This document provides an overview of cardiovascular disorders and ischemic heart disease (IHD). It defines IHD as heart weakening caused by reduced blood flow to the heart, typically due to coronary artery disease where the coronary arteries narrow. It discusses the anatomy of the heart including the four chambers, great vessels, valves, and cardiac muscle cells. It also covers ECGs, cardiac conduction, circulatory system functions, common cardiovascular diseases like IHD, strokes, peripheral artery disease, aortic disease, and high blood pressure, as well as types of angina.

1. Cardiovascular Disorders
Ahmad Thanin

2. Learning Objectives
By the end of this module the learner will be able to:
• Define Ischemic heart disease (IHD)
• Discuss pathophysiology of IHD
• Explain the steps and actions in the completion of a holistic
assessment of a patient’s IHD
• Identify the risk factors associated with IHD
• Evaluate the role of secondary prevention in IHD management
• Assess, plan, implement and evaluate a range of appropriate nursing
interventions for the patient with IHD and the family

3. Anatomy of the Heart
Cardiac Chambers.
Great Vessels.
Valves
Cardiac Muscle Cells

4. Cardiac
Chambers
• The heart has 4 chambers:
• the right atrium
• right ventricle
• left atrium
• left ventricle.

5. Great
Vessels
The main pulmonary artery, also known as the pulmonary
trunk, emerges from the right ventricle and delivers
deoxygenated blood to the pulmonary circulation and lungs.
The aorta emerges from the left ventricle and delivers
oxygenated blood to the rest of the body.
The superior vena cava and inferior vena cava are the main
veins that deliver deoxygenated venous blood from the rest of
the body back to the heart, specifically the right atrium.
The pulmonary veins are the main veins that deliver
oxygenated blood from the lungs back to the heart,
specifically the left atrium.

7. Valves
• There are 4 valves in the
heart:
• the tricuspid valve
• mitral valve
• pulmonic valve
• aortic valve.

9. Cardiac
Muscle Cells
• There are 2 main types of
cardiac myocytes (muscle
cells) in the myocardium:
• Conducting Cells
(Pacemaker Cells)
• Contractile Cells (Non-
Pacemaker Cells)

10. Cardiac Muscle Cells
The pacemaker cells have the capability of generating
spontaneous action potentials.
• They are located in the SA node, AV node, bundle of His, right and
left bundle branches, and the Purkinje fibers.
• They make up the conduction system of the heart.
The contractile cells are the muscle cells that lead to
contraction of the heart once depolarized.

11. Cardiac Conduction System
The cardiac conduction system is the electrical pathway of the heart that leads to atrial and
ventricular contraction.
The conduction system consists of pacemaker cells that generate spontaneous action
potentials, and then deliver those impulses throughout the heart.
The cardiac conduction system comprises the following structures in order:
• SA node,
• internodal pathway and Bachmann’s bundle,
• AV node,
• bundle of His,
• bundle branches, and
• Purkinje fibers.

12. Cardiac
Conduction
System

14. ECG Paper

15. Characteristics of the Normal
ECG-Measurements
• 60 - 90 bpm heart rate
calculation
Heart Rate:
• 0.12 - 0.20 sec
PR Interval:
• 0.06 - 0.10 sec
QRS
Duration:
• (QTc ≤ 0.40 sec)
QT Interval

16. How to calculate heart rate from ECG?

17. How to calculate
heart rate from
ECG?
Calculating the heart rate when the rhythm is
regular
• There are 300 large squares per minute
• If the rhythm is regular count the number of large squares
between two QRS complexes and divide it into 300

18. How to calculate
heart rate from
ECG?
Have a six second
strip, count the
QRS complexes
and multiple by 10.
6-
Second
Method:

19. Heart Rhythm
Heart Rhythm
• Regular
• Irregular
To accurately determine the regularity of the rhythm, measure the R-R
interval across the entire strip .
• Is the distance between R-R interval is constant?

20. P Wave
It is important to remember that the P wave represents the sequential activation of the right
and left atria, and it is common to see notched or biphasic P waves of right and left atrial
activation.
P duration < 0.12 sec
P amplitude < 2.5 mm
Frontal plane P wave axis: 0° to +75°
May see notched P waves in frontal plane

21. PR Interval
• Normal length of the PR Interval
is (0.12 – 0.20 Seconds , 3-5
small squares).
• Are PRI greater than 0.20
seconds?
• Are PRI smaller than 0.12
seconds?
• Are the PRI’s constant across
the ECG Strip?

22. Normal Duration: less than 0.12
seconds (less than 3 small
boxes).
QRS
Complex
Narrow
Supra
Ventricular
Wide
Ventricular

23. ST Segment and T
wave
• In a sense, the term "ST segment" is a misnomer,
because a discrete ST segment distinct from the T
wave is usually absent.
• More often the ST-T wave is a smooth,
continuous waveform beginning with the J-
point (end of QRS), slowly rising to the peak
of the T and followed by a rapid descent to
the isoelectric baseline or the onset of the U
wave.
• This gives rise to an asymmetrical T wave. In
some normal individuals, particularly
women, the T wave is symmetrical and a
distinct, horizontal ST segment is present.

24. ST Segment and T wave
• The normal T wave is usually in
the same direction as the QRS
except in the right precordial
leads.
• In the normal ECG the T wave is
always upright in leads I, II, V3-6,
and always inverted in lead aVR.

25. ST Segment and T wave
• Normal ST segment elevation:
• this occurs in leads with large S
waves (e.g., V1-3), and the normal
configuration is concave upward.
• ST segment elevation with concave
upward appearance may also be
seen in other leads;
• this is often called early
repolarization, although it's a term
with little physiologic meaning (see
example of "early repolarization" in
leads V4-6)

26. Circulatory (cardiovascular) system
• The circulatory system, also called cardiovascular system,
• is a vital organ system that delivers essential substances to all cells for
basic functions to occur.
• Also commonly known as the cardiovascular system, is a network composed
of the heart as a centralized pump, bloods vessels that distribute blood
throughout the body, and the blood itself, for transportation of different
substances.

27. Circulatory (cardiovascular) system
• The circulatory system is divided into two separate loops:
• The shorter pulmonary circuit that exchanges blood between the heart
and the lungs for oxygenation; and
• the longer systemic circuit that distributes blood throughout all other
systems and tissues of the body.
• Both of these circuits begin and end in the heart.

28. Functions Transport of gases, nutrients, electrolytes, wastes, hormones
Heart Layers - myocardium, endocardium, epicardium
Chambers - left and right atria, left and right ventricles
Blood vessels - arteries (oxygenated blood), veins (deoxygenated blood)
Blood vessels Arteries, veins, capillaries
Hierarchy: Heart -> arteries -> arterioles -> capillaries [gas exchange - oxygenated blood becomes
deoxygenated] -> venules -> veins -> heart
Circulations Pulmonary - superior and inferior vena cava (with deoxygenated blood) -> right atrium -> right ventricle ->
right and left pulmonary artery -> capillaries of each lung (oxygenation of the blood) -> pulmonary veins ->
left atrium -> systemic circulation
Systemic - left atrium -> left ventricle -> aorta and all of its branches -> capillaries -> veins -> superior and
inferior vena cava -> pulmonary circulation
Coronary - ascending aorta -> right coronary artery -> right marginal branch, posterior interventricular
artery, left coronary artery -> anterior interventricular branch (anastomoses with the posterior branch),
circumflex artery
Blood Plasma with cellular components:
Erythrocytes (red blood cells) - contain hemoglobine and carry oxygen throughout the blood vessels
Leukocytes (white blood cells) - immune system cells
Thrombocytes (platelets) - coagulation cells
Clinical relations Arteriosclerosis, cerebrovascular disease, peripheral artery disease, aneurysm, varices, arrhytmia, heart
failure

29. The heart
• The heart is continuously going through a series of
contractions and relaxations.
• Systole refers to when the ventricles of the heart
simultaneously contract, diastole is when the ventricles relax.
• During systole, blood is forcibly pumped out of the ventricles
into the outflow tracts of their corresponding circulation.
• The atria are filling with blood at the same time.
• During diastole, the ventricles are relaxed, and blood flows
from the atria into the corresponding ventricles.

30. Pulmonary circulation
• Deoxygenated blood from systemic circulation returns to the right
atrium via the superior and inferior vena cava.
• The coronary sinus, returning blood from the coronary circulation,
also opens into the right atrium.
• The blood in the right atrium flows into the right ventricle through
the right atrioventricular valve (tricuspid valve) during diastole.
• During systole, the right ventricle contracts, directing the blood
into the conus arteriosus at the base of the pulmonary trunk.
• Contraction of the ventricle causes the tricuspid valve to shut,
preventing backflow of blood into the right atrium.

31. Pulmonary circulation
• Between the conus arteriosus and the pulmonary trunk is a
valve; the pulmonary valve. In diastole, the valve closes to
prevent backflow of blood into the right ventricle.
• The pulmonary trunk splits into a right and a left
pulmonary artery, serving the right and left lung
respectively.
• Deoxygenated blood flows into the capillaries of each lung,
where it is then oxygenated.
• The pulmonary veins collect the newly oxygenated blood
from the lung, and return it to the left atrium, where it will
be passed into systemic circulation.

32. Systemic circulation
• Oxygenated blood enters the left atrium from the
pulmonary circulation via the pulmonary veins.
• During diastole, blood passes from the left
atrium to the left ventricle through the left
atrioventricular valve (bicuspid valve).
• In systole, the left ventricle contracts, forcing
blood into the aorta.
• The blood passes through the false into the
ascending aorta.

33. Systemic circulation
• The ascending aorta becomes the arch of the aorta,
where three large arteries branch from it:
• the brachiocephalic trunk, the left common
carotid artery and the left subclavian artery.
• These arteries supply oxygenated blood to the head
and neck, and to the upper limbs.

34. Coronary
circulation
The coronary circulation refers to the blood supply
to the heart itself. It is a component of the systemic
circulation.
The right and left coronary arteries branch directly
from the ascending aorta, immediately above the
aortic valve.
The right coronary artery passes to the right and
gives off two main branches:
• the right marginal branch along the right border of the heart
and the posterior interventricular (posterior descending)
artery, which descends along the interventricular septum on
the base of the heart.

35. Functions of the cardiovascular system
Blood circulates through a network of vessels throughout the body to provide individual
cells with oxygen and nutrients and helps dispose of metabolic wastes.
• The heart pumps the blood around the blood vessels.
Functions of blood and circulation:
• Circulates OXYGEN and removes Carbon Dioxide.
• Provides cells with NUTRIENTS.
• Removes the waste products of metabolism to the excretory organs for disposal.
• Protects the body against disease and infection.
• Clotting stops bleeding after injury.
• Transports HORMONES to target cells and organs.
• Helps regulate body temperature.

36. Cardiovascular disease
• Cardiovascular disease (CVD) is a general term for conditions affecting the
heart or blood vessels.
• It's usually associated with a build-up of fatty deposits inside the arteries
(atherosclerosis) and an increased risk of blood clots.
• It can also be associated with damage to arteries in organs such as the brain,
heart, kidneys and eyes

37. Coronary
heart
disease
Coronary heart disease occurs when the flow of oxygen-rich
blood to the heart muscle is blocked or reduced.
Coronary heart disease (CHD) occurs when your heart muscle's
blood supply is blocked or interrupted by a build-up of fatty
substances (atheroma) in the coronary arteries.
The coronary arteries are the major blood vessels that supply
your heart with blood.
This puts an increased strain on the heart, and can lead to:
•angina – chest pain caused by restricted blood flow to the heart muscle
•heart attacks – where the blood flow to the heart muscle is suddenly blocked
•heart failure – where the heart is unable to pump blood around the body
properly

38. Strokes and TIAs
A stroke is where the blood supply to part of the brain is cut off, which can cause brain damage and
possibly death.
A transient ischemic attack (also called a TIA or "mini-stroke") is similar, but the blood flow to the brain is
only temporarily disrupted.
The main symptoms of a stroke or TIA can be remembered with the word FAST, which stands for:
•Face – the face may have drooped on one side, the person may be unable to smile, or their mouth or eye may have dropped.
•Arms – the person may not be able to lift both arms and keep them there because of arm weakness or numbness in one arm.
•Speech – their speech may be slurred or garbled, they may not be able to talk at all or they may not be able to understand what you
are saying to them.
•Time – it's time to dial 999 immediately if you see any of these signs or symptoms.

39. Peripheral arterial disease
Peripheral arterial disease occurs when there's a blockage in the arteries to
the limbs, usually the legs.
This can cause:
• dull or cramping leg pain, which is worse when walking and gets better with rest
• hair loss on the legs and feet
• numbness or weakness in the legs
• persistent ulcers (open sores) on the feet and legs

40. Aortic disease
Aortic diseases are a group of conditions affecting the aorta.
This is the largest blood vessel in the body, which carries blood from the heart to the rest of the body.
The aorta is the largest blood vessel in the body.
It carries blood from heart to the rest of the body.
One of most common aortic diseases is an aortic aneurysm, where the aorta becomes weakened and bulges
outwards.

41. High blood pressure
High blood pressure (hypertension)
is one of the most important risk
factors for CVD.
If your blood pressure is too high, it
can damage your blood vessels.

42. Ischemic heart disease
• Ischemic heart disease refers to heart weakening caused by reduced
blood flow to the heart.
• Typically, this reduced blood flow is the result of coronary artery
disease, a condition that occurs when the coronary arteries narrow.
• Ischemic heart disease may also be called cardiac ischemia or
ischemic cardiomyopathy.

43. Ischemic heart disease
• Ischemia is a term that refers to an imbalance between supply and
demand resulting in one of many clinical syndromes.
• Ischemic heart disease
• Condition in which an imbalance between myocardial oxygen supply and
demand results in myocardial hypoxia and accumulation of waste
metabolites;
• most often due to atherosclerosis of the coronary arteries ("coronary artery
disease")

45. Angina
• is a type of chest pain caused by reduced blood flow to the heart.
• Angina is a symptom of coronary artery disease.
• Angina is also called angina pectoris.
• Angina pain is often described as squeezing, pressure, heaviness, tightness or
pain in the chest
• Pain/discomfort you feel in your chest may spread to other parts of your upper
body.
• These include your neck, jaw, shoulders, arms, back or belly.

46. angina
• Lack of oxygen to your heart can cause
other symptoms, known as “angina
equivalents.”
• These are symptoms that you don’t feel
in your chest, including:
• Fatigue.
• Nausea or vomiting.
• Shortness of breath.
• Sweating a lot.

47. What are the different types of angina?
There are four
main types of
angina:
Stable angina.
Unstable
angina.
Microvascular
angina.
Prinzmetal
(variant) angina.

48. What are the different types of angina?
Type of angina What it feels like When you might feel it Fast facts
Stable angina
• Pressure, pain, squeezing or
fullness in the center of
your chest.
• The feeling may spread to
your jaw, neck, back,
shoulder or arm.
• May feel like gas or
indigestion.
• Lasts five minutes or less.
• During physical exertion,
like walking up a hill or flight
of stairs.
• During periods of strong
emotions (anger, anxiety,
stress).
• In very hot or very cold
weather.
• After a big meal.
• Any time your heart has to
work harder.
• Rest or medicine make it go
away.
• It comes and goes in
predictable patterns for at
least two months.
• Pain episodes are similar.
• It’s a symptom of coronary
artery dise

50. What are the different types of angina?
Unstable angina
• Pain that feels different
from usual stable angina.
• Pain that’s more severe
or gets worse.
• May also have shortness
of breath.
• May last more than 20
minutes.
• May go away and then
return.
• When you’re resting or
sleeping.
• When you have light
physical activity.
• Rest or medicine doesn’t
make it go away.
• It hits you by surprise
(not predictable).
• It can get worse over
time.
• It may indicate you’re
having

51. What are the different types of angina?
Microvascular
angina
• Severe chest pain.
• May also feel
shortness of
breath, sweating or
fatigue or have
sleep problems.
• Lasts at least 10
minutes.
• During your
normal daily
routine.
• During physical
exertion.
• During periods of
strong emotions.
• Medicine may not
help right away.
• It’s a symptom of
coronary
microvascular
disease.

52. What are the different types of angina?
Prinzmetal (variant or
vasopastic) angina
• Severe chest pain.
• Vague pain or pressure
in your lower chest.
• Pain may spread to your
neck, jaw or left
shoulder.
• May have cold sweat,
nausea, dizziness or
fainting.
• When you’re resting or
sleeping, often between
midnight and 8 a.m.
• In a recurrent pattern.
• Medication relieves
pain.
• It’s the least common
form of angina.
• It affects people who are
younger (compared with
other forms of angina).
• It’s a symptom of a
coronary spasm.

53. What causes angina?
• Reduced blood flow to the heart (myocardial ischemia) causes angina.
• Several problems with coronary arteries can prevent the heart from
receiving enough blood. These include:
• Coronary artery disease (CAD):
• Coronary microvascular disease:
• Coronary artery spasm:

54. What causes angina?
Coronary artery disease (CAD):
•This is the most common cause of angina.
•It happens when plaque (a fatty, waxy substance) builds up in the coronary arteries, which supply blood to the heart.
•These arteries narrow or harden (atherosclerosis), reducing blood flow to the heart.
Coronary microvascular disease:
•This condition is more common among women and people assigned female at birth (AFAB) compared with men and people
assigned male at birth (AMAB).
•It damages the walls of tiny blood vessels that branch from the coronary arteries.
•These blood vessels aren’t seen on typical testing for
Coronary artery spasm:
•the coronary arteries repeatedly constrict (tighten) then open up.
•These spams temporarily restrict blood flow to the heart.
•The coronary spasms without having coronary artery disease.
•This may not be diagnosed with routine testing for CAD and may require special testing.

55. How is angina treated?
Common treatment options include:
• Anticoagulants or antiplatelet drugs to lower your risk of blood clots.
• Blood pressure medications.
• Cholesterol medications.
• Medications used specifically to treat angina.
• Lifestyle changes.
• Coronary artery bypass grafting (CABG).
• Percutaneous coronary intervention (PCI), also called coronary angioplasty and
stenting.

56. SYNDROM DESCRIPTION
Ischemic heart disease Condition in which an imbalance between myocardial oxygen supply and demand
results in myocardial hypoxia and accumulation of waste metabolites; most
often due to atherosclerotic disease of the coronary arteries ("coronary
artery disease")
Angina pectoris Uncomfortable sensation in the chest or neighboring anatomic structures
produced by myocardial ischemia
Stable angina Chronic pattern of transient angina pectoris, precipitated by physical
activity or emotional upset, relieved by rest within a few minutes; episodes
often associated with temporary depression of the ST segment, but permanent
myocardial damage does not result
Variant angina Typical anginal discomfort, usually at rest, which develops because of
coronary artery spasm, rather than an increase of myocardial oxygen demand;
episodes often associated with transient shifts of the ST segment (usually ST
elevation)
Unstable angina Pattern of increased frequency and duration of angina episodes, produced by
less exertion, or at rest; high frequency of progression to myocardial
infarction if untreated
Silent ischemia Asymptomatic episodes of myocardial ischemia; can be detected by EKG and other
laboratory techniques
Myocardial infarction (See Chapter
7)
Region of myocardial necrosis usually due to prolonged cessation of blood
supply; most often results from acute thrombus at site of coronary
atherosclerotic stenosis; may be first clinical manifestation of ischemic
heart disease, or there may be a history of angina pectoris

57. Myocardial oxygen supply
• Diastolic perfusion pressure
• Coronary vascular resistance
• external compression
• intrinsic regulation
local metabolites
endothelial factors
neural innervation
• O2-carrying capacity
Myocardial oxygen demand
• Wall Tension ( P x r / 2h )
• Heart rate
• Contractility

58. ACUTE MYOCARDIAL
INFARCTION
An abrupt disruption of the coronary artery
plaque, leading to occlusive thrombus formation
is the most common cause of acute myocardial
infarction.
This initiates an "ischemic cascade", which
progresses as outlined below:
•Decreased diastolic compliance (diastolic dysfunction)
•Decreased systolic function (usually localized)
•Ischemic electrocardiographic changes
•Clinical symptoms of chest discomfort or other "anginal
equivalents“
•Release of breakdown products due to cell death, i.e. CPK,
LDH, troponin-i enzymes.

59. • Pathologic Time course in Transmural Infarction
TIME EVENT
Early changes
1 - 2min ATP levels fall; cessation of contractility
10 min 50% depletion of ATP; cellular edema, decreased membrane potential and susceptibility to arrhythmias
20 - 24 min Irreversible cell injury
1 - 3 hours Wavy myofibers
4 - 12 hours Hemorrhage, edema, PMN infiltration
18 - 24 hours
Coagulation necrosis (pyknotic nuclei with eosinophilic
cytoplasm), edema
2-4 days Total coagulation necrosis (no nuclei or striations, rimmed by hyperemic tissue); monocytes appear

60. • Pathologic Time course in Transmural Infarction
TIME EVENT
Late Changes
5 - 7 days Yellow-softening from resorption of dead tissue by macrophages
7 days + Ventricular remodeling
7 weeks Fibrosis and scarring complete

61. Clinical presentation of acute MI
Chest discomfort, characteristically described as "pressure" rather than pain or as tightness or heaviness
•Usually located in the center of the chest over an area the size of a fist rather than in a localized point.
•There is often radiation of discomfort to either or both upper arms or shoulders, sometimes to the neck and into the jaw or into
the back.
•There is often accompanying diaphoresis (sweatiness), shortness of breath, and nausea or vomiting.
•The physical exam may be entirely unremarkable but may demonstrate an S4 gallop, occasionally an S3 gallop if myocardial
infarction is large and leads to significant left ventricular dysfunction.
•Occasionally a dyskinetic apical impulse may be present if an extensive antero-apical MI occurs.
•A systolic murmur may occur with acute mitral regurgitation or ventricular/septal defect.
•Jugular venous distention (JVD) may be present in the setting of right ventricular infarct or when there is significant biventricular
heart failure.
•Pulmonary rales may be present if left ventricular failure is present.
•Electrocardiographic changes include ST segment elevation followed ultimately by T-wave inversion and evolution of Q-waves
over a time course of 24 to 48 hours.
•The location of the myocardial infarction is dependent on the site of coronary thrombosis as are the potential complications
which may follow. Coronary artery anatomy is reviewed below

62. Symptoms of a heart attack that people
describe most often include
Chest pain (angina).
• This can be mild and feel like discomfort or heaviness, or it can be severe and feel like crushing pain.
• It may start in your chest and spread (or radiate) to other areas like your left arm (or both arms), shoulder, neck, jaw, back or down toward your waist.
Shortness of breath or trouble breathing.
Fatigue.
Trouble sleeping (insomnia).
Nausea or stomach discomfort.
• Heart attacks can often be mistaken for indigestion or heartburn.
Heart palpitations.
Anxiety or a feeling of “impending doom.”
Sweating.
Feeling lightheaded, dizzy or passing out.

63. Inherited (genetic) factors-Who is most at
risk?Mycardial Infraction
People with inherited high blood pressure (hypertension)
People with inherited low levels of HDL cholesterol, high levels of LDL cholesterol, or high levels of triglycerides
People with a family history of heart disease.
•This is especially true if the heart disease started before age 55.
Older men and women
People with type 1 diabetes
Women who have gone through menopause. Generally, men are at risk at a younger age than women.
•After menopause, women are equally at risk.

64. Acquired risk factors: Who is most at risk?
These groups are most at risk:
People with acquired high blood pressure (hypertension)
People with acquired low levels of HDL cholesterol, high levels of LDL cholesterol, or high levels of triglycerides
Cigarette smokers
People who are under a lot of stress
People who drink too much alcohol
People who lead a sedentary lifestyle
People overweight by 30% or more
People who eat a diet high in saturated fat
People with type 2 diabetes

65. Symptoms of a Heart Attack
Severe pressure, fullness, squeezing, pain, or discomfort in the center of the chest that lasts for more than a few minutes
Pain or discomfort that spreads to the shoulders, neck, arms, or jaw
Chest pain that gets worse
Chest pain that doesn't get better with rest or by taking nitroglycerin
Chest pain that happens along with any of these symptoms:
Sweating, cool, clammy skin, or paleness
Shortness of breath
Nausea or vomiting
Dizziness or fainting
Unexplained weakness or fatigue
Rapid or irregular pulse

66. Treatment for a heart attack
The goal of treatment for a heart attack is to relieve pain, preserve the heart muscle
function, and prevent death.
Treatment in the emergency department may include:
• Intravenous therapy, such as nitroglycerin and morphine
• Continuous monitoring of the heart and vital signs
• Oxygen therapy to improve oxygenation to the damaged heart muscle
• Pain medicine to decrease pain.
• Cardiac medicine such as beta-blockers to promote blood flow to the heart, improve the blood supply,
prevent arrhythmias, and decrease heart rate and blood pressure
• Fibrinolytic therapy. This is the intravenous infusion of a medicine that dissolves the blood clot, restoring
blood flow.

67. Treatment for a heart attack
• This is used to prevent further blood clotting.
Antithrombin or antiplatelet therapy with aspirin or clopidogrel.
• These medicines lower lipids (fats) in the blood, particularly low density lipid (LDL)
cholesterol.
• Statins are a group of antihyperlipidemic medicines.
• They include simvastatin, atorvastatin, and pravastatin.
• Bile acid sequestrants—colesevelam, cholestyramine, and colestipol—and nicotinic
acid (niacin) are two other types of medicines that may be used to lower
cholesterol levels.
Antihyperlipidemics.

68. Acute Coronary Syndromes-Priorities of care
Administration of
high flow high
concentration
oxygen
Pain relief by
administering
Morphine
Sublingual
nitroglycerine
Asprin and
clopidogrel
Heparinization Nitrates
Beta blockade
unless
contraindicated

69. Principles
of
care
Rest :
• if the pain does not resolve by rest this is unstable angina
Relief of anxiety :
• reassurance in the form of competent nursing care, Appropriate information
and emphatic listening
Drug therapy:
• unless a drug type is specifically contraindicated, medical therapy of unstable
angina will consist of :
MONA :
• Morphine , Oxygen , Nitrates , Asprin
If symptoms do not improve an infusion of IIb/IIIa inhibitor
should be performed and urgent angiography done

70. Investigations
12 lead ECG
Cardiac enzymes
Stress testing
Echocardiography
Thalium scanning
Angiography (PCI)

71. Biochemical
Markers:
(Cardiac
Enzymes)
Biochemical evidence of myocardial infarction
involves a typical pattern of elevation followed by
a gradual fall of troponins (either I or T) or of
creatine kinase MB fraction (CK-MB).
CK-MB increases more rapidly than the troponins
and provides early evidence of myocardial
infarction
But, CK-MB is a less sensitive and less specific
marker of myocyte damage

72. Biochemical Markers

73. Pharmacological treatment
• Patients with stable and unstable angina are treated initially with antiplatelet therapy
(aspirin) to reduce the likelihood of clot formation and therefore to reduce the chance of
acute MI
Antiplatelets
• Intravenous heparin is essential in the treatment of unstable angina and works by inhibiting
further clot formation.
Heparin
• include several intravenously administered potent inhibitors of platelet aggregation such as
IIb/IIIa inhibitors (clopidogrel (plavex))
Newer anti-platelet agents-Newer anti-platelet agents

74. Pharmacological treatment
• Beta-blockers can be administered orally or intravenously to decrease
myocardial oxygen demand by reducing heart rate and contractility and, by
reduction of blood pressure, and wall tension.
Beta-blockers-
• Nitrates are effective in reducing venous return to the heart (pre-load)
thereby reducing wall tension.
• Another effect of organic nitrates is to cause a direct vasodilatation of the
coronary arteries, thereby increasing coronary perfusion.
Nitrates

75. Pharmacological treatment
• Calcium channel blockers are a large class of
agents which act by different mechanisms.
• Some of them act more through peripheral
vasodilatation and reduction of blood pressure, i.e.
wall tension
• Others act by reducing heart rate and reducing
oxygen demand.
• All of them cause some coronary vasodilatation,
resulting in increased coronary blood flow.
Calcium channel blockers

76. Reperfusion
Urgent reperfusion of the ischemic myocardium by restoration of flow in occluded coronary artery is the
primary therapeutic goal in patients with ST-elevation ACS who present within 12 hours of symptom onset.
The earlier reperfusion therapy is initiated after the onset of symptoms, the smaller the infarct size and the
greater the survival benefit.
When flow is restored within 30 minutes of occlusion, myocardial infarction can be aborted.
If flow is achieved within 2 hours, considerable myocardial salvage can occur.
When reperfusion is achieved after 2 to 3 hours, myocardial salvage is progressively reduced
Beyond 6 hours, myocardial salvage is minimal or absent.

77. Pharmacologic Reperfusion: Thrombolytic
(fibrinolytic) therapy
Thrombolytic therapy remains the most important modality for the
treatment of acute myocardial infarction and, in the absence of
contra-indications, is recommended for all patients presenting within
the first several (4-6hrs up to 12hrs) hours of myocardial infarction.
This is done through the administration of a thrombolytic agent to
dissolve the clot leading to recanalization of the coronary artery and
reperfusion of the myocardium this will be effective only if complete
infarction has not occurred.

78. Thrombolytic
Naturally occurring products:
•Streptokinase longer acting and less expensive but may cause anaphylactic reactions and are not specific to the clot
Recombinant products :
•recombinant tissue plasminogen activator :
•specific to the clot, and less likely to produce allergic or anaphylactic reactions but expensive and has a shorter half life.
Contraindications to streptokinase
Previous reaction
Previously treated with streptokinase within the last 2 months
Recent streptococcal infection
Scheduled surgical or invasive procedure

79. Contraindications to thrombolysis - Absolute
contraindications
Active GIT bleeding
Aortic dissection
Neurosurgery / Head injury/ cerebrovascular accident within 2 months
Intracranial neoplasm or aneurysm
Proliferative diabetic retinopathy
Serious trauma / major surgery within 10 days
Systolic blood pressure > 200mmHg

80. Contraindications
to thrombolysis -
Relative
contraindications
:
Prolonged CPR
Recent delivery
Prior organ biopsy
Bleeding tendency
Recent puncture of major vessel

81. Non-Pharmacological Reperfusion
Percutaneous transluminal coronary angioplasty (PTCA)
Coronary artery bypass grafting (CABG)
• These modalities are usually reserved for those patients who are
refractory to conventional medical therapy.
• PTCA is reserved for patients with one-vessel and sometimes two-
vessel coronary artery disease
• CABG is often recommended for patients with triple-vessel coronary
artery disease or disease of the left main coronary artery.

82. Percutaneous Coronary Intervention
A cardiac catheter is introduced via an arterial sheath (a small tube inserted
into the artery to provide arterial access).
The cardiac catheter enters a main artery (femoral or radial) and is advanced
towards the coronary arteries under X-ray guidance.
Once the cardiac catheter is in place, a radio opaque dye is injected into each
of the coronary arteries and its flow rate is monitored.
The severity of disease will dictate further treatment such as drug therapy,
PTCA and coronary artery bypass grafting.

83. PTCA
PTCA can be carried out either electively in a patient with stable angina, or as
an emergency in high-risk patients with unstable angina.
It can also be used in patients following an acute myocardial infarction to aid
reperfusion of the myocardium instead of thrombolysis (dissolution of a blood
clot by an enzyme such as streptokinase), or if thrombolysis has failed.
To ensure the continued viability of the artery, a coronary stent (a cylindrical
tube) may then be inserted at the plaque site

84. Nursing care after PTCA and stent insertion
Immediately after the procedure, the patient is at risk of arrhythmia and myocardial infarction.
When the patient returns to the ward or department following the procedure, cardiac
monitoring should be commenced to detect any arrhythmias, and the patient should be
observed for signs of chest pain.
A 12-lead electrocardiogram should be recorded to identify any changes which could indicate
the presence of ischemia or stent occlusion.
Observations of blood pressure (BP), heart rate, respirations and temperature, (Initially
measurement of BP, pulse and respirations every 30 minutes, and temperature every four
hours).

85. Nursing care after PTCA and stent insertion
(cont’d)
The limb that has been used for the procedure needs to be closely monitored for signs of poor
arterial circulation.
Color and warmth of the limb should be checked.
Pulses, distal to the puncture site, should be monitored at regular intervals to ensure adequate
blood flow (dorsalis pedis pulses if a femoral approach).
The nurse will observe the puncture site for signs of hematoma or bleeding.
Patients may experience pain from the puncture site and discomfort from their prolonged period of
immobility, so analgesia may be required.