Cardiovascular System

1. The Heart
The heart is a four-chamber organ located
in the upper left thoracic cavity.
Purpose
Pumps the blood around the body so that
oxygen and nutrients can be distributed to all
areas of the body
Maintains the blood pressure at an acceptable
level

2. Angina pectoris, commonly known as angina, is
the sensation of chest pain, pressure, or
squeezing, often due to ischemia of the heart
muscle from obstruction or spasm of
the coronary arteries. While angina pectoris can
derive from anemia, cardiac
arrhythmias and heart failure, its main cause
is coronary artery disease,
an atherosclerotic process affecting
the arteries feeding the heart. The term derives
from the Latin angere ("to strangle")
and pectus ("chest"), and can therefore be
translated as "a strangling feeling in the chest

3. Major risk factors
Age (≥ 45 years for men, ≥ 55 for women)
Cigarette smoking
Diabetes mellitus (DM)
Dyslipidemia
Family history of premature cardiovascular
disease (men <55 years, female <65 years old)
Hypertension (HTN)
Kidney disease (microalbuminuria or GFR<60
mL/min)
Obesity
Physical inactivity
Prolonged psychosocial stress

4. Conditions that exacerbate or provoke
(stimulate) angina Medications
Vasodilators
Excessive thyroid replacement
Vasoconstrictors
Polycythemia which thickens the blood causing it
to slow its flow through the heart muscle
Hypothermia
Hypovolaemia
Hypervolaemia

5. The most specific medicine to treat angina is nitroglycerin. It is a
potent vasodilator that makes more oxygen available to the heart
muscle. Betablockers (e.g., carvedilol, propranolol, atenolol) and
calcium channel blockers (such as nifedipine (Adalat)
and amlodipine) act to decrease the heart's workload, and thus its
requirement for oxygen. isosorbide mononitrate and nicorandil are
vasodilators commonly used in chronic stable angina .Nitroglycerin
should not be given if certain inhibitors such
as Sildenafil (Viagra), Tadalafil(Cialis), or Vardenafil (Levitra) have
been taken within the previous 12 hours as the combination of the
two could cause a serious drop in blood pressure. Treatments for
angina are balloon angioplasty, in which the balloon is inserted at
the end of a catheter and inflated to widen the
arterial lumen. Stents to maintain the arterial widening are often
used at the same time. Coronary bypass surgery involves bypassing
constricted arteries with venous grafts. This is much more invasive
than angioplasty.

6. A new therapeutic class, called If inhibitor, has recently
been made available: Ivabradine provides pure heart rate
reduction leading to major anti-ischemic and antianginal
efficacy. ACE inhibitors are also vasodilators with both
symptomatic and prognostic benefit. Statins are the most
frequently used lipid/cholesterol modifiers, which
probably also stabilize existing atheromatous plaque. Low-
dose aspirin decreases the risk of heart attack in patients
with chronic stable angina, and was part of standard
treatment. However, in patients without established
cardiovascular disease, the increase in haemorrhagic
stroke and gastrointestinal bleeding offsets any benefits
and it is no longer advised unless the risk of myocardial
infarction is very high.

7. Exercise is also a very good long-term treatment for the angina
(but only particular regimens - gentle and sustained exercise
rather than intense short bursts), probably working by complex
mechanisms such as improving blood pressure and promoting
coronary artery collateralisation.
Identifying and treating risk factors for further coronary heart
disease is a priority in patients with angina. This means testing
for elevated cholesterol and other fats in the
blood,diabetes and hypertension (high blood pressure), and
encouraging smoking cessation and weight optimisation.
The calcium channel blocker nifedipine prolongs cardiovascular
event- and procedure-free survival in patients with coronary
artery disease. New overt heart failures were reduced by 29%
compared to placebo; however, the mortality rate difference
between the two groups was statistically insignificant

8. Antiarrhythmics and Antianginals
:Cardiac illnesses
Cardiac stimulants
Cardiac depressants
Treatment of Heart Failure:
Cardiac glycosides
Digoxin
Treat arrhythmias

9. Cardiac arrhythmia, also known as cardiac
dysrhythmia or irregular heartbeat, is a group of
conditions in which the heartbeat is irregular, too
fast, or too slow. A heartbeat that is too fast - above
100 beats per minute in adults - is
called tachycardia and a heartbeat that is too slow -
below 60 beats per minute - is
called bradycardia. Many arrhythmias have no
symptoms. When symptoms are present these may
include palpitations or feeling a pause between
heartbeats. More seriously there may be
lightheadedness, passing out, shortness of breath,
or chest pain While most arrhythmias are not
serious some predispose a person to complications
such as stroke or heart failure .

10. There are four main types of arrhythmias: extra
beats, supraventricular tachycardias, ventricular
arrhythmias, andbradyarrhythmias. Extra beats
include premature atrial contractions and premature
ventricular contractions. Supraventricular
tachycardias include atrial fibrillation, atrial flutter,
and paroxysmal supraventricular tachycardia.
Ventricular arrhymias includeventricular
fibrillation and ventricular tachycardia. Arrhythmias
are due to problems with the electrical conduction
system of the heart.Arrhythmias may occur in
children; however, the normal range for the heart
rate is different and depends on age. A number of
tests can help with diagnosis including
an electrocardiogram (ECG) and holter monitor

11. Most arrhythmias can be effectively treated.
Treatments may include medications, medical
procedures such as a pacemaker, and surgery.
Medications for a fast heart rate may include beta
blockers or agents that attempt to restore a normal
heart rhythm such as procainamide. This later group
may have more significant side effects especially if
taken for a long period of time. Pacemakers are often
used for slow heart rates. Those with an irregular
heartbeat are often treated with blood thinners to
reduce the risk of complications. Those who have
severe symptoms from an arrhythmia may be treated
emergently with a jolt of electricity in the form
of cardioversion or defibrillation

12. Digoxin:
Decreases electrical conduction
Prolongs refractory period
Increases the force of the myocardial contraction
Positive inotropic (by inoculation) action.
Dose Considerations:
Duration of action
Method of administration
Other
Physical size of the client
Other medications
Renal or hepatic function
Advanced age
Presence of other illnesses

13. Antiarrhythmics and Antianginals
Require a digitalizing dose
To bring serum levels to a therapeutic level
All glycosides have a low therapeutic level
Side Effects
Gastrointestinal effects
Nausea and vomiting
Anorexia
Diarrhea-
Cardiac effects
Cardiac arrhythmias

14. Side Effects
Neurological effects
Restlessness
Irritability
Drowsiness
Vision changes
Headache
Cardiac Glycoside ToxicityTreatment
Stop the drug
Physical assessment
Check potassium level
Administer if needed
Monitor heart rate
Administer antiarrhythmics

15. Antiarrhythmic and Antidysrhythmic Drugs
Grouped together according to their similar
actions
Antiarrhythmics and Antianginals: Drug
Action:
Work three ways:
1/Decrease the automaticity of cardiac tissues
in the ectopic sites.
2/Alter the rate of conduction of electrical
impulses through the heart.
3/Alter the refractory period of cardiac muscle
between consecutive contractions.

16. Antidysrhythmic Agents
1/Group 1, 1A, 1B, 1C: decrease the influx
of sodium ions, stabilizing membranes
2/Group 2: depress phase 4 in
depolarization
/Group 3: prolong repolarization in phase3
4/Group 4: depress phase 4 depolarization
and prolong repolarization of phases 1 and
2

17. Beta-adrenergic Blocking Agents
Inhibit beta1 and beta2 sympathetic
receptors.
Reduce heart rate.
Reduce contractility.
Decrease supraventricular and ventricular
rhythms.
Decrease blood pressure.

18. Antidysrhythmic Agents
Adverse effects
Cause bronchoconstriction
Cause heart failure
Examples: propanolol (Inderal),
esmolol, bretylium tosylate (Bretylol)

19. Calcium Channel Antagonists
Reduce the influx of calcium into the
cell:
Prevention or reversal of spasms of the
coronary blood vessels
Coronary artery dilation
Reduction of myocardial oxygen
consumption
Example: verapamil

20. Adenosine
Slow conduction through the AV node
Cardioverts paroxysmal supraventricular
tachycardia (PSVT)
Side effects
Facial flushing
Shortness of breath
Headache
Nausea and vomiting

21. Adrenergic or Sympathomimetic
Drugs
Affect alpha- or beta-adrenergic receptors
Treat shock
Mimic epinephrine and/or norepinephrine
Cause increase in heart rate
Cause vasoconstriction
Reverse hypotension from shock

22. Myocardial infarction (MI) or acute myocardial
infarction (AMI), commonly known as a heart attack,
occurs when blood flowstops to a part of the heart
causing damage to the heart muscle. The most common
symptom is chest pain or discomfort which may travel
into the shoulder, arm, back, neck, or jaw. Often it is in
the center or left side of the chest and lasts for more than
a few minutes. The discomfort may occasionally feel
like heartburn. Other symptoms may include shortness of
breath, nausea, feeling faint, a cold sweat, or feeling
tired. About 30% of people have atypical symptoms,[
with women more likely than men to present
atypically.[Among those over 75 years old, about 5% have
had an MI with little or no history of symptoms. An MI
may causeheart failure, an irregular heartbeat, or cardiac
arrest

23. Most MIs occur due to coronary artery disease. Risk
factors include high blood pressure, smoking, diabetes,
lack of exercise,obesity, high blood cholesterol, poor
diet, and excessive alcohol intake, among others. The
mechanism of an MI often involves the rupture of
an atherosclerotic plaque MIs are less commonly
caused bycoronary artery spasms, which may be due
to cocaine, significant emotional stress, and extreme
cold, among others. A number of tests are useful to
help with diagnosis,
including electrocardiograms (ECGs), blood tests,
and coronary angiography.[11] An ECG may confirm
an ST elevation MI if ST elevation is present.Commonly
used blood tests include troponin and
lessoften creatine kinase MB.[

24. Aspirin is an appropriate immediate treatment for a suspected
MI. Nitroglycerin or opioids may be used to help with chest pain;
however, they do not improve overall outcomes . Supplemental
oxygen should be used in those with low oxygen levels or
shortness of breath. In ST elevation MIs treatments which attempt
to restore blood flow to the heart are typically recommended and
include angioplasty, where the arteries are pushed open,
or thrombolysis, where the blockage is removed using
medications. People who have a non-ST elevation myocardial
infarction (NSTEMI) are often managed with the blood
thinner heparin, with the additional use angioplasty in those at
high risk . In people with blockages of multiple coronary arteries
and diabetes, bypass surgery (CABG) may be recommended rather
than angioplasty. After an MI, lifestyle modifications, along with
long term treatment with aspirin, beta blockers, and statins, are
typically recommended.

25. Complications may occur immediately following the
heart attack (in the acute phase), or may need time to
develop (a chronic problem). Acute complications may
include heart failure if the damaged heart is no longer
able to pump blood adequately around the
body; aneurysm of the left ventricle myocardium;
ventricular septal rupture or free wall rupture; mitral
regurgitation, in particular if the infarction causes
dysfunction of the papillary muscle; Dressler's
syndrome (is a secondary form of pericarditis that
occurs in the setting of injury to the heart or
the pericardium); and abnormal heart rhythms, such as
ventricular fibrillation, ventricular tachycardia, atrial
fibrillation, and heart block. Longer-term complications
include heart failure, atrial fibrillation, and an
increased risk of a second MI.

26. Hyperlipidemia
Hyperlipidemia is defined as an elevation of
one or more of the following: cholesterol,
cholesterol esters, phospholipids, or
triglycerides. Hyperlipoproteinemia
describes an increased concentration of the
lipoprotein macromolecules that transport
lipids in the plasma.

27. Pathophysiology of Hyperlipidemia :
Cholesterol, triglycerides, and phospholipids are
transported in the bloodstream as complexes of lipid
and proteins known as lipoproteins. Elevated total and
low-density lipoprotein (LDL) cholesterol and reduced
high-density lipoprotein (HDL) cholesterol are
associated with the development of coronary heart
disease (CHD).
Atherosclerotic lesions are thought to arise from
transport and retention of plasma LDL through the
endothelial cell layer into the extracellular matrix of
the subendothelial space. Once in the artery wall, LDL
is chemically modified through oxidation and
nonenzymatic glycation. Mildly oxidized LDL then
recruits monocytes into the artery wall. These
monocytes then become transformed into
macrophages that accelerate LDL oxidation.

28. The extent of oxidation and the
inflammatory response are under
genetic control, and primary or genetic
lipoprotein disorders are classified into
six categories for the phenotypic
description of hyperlipidemia.
Secondary forms of hyperlipidemia also
exist, and several drug classes may
elevate lipid levels (e.g., progestins,
thiazide diuretics, glucocorticoids, β
blockers, isotretinoin, protease
inhibitors, cyclosporine, mirtazapine,
sirolimus).

29. Diagnosis of Hyperlipidemia :
A fasting lipoprotein profile (FLP) including
total cholesterol, LDL, HDL, and triglycerides
should be measured in all adults 20 years of
age or older at least once every 5 years.
Measurement of plasma cholesterol (which
is about 3% lower than serum
determinations), triglyceride, and HDL levels
after a 12-hour or longer fast is important,
because triglycerides may be elevated in
nonfasted individuals; total cholesterol is
only modestly affected by fasting.

30. After a lipid abnormality is confirmed, major
components of the evaluation are the history
(including age, gender, and, if female, menstrual
and estrogen replacement status), physical
examination, and laboratory investigations.
Because total cholesterol is composed of
cholesterol derived from LDL, VLDL, and HDL,
determination of HDL is useful when total
plasma cholesterol is elevated. HDL may be
elevated by moderate alcohol ingestion (fewer
than two drinks per day), physical exercise,
smoking cessation, weight loss, oral
contraceptives, phenytoin, and terbutaline. HDL
may be lowered by smoking, obesity, a
sedentary lifestyle, and drugs

31. Treatment of hyperlipidemia
Pharmacologic treatment of hyperlipidemia in
conjunction with therapeutic lifestyle changes can
be used for both primary and secondary prevention
of cardiovascular disease. Statins have the most
convincing data for primary prevention, especially
for higher risk patients. Therefore, risk stratification
is essential. Statin therapy is also recommended for
secondary prevention in all patients with known
cardiovascular disease or the risk equivalent. High-
dose statins should be initiated in patients with
acute coronary syndrome.

32. Omega-3 fatty acids may be a good alternative after
myocardial infarction for patients who cannot
tolerate statins. Fibrates and niacin have not been
shown to reduce all-cause mortality in secondary
prevention, but may be useful adjuncts when statins
alone cannot adequately control lipid levels. Other
cholesterol-lowering medications used for primary or
secondary prevention of cardiovascular disease have
not been shown to consistently improve patient-
oriented outcomes. There is good evidence for using
statins in the secondary prevention of stroke and
peripheral arterial disease.

33. Hyperlipidemia is a common risk
factor for CVD, with 53.4 percent of
adults having abnormal cholesterol
values and 32 percent having
elevated low-density lipoprotein
(LDL) cholesterol levels.

34. Primary Prevention
Primary prevention of CVD consists of
treating patients with hyperlipidemia before
clinical CHD manifests (e.g., myocardial
infarction). The evidence supporting
treatment of hyperlipidemia for primary
prevention is inconsistent. Patients with the
highest baseline risk are most likely to
benefit. Medications should be chosen
based on a favorable balance between the
likelihood of benefits (e.g., patient-oriented
outcomes, mortality, CVD events, functional
status, quality of life) and harm (adverse
effects), as well as cost.

35. Characteristics of Medications to Treat Lipid
Disorders
Bile acid–binding resins
Contraindicated in complete biliary or bowel
obstruction
Constipation, nausea, and bloating are common,
leading to poor adherence in most patients
May increase triglycerides; use with caution when
triglyceride level is > 200 mg per dL (2.26 mmol per L)
Combined primary/secondary prevention: reduces
relative risk of cardiovascular mortality by 30 percent
Primarily reduces LDL cholesterol by 15 to 30 percent
Generic
Cholestyramine
Colestipol

36. Ezetimibe
No serious safety concerns with monotherapy
Well tolerated as monotherapy; side effect profile
similar to placebo
Arthralgias and myalgias more common when
combined with a statin
Lacks clinical outcome data (monotherapy or
combined with a statin)
Monotherapy reduces LDL cholesterol by 18 percent
May increase likelihood of attaining LDL cholesterol
goals when combined with a statin
No generic available
Brand
Zetia
Vytorin (ezetimibe/simvastatin)

37. Fibrates
Contraindicated in severe hepatic or renal disease
Gastrointestinal upset, rash, and abdominal pain are common
Decreased renal function and myopathies are rare
Increases risk of gallstones by 1 to 2 percent
No effect on all-cause mortality
Combined primary/secondary prevention: NNT = 46 to 125 to
prevent one coronary event; NNT = 53 to 150 to prevent one
nonfatal myocardial infarction
Generic
Gemfibrozil†
Micronized fenofibrate
Brand
Multiple prescription preparations (fenofibrate)

38. HMG-CoA reductase inhibitors (statins)
Contraindicated in active liver disease and pregnancy
Generally better tolerated than other agents
Myopathies occur in less than 1 percent of patients; increased incidence when used with
fibrates
Rhabdomyolysis occurs in less than 0.2 percent of patients
Liver function test results greater than three times the upper limit of normal occur in less than
2 percent of patients
Primary prevention: NNT = 81 for four years to prevent one coronary event; NNT = 244 for
four years to prevent one cerebrovascular event
Secondary prevention: NNT = 50 for five years to prevent one death
Acute coronary syndrome: NNT = 77 treated with high-dose statins for two years to prevent
one death
Generic
Lovastatin†
Pravastatin†
Simvastatin
Brand
Atorvastatin (Lipitor)
Fluvastatin (Lescol)
Rosuvastatin (Crestor)

39. Nicotinic acid (niacin)
Contraindicated in severe peptic ulcer disease, chronic liver
disease, and severe gout
Flushing is common; may be reduced with aspirin
pretreatment
May increase uric acid and glucose levels
Does not affect all-cause mortality
When combined with statins, improves disease-oriented
outcomes‡
Primarily increases HDL cholesterol by 15 to 35 percent
Generic
Multiple OTC preparations (immediate or controlled
release)
Brand
Multiple prescription preparations (controlled release)

40. Omega-3 fatty acids
Use with caution in patients with fish
allergy
Dyspepsia, burping, and fishy taste
most common
Generic
Multiple OTC preparations
Brand
Multiple prescription preparations