The cardiovascular system consists of the heart and blood vessels. The heart has four chambers - two atria and two ventricles. It is surrounded by layers including the pericardium, myocardium, and endocardium. There are four valves in the heart that allow blood flow in only one direction. Blood vessels include arteries, which carry blood away from the heart; veins, which carry blood back to the heart; and capillaries, where gas exchange occurs. The circulatory system can be divided into systemic circulation and pulmonary circulation. Cholesterol is carried through the bloodstream by lipoproteins including LDL, VLDL, HDL, and chylomicrons.

1. TRAINING
Cardiovascular System

2. Cardiovascular System:
The cardiovascular system, also known as the
circulatory system, is the system of heart and
blood vessels that transport blood, oxygen, and
nutrients to the tissues, and remove waste
products and carbon dioxide from the tissues of
the body.

3. Anatomy and Physiology of the
Cardiovascular System

4. CVS consists of:
Heart,
Arteries,
Veins,
Capillaries

5. Heart:

6. Position of the heart in the body:

7. Size, location and Composition
Size:
• Approximately the size of your fist.
• Length:12 cm
• Width: 9 cm
• Weight: 250-350 gm. (1 Pound)
Location:
 Superior surface of diaphragm
 Left of the midline
 Anterior to the vertebral column,
 Posterior to the sternum
 Between 2nd and 6th ribs

8. Composition:

9. Chambers:
The heart consists of four chambers:
2 Atria:
Right Atrium
Left Atrium
2 Ventricles:
Right Ventricle
Left Ventricle

10. Right Atrium:
 Thin walled,
 Low pressure,
 Receiving chamber,
 Receive venous blood via 2 large veins:
1. Superior Vena cava (head, neck and upper limbs)
2. Inferior Vena cava (lower parts of the body)

11. Right Ventricle:
 Thick walled,
 Receives venous blood from the right atrium,
 Pump the blood to the lungs through Pulmonary artery,
 Communicates with the right atrium through “Tricuspid valve”.

12. Left Atrium:
 Thin walled,
 Low pressure,
 Receiving chamber,
 Receives oxygenated blood from the lungs
through Pulmonary veins,

13. Left Ventricle
 Very thick walled,
 Muscular walls,
 Pumping chamber,
 Communicates with the left atrium through “Bicuspid Valve’’ (mitral valve),
 Receives the oxygenated blood from left atrium,
 Pump the oxygenated blood to different parts of the body through Systemic aorta.

14. Valves of the heart
There are 4 valves in human heart.
1. Two Atrioventricular Valves
2. Two Semilunar Valves
All these valves of the heart permit the flow of blood through the heart in only one direction.

15. Atrioventricular valves:
1. Left AV valve (Bicuspid valve)
2. Right AV valve (Tricuspid valve)

16. Left AV valve (Bicuspid Valve):
 Also known as Bicuspid valve or Mitral valve,
 Formed by 2 valvular cusps or flaps,
 Lie between the left atrium and left ventricle,
 Chordae tendineae anchor AV valves to papillary muscles,
 The papillary muscles arise from the inner surface of the ventricles,
 The papillary muscles play an important role in the closure of cusps and in preventing
the back flow of blood from ventricle to atria during ventricular contraction.

17. Right AV valve (Tricuspid Valve):
 Also known as Tricuspid valve,
 Formed by 3 valvular cusps,
 Lie in between right atrium and right ventricle,
 Prevents the blood from flowing back into the right
atrium when the right ventricle contracts.

18. The anatomy of the valves of heart:

19. The anatomy of the valves of heart:

20. AV valves = Closed
SL Valves = Open

21. Semilunar Valves:
 Because of the half moon shape, these two valves are called Semilunar Valves,
 Both the semilunar valves are similar in structure,
 Each valve has 3 flaps,
 Semilunar valves prevent backflow of blood into the ventricles,
 There are 2 types of Semilunar valves:
1. Pulmonary Valve
2. Aortic Valve

22. Pulmonary Valve:
 P. Valve lies between the right ventricle and pulmonary
trunk,
 Lies on the right side of heart,
 Prevents blood from flowing back into the right
ventricle.

23. Aortic valve:
 Aortic valve lies between the left ventricle and the
aorta,
 Lies on the left side of heart,
 Prevents blood from flowing back into the left ventricle,

24. Layers of wall of the heart:
Heart is made up of 3 layers of tissues:
1. Pericardium
2. Myocardium
3. Endocardium

25. Pericardium
• Outermost covering of the heart,
• Made up of 2 layers:
1. Parietal Pericardium
2. Visceral Pericardium

26. 1. Parietal Pericardium
 Outer layer,
 Forms a strong protective sac for the heart,
 Helps to anchor the heart within the mediastinum,
 Made up of 2 layers:
i. Fibrous layer
ii. Serous layer

27. i. Fibrous layer
 Formed by thick fibrous Connective tissue,
 Attached to the diaphragm,
 Protects the heart from over stretching.

28. ii. Serous layer
 Formed by mesothelium + small amount of CT,
 Mesothelium contains squamous epithelial cells,
 Epithelial cells secrete a small amount of fluid which lines the pericardial space,
 The fluid prevent friction and allows free movement of heart within the pericardium
when it contracts and relaxes,
 The total volume of this fluid is about 25-35 mL.

29. 2. Visceral Pericardium
 Inner layer,
 Closely lines the surface of the myocardium,
 Made up of flattened epithelial cells,
 Also known as “Epicardium”.

30. Pericardial cavity
 Potential space between the Parietal Pericardium and Visceral Pericardium,
 Contains fluid of about 25-35 mL,
 In healthy conditions, the 2 layers of Pericardium lie in close approximation separated
by a thin film of fluid.

32. Myocardium
 Middle layer of the wall of heart,
 Formed by Cardiac muscle fibers,
 Responsible for pumping action of heart,
 Forms the bulk of heart,
 3 types of CMF are present in myocardium:
i. Which form the contractile unit of the heart
ii. Which forms Pacemaker
iii. Which forms the conductive system.

33. Endocardium
 Inner most layer of the heart wall,
 Thin,
 Smooth,
 Glistering,
 Formed by a single layer of endothelial cells,
 Endocardium continues as endothelium of the blood vessels.

34. Different layers of Pericardium

35. Septa of the heart
Two types of septa are present in the heart:
1. Interatrial Septum:
Atria of the heart are separated from one another by a
fibrous septum called interatrial septum.
2. Interventricular Septum:
The ventricles are separated from one another by septum
called interventricular septum.

36. Actions of the heart
The actions of the heart are classified into 4 types.
1. Chronotropic action (Frequency of heartbeat)
2. Inotropic action (Force of contraction of heart)
3. Dromotropic action (Conduction of Impulse)
4. Bathmotropic action (Excitability of Cardiac muscle)

37. Blood Vessels
There are 3 main types of blood vessels:
1. Arteries
2. Veins
3. Capillaries

38. Arteries
 Carry blood away from the heart to the capillaries,
 Diameter: 4 mm
 Thickness of the wall: 1 mm
 Strongest of the blood vessels,
 These are the distributors,
 Walls of arteries are the thickest,
 Lumens of arteries are narrower than that of veins,
 Blood moves under high pressure,
 The elastic fibres allow the artery to stretch under pressure.

39. Arterioles
 The arterial branches become narrower and their walls
become thinner reaching the periphery called arterioles,
 Diameter: 30 micron,
 Thickness: 6 micron,
 These are called the resistant vessels because peripheral
resistance is offered to the blood flow in the arterioles,
 The arterioles connect to the capillaries.

40. Aorta
 Leaves left ventricle,
 Takes blood from the heart to the body,
 Diameter: 25 mm,
 Thickness of the wall: 2 mm,
 Has 4 portions:
1. Ascending Aorta
2. Arch of Aorta
3. Thoracic Aorta
4. Abdominal Aorta

42. Vein
 Carry blood from capillaries back to the heart,
 Diameter: 5 mm,
 Thickness of the wall: 0.5 mm,
 Veins contain valves that ensure blood flow in one direction only,
 Pressure in the veins is low so they rely on skeletal muscles to aid in venous blood
flow,
 Great ability to stretch (capacitance),
 Lumens of veins are wider than that of arteries,

44. Venules
 The venules are smaller vessels with thin muscular wall,
 Connecting the capillaries with the larger systemic veins,
 Diameter: 20 micron,
 Thickness of the wall: 1 micron.

45. Vena Cava
 Carry deoxygenated blood to the right atrium,
 Diameter: 30 mm,
 Thickness of the wall: 1.5 mm,
 Two types:
1. Superior Vena cava
2. Inferior Vena cava

46. Capillaries
 Microscopic vessels where exchange between cells and blood
takes place,
 Capillaries are the smallest blood vessels,
 Only about one cell layer thick,
 Speed of blood flow decreases to increase contact time,
 Connect arterioles to venules,
 Diameter: 8 micron,
 Thickness of the wall: 0.5 micron.

48. Anatomy of blood vessels
The walls of blood vessels are made up of 3 layers.
1. Tunica adventitia,
2. Tunica media,
3. Tunica intima.

49. Tunica adventitia
 Outermost layer,
 Made up of fibrous connective tissue,
 Holds vessels open,
 Prevents tearing of vessels walls during body
movements,
 Larger in veins than the arteries.

50. Tunica media
 Middle layer,
 Formed by Smooth muscle and elastic CT,
 Helps vessels constrict and dilate,
 Larger in arteries.

51. Tunica intima
 Innermost layer,
 Composed of endothelium,
 One cell thick in capillaries,
 Continuation of endocardium.

55. Difference b/w arteries and veins

57. Blood
 Blood separates into two main parts:
1. Plasma
2. Elements
 Plasma accounts for 55% and elements 45% of
blood volume.

60. Division of circulation
The blood flows through 2 divisions of circulatory
system.
1. Systemic circulation
2. Pulmonary circulation

61. Systemic circulation
 The system of blood vessels that carries oxygenated blood from the left ventricle to
the tissues of the body and deoxygenated blood back to the right atrium of the heart.
 Known as greater circulation,

62. Pathway
 Left side of heart
 Receives blood from lungs
 Ejects blood into aorta
 Systemic arteries, arterioles
 Gas and nutrient exchange in systemic capillaries
 Systemic venules and veins lead back to right atrium
Left atrium  Left ventricle  Aorta  Arteries  Arterioles 
Capillaries  Venules  Veins  Vena cava  Heart (right atrium)

63. Pulmonary circulation
 The system of blood vessels that carries
deoxygenated blood from right ventricle to the
lungs and oxygenated blood back to left atrium of
the heart.
 Known as lesser circulation.

64. Pathway
 Right side of heart
 Receives blood from systemic circulation
 Ejects blood into pulmonary trunk then pulmonary
arteries
 Gas exchange in pulmonary capillaries
 Pulmonary veins takes blood to left atrium
Right Atrium  Right Ventricle  Pulmonary Artery trunk  Pulmonary Arteries  Lungs 
Pulmonary Veins  Heart (left atrium)

67. Blood flow in the body
Right
Atrium
Right
Ventricle
Pulmonary
Semilunar
Valve
Left
Atrium
Bicuspid
Valve
Left
Ventricle
Pulmonary
Valve
Tricuspid
Valve
Aortic
Semilunar
Valve
Lungs
Body

68. Cardiac Cycle
One complete heartbeat, consisting of one
contraction (Systole) and one relaxation
(diastole) of the heart.

69. Cardiac Cycle

70. Basic terminologies
 Blood Pressure: Blood pressure (BP) is the pressure exerted by circulating blood
upon the walls of blood vessels.
 Systole: Contraction of the heart, especially of the ventricles, by which blood is driven
through the aorta and pulmonary artery.
 Diastole: Relaxation and dilatation of the heart chambers, especially the ventricles,
during which they fill with blood.

71. Calculation of blood pressure
Blood pressure can be calculated as:
 BP = Cardiac Out Put (CO) x Total Peripheral Resistance (TPR)
 CO = Stroke Vol. x Heart Rate
 Cardiac out put: The amount of blood ejected from left ventricle per minute
 Stroke Volume: The amount of blood ejected from left ventricle per stroke (beat)
 Heart Rate: Number of heart beat per minute
 Total Peripheral Resistance: the sum of the resistance of all peripheral
vasculature in the systemic circulation.

72. Cholesterol
 A waxy substance found in your body,
 Steroid metabolites,
 Found in the cell membrane,
 Comes from 2 sources:
i. Liver (Endogenous)
ii. Food (Exogenous)

73. Cholesterol
Exogenous source:
It involves dietary cholesterol which is absorbed from the intestine and is converted into
Chylomicrons (CMs).
Endogenous source:
It involves the synthesis of cholesterol in the liver which is transported to blood as HDL,
LDL and VLDL.

74. Cholesterol
 Necessary for the formation of:
 bile acids
 cell membranes
 steroid hormones (Estrogen, testosterone, cortisol)
 Fat soluble vitamins (ADEK)
 75% synthesized by body(mostly liver)
 25% obtained from diet
 Insoluble in water

75. Cholesterol
 140 g of cholesterol is present in human body.
 1.5 g of cholesterol is synthesized by liver per
day.
 Transported as lipoproteins (LDL, HDL, VLDL).

76. Lipoproteins
• They are the molecules of proteins + fats.
• They carry cholesterol through the blood.
• As cholesterol doesn’t dissolve well in blood, it needs to attach itself to fatty proteins to
circulate through the body.
• They are non-polar from the inside and polar at the outside so they can contact with
water of blood for transportation.

77. Types of cholesterol
1. Low Density Lipoproteins (LDL)
2. Very Low Density Lipoprotein (VLDL)
3. High Density Lipoproteins (HDL)
4. Chylomicrons (CMs)

78. Low Density Lipoproteins (LDL)
 Also known as the "bad cholesterol".
 They are produced by the liver.
 Carry cholesterol from the liver to different areas of the body like heart, muscles,
tissues and organs.
 Collects in the walls of blood vessels thus causes blockage.

79. Very Low Density Lipoproteins (VLDL)
 They carry cholesterol from the liver to organs
and tissues in the body.
 They are formed by a combination of cholesterol
and triglycerides.
 VLDL are heavier than LDL.

80. High Density Lipoproteins (HDL)
 They are considered the "good" cholesterol.
 They are cholesterol scavengers.
 They Reduce, Re-use and Re-cycle the LDL by transporting them back to the liver for
degradation.
 They act as maintenance crew for inner walls (endothelium) of blood vessels.
 High levels of HDL are a good indicator of a healthy heart, because less cholesterol is
available in your blood to attach to blood vessels and cause plaque formation.

81. HDL: Good Cholesterol:Scavenger

82. Chylomicrons (CMs)
Large lipoprotein particles that consist of:
• triglycerides (85-92%),
• phospholipids (6-12%),
• cholesterol (1-3%) and
• proteins (1-2%).
They transport dietary lipids from the intestines to
other locations in the body.

83. Triglycerides (TGs)
o Type of fat (lipid) found in blood.
o Body converts any calories that doesn’t need to use into TGs.
o TGs are stored in Fat cells.
o If you regularly eat more calories than you burn, you may have high triglycerides
(hypertriglyceridemia).

84. Biosynthesis of cholesterol
 Biosynthesis of cholesterol takes place in the ER
of hepatic cells.
 Biosynthesis begins with Acetyl-CoA.
 Acetyl-CoA is derived from the oxidation
reaction in mitochondria.

85. Biosynthesis of cholesterol

86. Mechanism of action of STATINS
o STATINS are the selective and competitive
inhibitor of 3-hydroxy–3–methyl–glutaryl–
coenzyme A (HMG-CoA) reductase.
o The enzyme catalyzes the conversion of HMG-
CoA to mevalonate, an early and rate-limiting
step in cholesterol biosynthesis

89. Normal values of Lipid profile
Total Cholesterol Level Category
Less than 200 mg/dL
Desirable level that puts you at lower risk for coronary heart disease. A
cholesterol level of 200 mg/dL or higher raises your risk.
200 to 239 mg/dL Borderline high
240 mg/dL and above
High blood cholesterol. A person with this level has more than twice the
risk of coronary heart disease as someone whose cholesterol is below
200 mg/dL.
HDL Cholesterol Level Category
Less than 40 mg/dL (for men)
Less than 50 mg/dL (for women)
Low HDL cholesterol. A major risk factor for heart disease.
60 mg/dL and above
High HDL cholesterol. An HDL of 60 mg/dL and above is considered
protective against heart disease.
LDL Cholesterol Level Category
Less than 100 mg/dL Optimal
100 to 129 mg/dL Near or above optimal
130 to 159 mg/dL Borderline high
160 to 189 mg/dL High
190 mg/dL and above Very high
Triglyceride Level Category
Less than 150 mg/dL
150–199 mg/dL Borderline high
200–499 mg/dL High
500 mg/dL and above Very high

90. Metabolic syndrome
 A cluster of conditions.
 Metabolic syndrome is present if three or more of the following five criteria are met.
Risk Factor Defining Level
1. Abdominal obesity
 Men Waist  40 inches
 Women Waist  35 inches
2. Triglycerides  150 mg/dL
3. HDL cholesterol
 Men  40 mg/dL
 Women  50 mg/dL
4. Blood pressure  130/  85 mm Hg
5. Fasting glucose  110 mg/dL

91. Pathology of CVS
The common types of heart and vascular diseases are:
1. Heart attack (MI)
2. Arrhythmia
3. Heart failure
4. Left Ventricular hypertrophy
5. Angina Pectoris
6. Atherosclerosis
7. Stroke
8. Hypertension
9. Coronary Artery Disease
10. Cardiomyopathy
11. Ischemic heart disease

92. Coronary Artery disease
 This type of cardiovascular disease involves atherosclerosis—hardening and
narrowing—of the coronary arteries, producing blockages in the vessels that carry blood
to the heart.
 Partially blocked it causes angina.
 Fully blocked it causes a myocardial infarction or a heart attack!

93. Coronary arteries

94. Atherosclerosis
Deposition of Fatty substances especially Cholesterol or fatty acids in arteries.
Risks Factors include:
 Hypertension
 Hyperlipidemia
 Obesity
 Carbon Monoxide in Smoke

95. Mechanism of atherosclerosis
Atherosclerosis is also known as arteriosclerotic vascular disease or ASVD.
 Atherosclerosis develops from low-density lipoprotein molecules (LDL) becoming oxidized
(LDL-ox) by free radicals.
 When oxidized LDL comes in contact with an artery wall, a series of reactions occur to repair
the damage to the artery wall caused by oxidized LDL.
 The body's immune system responds to the damage to the artery wall caused by oxidized
LDL by sending specialized white blood cells (macrophages and T-lymphocytes) to absorb
the oxidized-LDL forming specialized foam cells.
 These white blood cells are not able to process the oxidized-LDL, and ultimately grow then
rupture, depositing a greater amount of oxidized cholesterol into the artery wall. This triggers
more white blood cells, continuing the cycle.
 Eventually, the artery becomes inflamed. The cholesterol plaque causes the muscle cells to
enlarge and form a hard cover over the affected area. This hard cover is what causes a
narrowing of the artery, reduces the blood flow and increases blood pressure.
 A complete blockage leads to ischemia of the myocardial (heart) muscle and
damage. This process is the myocardial infarction or "heart attack."

96. Pathophysiology of atherosclerosis

97. Atherosclerosis Timeline
Phase I: Initiation
LDL-C plays a major role in
initiating the development
of atherosclerotic plaque.
Media
Intima
Phase II: Progression
Disease progression results
in the remodeling of the
vascular wall so that the
size of the lumen does
not change significantly.
LDL-C
Phase III: Complication
Extensive lipid accumulation
and a greater inflammatory
component can pose the
threat of plaque rupture.
Lumen Unstable
Stable
Libby P. In: Heart Disease: A Textbook of Cardiovascular Medicine. 6th ed.
Philadelphia, Pa: WB Saunders Co; 2001:995-1009;
Libby P. J Intern Med. 2000;247:349-358.

98. ATHEROTHROMBOSIS
The Leading Cause of Death Worldwide*
Atherothrombosis
(vascular disease)
Infectious disease
Pulmonary disease
Cancer
Violent deaths
AIDS
Number of deaths (x 106)
0 2 4 6 8 10 12 14 16
Murray et al. Lancet 1997;349:1269-1276.
*In eight defined regions of the world, including developed and developing areas.

99. Myocardial ischemia
Whenthe blood flow demands of the heart exceed the
blood supplied by the coronary arteries.
Causes:
a) Atherosclerosis
b) Blockage of coronary arteries due to the
accumulation of lipid plaques and/or thrombus.

100. Imbalance b/w Supply and Demand

101. Heart attack (MI)
 Myocardial infarction refers to the process by
which myocardial tissue is destroyed in regions of
the heart that are deprived of an adequate blood
supply because of a reduced coronary blood flow
 A prolonged lack of myocardial oxygenation
leading to necrosis of a portion of the heart
muscle.

102. Heart attack risk factors include:
• Age. Men age 45 or older and women age 55 or older are more likely to have a heart attack than are younger men and women.
• Tobacco. This includes smoking and long-term exposure to secondhand smoke.
• High blood pressure. Over time, high blood pressure can damage arteries that feed your heart. High blood pressure that occurs with
other conditions, such as obesity, high cholesterol or diabetes, increases your risk even more.
• High blood cholesterol or triglyceride levels. A high level of low-density lipoprotein (LDL) cholesterol (the "bad" cholesterol) is most
likely to narrow arteries. A high level of triglycerides, a type of blood fat related to your diet, also ups your risk of heart attack. However, a
high level of high-density lipoprotein (HDL) cholesterol (the "good" cholesterol) lowers your risk of heart attack.
• Obesity. Obesity is associated with high blood cholesterol levels, high triglyceride levels, high blood pressure and diabetes. Losing just
10 percent of your body weight can lower this risk, however.
• Diabetes. Not producing enough of a hormone secreted by your pancreas (insulin) or not responding to insulin properly causes your
body's blood sugar levels to rise, increasing your risk of heart attack.
• Metabolic syndrome. This occurs when you have obesity, high blood pressure and high blood sugar. Having metabolic syndrome
makes you twice as likely to develop heart disease than if you don't have it.
• Family history of heart attack. If your siblings, parents or grandparents have had early heart attacks (by age 55 for male relatives and
by age 65 for female relatives), you might be at increased risk.
• Lack of physical activity. Being inactive contributes to high blood cholesterol levels and obesity. People who exercise regularly have
better cardiovascular fitness, including lower high blood pressure.
• Stress. You might respond to stress in ways that can increase your risk of a heart attack.
• Illicit drug use. Using stimulant drugs, such as cocaine or amphetamines, can trigger a spasm of your coronary arteries that can cause
a heart attack.
• A history of preeclampsia. This condition causes high blood pressure during pregnancy and increases the lifetime risk of heart
disease.
• An autoimmune condition. Having a condition such as rheumatoid arthritis or lupus can increase your risk of heart attack.

103. Etiology and pathophysiology
1. Atherosclerosis:
o Narrowing of a coronary artery.
2. Arterial Thrombosis:
 Thrombus is a solid mass (Abnormal clot),
 Usually due to atherosclerosis.
3. Arterial Embolism:
 Embolus is a Floating clot,
 Breaks off from thrombi (Piece of thrombus.
(Plaque that accumulates on the inner walls of your arteries is made from various
substances that circulate in your blood. These include calcium, fat, cholesterol and
fibrin, a material involved in blood clotting).

104. Signs and symptoms
 Pain
 Anxiety
 Nausea and vomiting
 Breathlessness
 Collapse/syncope
 Chest discomfort
 Paleness

105. Diagnosis
 Electrocardiogram (ECG)
 Blood test (Cardiac enzymes)
 Echocardiogram
 Nuclear scan
 Chest radiographs
 Coronary angiography
 Exercise stress test.
 Cardiac computerized tomography (CT) or magnetic resonance imaging
(MRI).

106. Common diagnostic procedures include:
• Angioplasty. An angioplasty opens the blocked artery by using a balloon or by
removing the plaque buildup.
• Stent. A stent is a wire mesh tube that’s inserted into the artery to keep it open after
angioplasty.
• Heart bypass surgery. In bypass surgery, your doctor reroutes the blood around the
blockage.
• Heart valve surgery. In valve replacement surgery, your leaky valves are replaced to
help the heart pump.
• Pacemaker. A pacemaker is a device implanted beneath the skin. It’s designed to help
your heart maintain a normal rhythm.
• Heart transplant. A transplant is performed in severe cases where the heart attack
has caused permanent tissue death to most of the heart.

107. Medical management
 Analgesic (morphine sulphate) & antiemetic
 Antithrombotic therapy (Antiplatelet therapy, anticoagulants)
 Anti-anginal therapy
 Surgical therapy

108. Treatment
1. Pain relief (Morphine or Pethidine)
2. Oxygen (To relive dyspnoea)
3. Nitrates (To relieve ischemic pain)
4. Beta blockers
5. Thrombolytic therapy (Streptokinase)

109. Arrhythmia
Arrhythmia refers to:
 Irregular heartbeat or
 Disturbance in the rhythm of heart.
In arrhythmia heartbeat may be:
 Fast or
 Slow or
 There may be an extra beat or
 Missed beat.

110. Types of arrhythmia
1. Arrhythmias Originating in the Atria
 Atrial fibrillation
 Atrial flutter
 Sinus arrhythmia
 Sinus tachycardia
2. Arrhythmias Originating in the Ventricles
o Ventricular Fibrillation
o Ventricular Tachycardia

111. Atrial fibrillation
 It is characterized by rapid and irregular atrial contractions at the rate of
300-400 beats/minute.
 It is mostly due to circus movement of impulses within atrial musculature.
 P wave is absent in ECG.
 Common in old people and patients with heart diseases.
 Not life threatening.
 If continues for long time, it may cause blood clot and blockage of blood
flow to vital organs.

112. Atrial flutter
 It is characterized by rapid ineffective atrial contractions caused by
ectopic foci originating from atrial musculature.
 Both the atria beat rapidly like the wings of a bird hence the name
atrial flutter.
 Atrial rate is about 250-350/minute.
 The ratio b/w atrial beats and ventricular beats is 2:1 or sometimes
3:1.
 Common in patients suffering from cardiovascular diseases such as
hypertension and CAD.

113. Ventricular fibrillation
 It is the dangerous cardiac arrhythmia characterized by rapid and irregular twitching
of ventricles.
 It is mostly due to circus movement of impulses within ventricular muscle.
 The rate reaches to 400-500/minute.
 It is serious type of arrhythmia and lead to death since the ventricles can not pump
blood.
 Common during electric shock and coronary occlusion.

114. Ventricular tachycardia
 It is the sudden increase in heart rate caused by ectopic foci arising from ventricular
musculature.
 Sometimes, a part of ventricular muscle, particularly an ischemic area is excited
abnormally followed by a series of extrasystole.
 This condition is dangerous as the circus movement is developed within ventricular
muscle.

115. Heart failure
 It is a serious condition, heart failure does not mean that the heart is no longer working.
 Heart failure is when the heart’s ability to pump is weaker than normal.
 Blood moves through the heart and body at a slower rate, pressure increases in the
heart, and the heart can’t supply enough blood and oxygen to the body’s cells, resulting
in fatigue and shortness of breath.

116. Heart failure can be caused by:
o Cardiomyopathies (diseases that damage the heart muscles)
o Coronary Artery Disease
o Diabetes
o Diseases of the Heart Valves
o Heart Defects present at Birth
o High Blood Pressure
o Lung Disease such as Emphysema
o Past Heart Attacks

117. Congenital heart defects
 Different than other types of heart conditions.
 Congenital heart defects are present at birth.
 These defects are not a disease, but rather an abnormality that occurs while a foetus is
developing.
 Examples include a leaky heart valve or malformations in the walls that separate the
heart chambers.
 Some heart defects may produce symptoms at birth or during childhood, while others
aren’t discovered until a person is an adult. Treatment may or may not be needed,
depending on the severity of the defect.

118. Cardiomyopathy
 A progressive disease that causes the heart to
become abnormally enlarged, thickened, and/or
stiffened,
 Cardiomyopathy limits the heart muscle’s ability to
pump blood effectively.
 This often leads to other heart conditions such as
heart failure or arrhythmia.

119. Stroke
A stroke occurs when blood flow
to the brain is interrupted by a
blocked or burst blood vessel.

120. Stroke (Definition)
Stroke is a clinical syndrome of sudden
focal or global cerebral dysfunction
lasting more than 24 hours, of presumed
vascular origin.

121. Risk factors of stroke
 Hypertension (a major factor, no critical BP level).
 Cardiac disease (cardiac enlargement, failure, arryhthmias, rheumatic heart
disease, patent foramen ovale)
 Diabetes (the risk of cerebral infarction is increased twice).
 Heredity
 Hypercholesterolemia
 Haematocrit (a  Hb concentration,  fibrinolysis)
 Oral contraceptives

122. Causes of Stroke
 Occlusion (50%)
 Embolisation (25%)
 Haemorrhage (20%)

123. Two major types of stroke

124. Ischemic Stroke
 It is the sudden loss of blood circulation to an
area of the brain, resulting in a loss of
neurologic functions.
 It is caused by thrombotic or embolic occlusion
of cerebral artery.

125. Haemorrhagic stroke
 It develops as a result of involuntary break of intracerebral vessel and is accompanied
by forming of hematoma.
 The usual mechanism is thought to be leakage from small intracerebral arteries
damaged by chronic hypertension.

126. Angina Pectoris
 It is a clinical syndrome characterized by intermittent chest pain caused by reversible
myocardial ischemia.
 It lasts for several minutes.
Types of Angina pectoris:
1. Stable Angina
2. Variant Angina
3. Unstable Angina

127. Symptoms of Angina
Angina symptoms include:
• Chest pain or discomfort, possibly described as pressure, squeezing, burning
or fullness
• Pain in your arms, neck, jaw, shoulder or back accompanying chest pain
• Nausea
• Fatigue
• Shortness of breath
• Sweating
• Dizziness

128. Risk factors of Angina
• Tobacco use. Chewing tobacco, smoking and long-term exposure to secondhand smoke damage the interior walls of arteries — including arteries to your heart — allowing
deposits of cholesterol to collect and block blood flow.
• Diabetes. Diabetes is the inability of your body to produce enough or respond to insulin properly. Insulin, a hormone secreted by your pancreas, allows your body to use
glucose, which is a form of sugar from foods. Diabetes increases the risk of coronary artery disease, which leads to angina and heart attacks by speeding up atherosclerosis
and increasing your cholesterol levels.
• High blood pressure. Blood pressure is determined by the amount of blood your heart pumps and the amount of resistance to blood flow in your arteries. Over time, high
blood pressure damages arteries by accelerating hardening of the arteries.
• High blood cholesterol or triglyceride levels. Cholesterol is a major part of the deposits that can narrow arteries throughout your body, including those that supply your
heart. A high level of the wrong kind of cholesterol, known as low-density lipoprotein (LDL) cholesterol (the "bad" cholesterol), increases your risk of angina and heart attacks.
A high level of triglycerides, a type of blood fat related to your diet, also is undesirable.
• Family history of heart disease. If a family member has coronary artery disease or has had a heart attack, you're at a greater risk of developing angina.
• Older age. Men older than 45 and women older than 55 have a greater risk than do younger adults.
• Lack of exercise. An inactive lifestyle contributes to high cholesterol, high blood pressure, type 2 diabetes and obesity. However, it is important to talk with your doctor before
starting an exercise program.
• Obesity. Obesity raises the risk of angina and heart disease because it's associated with high blood cholesterol levels, high blood pressure and diabetes. Also, your heart has
to work harder to supply blood to the excess tissue.
• Stress. Stress can increase your risk of angina and heart attacks. Too much stress, as well as anger, also can raise your blood pressure. Surges of hormones produced
during stress can narrow your arteries and worsen angina.

129. Stable Angina
 It occurs due to increased demand of myocardial
Oxygen during exertion in a patient of narrow
coronary arteries.
 It is relived by rest and nitroglycerine.

130. Characteristics of stable angina
• Develops when your heart works harder, such as when you exercise or climb
stairs
• Can usually be predicted and the pain is usually similar to previous types of
chest pain you've had
• Lasts a short time, perhaps five minutes or less
• Disappears sooner if you rest or use your angina medication

131. Causes of Stable Angina
Stable angina is usually triggered by physical exertion. When you climb stairs,
exercise or walk, your heart demands more blood, but it's harder for the muscle to
get enough blood when your arteries are narrowed. Besides physical activity, other
factors such as emotional stress, cold temperatures, heavy meals and smoking
also can narrow arteries and trigger angina.

132. Variant Angina
 Occurs at rest,
 Documented to be due to arterial spasm,
 Unrelated to physical activity, heart rate or
blood pressure,
 Generally responds to vasodilators.

133. Characteristics of variant angina
• Usually happens when you're resting
• Is often severe
• May be relieved by angina medication

134. Causes of Variant Angina
 This type of angina is caused by a spasm in a coronary artery in which the
artery temporarily narrows. This narrowing reduces blood flow to your heart,
causing chest pain. Emotional stress, smoking and use of the illegal drug
cocaine may trigger this type of angina.

135. Unstable Angina
 Pain occurs with progressively increasing
frequency and tends to be more prolonged.
 Associated with disruption of the atherosclerotic plaque, with superimposed
thrombosis, embolization or spasm.
 Predictor of Myocardial Infarction.

136. Characteristics of unstable angina
(a medical emergency)
• Occurs even at rest
• Is a change in your usual pattern of angina
• Is unexpected
• Is usually more severe and lasts longer than stable angina, maybe 30 minutes
or longer
• May not disappear with rest or use of angina medication
• Might signal a heart attack

137. Causes of Unstable Angina
 If fatty deposits (plaques) in a blood vessel rupture or a blood clot forms, it can quickly block or reduce
flow through a narrowed artery, suddenly and severely decreasing blood flow to your heart muscle.
Unstable angina can also be caused by blood clots that block or partially block your heart's blood
vessels.
 Unstable angina worsens and isn't relieved by rest or your usual medications. If the blood flow doesn't
improve, your heart is deprived of oxygen and a heart attack occurs. Unstable angina is dangerous and
requires emergency treatment.

138. Left ventricular hypertrophy
 Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart's main
pumping chamber (left ventricle).
 Left ventricular hypertrophy can develop in response to some factor — such as high blood pressure or a
heart condition — that causes the left ventricle to work harder. As the workload increases, the muscle
tissue in the chamber wall thickens, and sometimes the size of the chamber itself also increases. The
enlarged heart muscle loses elasticity and eventually may fail to pump with as much force as needed.
 Left ventricular hypertrophy is more common in people who have uncontrolled high blood pressure. But no
matter what your blood pressure is, developing left ventricular hypertrophy puts you at higher risk of a
heart attack and stroke.
 Treating high blood pressure can help ease your symptoms and may reverse left ventricular hypertrophy.

139. Symptoms of Left ventricular hypertrophy
Left ventricular hypertrophy usually develops gradually. You may experience no
signs or symptoms, especially during the early stages of the condition. As left
ventricular hypertrophy progresses, you may experience:
• Shortness of breath
• Fatigue
• Chest pain, often after exercising
• Sensation of rapid, fluttering or pounding heartbeats (palpitations)
• Dizziness or fainting

140. Causes of Left ventricular hypertrophy
Left ventricular hypertrophy can occur when some factor makes your heart work harder than normal to pump
blood to your body.
Factors that can cause your heart to work harder include:
• High blood pressure (hypertension). This is the most common cause of left ventricular hypertrophy. More
than one-third of people show evidence of left ventricular hypertrophy at the time of their diagnosis with
hypertension.
• Aortic valve stenosis. This disease is a narrowing of the aortic valve that separates the left ventricle from the
large blood vessel leaving your heart (aorta). The narrowing of the aortic valve requires the left ventricle to
work harder to pump blood into the aorta.
• Hypertrophic cardiomyopathy. This genetic disease occurs when the heart muscle becomes abnormally
thick, even with completely normal blood pressure, making it harder for the heart to pump blood.
• Athletic training. Intense, prolonged endurance and strength training can cause the heart to adapt to handle
the extra workload. It's unclear whether this athletic type of left ventricle hypertrophy can lead to stiffening of
the heart muscle and disease.

142. Hypertension
> 140 mmHg > 90 mmHg

143. Hypertension
HYPERTENSION: Hypertension is a persistent elevation in blood pressure.
STAGES of HYPERTENSION
Blood pressures are generally classified in adults as follows:
 Normal blood pressure - a systolic of less than 120 and diastolic of less than 80 mm
Hg
 Pre-hypertension (a state of blood pressure that is elevated above normal and that may
eventually become hypertension) - a systolic pressure between 120-139 and/or a
diastolic between 80-89 mm Hg
 Hypertension, Stage 1 - a systolic of 140-159 and/or a diastolic of 90-99 mm Hg
 Hypertension, Stage 2 - a systolic of 160-179 and/or a diastolic of 100-109 mm Hg
 Severe hypertension, Stage 3 – a systolic greater than or equal to180 and/or a diastolic
greater than or equal to 110 mm Hg

144. What Causes High Blood Pressure?
The exact causes of high blood pressure are not known, but several things may play a role, including:
 Smoking
 Being overweight or obese
 Lack of physical activity
 Too much salt in the diet
 Too much alcohol consumption (more than 1 to 2 drinks per day)
 Stress
 Older age
 Genetics
 Family history of high blood pressure
 Chronic kidney disease
 Adrenal and thyroid disorders
 Diabetes

145. Causes of Hypertension

146. Causes of Cardiovascular Disease
Genetics Smoking
Atherosclerosis
Myocardial Ischemia
Arrhythmia, Angina, Heart Attacks
Heart Failure

147. Types of hypertension
1. Essential hypertension
2. Secondary hypertension

148. Essential hypertension
 Unknown origin
 Most common
 About 90% of clients.
Contributing Factors:
 family hx,
 hyperlipidemia,
 African American background,
 Diabetes,
 Obesity,
 Aging,
 Stress,
 Smoking

149. Secondary hypertension
 Less common (affecting only 5% of hypertensive patients)
 Identifiable cause,
 Due to specific organ pathology i.e. kidney, arteries, heart, endocrine system.

150. Classification of Anti-hypertensive drugs:
AABCDES
1. ACE inhibitors,
2. ARBs,
3. Blockers,
4. Calcium Channel blockers,
5. Diuretics,
6. Emergency drugs,
7. Sympathoplegics.

151. ACE inhibitors
Mechanism of Action
1.Blocks the enzymes that convert AT-I to AT-II,
(AT-II causes Vasoconstriction)
2. Inhibit the breakdown of Bradykinins,
Bradykinins increase the production of:
• Nitric oxide
• Prostacyclin
(Both are Vasodilators)
3. Decrease the secretion of Aldosterone.
(Causes a decrease in Sodium/Water retention)

152. Drugs: (-pril family)
 Captopril
 Enalapril
 Ramipril
 Lisinopril

153. Indications of ACEIs
 Hypertension
 Congestive Heart Failure
 Myocardial Infarction
 Diabetic Nephropathy
 CAD

154. Special instructions (ACEIs)
 Used alone or in combination:
When used alone:
Effective in hypertensive patients who are white and young.
When used in combination with Diuretic:
Effective in both white and black patients.
 Should never be used during pregnancy.

155. ARBs (Angiotensin-II Receptor Blockers)
Mechanism of Action
 ARBs are alternatives to ACEIs.
 The pharmacological effects of ARBs are
similar to those of ACEIs.
 But unlike ACEIs, the ARBs don’t increase
Bradykinin levels.

157. Drugs: (-tan family)
• Losartan
• Valsartan
• Telmisartan
• Candesartan

158. Indications of ARBs
 Similar as ACEIs.
 These are the substitutes for ACEIs in those
patients with severe cough.

159. Blockers
1. Alpha blockers
2. Beta blockers
3. Alpha & Beta blockers

160. Alpha blockers
Mechanism of Action:
Blocking of alpha adrenergic receptors in
arterial and venous smooth muscles causes
Vasodilatation and decrease peripheral
vascular resistance.

161. Drugs: (-zosin family)
 Terazosin
 Prazosin
 Doxazosin

162. Indications of alpha blockers
 Alpha blockers are used to treat mild to moderate hypertension and is prescribed in
combination with propranolol or a diuretic for additive effects.
 Alternative if B-blockers and diuretics do not work.
 Because of the side-effect profile, development of tolerance and the advent of safer
antihypertensives, alpha blockers are seldom used as monotherapy in the treatment of
hypertension.

163. Beta blockers
Binds to beta receptors and block the activity:
1. Block beta 1 adrenoceptors on heart and thus
decrease cardiac output leading to a decrease
in blood pressure.
2. Block beta 1 adrenoceptors on kidney and thus
decrease the release of Renin from kidney.

164. Beta 1 adrenoceptor blockers
Generally, they antagonize effects of
catecholamines on the heart.

165. Mechanism of action Beta-blockers
 Beta-blockers block the effects of sympathetic nerve stimulation or circulating
catecholamines at beta-adrenoceptors which are widely distributed throughout body
systems.
 Beta1-receptors are predominant in the heart (and kidney) while beta2-receptors are
predominant in other organs such as the lung, peripheral blood vessels and skeletal
muscle.
 Kidney: Blockade of beta1-receptors inhibit the release of renin from juxta-glomerular
cells and thereby reduce the activity of the renin-angiotensin-aldosterone system.
 Heart: Blockade of beta1-receptors in the sino-atrial node reduces heart rate (negative
chronotropic effect) and blockade of beta1-receptors in the myocardium decrease cardiac
contractility (negative inotropic effect).

166. Mechanism of action of beta-adrenoblockers
(anaprilin, atenolol, methoprolol etc.)
in case of arterial hypertension
β-
adrenoblockers
activation of
β1-adrenoreceptors
of heart
Cardiac
output
Angiotensine ΙΙ
Renin
Aldosterone
Holding sodium
and water
Peripheral resist-
ance of vessels
Volume of
blood
circulation
Decreasing of
blood pressure

167. Drugs: (-olol family)
 Propranolol
 Atinolol
 Bisoprolol
 Penbutolol
 Oxpranonlol
 Nebivolol

168. Indications of beta blockers
 Useful in treating conditions that may coexist with hypertension such as:
 Supraventricular tachyarrhythmia
 Previous MI
 Angina Pectoris
 Chronic heart failure
 Also used to prevent migraine and cluster headaches.

169. Special instructions for beta blockers
Beta blockers are more effective for
treating hypertension in white than in
black patients and in young compared to
elderly patients.

170. Calcium Channel blockers
Calcium channel antagonists block the inward
movement of calcium by binding to L-type calcium
channels in the heart and in the smooth-muscle of
the coronary and peripheral vasculature. This causes
vascular smooth muscle to relax, dilating mainly
arterioles.

171. Drugs: (-dipine family)
 Amlodipine
 Nifidipine
 Nicardipine
 Nisoldipine
 Verapamil

172. Indications of CCB
 Useful in the treatment of hypertensive patients who have:
 Asthma
 Diabetes
 Angina
 Peripheral Vascular disease
 Black hypertensive patients respond well to CCBs.

173. Diuretics
There are 3 classes of diuretics:
1. Thiazide diuretics
2. Loop diuretics
3. Potassium-sparing diuretics

174. 1. Thiazide diuretics
Lowers the blood pressure by increasing Sodium
and Water excretion leading to:
 Decrease in Blood volume,
 Decrease in Cardiac output,
 Decrease in Renal blood flow,
 Decrease in Blood pressure.

175. Drugs: (-azide family)
 Chlorthiazide
 Cyclothiazide
 Polythiazide

176. Indications of Thiazides
 Used to treat mild to moderate HTN,
 Most suitable diuretics for long–lasting treatment of hypertension,
 Diabetes insipidus, (Anti-diuretic in nephrogenic diabetes insipidus)
 In the treatment of heart failure when used in combination with loop diuretics.

177. Special instructions
 Potassium sparing diuretics are often used in combination with thiazides to reduce the amount of potassium induced
by the thiazide diuretics.
 As diuretics induce hyperglycaemia, therefore, diuretics should be avoided in the treatment of hypertensive diabetes.
 The hypotensive actions of ACEIs are enhanced when give in combination with the Thiazides.

178. 2. Loop diuretics
 Block active reabsorption of Na+, Cl-, K+ from ascending limb.
 Loop diuretics cause:
 Decreased renal vascular resistance
 Increased renal blood flow.

179. Drugs: (-mide family)
• Furosemide
• Torsemide
• Bumetanide

180. Indications of loop diuretics
 The loop diuretics act promptly, even in patients
who have poor renal function or who have not
responded to thiazides or other diuretics.
 Acute pulmonary edema of heart failure,
 For the treatment of severe HTN, or with CHF.

181. 3. Potassium sparing diuretics
o Spironolactone antagonizes Aldosterone at intracellular cytoplasmic receptors sites by forming SR-Complex.
o Thus it prevents translocation of the receptor complex into the nucleus of the target cell and therefore can’t bind to
DNA.
o This results in a failure to produce proteins that are normally synthesized in response to Aldosterone.
o These mediator proteins normally stimulate the Na/K-exchange sites of the collecting tubule.
o Thus the lack of mediator proteins prevents Na-reabsorption and therefore Potassium and proton secretion.

182. Drugs:
 Spironolactone
 Amiloride
 Triamterene

183. Indications of K-sparing diuretics
 Diuretic of choice in patients with
hepatic cirrhosis.
 Diminishing Cardiac remodeling
that occurs in Heart failure.

184. Emergency drugs (Vasodilators)
Two classes:
1. Oral vasodilators
 Minoxidil
 Hydrazine
2. Parenteral vasodilators
 Sodium Nitropruside
 Diazoxide

185. Minoxidil
 Dilate arterioles.
 Decrease systemic resistance leading to a decrease
in blood pressure.
 For the treatment of severe to malignant
hypertension.
 Causes hypertrichosis (the growth of hairs on
body).

186. Sodium Nitroprusside
 It causes prompt vasodilation of blood vessels by relaxing arterial and venous smooth
muscles.
 As it also acts on veins, therefore it reduces cardiac preload.
 It metabolizes rapidly, therefore, require continues infusion to maintain its hypotensive
action.
 It is poisonous if given orally because of its hydrolysis to Cyanides.

187. Indications
 Indicated for the immediate reduction of blood
pressure in hypertensive crises.
 Indicated for producing controlled hypotension to
reduce bleeding during surgery.
 Indicated for the treatment of acute congestive
heart failure.

188. Thank you