Cardiac Disorders..

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CREATED BY: MRS. PALLAVI CHAUHAN

2. HYPERTENSION

7. DEFINITION
• IT is defined as a persistent elevation of the
systolic blood pressure at a level of
140mmhg or a higher and diastolic pressure
at a level of 90mmhg or higher.

10. TYPES OF HYPERTENSION
PRIMARY
HYPERTENSION
DIASTOLIC IS 90/100
SYSTOLIC IS 130/140
CAUSES:
• EXCESS SODIUM
INTAKE
• HYPER INSULLINEMIA
• GENETIC
• INCREASED CARDIAC
OUT PUT
SECONDARY
HYPERTENSION
DIASTOLIC IS 100
SYSTOLIC IS 160
CAUSES
• CONGENITAL
ANOMALIES
• ENDOCRINE
DISTURBANCES
• MEDICATIONS

13. SYSTEMIC VASCULER RESISTENCE

18. MANAGEMENT

21. • Reduce Na, fat, Caffeine intake.
• Lose weight
• Avoid alcohol, smoking
• Potassium supplements
• Antihypertensive Drugs
– Thiazide diuretics
– Loop diuretics, ACE inhibitors,
– ca channel blockers, vasodilators

28. • The assessment of patients with hypertension include:
a. Activity and rest include: weakness, fatigue, shortness of breath,
heart frequency increases, changes in heart rhythm.
b. Circulation includes: a history of hypertension, coronary heart
disease, episodes of palpitations, increased blood pressure,
tachycardia, sometimes sounding S2 heart sounds at the base of S3
and S4.
c. anxiety, depression, euphoria, irritability, facial muscle tension,
anxiety, respiratory haul, increased speech patterns.
d. Elimination include: history of kidney disease.
e. Food / fluids include: food preferences especially those containing
high salt, high fat, and cholesterol, nausea, vomiting, weight changes,
a history of diuretic drugs, presence of edema.

29. • f. Neuro-sensory include: complaints headache, throbbing, sub-occipital
headache, weakness on one side of the body, visual disturbances
(diplopia, blurred vision), epistaxis.
g. Pain / discomfort: include intermittent pain in the limbs, sub-occipital
headaches severe abdominal pain, chest pain.
h. Respiratory include: shortness of breath after activity, cough with or
without sputum, smoking history, medication use respiratory Bantu, additional
breath sounds, cyanosis.
i. Security include: gait disturbance, paresthesia, postural hypotension.
j. presence of family risk factors arearteriosclerosis, heart disease, diabetes,
kidney disease.

30. 1. Decreased Cardiac Output due to Inadequate blood pumped by the heart to
meet metabolic demands of the body
Goal: Maintain blood pressure within individually acceptable range, reduce blood pressure /cardiac workload.
Interventions :
• 1. Monitor blood pressure, measure in both arms/thighs three times, use correct cuff size and accurate
technique.
• Rationale : Comparison of pressures provides a more complete picture of vascular involvement/scope of
problem. Systolic hypertension also is an established risk factor for cerebrovascular disease and ischemic
heart disease, when diastolic pressure is elevated.
• 2. Note dependent/general edema.
Rationale : May indicate heart failure, renal or vascular impairment.
• 3. Note presence, quality of central and peripheral pulses.
Rationale : Pulses in the legs/feet may be diminished, reflecting effects of vasoconstriction (increased
systemic vascular resistance [SVR]) and venous congestion.
• 4. Observe skin color, moisture, temperature, and capillary refill time.

31. 2. Acute Pain due to an unpleasant sensory and emotional experience arising
from actual or potential tissue damage or described in terms of such
damage sudden or slow onset of any intensity.
Goal : pain is relieved/controlled.
Interventions :
• 1. Assess pain scale. Determine specifics of pain, e.g., location, characteristics.
Rationale : Helpful in evaluating effectiveness of therapy.
• 2. Encourage bedrest during acute phase.
Rationale : Minimizes stimulation/promotes relaxation.
• 3. Assist patient with ambulation as needed.
Rationale : Patient may also experience episodes of postural hypotension, causing
weakness when ambulating.
• 4. Minimize vasoconstricting activities that may aggravate headache.
Rationale : Activities that increase vasoconstriction accentuate the headache in the
presence of increased cerebral vascular pressure.

32. 3. Activity Intolerance due to Insufficient physiological or
psychological energy
Goal : increase in activity tolerance.
Interventions :
• 1. Encourage progressive activity/self-care when tolerated. Provide assistance
as needed.
Rationale : Gradual activity progression prevents a sudden increase in cardiac
workload. Providing assistance only as needed encourages independence in
performing activities.
• 2. Instruct patient in energy-conserving techniques, e.g., using chair when
showering, sitting to brush teeth or comb hair, carrying out activities at a
slower pace.
Rationale : Energy-saving techniques reduce the energy expenditure, thereby
assisting in equalization of oxygen supply and demand.

33. 4.Imbalanced Nutrition : more than body requirements related to
Intake of nutrients that exceeds metabolic needs
• Goal ; Maintain Nutritional Status:
• Interventions :
• 1. Discuss necessity for decreased caloric intake and limited intake of fats, salt, and sugar as
indicated.
Rationale : Excessive salt intake expands the intravascular fluid volume and may damage kidneys,
which can further aggravate hypertension.
• 2. Determine patient’s desire to lose weight.
Rationale : Motivation for weight reduction is internal. The individual must want to lose weight.
• 3. Review usual daily caloric intake and dietary choices.
Rationale : Identifies current strengths/weaknesses in dietary program.
• 4. Instruct and assist in appropriate food selections, such as a diet rich in fruits, vegetables, and low-
fat dairy foods.
Rationale : Avoiding foods high in saturated fat and cholesterol is important in preventing
progressing atherogenesis.

34. 5. Deficient Knowledge or Absence or deficiency of cognitive information
related to a specific topic
Goal : improve knowledge about topic.
Interventions :
1. Define and specify the desired blood pressure limits. Describe hypertension and its effect
on the heart, blood vessels, kidneys, and brain.
Rationale : Provides a basis for understanding blood pressure elevation, and describes
commonly used medical terms. Understanding that high blood pressure can occur
without symptoms is the center allows patients to continue treatment, even when it feels
good.
2. Assist patients in identifying the risk factors that can be modified, for example, obesity, a
diet high in sodium, saturated fat, and cholesterol, sedentary lifestyle, smoking, alcohol
consumption, stress lifestyle.
Rationale : Risk factors that have been shown to contribute to hypertension and
cardiovascular and renal disease.

35. RANAUD’S SYNDROME

38. What is Raynaud's phenomenon?
•Raynaud's (say "ray-NOHZ") phenomenon is a problem with blood flow. body
doesn't send enough blood to hands and feet, so they feel very cold and numb. In
most cases, this lasts for a short time when body overreacts to cold temperatures.
It may also hear this condition called Raynaud's syndrome or Raynaud's disease.

39. DEFINITIONS
• It is usually sensitivity to cold, emotional
stress or autoimmune disease. It intermittent
artero- vasoconstriction that results in
coldness, pain, pallor of finger tips or toes.
• It is also known as vasospastic disorder.

48. BURGER’S SYNDROME

49. It is also known thromboangitis obiterans
• It is an inflammatory disease of the small &
medium sized arteries and veins of
extremities.
• It is often seen in men who are smokers.

50. Clinical manifestations
• Pain, ulceration & pain from ischemia
• Color or temperature changes in finger.
• Parasthesia ,{ tingling sensation} pulsation
become weak
• Cyanotic or red
• Edema
• Changes in nail or skin

51. Diagnostic investigation
• History collection
• Physical examination
• Arteriography
• Biopsy

52. MANAGEMENT
• Relieve pain
• Vasodilators
• Emotional support
• Avoid smoking

53. CARDIOMYOPATHY

54. •It is a heart muscle disorder of unknown cause.
Three major types are:
-Dilated cardiomyopathy
-Hypertrophic cardiomyopathy
-Restrictive cardiomyopathy

55. Dilated cardiomyopathy
• It is characterized by ventricular dilation,
contractile dysfunction & heart failure.
Hypertrophic cardiomyopathy
-It is enlargement & stiffness of
interventriculer septum composed with the
free wall of the ventricles.
Restrictive cardiomyopathy
- It leads to impaired diastolic filling &
endocardial scarring.

56. Etiology /Risk factors
• Excessive intake of alcohol
• Systemic hypertension
• Infection etc.

57. Dilated cardiomyopathy
• In dilated cardiomyopathy usually both the left &
right ventricles dilate, the myocardial fibers
degenerate & fibrotic tissue replace viable tissue.
• Fibrotic tissue is not pliable, which leads to
reduced contractility & decreased stroke volume
& low cardiac out put with increase in heart rate.
• These changes eventually leads to heart failure
accompanied by lethal ventricular dysrhythmia.

58. Management
• Inotrophic agents : improve myocardial
contractility & to unload the heart.
• Nitroglycerine : used to decrease preload & after
load.
• Diuretics & Na restricted diet ; used to decrease
pulmonary congestion
• Anticoagulants : to prevent clots.
• Antidysrhthmic agents: to suppress ventricular
irritability.
• Rest : to improve cardiac function

59. Hypertrophic cardiomyopathy
• The disproportionate thickening of the
interventriculer septum in hypertrophic
cardiomyopathy leads to wall rigidity &
there by increase resistance to blood flow
from the left atrium.
• There is also obstruction of left ventriculer
out flow.

60. Clinical manifestation
• Dyspnea
• High pulmonary pressure
• Increase heart size
• Elevated left ventricular or diastolic
pressure

61. Management
• B-blockers
• Ca channels blockers : to reduce H.R.
• Nitrates
• Diuretics
• Anticoagulants agents
• Avoid alcohol

62. Restrictive cardiomyopathy
• It is impaired diastolic filling or endicardial
scarring.
• Any infiltrative process of the heart that results in
fibrosis &thickening can cause restrictive
cardiomyopathy,
• Deposition of eosinophilic fibrous protein in heart.

63. Clinical manifestation
• Chronic constructive pericarditis,
• cardiac out put falls
• Intra ventricular pressure rises

64. • Diagnostic investigation
– History collection’
– physical examination
– Chest x ray
– ECG
– Cardiac catheterization

65. Management
• Diuretics & digitalis
• Vasodilators
• Salt restriction
Surgical management
• Myotomy { cutting of muscles}
• Heart transplant

66. ATHEROSCLEROSIS

72. Pathophysiology
• D

76. ECHOCARDIOGRAM

79. ANGINA PECTORIS

80. It is chest pain resulting from myocardial ischemia
( inadequate blood supply to the myocardium).
It is common symptom of CHD.

84. Types

86. Types Of Angina Pectoris
1. Stable Angina
2. Unstable Angina
3. Variant Angina (Prinzmetal’s Angina)
4. Anginal Equivalent Syndrome
5. Syndrome- X
6. Silent Ischemia

87. STABLE ANGINA
• Predictable
• Occurs on exercise, emotion or eating.
• Caused by increase demand of the heart and by a
fixed narrowing of coronary vessels, almost
always by atheroma.
• Coronary obstruction is ‘fixed’
• Blood flow fails to increase during increased
demand despite the local factors mediated
‘vasodilation’ and so ischeamic pain is felt.

88. • So, the diastolic pressure increases and this
causes a endocrinal ‘crunch’ and thus causing
Ischeamatic pain in this region.
• Thus, a form of acutely developing and rapidly
reversible left ventricular failure results which
is relieved by taking rest and reducing the
myocardial workload.

89. UNSTABLE ANGINA
• This is characterized by Pain that occurs with less
excertion , cumulating pain at rest.
• The pathology is similar to that involved in
Myocardial Infraction, namely platelet-fibrin
thrombus associated with a ruptured atheromatous
plaque, but without complete
occulation of the vessels.
• The risk of infraction is
subtanial, and the main aim
of therapy is to reduce this.

90. VARIANT ANGINA (PRINZMETAL’S
ANGINA)
• Uncommon
• Occurs at rest generally during sleep
• Caused by Large Coronary Artery Spasm
• Usually associated with atheromatous
disease
• Abnormally reactive and
hypertrophied segments
in the Coronary Artery
• Drugs aimed at preventing
& relieving Coronary Spasm.

91. ANGINAL EQUIVALENT
SYNDROME
• Patient’s with exertional dyspnea rather than
exertional chest pain
• Caused by exercise induced left ventricular
dysfunction

92. ANGINA: SYNDROME X
• Typical , exertional angina with positive exercise
stress test
• Anatomically normal coronary arteries
• Reduced capacity of vasodilation in
microvasculature
• Calcium channel blockers and Beta
blockers are effective.

93. ANGINA: SILENT ISCHEMIA
• Very Common
• More episodes of Silent than Painful angina
in the same patient.
• Difficult to diagnose
• Gnerally Exercise testing.

95. Diagnostic investigations
• History collection
• Physical examination
• Lab teat investigations
• ANGIOGRAPGY
• ECG

96. 2. ELECTROCARDIOGRAM
(ECG)
• Measures electrical activity of the heart
• Provides info about the changes or damages to the heart
muscle
• Doesn’t detect the narrowing of the coronary arteries
• During an Anginal attack the ECG may show
1. S-T phase depression.
2. T- phase inversion and/or
3. Ventricular arrythmia
• ECG- more abnormal with Unstable Angina where the
elevation in S-T segment is found.

97. STABLE ANGINA
At
Rest
After
Exercise

98. Management
• To stable the angina.
• Provide anti-anginal medications.
• Provide education about risk factors
modifications.
• Avoid smoking & alcohol intake.

99. • A- aspirin & anti-anginal medications
• B- b blocker therapy & B.P. control.
• C- cigarette & cholesterol control
• D- diet & Diabetes control
• E- Education & Exersice.

100. Relieve the acute pain & restore
coronary blood flow.
• Analgesics/ opiate
• Morphine
• O2 therapy
• Nitrates
• Vasodilators
• B –adrenergic blockers, reduce workload
• Ca channel blockers- dilate coronary artery.
• Anti platelet agents
• Education

101. ANEURYSMS

102. Aneurysm
• An aneurysm is a distention of an artery brought
about by a weakening/destruction of the arterial
wall. They are lined with intraluminal debris, such
as plaque and thrombi. Because of the high
pressure in the arterial system, aneurysms can
enlarge, producing complications by compressing
surrounding structures; left untreated, they may
rupture, causing a fatal hemorrhage.

104. • The aorta is the most common site for
aneurysms; however, they may form in any
vessel. Peripheral vessel aneurysms may
involve the renal artery, subclavian artery,
popliteal artery (knee), or any major artery.
These produce a pulsating mass and may
cause pain or pressure on surrounding
structures.

105. CAUSES
• Aneurysms may form as the result of:
– Atherosclerosis.
– Heredity.
– Infection.
– HYPERTENSION
– Trauma.
– Immunologic conditions.

106. CLASSIFICATION
• Aneurysms may be classified as follows:
– Saccular distention of a vessel projecting from one side
– Fusiform distention of the whole artery (ie, entire circumference
is involved)
– Dissecting hemorrhagic or intramural hematoma, separating the
medial layers of the aortic wall
– Abdominal aortic aneurysms are described as infra renal, when the neck of the
aneurysm is located below the level of the renal arteries, or suprarenal, when the
aneurysm is located above the level of the renal arteries or involves the renal
arteries.

107. Clinical Manifestations
• From the aortic arch to the level of the diaphragm. At first, no symptoms; later, symptoms may come
from heart failure or a pulsating tumor mass in the chest.
•
Pulse and BP difference in upper extremities if aneurysm interferes with circulation in left
subclavian artery
• Pain and pressure symptoms , Constant, because of pressure
• Intermittent and neuralgic pain because of impingement on nerves
• Dyspnea, causing pressure against trachea
• Cough, often paroxysmal and brassy in sound
• Hoarseness, voice weakness, or complete aphonia, resulting from pressure against recurrent
laryngeal nerve
• Dysphagia due to impingement on esophagus
• Edema of chest wall — infrequent
• Dilated superficial veins on chest
• Cyanosis because of vein compression of chest vessels

108. Abdominal Aneurysm
• Many of these patients are asymptomatic
• Abdominal pain is most common, either persistent or intermittent —
often localized in middle or lower abdomen to the left of midline
• Lower back pain
• Feeling of an abdominal pulsating mass, palpated as a thrill,
Auscultate as a bruit
• Hypertension
• Distal variability of BP, pressure in arm greater than thigh
• If rupture, will present with hypotension and/or hypovolemic shock

109. Diagnostic Evaluation
• Abdominal or chest X-ray may show calcification that outlines
aneurysm.
• CT scanning and ultrasonography are used to detect and monitor size
of aneurysm.
• MRI/MRA.
• Spiral CT gives three-dimensional view of the aneurysm and any
attendant atherosclerosis
• Arteriography allows visualization of aneurysm and vessel

110. Management
• May follow small aneurysms (4 cm or less) with CT scanning or
ultrasound every 6 months and aggressively control BP.
• The prognosis is poor for untreated patients as aneurysm enlarges. It is
especially true if it enlarges 5mm in 3 months, or in patients with
chronic obstructive pulmonary disease.
• Surgery:
– Resection of the aneurysm via abdominal incision and placement of a
prosthetic graft to restore vascular continuity.
– Endovascular grafting repair of aneurysm using a stent graft, which is
deployed via the femoral artery. It attaches above and below the aneurysm
and provides a new channel for the blood.
– Thoracic aneurysms are the most difficult to treat and require use of atrial-
femoral circulatory bypass intraoperatively.

111. INFLAMMATORY HEART
DISEASE

114. RHEUMATIC HEART DISEASE/
RHEUMATIC ENDOCARDITIS

117. DEFINITION
• Rheumatic endocarditis is an acute, recurrent
inflammatory disease that causes damage to the heart as a
sequela to group A beta-hemolytic streptococcal infection,
particularly the valves, resulting in valve leakage
(insufficiency) and/or obstruction (narrowing or stenosis).
• There are associated compensatory changes in the size of
the heart's chambers and the thickness of chamber walls.

118. Rheumatic fever is a sequel to group A streptococcal infection

120. Clinical Manifestations
• Symptoms of streptococcal Pharyngitis may precede rheumatic symptoms
– Sudden onset of sore throat; throat reddened with exudates
– Swollen, tender lymph nodes at angle of jaw
– Headache and fever 101° to 104° F (38.9° to 40° C)
– Abdominal pain (children)
– Some cases of streptococcal throat infection are relatively asymptomatic
• Warm and swollen joints (polyarthritis)
• Chorea (irregular, jerky, involuntary, unpredictable muscular movements)
• Erythema marginatum (transient meshlike macular rash on trunk and
extremities in about 10% of patients)
• Subcutaneous nodules (hard, painless nodules over extensor surfaces of
extremities; rare)
• Fever
• Prolonged PR interval demonstrated by ECG
• Heart murmurs; pleural and pericardial rubs

121. Diagnostic Evaluation
• Throat culture to determine presence of
streptococcal organisms
• Sedimentation rate, WBC count and differential,
and CRP increased during acute phase of infection
• ECG-prolonged PR interval or heart block

122. Management
• Antimicrobial therapy penicillin is the drug of choice
• Rest to maintain optimal cardiac function
• Salicylates or NSAIDs to control fever and pain
• Prevention of recurrent episodes through long-term
penicillin therapy for 5 years after initial attack in most
adults; periodic prophylaxis throughout life if valvular
damage

123. INEFECTIVE ENDOCARDITIS

125. INFECTIVE ENDOCARDITIS
• Infective endocarditis (IE;
bacterial endocarditis) is an
infection of the inner lining
of the heart caused by
direct invasion of bacteria
or other organisms leading
to deformity of the valve
leaflets.

127. Causal organisms include:
– Bacteria
• Streptococcus viridans bacteremia occurs after dental work or upper
respiratory infection.
• Staphylococcus aureus bacteremia occurs after cardiac surgery or parenteral
drug abuse.
• Staphylococcus epidermidis bacteremia due to prosthetic heart valves and I.V.
access procedures.
• Enterococci (penicillin-resistant group D streptococci)—bacteremia usually
occurs in elderly patients (over age 60) with genitourinary tract infection.
– Fungi (Candida albicans, Aspergillus)
– Rickettsiae
– By rheumatic fever, congenital defects, on abnormally
vascularized valves, normal heart valves, and mechanical and
biological heart valves

128. PATHOPHYSIOLOGY
• When the inner lining of the heart (endocardium) becomes inflamed, a fibrin clot
(vegetation) forms.
• The fibrin clot may become colonized by pathogens during transient episodes of
bacteremia resulting from invasive procedures indwelling catheters, urinary tract
infections, and wound and skin infections.
• Platelets and fibrin surround the invading microorganisms, forming a protective covering
and causing the infected vegetation to enlarge.
– The enlarged vegetation (the basic lesion of endocarditis) can deform, thicken, stiffen, and scar
the free margins of valve leaflets as well as the fibrous ring (annulus) supporting the valve.
– The vegetations may also travel to various organs and tissues

129. CLINICAL MANIFESTATION
General Manifestations
• Fever, chills, sweats (fever may be absent in elderly patients or those with
uraemia)
• Anorexia, weight loss, weakness
• Cough, back and joint pain
• Splenomegaly
Skin and Nail Manifestations
• Petechiae conjunctiva, mucous membranes
• Splinter hemorrhages in nail beds
• Osler's nodes ,painful red nodes on pads of fingers and toes; usually late sign
of infection and found with a sub acute infection
• Janeway's lesions, light pink macules on palms or soles, nontender, may
change to light tan within several days, fade in 1 to 2 weeks; usually an early
sign of endocardial infection

130. Heart Manifestations
• New pathologic or changing murmur , no murmur with other signs and
symptoms may indicate right heart infection
• Tachycardia related to decreased CO
Central Nervous System Manifestations
• Localized headaches
• Transient cerebral ischemia
• Altered mental status, aphasia
• Hemiplegia
• Roth's spots on fundi (retinal hemorrhages)
Pulmonary Manifestations
• Usually occur with right-sided heart involvement
• Pneumonitis, pleuritis, pulmonary edema.

131. DIAGNOSTIC INVESTIGATION
• Blood cultures at least two positive serial blood cultures
• Endocardial involvement (diagnosed with echocardiography),
identification of vegetations and assessment of location and size of
lesions
• Echocardiogram ,consistent with disease

132. Management
• I.V. antimicrobial therapy, based on sensitivity of causative agent, for 4 to 6
weeks.
• PROVIDE antibiotics like penicillin, gentamycin etc.
• Urine cultures obtained after 48 hours to assess efficacy of drug therapy
• Repeat blood cultures obtained after 48 hours to assess efficacy of drug
therapy
• Close follow-up by cardiologist
• Supplemental nutrition

133. MYOCARDITIS

138. Fatigue and dyspnea., Palpitations
Occasional precordial discomfort
Cardiac enlargement.
Abnormal heart sounds: murmur, S3 or S4, or friction rubs.
Signs of heart failure (eg, dyspnea, crackles).
Fever with tachycardia.

143. PERICARDITIS

146. DEFINITION
• Pericarditis is an inflammation of the
pericardium, the membranous sac
enveloping the heart. It is usually a
manifestation of a more generalized disease.
• Pericardial effusion is an outpouring of
fluid into the pericardial cavity seen in
pericarditis.

147. CAUSES
• Infection
– Viral , influenza ETC.
– Bacterial ,Staphylococcus, meningococcus,
Streptococcus, pneumococcal, gonococcus,
Mycobacterium tuberculosis
– Fungal
– Parasitic
• Connective tissue disorders

149. CLINICAL MANIFESTATION
• Pain in anterior chest, aggravated by thoracic motion may
vary from mild to sharp and severe; located in precordial
area (may be felt beneath clavicle, neck, scapular region)
may be relieved by leaning forward
• Pericardial friction rub scratchy, grating, or creaking sound
occurring in the presence of pericardial inflammation
• Dyspnea from compression of heart and surrounding
thoracic structures
• Fever, sweating, chills due to inflammation of pericardium
• Dysrhythmias

150. Diagnostic Evaluation
• Echocardiogram most sensitive method for detecting pericardial effusion.
• Chest X-ray may show heart enlargement
• ECG to evaluate for MI
• Pericardiocentesis For examination of pericardial fluid for etiologic diagnosis

155. • Bacterial pericarditis penicillin or other antimicrobial agents
• Rheumatic fever penicillin G and other antimicrobial agents
• Tuberculosis antituberculosis chemotherapy.
• Fungal pericarditis amphotericin B and fluconazole
• Corticosteroids
• Renal pericarditis ,dialysis.
• Neoplastic pericarditis: Intrapericardial instillation of
chemotherapy; radiotherapy
• Bed rest, aspirin.
• Partial pericardiectomy or total pericardiectomy for recurrent
constrictive pericarditis

157. CARDIAC TAMPONADE

167. DIAGNOSTIC INVESTIGATION

176. CORNARY ARTERY DISEASE
PRESENTED BY: MRS. PALLAVI CHAUHAN

181. INTRODUCTION
• Coronary artery disease (CAD),
also known as ischemic heart
disease (IHD), is a group of
diseases that includes: stable
angina, unstable
angina, myocardial infarction,
and sudden coronary death

182. – The arteries, which is
smooth and elastic, become
narrow and rigid,
restricting blood flow to
the heart. The heart becomes
starved of oxygen and the
vital nutrients ,which needs
to pump properly.

184. ATHEROSCLEROSIS
• A disease of the arteries characterized by the
deposition of fatty material on their inner walls.

185. ARTERIOSCLEROSIS
The thickening and hardening of the walls of the
arteries.

186. DEFINITION :DEFINITION :
It is an abnormal
accumulation of the lipids or
fatty substances and fibrous
tissue in the vessel wall.
which blocks and narrow the
blood vessel, reducing the
blood flow to myocardium.

187. • CAD is characterized by
accumulation of plaque with in layer
of coronary artery. The plaque
progressively enlarge, thickens and
calcify causing a critical narrowing
of the coronary artery lumen,
resulting decrease in blood flow.

188. • What Is Ischemia?
– Ischemia is a condition in which the blood
flow (and thus oxygen) is restricted or
reduced in a part of the body. Cardiac
ischemia is the name for decreased blood
flow and oxygen to the heart muscle.
– Cardiac ischemia occurs when plaque and
fatty matter narrow the inside of an artery
to a point where it cannot supply enough
oxygen-rich blood to meet heart's needs.

190. RISK FACTORS :RISK FACTORS :
MODIFIABLE :
• HIGH BLOOD CHOLESTROL LEVEL.
• CIGARETTE SMOKING AND TOBACCO CHEWING.
• HYPERTENSION
• DM.
• PHYSICAL INACTIVITY.
• OBESITY
NON MODIFIABLE:
• FAMILY HISTORY
• INCREASING AGE
• GENDER
• RACE

191. PATHOPHYSIOLOGY:PATHOPHYSIOLOGY:
ETIOLOGICAL FACTORSETIOLOGICAL FACTORS
ACCUMULATION OF LIPIDSACCUMULATION OF LIPIDS
NARROWING OF LUMEN AND DECREASED IN BLOODNARROWING OF LUMEN AND DECREASED IN BLOOD
FLOW.FLOW.
FORMATION OF THROMBUS.FORMATION OF THROMBUS.
OBSTRUCTION IN BLOOD FLOW.OBSTRUCTION IN BLOOD FLOW.
CADCAD

192. CLINICAL MANIFESTATION:
• ACUTE ONSET OF CHEST PAIN.
•NAUSEA AND VOMITING.
•INDIGESTION
•FAINTING
•CHANGES IN ECG.
•HIGHER LEVEL OF CARDIAC ENZYME.

193. • A common symptom is chest
pain or discomfort which may
travel into the shoulder, arm, back,
neck, or jaw.
• Occasionally it may feel
like heartburn. Usually symptoms
occur with exercise or emotional
stress, last less than a few minutes,
and get better with rest.
• Shortness of breath may also occur
and sometimes no symptoms are
present
• irregular heartbeat

194. DIAGNOSTIC EVALUATION:
• ECG
• STRESS TESTING
• BLOOD TEST
• ANGIOGRAPHY
• CARDIAC
CATHETERIZATION
• PET (POSITRON EMISION TOMOGRAPHY)

195. ECG
•P = contractions of the atria
•QRS= ventricular contractions..
•T and U = follow the ventricular
contractions.

196. ECG FINDINGS

197. TREADMILL STRESS TEST
• This is the commonest test done to screen for heart
problem.
• It involves placing electrodes on body and a blood
pressure cuff on arm, then have to walk on a
treadmill.
• This is to make heart work hard so that any blockage
in artery will show up as an abnormality in ECG.

198. TREADMILL STRESS TEST

199. ECHOCARDIOGRAMS
• An echocardiogram is a non invasive test that uses ultrasound images
of the heart. This test is more expensive than an ECG, but it can be
very valuable, particularly in identifying damage of the heart muscle.

200. RADIONUCLIDE IMAGING
• Radionuclide procedures use imaging techniques and computer
analyses to plot and detect the passage of radioactive tracers
through the region of the heart & given intravenously.
Radionuclide imaging is useful for diagnosing and determining:
• Severity of chronic coronary artery disease
• Severity of unstable angina when less expensive diagnostic
approaches are unavailable or unreliable
• Success of surgeries for coronary artery disease.

201. RADIONUCLIDE IMAGING

202. ANGIOGRAPHY
• Angiography is an invasive test.
• In an angiography procedure: A narrow tube is
inserted into an artery, usually in the leg or arm,
and then threaded up through the body to the
coronary arteries.
• A dye is injected into the tube, and an x-ray
records the flow of dye through the arteries.
This process provides a map of the coronary
circulation, revealing any blocked areas.

206. Magnetic Resonance Angiography
• MRA is a newer non invasive imaging technique that can
provide three-dimensional images of the major arteries to the
heart.

208. COMPUTED TOMOGRAPHY
• Computed tomography (CT) scans may be used to evaluate coronary artery
disease.

209. BLOOD TEST INVESTIGATIONS

210. • Complete Blood Count : The CBC can help detect blood diseases and
disorders, such as anaemia, infections, clotting problems, blood cancers, and
immune system disorders.
– Red Blood Cells : (4.4-5.8 million/ml)
– White Blood Cells: (3800-10.800/ml)
– Platelets : are blood cell fragments that help to blood clot. (130.000-400.000/ml)
– Blood Glucose : Abnormal glucose levels in your blood may be a sign of diabetes.

211. • Blood Enzyme Tests : Enzymes are chemicals that help control chemical
reactions in body. There are many blood enzyme tests. This section focuses on
blood enzyme tests used to check for heart attack.
– Troponin: (25.92ng/ml) Troponin is a muscle protein that helps your muscles
contract. When muscle or heart cells are injured, troponin leaks out, and its levels in
your blood rise.
– Creatine Kinase: (141.8ng/ml ) A blood product called CK is released when the
heart muscle is damaged. High levels of CK in the blood can mean that a heart
attack.

212. Cholesterol test
• A cholesterol test, also called a lipid panel or lipid profile, measures the fats
(lipids) in blood.
– Total cholesterol : less than 200 (mg/dL)
– Low-density lipoprotein cholesterol ( less than 130, mg/dL & under 100 mg/dL)
– High-density lipoprotein cholesterol (35-45 mg/dL}
– Triglycerides ( 30-150 mg/Dl)

213. POSITRON EMISSION TOMOGRAPHY
• Positron emission tomography (PET) is a
test that uses a special type of camera and
a tracer (radioactive chemical) to look at
organs in the body.
• During the test, the tracer liquid is put into
a vein in arm. The tracer moves through
body, where much of it collects in the
specific organ or tissues.
• The tracer gives off tiny positively charged
particles (positrons). The camera records
the positrons and turns the recording into
pictures on a computer.
• A PET scan may be used to look
for cancer, check blood flow, or find out
how well organs are working.

215. TREATMENT

216. MANAGEMENT:
MEDICAL MANAGEMENT:-
PREVENTION OF RISK FACTORS
NTG. (NITROGLYCERIN)
BETA ADRENERGIC BLOCKING AGENT (PROPANALOL)
CALCIUM CHANNEL BLOCKERS. (AMLODEPINE)
ANTI PLATELETS AND ANTI COAGLULANTS. (ASPIRIN AND HEPARIN)
THROMBOLYTIC AGENT.(STREPTOKAINASE)
ANALGESICS.(MORPHIN SULPHATE)
Aspirin or other antiplatelets to help prevent blood clots.
An ACE inhibitor or a beta-blocker to help lower blood pressure
A statin to help lower cholesterol.

217. SURGICAL TREATMENT
• PTCA
• STENT PROCEDURE
• ANGIOPLASTY
• ATHERECTOMY
• BYPASS SURGERY
{CABG}
• MIDCAB

218. PERCUTANEOUS TRANSLUMINAL CORONARY
ANGIOPLASTY
• In this procedure injecting some local anaesthesia into the
groin area and putting a needle into the femoral artery, the
blood vessel that runs down the leg.
• A guide wire is placed through the needle and the needle is
removed.
• An introducer is then placed over the guide wire, after which
the wire is removed. A different sized guide wire is put in its
place.
• Next, a long narrow tube is introducer over the guide wire, into
the blood vessel and after that the guide wire is removed. Once
the catheter is placed in the coronary arteries, injects dye and
takes an x-ray.
• If a treatable blockage is noted, then a balloon catheter is
advanced to the blockage site. The balloon is inflated for a few
seconds to compress the blockage against the artery wall. Then
the balloon is deflated.

219. PCTA

220. STENT

222. ATHERECTOMY
• Atherectomy is a minimally invasive endovascular
surgery technique for removing atherosclerosis from blood
vessels within the body
• Atherectomy involves techniques similar to those used
for angioplasty.
• The difference is that atherectomy uses special tools to
remove the plaque buildup from the artery wall.

223. • A DIRECTIONAL ATHERECTOMY device
cuts away plaque, which is then collected in the tip
of the device.

224. • A ROTATIONAL CUTTING DEVICE spins at
a high speed and pulverizes plaque, which is then
safely washed away in your bloodstream.

225. • A TRANSLUMINAL EXTRACTION device
cuts away plaque using tiny rotating blades. The
loose plaque is sucked into a tube through a
vacuum.

226. CABG
Coronary artery bypass grafting (CABG) is a type of surgery that improves blood
flow to the heart. Surgeons use CABG to treat people who have severe coronary
heart disease (CHD).
There are a number of sites from which the conduit can be harvested, including
the following:
•Saphenous vein
•Radial artery
•Left internal thoracic (mammary) artery (LITA)
•Right internal thoracic (mammary) artery (RITA)
•Inferior epigastric artery
•Splenic artery

228. MINIMALLY INVASIVE HEART BYPASS SURGERY
• Minimally Invasive Direct Coronary Artery Bypass (MIDCAB) is a minimally
invasive surgery. MIDCAB is beating heart surgery, which means that stopping the heart
(cardioplegia) is not necessary and a heart-lung machine is not required.
• MIDCAB surgery can be performed through a 3"-5" incision placed between the ribs, or
may be done with several small incisions.
• MIDCAB surgery results in a faster recovery, fewer complications, and less pain after
surgery.
• It is indicated for use when bypassing one or two coronary arteries. For bypassing three
or more arteries, a conventional CABG is indicated.

230. Provide healthy diet { fat free}
Low sodium diet

231. Nursing management
MONITRING:
 BP.
 PULSE.
 CARDIAC MONITRING.
 HOURLY INTAKE OUTPUT.
 NAIL BEDS, LIPS, OR FOR CYANOSIS
 GIVE SEMI FOWLER POSITION
 MAILTAIN FLUID ELECTROLYTE BALANCE
 BED REST
 CVP MONITORING

232. COMPLICATION
• MI
• CARDIAC DEATH
• CARDIAC FAILURE

233. RESEARCH FINDINGS

234. • Coronary heart disease in rural population of Himachal--a population based study.
BACKGROUND: Cardiovascular disease has emerged as a major health burden worldwide. There
is no study in Himachal about the prevalence of coronary heart disease (CHD), hence the purpose of
the study.
• MATERIAL AND METHODS: Population based study was done in 3 different villages of
different districts of Himachal Pradesh. The people were well notified about the survey in advance.
They cover all persons above the age of 30 years. Total 812 persons were examined. History &
Detailed physical examination regarding presence and nature of chest pain was taken.. ECG of all
patients was taken.
• RESULTS: 812 patients were examined. 399 were males and 413 were females. 33 patients were
found to have coronary heart disease, giving the prevalence of 4.06%. Twenty six of 399 males had
CHD and 19 of 413 females had CHD . 17 of these CHD patients were hypertensive, two were
diabetic and 10 patients had family history of CHD.
• CONCLUSION: The prevalence of CHD was low in rural population of Himachal Pradesh, being
around 4%, more in males than in females.

235. SUMMARIZATION

236. MYOCARDIAL INFARCTION

237. INTRODUCTION
• Myocardial infarction (MI)
refers to the process by which
areas of myocardial cells in the
heart are permanently destroyed.
• It occurs when myocardial
tissues are abruptly and
severely deprived of oxygen.

238. DEFINITION
• Myocardial infarction is a
diseased condition which is
caused by reduced blood flow
in a coronary artery due to
atherosclerosis and occlusion
of an artery by an embolus or
thrombus.

240. CORONARY ARTERIES OF HEART

241. LOCATION / TYPES OF MYOCARDIAL
INFARCTION
 Obstruction of the left anterior descending artery (LAD)
results in anterior or septal wall MI.

243. Contd…..
 Obstruction of the circumflex artery results in posterior wall
MI or lateral wall MI.
 Obstruction of the right coronary artery results in inferior wall
MI.

244. ETIOLOGY

245. NON-MODIFIABLE
RISK
FACTORS
MODIFIABLE
RISK
FACTORS
ETIOLOGY

246. NON-MODIFIABLE RISK
FACTORS

247. AGE: More than 40 years.
FAMILY HISTORY:
Myocardial infarction can
be inherited from parents
to children.
GENDER: Myocardial
infarction is 3 times more
in men than women.

248. MODIFIABLE RISK FACTORS

249. HIGH BLOOD CHOLESTROL LEVEL
LOW DENSITY
LIPOPROTEIN
(LDL)
DANGEROUS
HIGH DENSITY
LIPOPROTEIN
(HDL)
LIPIDS
(LIPOPROTIENS)

250. HDL is not dangerous because it contains
more proteins & very less lipids.
Secondly it carry lipids away from arteries
to the liver for metabolism. So it prevents
lipids accumulation within arteries.
LDL is dangerous because it contains more
lipids & has capacity to deposit fat within
arteries.
So, LDL level more than 160mg/dl will
place a person at a risk of myocardial
infarction.

251. HYPERTENSION
If a person’s blood pressure is more than
140/90 mmHg continuously for 4-5 years
Sustained stress on arterial walls injury
to endothelial lining atherosclerosis
narrowed & thickened arterial walls
risk of M.I.
Also salt consumption 5gms/ day cause M.I.

252. SMOKING
Smoking nicotine catecholamine
(epinephrine & nor epinephrine) release
increases heart rate & blood pressure increases
cardiac workload.
+
CO decreases O2 available to myocardium
Injury to myocardium

253. PHYSICAL INACTIVITY
Improper lipid metabolism
LDL level increases
Starts accumulating
in blood vessels
Risk of M.I.

254. OBESITY
More lipids are produced
LDL level increases
Atherosclerosis
Risk of M.I.

255. DIABETES MELLITUS
Glucose molecules may stick to
lumen of artery
Blockage of artery
Risk of having M.I.

256. STRESS
SNS stimulation
Release of catecholamine
Increases heart rate & intensify the force of
myocardial contraction
Increases O2 demand
Cell death
Risk of M.I.

257. PATHOPHYSIOLOGY

258. • Due to causing factors
• A build up of fatty deposits called plaque
• Plaque clogs & narrow the arteries & other blood vessels
• Slows or block the flow of blood to the heart
• Sometimes the surface of plaque can rupture or tear, which can cause blood
clots to form the block arteries.
• A complete or near complete blockage of cornary arteries results heart failure.

259. Causative factor: Obesity
Atherosclerosis
Narrowing of lumen
ed heart insufficient blood flow to myocardium
Contractility ed O2demand of myocardial cells
Inadequate creates an O2deficit
Blood supply
myocardial cell death inflammation
Oliguria
CK-MB & Troponine released Fever

260. Anaerobic glycolysis
Accumulation of lactic acid
Irritation of myocardial nerve fibers
Transmission of pain massage to
myocardium
Chest pain & radiation towards shoulder &

261. Stimulation of vomiting SNS Stimulation
center
increased
Nausea & Vomiting catecholamine
Diaphoresis Increased
(perfuse sweating) Heart Rate
Cold & Clammy skin
“Cold Sweat”

262. CLINICAL MANIFESTATIONS
 Cardiovascular-
 Chest pain/Discomfort
 Palpitations
 Elevated BP
 ECG may show tachycardia, bradycardia and
dysarrythmia

264. PAIN
Characteristics: Severe,
immobilizing chest pain.
Usually prescribed as heaviness,
pressure, tightness, burning.
Location: Substernal,
Retrosternal or Epigestric.
Radiation: It may radiate to
neck, jaw, arm or back.
Duration: Lasts for 20 minutes
or more.

265. NAUSEA & VOMITING
Stimulation of vomiting center by severe
pain causes nausea & vomiting.
FEVER
100.4 to 102.2°F
It is due to inflammatory process caused
by Myocardial cell death.

266. CONTD…..
 Respiratory-
 Shortness of breath
 Dyspnea/Tachypnea
 Crackles
 Pulmonary edema-may be present
 Gastrointestinal-
 Nausea
 Vomiting

267. CONTD…..
 Genitourinary-
 Decreased urinary output
 Skin-
 Cool, clammy skin
 Diaphoresis
 Pallor, Cyanosis
 Coolness of extremities

268. CONTD…..
 Neurogenic-
 Anxiety, restleness
 Light- headedness
 Headache
 Visual Disturbances
 Altered speech
 Altered motor functions
 Altered level of consciousness

269. CONTD…..
 Psychosocial-
 Fear feeling
 Pt. may deny that anything is
wrong

270. SYMPATHETIC NERVOUS SYSTEM
STIMULATION
Increased catecholamine releases.
Diaphoresis (perfuse sweating).
Cold & clammy skin (“cold sweat”).

271. CARDIOVASCULAR MANIFESTATIONS
Hypotension
Decrease cardiac output
Shock
Urine output (Oliguria): <30ml/day.
Dyspnoea

272. DIAGNOSTIC TESTS

273. ASSESSMENT/DIAGNOSTIC
FINDINGS
 It is generally based on presenting symptoms, ECG and
laboratory test results.
 Patient history-it includes
• Description of presenting
symptoms
• History of previous illness,
family health history

274. CONTD…..
 Electrocardiogram-
ECG provides information that
assists in diagnosing acute MI.
 The classic ECG changes are-
 T wave inversion
 ST segment elevation
 Abnormal Q wave

276. CONTD…..

277. Contd…..

278. SERUM CARDIAC
MARKERS
CK-MB (ENZYME)
TROPONINE-T
(PROTEIN)

279. • CK-MB- increases 3-6 hrs after onset of
chest pain, peaks in 12-18 hrs & return to
normal within 3-4 days.
• Cardiac troponin T- increases 7-14 hrs after
MI & persists for 5-7 days.

280. ECHOCARDIOGRAM
PURPOSE: it is useful to assess the ability of
heart muscles to contract & relax.
It is done to evaluate ventricular function by
checking ejection rate.
MEGNATIC RESONANCE IMAGING
(MRI)
PURPOSE: To detect site & extent of
myocardial cells.

281. ANGIOGRAPHY
To detect percentage of blockage & type of MI.
CHEST X-RAY
To detect cardiomegaly.
• Positron emission tomography- (PET scan)
• It is used to evaluate cardiac
metabolism & to assess tissue perfusion.

282. MEDICAL MANAGEMENT
DRUG
THERAPY
FIBRINOLYTIC
THERAPY
MEDICAL
MANAGEMENT

283. MEDICAL MANAGEMENT
 The goal of medical management is to minimize myocardial
damage, preserve myocardial function and prevent
complications.
 Pharmacological management- MONA
 M-MORPHINE
 O-O2 & OPIODS
 N- NITRATES
 A- ASPIRIN
 Thrombolytics
 Analgesics
 ACE Inhibitors(ACE-I)

284. DRUG THERAPY
ANALGESIC: Morphine Sulphate.
NITRATES
I/V Nitroglycerine: 4 ampules of NTG are dissolved in
100 ml normal saline to reduce pain by dilating
coronary arteries.
Sublingual Nitroglycerine: (Sorbitrate)
At one time patient can take 3 tablets.
if pain relieved If pain not relieved
Take second Tab. After 10 take next Tab. at same time
minutes

285. BETA ADRENERGIC BLOCKERS
(Propanolol) it inhibit SNS stimulation of heart.
reduces both heart rate & contractility
CALCIUM CHANNEL BLOCKERS
(Verapamil, Nifedipine)
It causes coronary artery vasodilatation & decreases
myocardial contractility.
Increases blood supply to myocardium & decreases
O2 demand of myocardium.
LOW-MOLECULAR-WEIGHT HEPARIN
(Fragmine)
These inhibit conversion of fibrinogen into fibrin.

286. FIBRINOLYTIC THERAPY
TIME OF
ADMINISTRATION:
Thrombolytic are given
to the patient upto 12
hours of onset of chest
pain but for best results it
should be given within 1
hr after onset of chest
pain.
ACTION: These will dissolve & lysis of thrombus
in coronary artery.
It includes streoptokinase, urokinase, t-PA,
alteplase.
After thrombolytic therapy, IV heparin is
continued.

287. SURGICAL MANAGEMENT
PTCA (Percutaneous
Transluminal
Coronary
Angioplasty)

288. STENT PLACEMENT

289. ATHERECTOMY
With Atherectomy the plaque is shaved off using a type
of rotational blade.

290. CORONARY
ARTERY
BYPASS
GRAFT (CABG)
A portion of
saphenous vein
from leg is
removed & is
anastmosed
proximally to the
ascending aorta &
distally to
coronary artery.

293. THANK YOU
Eat good, Workout for a Strong Heart