gradient of increasing anticoagulation
towards the fluid phase (circulating blood)[28]. Though it seems counterintuitive that increasing
injury severity is associated with progressive hypocoagulability and hyperfibrinolysis[28, 29],
this may from an evolutionary perspective exert a survival advantage by preserving blood flow
through the progressively more damaged and procoagulant microvasculature[28] In alignment
with this, we found that in trauma patients upon hospital admission, a high level of syndecan-1, a
marker of endothelial glycocalyx degradation, was associated with high sympathoadrenal
activity and increased mortality, even after adjusting for injury severity score[30]. Also, only in
patients with high syndecan-1 levels, was increasing injury severity associated with increased
tissue and endothelial damage, protein C depletion, hyperfibrinolysis and inflammation[30].
Consumptive coagulopathy
Tissue injury secondary to trauma induce immediate activation of the coagulation system
through upregulation of tissue factor (TF) expression and extensive thrombin generation. Tissue
injury in association with extensive endothelial injury, massive soft tissue damage, and fat
embolization from long bone fractures, may be associated with consumption of coagulation
factors and platelets and, hence development of coagulopathy. Disseminated intravascular
coagulation (DIC) is the most extreme form of consumptive coagulopathy and is characterized
by systemic activation of pathways leading to and regulating coagulation, which can result in the
generation of fibrin clots that may cause organ failure with concomitant consumption of platelets
and coagulation factors that may result in clinical bleeding[31, 32]. We recently reported that
disseminated intravascular coagulation (DIC) was not a part of the early coagulopathy secondary
to trauma[33] though this may develop later in the course of resuscitation as described by Gando
et al.[34].

Hyperfibrinolysis
Increased fibrinolysis is observed in patients with profound endothelial activation and damage
secondary to trauma, surgery and ischemia-reperfusion injury where tissue-type plasminogen
activator (tPA) is released from the Weibel-Palade bodies of the endothelial cells. In trauma,
increased fibrinolysis has been reported in the most severely injured patients and this correlates
with poor outcome[29, 35–38]. The presence of increased fibrinolysis with increasing injury
severity probably reflects an evolutionary mechanism aiming at preventing fatal intravascular
coagulation secondary to systemic hypercoagulation induced by the trauma, as reported recently
by us[28].

Anticoagulation
Vitamin K antagonists are frequently used by patients with atrial fibrillation or artificial cardiac
valves and warfarin has been reported to be associated with about 21,000 visits for bleeding
complications per year in the US alone[39], and these data are consistent with reports of major
bleeding frequencies for warfarin as high as 10% to 16%[40]. The use of International
Normalized Ratio (INR, a plasmatic coagulation analysis) to monitor the degree of
anticoagulation by warfarin may in part explain this problem. The lack of adequate hemostatic
monitoring is also evident with regards to the newer pharmaceutical agents used for secondary
prevention and postoperative thromboprophylaxis such as the direct thrombin inhibitor
dabigatran[41], the indirect FXa inhibitors apixaban[42] and rivaroxaban[43]. Furthermore, as
for now it is recommended that treatment with these agents do not require hemostatic
monitoring[44]. Despite this, however, reports of severe bleedings in patients taking these
medications are being reported, including trauma,and since no antidote exists treatment of these
patients is a major challenge[45].
Apart from coagulopathy due to iatrogenic heparinization, critically ill patients, including trauma
patients, may become endogenously heparinized due to degradation of the endothelial
glycocalyx[30, 46], the antiadhesive and anticoagulant carbohydrate-rich surface layer that
covers and protects the endothelial cells and contains significant amounts of heparin-like
substances[47–53].

Platelet inhibitors
An important cause of excessive bleeding in trauma patients is platelet inhibitors, which an
increasing proportion of the population today uses as secondary prevention. Currently, the most
important are the platelet ADP receptor inhibitors clopidogrel and lately also the even more
potent prasugrel that irreversibly inhibits platelet activation through the platelet ADP receptor
and confers more potent platelet inhibition than acetylsalicylic acid

Importantly, the enhanced antiplatelet activity and greater efficacy seen with prasugrel when
compared to clopidogrel in clinical trials has been accompanied by increased bleeding risk and
the FDA advisory committee issued guidance to physicians about increased risk in low-weight or
elderly patients[54].

Burn treatment depends on the type of burn.

 First-degree burns can usually be treated with skin

care products like aloe vera cream or an antibiotic
ointment and pain medication such
as acetaminophen (Tylenol).
 Second-degree burns may be treated with an
antibiotic cream or other creams or ointments
prescribed by a doctor.
 Third-degree and fourth-degree burns may need more
intensive treatments such as intravenous
(IV) antibiotics to prevent infection or IV fluids to
replace fluids lost when skin was burned. They may
also need skin grafting or the use of synthetic skin.
Medical treatment
After you have received first aid for a major burn, your medical care may include
medications and products that are intended to encourage healing.

 Water-based treatments. Your care team may use techniques such as ultrasound
mist therapy to clean and stimulate the wound tissue.

 Fluids to prevent dehydration. You may need intravenous (IV) fluids to prevent
dehydration and organ failure.

 Pain and anxiety medications. Healing burns can be incredibly painful. You may
need morphine and anti-anxiety medications — particularly for dressing changes.

 Burn creams and ointments. If you are not being transferred to a burn center,
your care team may select from a variety of topical products for wound healing,
such as bacitracin and silver sulfadiazine (Silvadene). These help prevent infection
and prepare the wound to close.

 Dressings. Your care team may also use various specialty wound dressings to
prepare the wound to heal. If you are being transferred to a burn center, your
wound will likely be covered in dry gauze only.

 Drugs that fight infection. If you develop an infection, you may need IV
antibiotics.

 Tetanus shot. Your doctor might recommend a tetanus shot after a burn injury.

Treatment for Poisoning

Some people who have swallowed a poisonous substance or overdosed on medication
will be admitted to hospital for examination and treatment.

Possible treatments that can be used to treat poisoning include:

 activated charcoal – sometimes used to treat someone who's been poisoned; the
charcoal binds to the poison and stops it being further absorbed into the blood
 antidotes – these are substances that either prevent the poison from working or
reverse its effects
 sedatives – may be given if the person is agitated
 a ventilator (breathing machine) – may be used if the person stops breathing
 anti-epileptic medicine – may be used if the person has seizures (fits)
Treatments for COVID-19
What helps, what doesn't, and what's in the pipeline

Updated: November 23, 2020Published: March, 2020

Most people who become ill with COVID-19 will be able to recover at home. Some of the same
things you do to feel better if you have the flu — getting enough rest, staying well hydrated, and
taking medications to relieve fever and aches and pains — also help with COVID-19.

The antiviral drug remdesivir was FDA approved in October 2020 to treat certain hospitalized
patients with COVID-19. And scientists are working hard to develop other effective treatments.
Therapies that are under investigation include drugs that have been used to treat autoimmune
diseases; additional antiviral drugs, and antibodies from people who have recovered from
COVID-19.

What are monoclonal antibodies? Can they help treat COVID-19?

The FDA has granted emergency use authorization (EUA) to two new treatments for COVID-19.
Both are monoclonal antibodies. And both have been approved to treat non-hospitalized adults
and children over age 12 with mild to moderate symptoms who have recently tested positive for
COVID-19, and who are at risk for developing severe COVID-19 or being hospitalized for it.
This includes people over 65, people with obesity, and those with certain chronic medical
conditions.

The FDA granted EUA to the first treatment, a monoclonal antibody called bamlanivimab made
by Eli Lilly, based on an interim analysis of results from a well-designed but small clinical trial.
The study looked at 465 non-hospitalized adults with mild to moderate COVID-19 symptoms
who were at high risk of severe disease. A placebo was given to 156 of these patients. The
remaining patients were given one of three different doses of bamlanivimab. Patients treated with
the monoclonal antibody had a reduced risk (3% versus 10%) of being hospitalized or visiting
the ER within 28 days after treatment, compared to patients given a placebo. This is a single-
dose treatment that must be given intravenously and within 10 days of developing symptoms.

The FDA has also granted EUA to a combination therapy consisting of two monoclonal
antibodies, casirivimab and imdevimab, made by Regeneron. The EUA was based on results
from a clinical trial that enrolled 799 non-hospitalized adults with mild to moderate COVID-19
symptoms. The participants were divided into three groups, two of which received the
casirivimab-imdevimab combination but at different doses. The third group received a placebo.
For patients at high risk for severe disease, those treated with the monoclonal antibody treatment
had a reduced risk (3% versus 9%) of being hospitalized or visiting the ER within 28 days of
treatment. This treatment must also be given intravenously in a clinic or hospital.

Monoclonal antibodies are manmade versions of the antibodies that our bodies naturally make to
fight invaders, such as the SARS-CoV-2 virus. Both of these FDA-approved therapies attack the
coronavirus's spike protein, making it more difficult for the virus to attach to and enter human
cells.

These treatments are not authorized for hospitalized COVID-19 patients or those receiving
oxygen therapy. They have not shown to benefit these patients and could lead to worse outcomes
in these patients.

What is convalescent plasma? Does it help people with COVID-19?

When people recover from COVID-19, their blood contains antibodies that their bodies produced
to fight the coronavirus and help them get well. Antibodies are found in plasma, a component of
blood.

Convalescent plasma — literally plasma from recovered patients — has been used for more than
100 years to treat a variety of illnesses from measles to polio, chickenpox, and SARS. It is
widely believed to be safe.

In the current situation, antibody-containing plasma from a recovered patient is given by

transfusion to a patient who is suffering from COVID-19. The donor antibodies may help the
patient fight the illness, possibly shortening the length or reducing the severity of the disease.

Though convalescent plasma has been used for many years, and with varying success, not much
is known about how effective it is for treating COVID-19. A recent analysis of 35,000
hospitalized patients who received convalescent plasma to treat severe COVID-19 suggests that
the therapy may reduce the risk of dying. The data comes from the ongoing Expanded Access
Program (EAP) led by the Mayo Clinic. The researchers found that patients with (or at risk of)
severe COVID-19 who received convalescent plasma within three days of diagnosis were less
likely to die than patients who received convalescent plasma later in their illness.
The problem? The study has no control group. All patients who are eligible to get convalescent
plasma under the EAP receive that treatment. As a result, questions remain as to whether, or the
degree to which, convalescent plasma is effective for treating COVID-19; who would benefit
from this treatment; and when in the course of illness convalescent plasma is most effective.
(High demand to enroll in the program may have also unintentionally driven down enrollment in
randomized, controlled studies of convalescent plasma across the country.)

Despite this, the FDA has issued an emergency use authorization (EUA) for convalescent
plasma, which will make it easier for hospitals to provide the treatment to their patients.

Who can donate plasma for COVID-19?

In order to donate plasma, a person must meet several criteria. They have to have tested positive
for COVID-19, recovered, have no symptoms for 14 days, currently test negative for COVID-19,
and have high enough antibody levels in their plasma. A donor and patient must also have
compatible blood types. Once plasma is donated, it is screened for other infectious diseases, such
as HIV.

Each donor produces enough plasma to treat one to three patients. Donating plasma should not
weaken the donor's immune system nor make the donor more susceptible to getting reinfected
with the virus.

Is there an antiviral treatment for COVID-19?

In October 2020, the FDA approved the antiviral drug remdesivir to treat COVID-19. The drug
may be used to treat adults and children ages 12 and older and weighing at least 88 pounds, who
have been hospitalized for COVID-19. Clinical trials suggest that in these patients, remdesivir
may modestly speed up recovery time.

Other antiviral drugs are also being tested to see if they might be effective against the virus that
causes COVID-19.

Why is it so difficult to develop treatments for viral illnesses?

An antiviral drug must be able to target the specific part of a virus's life cycle that is necessary
for it to reproduce. In addition, an antiviral drug must be able to kill a virus without killing the
human cell it occupies. And viruses are highly adaptive. Because they reproduce so rapidly, they
have plenty of opportunity to mutate (change their genetic information) with each new
generation, potentially developing resistance to whatever drugs or vaccines we develop.

What treatments are available to treat coronavirus?

In October 2020, the FDA approved the antiviral drug remdesivir to treat certain patients
hospitalized with COVID-19.

In November 2020, the FDA granted emergency use authorization to two monoclonal antibody
treatments (bamlanivimab, made by Eli Lilly; and a combination of casirivimab and imdevimab,
made by Regeneron). Both treatments have been approved for non-hospitalized adults and
children over age 12 with mild to moderate COVID-19 symptoms who are at risk for developing
severe COVID-19 or being hospitalized for it. In these patients, the approved treatments can
reduce the risk of hospitalization and emergency room visits. These therapies must be given
intravenously (by IV) soon after developing symptoms.

Other treatments, still under investigation, may also be available to people who are being treated
for COVID-19 in the hospital.

If you are recovering at home, these measures can help:

While you don't need to stay in bed, you should get plenty of rest.
Stay well hydrated.
To reduce fever and ease aches and pains, take acetaminophen. Be sure to follow directions. If
you are taking any combination cold or flu medicine, keep track of all the ingredients and the
doses. For acetaminophen, the total daily dose from all products should not exceed 3,000
milligrams.
Is dexamethasone effective for treating COVID-19?
A recent report on a clinical trial showed that the corticosteroid drug dexamethasone decreased
the risk of dying in very ill hospitalized COVID-19 patients. The report was released prior to
publication of the study in a medical journal, which means the research results have not gone
through the usual careful review.

Many doctors, including those in the United States, have been treating very ill COVID-19
patients with corticosteroids since the pandemic began. It makes biologic sense for those patients
who have developed a hyper-immune response (a cytokine storm) to the viral infection. In these
cases, it is the immune system's overreaction that is damaging the lungs and other organs, and
too often leading to death.

Dexamethasone and other corticosteroids (prednisone, methylprednisolone) are potent anti-

inflammatory drugs. They are readily available and inexpensive.

A key question if dexamethasone is effective for some COVID-19 patients: when should it be
started? If you start too soon you blunt the body's natural defense system, and that could allow
the virus to thrive. What might make the most biological sense is to give dexamethasone when
laboratory studies suggest an immune system in overdrive after the amount of virus in the body
has started to decrease.

But we will need more studies beyond this most current report to confirm the drug's
effectiveness.

Is it safe to take ibuprofen to treat symptoms of COVID-19?

Some French doctors advise against using ibuprofen (Motrin, Advil, many generic versions) for
COVID-19 symptoms based on reports of otherwise healthy people with confirmed COVID-19
who were taking an NSAID for symptom relief and developed a severe illness, especially
pneumonia. These are only observations and not based on scientific studies.

The WHO initially recommended using acetaminophen instead of ibuprofen to help reduce fever
and aches and pains related to this coronavirus infection, but now states that either
acetaminophen or ibuprofen can be used. Rapid changes in recommendations create uncertainty.
Since some doctors remain concerned about NSAIDs, it still seems prudent to choose
acetaminophen first, with a total dose not exceeding 3,000 milligrams per day.

However, if you suspect or know you have COVID-19 and cannot take acetaminophen, or have
taken the maximum dose and still need symptom relief, taking over-the-counter ibuprofen does
not need to be specifically avoided.

Are chloroquine/hydroxychloroquine and azithromycin safe and effective for treating COVID-
19?
Early reports from China and France suggested that patients with severe symptoms of COVID-
19 improved more quickly when given chloroquine or hydroxychloroquine. Some doctors were
using a combination of hydroxychloroquine and azithromycin with some positive effects.

Hydroxychloroquine and chloroquine are primarily used to treat malaria and several
inflammatory diseases, including lupus and rheumatoid arthritis. Azithromycin is a commonly
prescribed antibiotic for strep throat and bacterial pneumonia. Both drugs are inexpensive and
readily available.

Hydroxychloroquine and chloroquine have been shown to kill the COVID-19 virus in the
laboratory dish. The drugs appear to work through two mechanisms. First, they make it harder
for the virus to attach itself to the cell, inhibiting the virus from entering the cell and multiplying
within it. Second, if the virus does manage to get inside the cell, the drugs kill it before it can
multiply.

Azithromycin is never used for viral infections. However, this antibiotic does have some anti-
inflammatory action. There has been speculation, though never proven, that azithromycin may
help to dampen an overactive immune response to the COVID-19 infection.

The jury is still out regarding whether these drugs, alone or in combination, can treat COVID-19
viral infection. While recent human studies suggest no benefit and possibly a higher risk of death
due to lethal heart rhythm abnormalities, two studies supporting these conclusions have been
retracted by the authors because of irregularities in how results were collected and analyzed.

Regarding the effectiveness of hydroxychloroquine alone to prevent coronavirus infection, the

results of a clinical trial just published in the New England Journal of Medicine found that it did
not prevent infection. However, how this study was conducted has been questioned by some
experts.

Where does that leave us? The recommendation has not changed. Chloroquine or
hydroxychloroquine with or without azithromycin should not be used to prevent or treat COVID-
19 infection unless it is being prescribed in the hospital or as part of a clinical trial.

Clinical trials that were ongoing and about to be started to evaluate the effectiveness of these
drugs are resuming.
Is the antiviral drug remdesivir effective for treating COVID-19?
Scientists all over the world are testing whether drugs previously developed to treat other viral
infections might also be effective against the new coronavirus that causes COVID-19.

One drug that has received a lot of attention is the antiviral drug remdesivir. The drug appears to
be effective in the laboratory dish, in protecting cells against infection by the COVID virus.

Human studies are also underway. One well-designed study was published in the New England
Journal of Medicine in May 2020. In comparing remdesivir to a placebo in more than 1,000
people hospitalized with COVID-19, it found that patients who received remdesivir recovered
more quickly than those taking a placebo (a median of 11 days for remdesivir, compared to a
median of 15 days for placebo). This was a statistically significant difference. Remdesivir was
less effective in sicker COVID-19 patients, including those on a ventilator or on a heart-lung
machine.

However, a large study conducted as part of the WHO Solidarity trial found that treating
hospitalized COVID-19 patients with remdesivir did not significantly reduce their risk of death
or shorten the length of their hospitalizations. Some experts have questioned if too many of the
patients received the drug too late in their disease, and therefore would not be expected to
benefit.

In October 2020, the FDA approved remdesivir as a treatment for adults and children ages 12
and older and weighing at least 88 pounds, who have been hospitalized for COVID-19.

Does vitamin D protect against COVID-19?

There is some evidence to suggest that vitamin D might help protect against becoming infected
with, and developing serious symptoms of, COVID-19. We know, for example, that people with
low vitamin D levels may be more susceptible to upper respiratory tract infections. One meta-
analysis found that people who took vitamin D supplements, particularly those who had low
vitamin D levels, were less likely to develop acute respiratory tract infections than those who
didn't.

Vitamin D may protect against COVID-19 in two ways. First, it may help boost our bodies'
natural defense against viruses and bacteria. Second, it may help prevent an exaggerated
inflammatory response, which has been shown to contribute to severe illness in some people
with COVID-19.

Our bodies make vitamin D when exposed to sunshine. Five to 10 minutes of sun exposure on
some or most days of the week to the arms, legs, or back without sunscreen will enable you to
make enough of the vitamin. Good food sources of vitamin D include fatty fish (such as tuna,
mackerel, and salmon), foods fortified with vitamin D (such as dairy products, soy milk, and
cereals), cheese, and egg yolks.

The recommended dietary dose of vitamin D is 600 IU each day for adults 70 and younger and
800 IU each day for adults over 70. A daily supplement containing 1,000 to 2,000 IU of vitamin
D is likely safe for most people. For adults, the risk of harmful effects increases above 4,000 IU
per day.

I've heard that high-dose vitamin C is being used to treat patients with COVID-19. Does it work?
And should I take vitamin C to prevent infection with the COVID-19 virus?
Some critically ill patients with COVID-19 have been treated with high doses of intravenous
(IV) vitamin C in the hope that it will hasten recovery. However, there is no clear or convincing
scientific evidence that it works for COVID-19 infections, and it is not a standard part of
treatment for this new infection. A study is underway in China to determine if this treatment is
useful for patients with severe COVID-19; results are expected in the fall.

The idea that high-dose IV vitamin C might help in overwhelming infections is not new. A 2017
study found that high-dose IV vitamin C treatment (along with thiamine and corticosteroids)
appeared to prevent deaths among people with sepsis, a form of overwhelming infection causing
dangerously low blood pressure and organ failure. Another study published last year assessed the
effect of high-dose vitamin C infusions among patients with severe infections who had sepsis
and acute respiratory distress syndrome (ARDS), in which the lungs fill with fluid. While the
study's main measures of improvement did not improve within the first four days of vitamin C
therapy, there was a lower death rate at 28 days among treated patients. Though neither of these
studies looked at vitamin C use in patients with COVID-19, the vitamin therapy was specifically
given for sepsis and ARDS, and these are the most common conditions leading to intensive care
unit admission, ventilator support, or death among those with severe COVID-19 infections.

Regarding prevention, there is no evidence that taking vitamin C will help prevent infection with
the coronavirus that causes COVID-19. While standard doses of vitamin C are generally
harmless, high doses can cause a number of side effects, including nausea, cramps, and an
increased risk of kidney stones.

What is serologic (antibody) testing for COVID-19? What can it be used for?
A serologic test is a blood test that looks for antibodies created by your immune system. There
are many reasons you might make antibodies, the most important of which is to help fight
infections. The serologic test for COVID-19 specifically looks for antibodies against the
COVID-19 virus.

Your body takes at least five to 10 days after you have acquired the infection to develop
antibodies to this virus. For this reason, serologic tests are not sensitive enough to accurately
diagnose an active COVID-19 infection, even in people with symptoms.

However, serologic tests can help identify anyone who has recovered from coronavirus. This
may include people who were not initially identified as having COVID-19 because they had no
symptoms, had mild symptoms, chose not to get tested, had a false-negative test, or could not get
tested for any reason. Serologic tests will provide a more accurate picture of how many people
have been infected with, and recovered from, coronavirus, as well as the true fatality rate.

Serologic tests may also provide information about whether people become immune to
coronavirus once they've recovered and, if so, how long that immunity lasts. In time, these tests
may be used to determine who can safely go back out into the community.

Scientists can also study coronavirus antibodies to learn which parts of the coronavirus the
immune system responds to, in turn giving them clues about which part of the virus to target in
vaccines they are developing.

Serological tests are starting to become available and are being developed by many private
companies worldwide. However, the accuracy of these tests needs to be validated before
widespread use in the US.

Chemotherapy is one of the most common treatments for cancer. It uses certain drugs to
kill cancer cells or to stop them from growing and spreading to other parts of your body. Your
doctor might prescribe chemo by itself or with surgery or radiation therapy. You might also take
newer kinds of cancer-fighting drugs along with chemotherapy.

You can take chemo as pills or shots. You might go to a clinic or hospital so you can get the
drugs through an IV, what doctors call an infusion.

To help your body regain strength and grow new, healthy cells, you might take the drugs over a
few weeks. You might take doses every day, every week, or every month. It depends on the
type of cancer you have and how severe it is.

Your cancer doctor, called an oncologist, may prescribe one chemo drug or a mix of different
ones, depending on:

Your type of cancer

Whether you’ve had cancer before
If you have other health problems like diabetes or heart, kidney, or liver disease
Why You Need Chemotherapy
Even after surgery to remove a tumor, your body might still have cancer cells. These cells can
grow new tumors or spread the cancer to other parts of your body.

Chemotherapy drugs help destroy, shrink, or control those cells. It might also treat symptoms
the cancer causes, like pain. You might also get chemo to shrink a tumor before your doctor
removes it in surgery.

How It Works
Chemotherapy drugs work in a few different ways. They can:

Kill both cancerous and healthy cells

Fight only cancer cells
Keep tumors from growing blood vessels, which help them thrive
Attack the cancer cells’ genes so the cells die and can’t grow into new tumors
Common Chemotherapy Drugs
There are dozens of chemotherapy drugs that doctors can prescribe. They’re often divided into
groups based on how they work and what they’re made of. Each group of drugs destroys or
shrinks cancer cells in a different way.

Some drugs damage the DNA of cancer cells to keep them from making more copies of
themselves. They are called alkylating agents, the oldest type of chemotherapy. They treat
many different types of cancer, such as leukemia, lymphoma, Hodgkin's disease, multiple
myeloma, and sarcoma, as well as breast, lung, and ovarian cancers. Some examples of
alkylating agents are cyclophosphamide, melphalan, and temozolomide. As they kill bad cells,
though, they can also destroy your bone marrow in the process, which can cause leukemia
years later. To lower this risk, you can take the drugs in small doses. One type of alkylating
agent -- platinum drugs like carboplatin, cisplatin, or oxaliplatin -- has a lower risk of causing
leukemia.
One type of chemo drug interferes with the normal metabolism of cells, which makes them
stop growing. These drugs are called antimetabolites. Doctors often use them to treat leukemia
and cancer in the breasts, ovaries, and intestines. Drugs in this group include 5-fluorouracil, 6-
mercaptopurine, cytarabine, gemcitabine, and methotrexate, among many others.
Anthracycline chemotherapy attacks the enzymes inside cancer cells’ DNA that help them
divide and grow. They work for many types of cancer. Some of these drugs are actinomycin-D,
bleomycin, daunorubicin, and doxorubicin, among others. High doses of anti-tumor antibiotics
can damage your heart or lungs. So your doctor will have you take them for a short time.
Drugs called mitotic inhibitors stop cancer cells from making more copies of themselves. They
can also stop your body from making the proteins that cancer cells need to grow. Doctors might
prescribe them for breast and lung cancers and types of myeloma, leukemia, and lymphoma.
Mitotic inhibitors include docetaxel, estramustine, paclitaxel, and vinblastine.
Another type of medicine, called topoisomerase inhibitors, also attacks enzymes that help
cancer cells divide and grow. They treat some types of leukemia and cancer of the lung, ovaries,
and intestines, among other types. This group of medicine includes etoposide, irinotecan,
teniposide, and topotecan. Some of them, though, may raise your odds of getting a second
cancer a few years later.
Steroids are drugs that act like your body’s own hormones. They are useful in treating many
types of cancer, and they can keep you from having nausea and vomiting after a round of
chemo. They can also prevent allergic reactions to some of the drugs. Some of the steroids your
doctor might prescribe are prednisone, methylprednisolone, and dexamethasone.
Chemotherapy is one of the most common treatments for cancer. It uses certain drugs to
kill cancer cells or to stop them from growing and spreading to other parts of your body. Your
doctor might prescribe chemo by itself or with surgery or radiation therapy. You might also take
newer kinds of cancer-fighting drugs along with chemotherapy.

You can take chemo as pills or shots. You might go to a clinic or hospital so you can get the
drugs through an IV, what doctors call an infusion.

To help your body regain strength and grow new, healthy cells, you might take the drugs over a
few weeks. You might take doses every day, every week, or every month. It depends on the
type of cancer you have and how severe it is.

Your cancer doctor, called an oncologist, may prescribe one chemo drug or a mix of different
ones, depending on:

Your type of cancer

Whether you’ve had cancer before
If you have other health problems like diabetes or heart, kidney, or liver disease
Why You Need Chemotherapy
Even after surgery to remove a tumor, your body might still have cancer cells. These cells can
grow new tumors or spread the cancer to other parts of your body.

Chemotherapy drugs help destroy, shrink, or control those cells. It might also treat symptoms
the cancer causes, like pain. You might also get chemo to shrink a tumor before your doctor
removes it in surgery.
How It Works
Chemotherapy drugs work in a few different ways. They can:

Kill both cancerous and healthy cells

Fight only cancer cells
Keep tumors from growing blood vessels, which help them thrive
Attack the cancer cells’ genes so the cells die and can’t grow into new tumors
Common Chemotherapy Drugs
There are dozens of chemotherapy drugs that doctors can prescribe. They’re often divided into
groups based on how they work and what they’re made of. Each group of drugs destroys or
shrinks cancer cells in a different way.

Some drugs damage the DNA of cancer cells to keep them from making more copies of
themselves. They are called alkylating agents, the oldest type of chemotherapy. They treat
many different types of cancer, such as leukemia, lymphoma, Hodgkin's disease, multiple
myeloma, and sarcoma, as well as breast, lung, and ovarian cancers. Some examples of
alkylating agents are cyclophosphamide, melphalan, and temozolomide. As they kill bad cells,
though, they can also destroy your bone marrow in the process, which can cause leukemia
years later. To lower this risk, you can take the drugs in small doses. One type of alkylating
agent -- platinum drugs like carboplatin, cisplatin, or oxaliplatin -- has a lower risk of causing
leukemia.
One type of chemo drug interferes with the normal metabolism of cells, which makes them
stop growing. These drugs are called antimetabolites. Doctors often use them to treat leukemia
and cancer in the breasts, ovaries, and intestines. Drugs in this group include 5-fluorouracil, 6-
mercaptopurine, cytarabine, gemcitabine, and methotrexate, among many others.
Anthracycline chemotherapy attacks the enzymes inside cancer cells’ DNA that help them
divide and grow. They work for many types of cancer. Some of these drugs are actinomycin-D,
bleomycin, daunorubicin, and doxorubicin, among others. High doses of anti-tumor antibiotics
can damage your heart or lungs. So your doctor will have you take them for a short time.
Drugs called mitotic inhibitors stop cancer cells from making more copies of themselves. They
can also stop your body from making the proteins that cancer cells need to grow. Doctors might
prescribe them for breast and lung cancers and types of myeloma, leukemia, and lymphoma.
Mitotic inhibitors include docetaxel, estramustine, paclitaxel, and vinblastine.
Another type of medicine, called topoisomerase inhibitors, also attacks enzymes that help
cancer cells divide and grow. They treat some types of leukemia and cancer of the lung, ovaries,
and intestines, among other types. This group of medicine includes etoposide, irinotecan,
teniposide, and topotecan. Some of them, though, may raise your odds of getting a second
cancer a few years later.
Steroids are drugs that act like your body’s own hormones. They are useful in treating many
types of cancer, and they can keep you from having nausea and vomiting after a round of
chemo. They can also prevent allergic reactions to some of the drugs. Some of the steroids your
doctor might prescribe are prednisone, methylprednisolone, and dexamethasone.