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on your heart and often relieve symptoms of chest pain. Beta blockers reduce the
risk of heart attacks and some heart rhythm problems.
Angiotensin-converting enzyme (ACE) inhibitors: These medications may help
slow the progression of atherosclerosis by lowering blood pressure and producing
other beneficial effects on the heart arteries. ACE inhibitors can also reduce the risk
of recurrent heart attacks.
Calcium channel blockers: These medications lower blood pressure and are
sometimes used to treat angina.
Water pills (diuretics): High blood pressure is a major risk factor for
atherosclerosis. Diuretics lower blood pressure.
Fibrates to Reduce Triglycerides: Fibrates are drugs that reduce triglyceride
levels. Triglycerides are not cholesterol, but they are fats that contribute to
atherosclerosis. There are two fibrates used:
Gemfibrozil
Fenofibrate
than 140 over 90. For people with atherosclerosis, the goal may be below 130 over
80.
2. Classify drugs used in atherosclerosis with suitable examples. What is the nonpharmacological treatment of atherosclerosis
DRUGS USED IN ATHEROSCLEROSIS:
There are several medications available to treat many of the underlying causes of
atherosclerosis, such as a high cholesterol level and high blood pressure
(hypertension).
High blood pressure (hypertension)
The most widely used medications for treating high blood pressure are outlined
below.
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin-converting enzyme (ACE) inhibitors work by blocking the actions of
some of the hormones that help regulate blood pressure. By stopping these
hormones from working, ACE inhibitors reduce the amount of water in your blood as
well as widening your arteries, both of which will lower your blood pressure.
ACE inhibitors are not suitable for:
people with conditions that affect the blood supply to their kidneys
The side effects of ACE inhibitors include dizziness, tiredness and headaches. If the
side effects of ACE inhibitors become troublesome, angiotensin-2 receptor
antagonists may be recommended. They work in a similar way to ACE inhibitors.
situation (blood or serum infusions), renal diseases, chronic severe anemia, beriberi
(vitamin B1/thiamine deficiency), thyrotoxicosis, Paget's disease, arteriovenous
fistulae, or arteriovenous malformations.
A study of healthy adults in the United States found the following risk factors:
1. Ischaemic heart disease 62%
2. Cigarette smoking 16%
3. Hypertension (high blood pressure) 10%
4. Obesity 8%
5. Diabetes 3%
6. Valvular heart disease 2% (much higher in older populations)
Italians had the following underlying causes:
1. Ischaemic heart disease 40%
2. Dilated cardiomyopathy 32%
3. Valvular heart disease 12%
4. Hypertension 11%
5. Other 5%
Rarer causes of heart failure include:
Arrhythmias.
Ace inhibitors
Ace inhibitors (ACEI) are drugs that relax the blood vessels. Some commonly
prescribed ACEI include: Capoten (captopril); Vasotec (enalapril); Prinivil/Zestril
(lisinopril); Accupril (quinapril); Altace (ramipril); and Monopril (fosinopril).
Beta-blockers
Beta-blockers help lower blood pressure and slow your heart rate. They also block
the harmful effects of some of the hormone-like substances that advance heart
damage. Over time, Beta-blockers may also improve the pumping action of the
heart . Commonly prescribed beta-blockers include Coreg (carvedilol) and
Lopressor/Toprol (metoprolol).
Taking an ACEI or beta-blocker will improve heart function over time (months and
years). Both drugs, either taken alone or together, have been very useful in
improving heart conditions.
Diuretics
Diuretics or "water pills" help rid the body of excess fluid that may collect in your
lungs, stomach, or feet and ankles. Less fluid in your body will decrease the
workload of your heart.
In addition to excess fluid, diuretics may also deplete your body of potassium.
Potassium is a mineral that, among other things, helps to balance the fluid in your
body's cells. It is important for your muscles to work properly. The richest sources of
potassium are fruits and vegetables, especially bananas, dried prunes, raisins,
baked potatoes (with skin), and tomato juice.
Side effects include dizziness, weakness, gout and muscle cramps (usually due to
low potassium). Common diuretics include: Lasix (furosemide); Bumex
(bumetanide); Demadex (torsemide); and HCTZ (hydrochlorothiazide).
Spironolactone is a weak "water pill" but helps prevent loss of potassium and
scarring of the heart muscle.
Digoxin
Digoxin (lanoxin) is a medication that can help the heart muscle pump blood more
effectively. It can also regulate a heartbeat that is too rapid or irregular. However, if
your body's Digoxin level gets too high, you may have loss of appetite, nausea,
bluish or yellowish vision or rapid, forceful heartbeats.
4. Describe the pathophysiology and symptoms of cardiac arrhythmia
Discuss the therapeutic approach employed in the management of major cardiac
arrhythmias
SYMPTOMS OF CARDIAC ARRHYTHMIA:
The most common symptom of arrhythmia is an abnormal awareness of heartbeat,
called palpitations. These may be infrequent, frequent, or continuous. Some of
these arrhythmias are harmless (though distracting for patients) but many of them
predispose to adverse outcomes.
Some arrhythmias do not cause symptoms, and are not associated with increased
mortality. However, some asymptomatic arrhythmias are associated with adverse
events. Examples include a higher risk of blood clotting within the heart and a
higher risk of insufficient blood being transported to the heart because of weak
heartbeat. Other increased risks are of embolisation and stroke, heart failure and
sudden cardiac death.
If an arrhythmia results in a heartbeat that is too fast, too slow or too weak to
supply the body's needs, this manifests as a lower blood pressure and may cause
lightheadedness or dizziness, or syncope (fainting).
Some types of arrhythmia result in cardiac arrest, or sudden death.
Shortness of breath (dyspnea) occurs when the damage to the heart limits the
output of the left ventricle, causing left ventricular failure and consequent
pulmonary edema. Other symptoms include diaphoresis (an excessive form of
sweating), weakness, light-headedness, nausea, vomiting, and palpitations.
These symptoms are likely induced by a massive surge of catecholamines from
the sympathetic nervous system which occurs in response to pain and the
hemodynamic abnormalities that result from cardiac dysfunction. Loss of
consciousness (due to inadequate blood flow to the brain and cardiogenic shock)
and sudden death (frequently due to the development of ventricular fibrillation)
can occur in MIs.
The most common symptoms of MI in women include dyspnea, weakness, and
fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as
frequently occurring symptoms that may manifest as long as one month before
the actual clinically manifested ischemic event. In women, chest pain may be
less predictive of coronary ischemia than in men. Women may also experience
back or jaw pain during an episode.
Any group of symptoms compatible with a sudden interruption of the blood flow
to the heart are called an acute coronary syndrome.
Several groups of drugs slow conduction through the heart, without actually
preventing an arrhythmia. These drugs can be used to "rate control" a fast
rhythm and make it physically tolerable for the patient.
Some arrhythmias promote blood clotting within the heart, and increase risk of
embolus and stroke. Anticoagulant medications such as warfarin and heparins,
and anti-platelet drugs such as aspirin can reduce the risk of clotting.
Electricity
Dysrhythmias may also be treated electrically, by applying a shock across the
heart either externally to the chest wall, or internally to the heart via
implanted electrodes.Cardioversion is either achieved pharmacologically or via
the application of a shock synchronised to the underlying heartbeat. It is used for
treatment of supraventricular tachycardias. In elective cardioversion, the
recipient is usually sedated or lightly anesthetized for the procedure.
Defibrillation differs in that the shock is not synchronised. It is needed for the
chaotic rhythm of ventricular fibrillation and is also used for pulseless ventricular
tachycardia. Often, more electricity is required for defibrillation than for
cardioversion. In most defibrillation, the recipient has lost consciousness so there
is no need for sedation.
Defibrillation or cardioversion may be accomplished by an implantable
cardioverter-defibrillator (ICD).
Electrical treatment of dysrhythmia also includes cardiac pacing. Temporary
pacing may be necessary for reversible causes of very slow heartbeats, or
bradycardia, (for example, from drug overdose or myocardial infarction). A
permanent pacemaker may be placed in situations where the bradycardia is not
expected to recover.
Electrical cautery
Some cardiologists further sub-specialise into electrophysiology. In specialised
catheter laboratories, they use fine probes inserted through the blood vessels to
map electrical activity from within the heart. This allows abnormal areas of
conduction to be located very accurately, and subsequently destroyed with heat,
cold, electrical, or laser probes.
This pulmonary vein isolation may be completely curative for AV nodal reentrant
tachycardia and sometimes for atrial fibrillation, but for other forms of
arrhythmia the success rate remains disappointing.
DIAGNOSTIC TESTS OF ANGINA PECTORIS:
Electrocardiogram
The ECG is normal in about one-half of patients with angina who are not
experiencing an acute attack. Typical ST-Twave changes include depression, T-wave
inversion, and ST-segment elevation. Forms of ischemia other than exertional
angina may have ECG manifestations that are different; variant angina is associated
with ST-segment elevation, whereas silent ischemia may produce elevation or
depression. Significant ischemia is associated with STsegment depression of greater
than 2 mm, exertional hypotension,and reduced exercise tolerance.
Exercise Tolerance Testing
intravascular ultrasound is useful for directly imaging anatomy, calcified and fatty
plaques, and thrombosis superimposed on plaque as well as determining patency
following
revascularization procedures. Intravascular ultrasound guidance of stent
implantation may result in more effective stent expansion compared with
angiographic guidance alone.
7. Write the diagnosis of myocardial infarction
A cardiac troponin rise accompanied by either typical symptoms, pathological Q
waves, ST elevation or depression, or coronary intervention is diagnostic of MI.
WHO criteria formulated in 1979 have classically been used to diagnose MI; a
patient is diagnosed with MI if two (probable) or three (definite) of the following
criteria are satisfied:
1. Clinical history of ischemic type chest pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. Rise and fall of serum cardiac biomarkers
At autopsy, a pathologist can diagnose an MI based on anatomopathological
findings.
Classification
Myocardial infarctions are generally classified into ST elevation MI (STEMI) and nonST elevation MI (NSTEMI) A STEMI is the combination of symptoms related to poor
oxygenation of the heart with elevation of the ST segments on the
electrocardiogram followed by an increase in proteins in the blood related to heart
muscles death. They make up abut 25 to 40 percent of cases.
The phrase "heart attack" is often used non-specifically to refer to a myocardial
infarction and to sudden cardiac death. An MI is different from, but can cause
cardiac arrest, which is the stopping of the heartbeat. It is also distinct from heart
failure, in which the pumping action of the heart is impaired. However, an MI may
lead to heart failure.
A 2007 consensus document classifies MI into five main types:
Electrocardiogram
For a person to qualify as having a STEMI, in addition to reported angina, the ECG
must show new ST elevation in two or more adjacent ECG leads. This must be
greater than 2 mm (0.2 mV) for males and greater than 1.5 mm (0.15mV) in
females if in leads V2 and V3 or greater than 1 mm (0.1 mV) if it is in other ECG
leads. A left bundle branch block that is believed to be new used to be considered
the same as ST elevation; however, this is no longer the case. In early STEMIs there
may just be peaked T waves with ST elevation developing later.
Cardiac biomarkers
While there are a number of different biomarkers, troponins are considered to be
the best. Copeptin may be useful to rule out MI when used along with troponin.
Imaging
A chest radiograph and routine blood tests may indicate complications or
precipitating causes, and are often performed upon arrival to an emergency
department. New regional wall motion abnormalities on an echocardiogram are also
suggestive of an MI. Echo may be performed in equivocal cases by the on-call
cardiologist. In stable patients whose symptoms have resolved by the time of
evaluation, technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201
chloride can be used in nuclear medicine to visualize areas of reduced blood flow in
conjunction with physiological or pharmacological stress. Thallium may also be used
to determine viability of tissue, distinguishing whether nonfunctional myocardium is
actually dead or merely in a state of hibernation or of being stunned.
Medical societies recommend that the physician confirm a person is at high risk for
myocardial infarction before conducting imaging tests to make a diagnosis. Patients
who have a normal ECG and who are able to exercise, for example, do not merit
routine imaging. Imaging tests such as stress radionuclide myocardial perfusion
imaging or stress echocardiography can confirm a diagnosis when a patient's
history, physical exam, ECG, and cardiac biomarkers suggest the likelihood of a
problem.
Indication
Isosorbide
dinitrate
Treatment and
prevention of angina
Isosorbide
mononitrate
Treatment and
prevention of angina
Long-term management
of angina, to re-duce
frequency and severity
of anginal
episodes
atenolol
Long-term management
of angina, to re-duce
frequency and severity
of anginal
episodes
metoprolol
Long-term management
of angina, to re-duce
frequency and severity
of anginal
episodes
Nadolol
Long-term management
of angina, to re-duce
frequency and severity
of anginal
episodes
Calcium channel
blockers
Amlodipine
Bepridil
Diltiazem
Angina
Hypertension
Atrial fibrillation and
flutter PSVT
Hypertension
Hypertension
Angina
Hypertension
Nifedipine
Angina Hypertension
Nimodipine
Subarachnoid
hemorrhage
Nisoldipine
Hypertension
Verapamil
Angina
Atrial fibrillation or
flutter
PSVT
Hypertension
An electrophysiology (EP) study is a test performed to assess heart's electrical system or activity
and is used to diagnose abnormal heartbeats or arrhythmia.
The test is performed by inserting catheters and then wire electrodes, which measure electrical
activity, through blood vessels that enter the heart.
The Procedure
The EP study is performed in the electrophysiology laboratory of the hospital, where a person
will be placed on an X-ray table. A camera and television screens , heart monitors and various
instruments will be close by. Electrodes will be placed on chest and back to connect to
monitoring equipment. A blood pressure cuff will be placed on upper arm to monitor blood
pressure.
To prevent infection, shave and cleanse the groin and possibly neck area where the catheters will
be inserted. The area will be cleansed with an antiseptic. Sterile sheets will be draped over body.
Depending on the type of study medications may be given intraveniously, administered in yarm,
to sedate or make sleepy. These medications help reduce anxiety and relieve discomfort.
A local anesthetic will be administered with a tiny needle to numb the area where the catheters
are inserted.
One or more catheters, which are thin, long, flexible wires, will be inserted into a large vein in
groin or neck. The catheters will be guided to heart. The positioning of catheters inside heart
will be monitored on a screen. The incision site is less than a quarter of an inch.
There are two parts to the EP study:
Pacing the heart to bring on certain abnormal rhythms for observation under
controlled conditions
the heart muscle is starved of oxygen and dies), hypertension (which increases the
force of contraction needed to pump blood) and amyloidosis (in which protein is
deposited in the heart muscle, causing it to stiffen). Over time these increases in
workload will produce changes to the heart itself:
Reduced spare capacity. As the heart works harder to meet normal metabolic
demands, the amount cardiac output can increase in times of increased
oxygen demand (e.g. exercise) is reduced. This contributes to the exercise
intolerance commonly seen in heart failure. This translates to the loss of
one's cardiac reserve, or the ability of the heart to work harder during
strenuous physical activity. Since the heart has to work harder to meet the
normal metabolic demands, it is incapable of meeting the metabolic demands
of the body during exercise.
The general effect is one of reduced cardiac output and increased strain on the
heart. This increases the risk of cardiac arrest (specifically due to ventricular
dysrhythmias), and reduces blood supply to the rest of the body. In chronic disease
the reduced cardiac output causes a number of changes in the rest of the body,
some of which are physiological compensations, some of which are part of the
disease process:
Reduced perfusion (blood flow) to the kidneys stimulates the release of renin
an enzyme which catalyses the production of the potent vasopressor
angiotensin. Angiotensin and its metabolites cause further vasoconstriction,
and stimulate increased secretion of the steroid aldosterone from the adrenal
glands. This promotes salt and fluid retention at the kidneys.
The increased peripheral resistance and greater blood volume place further strain
on the heart and accelerates the process of damage to the myocardium.
Vasoconstriction and fluid retention produce an increased hydrostatic pressure in
the capillaries. This shifts the balance of forces in favour of interstitial fluid
formation as the increased pressure forces additional fluid out of the blood, into the
tissue. This results in edema (fluid build-up) in the tissues. In right-sided heart
failure this commonly starts in the ankles where venous pressure is high due to the
effects of gravity (although if the patient is bed-ridden, fluid accumulation may
begin in the sacral region.) It may also occur in the abdominal cavity, where the
fluid build-up is called ascites. In left-sided heart failure edema can occur in the
lungs this is called cardiogenic pulmonary edema. This reduces spare capacity for
ventilation, causes stiffening of the lungs and reduces the efficiency of gas
exchange by increasing the distance between the air and the blood. The
consequences of this are dyspnea (shortness of breath), orthopnea and paroxysmal
nocturnal dyspnea.
The symptoms of heart failure are largely determined by which side of the heart
fails. The left side pumps blood into the systemic circulation, whilst the right side
pumps blood into the pulmonary circulation. Whilst left-sided heart failure will
reduce cardiac output to the systemic circulation, the initial symptoms often
manifest due to effects on the pulmonary circulation. In systolic dysfunction, the
ejection fraction is decreased, leaving an abnormally elevated volume of blood in
the left ventricle. In diastolic dysfunction, end-diastolic ventricular pressure will be
high. This increase in volume or pressure backs up to the left atrium and then to the
pulmonary veins. Increased volume or pressure in the pulmonary veins impairs the
normal drainage of the alveoli and favors the flow of fluid from the capillaries to the
lung parenchyma, causing pulmonary edema. This impairs gas exchange. Thus, leftsided heart failure often presents with respiratory symptoms: shortness of breath,
orthopnea and paroxysmal nocturnal dyspnea.
In severe cardiomyopathy, the effects of decreased cardiac output and poor
perfusion become more apparent, and patients will manifest with cold and clammy
extremities, cyanosis, claudication, generalized weakness, dizziness, and syncope.
The resultant hypoxia caused by pulmonary edema causes vasoconstriction in the
pulmonary circulation, which results in pulmonary hypertension. Since the right
ventricle generates far lower pressures than the left ventricle (approximately 20
mmHg versus around 120 mmHg, respectively, in the healthy individual) but
nonetheless generates cardiac output exactly equal to the left ventricle, this means
that a small increase in pulmonary vascular resistance causes a large increase in
amount of work the right ventricle must perform. However, the main mechanism by
which left-sided heart failure causes right-sided heart failure is actually not well
understood. Some theories invoke mechanisms that are mediated by
neurohormonal activation.[33] Mechanical effects may also contribute. As the left
ventricle distends, the intraventricular septum bows into the right ventricle,
decreasing the capacity of the right ventricle.
PHARMACOTHERAPY OF CONGESTIVE HEART FAILURE:
Type
Angiotensinconverting
enzyme (ACE)
inhibitors
Drug
Benazepril
Captopril
Enalapril
Fosinopril
Lisinopril
Moexipril
Comments
Angiotensin II
receptor
blockers
Other
vasodilators
Perindopril
Quinapril
Ramipril
Trandolapril
Candesartan
Eprosartan
Irbesartan
Losartan
Telmisartan
Valsartan
Hydralazine
Beta-blockers
Cardiac
glycosides
Bisoprolol
Carvedilol
Metoprolol
Digitoxin
Digoxin
Loop diuretics
Potassiumsparing
diuretics
Thiazide and
thiazide-like
diuretics
Anticoagulants
Bumetanide
Ethacrynic acid
Furosemide
Amiloride
Spironolactone
Triamterene
Chlorthalidone
Heparin
Warfarin
Opioids
Positive
inotropic drugs
(drugs that
make muscle
contract more
forcefully)
Morphine
Inamrinone
Dobutamine
Dopamine
Milrinone
Fibric acid derivatives, the third group of antihyperlipidemic drugs, work in a variety
of ways. Clofibrate
Miscellaneous Antihyperlipidemic
Drug: Niacin
The mechanism by which niacin (nicotinic acid) lowers blood lipids is not fully
understood.
USES:
Bile Acid Sequestrants
The bile acid sequestrants are used as adjunctive therapy for the reduction of
elevated serum cholesterol in patients with hypercholesterolemia who do not have
an adequate response to a diet and exercise program. Cholestyramine may also be
used to relieve pruritus associated with partial biliary obstruction.
HMG-CoA Reductase Inhibitors
These drugs, along with a diet restricted in saturated fat and cholesterol, are used
to treat hyperlipidemia when diet and other nonpharmacologic treatments alone
have not resulted in lowered cholesterol levels.
Fibric Acid Derivatives
While the fibric acid derivatives have antihyperlipidemic effects, their use varies
depending on the drug.
For example, Clofibrate (Atromid-S) and gemfibrozil (Lopid) are used to treat
individuals with very high serum triglyceride levels who present a risk of abdominal
pain and pancreatitis and who do not experience a response to diet modifications.
Clofibrate is not used for the treatment of other types of hyperlipidemia and is not
thought to be effective for prevention of coronary heart disease. Fenofibrate (Tricor)
is used as adjunctive treatment for the reduction of LDL, total cholesterol, and
triglycerides in patients with hyperlipidemia.
Miscellaneous Antihyperlipidemic
Drug: Niacin
Niacin is used as adjunctive therapy for the treatment of very high serum
triglyceride levels in patients who present a risk of pancreatitis (inflammation of the
pancreas) and who do not experience an adequate response to dietary control.