1. Alterations In Oxygenation
Cardiac Disruptions

2. Cross Section of the Heart

3. Coronary Arteries & Veins

4. Blood Flow Through the Heart

5. Conduction System of the Heart

6. I. Overview of alterations in the cardiac system
A. Lack of blood supply
1. Consequences of decreased flow
Coronary arteries perfuse heart to meet O2 & nutritional needs
 Ischemia
 Stable angina pectoris
 Acute coronary Syndrome
 Myocardial infarction

7. 2. Conditions which cause this
type of cardiac disruption
Can be either: increased O2 demand
decreased O2 supply
a) atherosclerosis of the coronary arteries
b) thrombus within the coronary arteries
c) vasospasm of the coronary arteries
d) hypovolemia

8. Occlusion/Collateral Circulation
Vessel Occlusion with Collateral Circulation
A.Open, functioning coronary artery
B.Partial coronary artery closure with collateral circulation being established
C.Total coronary artery occlusion with collateral circulation bypassing the
occlusion to supply the myocardium

9. B. Infections of the heart
1. Consequences
Inflammation of the endocardium
2. Example of infectious conditions of the heart
a) Infective endocarditis

10. a) Infective endocarditis
 Most common causative agents are bacterial
 Must be:
 endothelial damage
 microorganisms invade and colonize structures -
cause inflammation
 vegetations - damage valves
 interfere with valve function and predispose to
embolus formation

11. Bacterial Endocarditis
mitral/bicuspid valve – destructive vegetations

12. C. Immune mediated inflammatory conditions
1. Consequences
 Immune attack on individual’s own tissue
 Can damage many tissues & organs
-including the heart

13. 2. Example of immune mediated
inflammatory condition
a) Rheumatic heart disease
 Diffuse, inflammatory disease caused by delayed
immune response to infection by group A beta-
hemolytic strep
 Antibodies directed against self tissues
 Acute rheumatic fever is febrile illness - inflammation
of joints, skin, nervous system, heart. Untreated,
causes scarring & deformity of cardiac structures 
rheumatic heart disease (10% occurrence)
 Primary lesion usually is at the mitral/bicuspid valves

14. Valve Disease
Disease of the aortic valve as viewed from the aorta
A.Stenosis of the valve opening
B.An incompetent or regurgitant valve that is unable to close completely

15. Rheumatic Valvulitis
Chronic rheumatic valvulitis. A view of the mitral valve from the left atrium shows
rigid, thickened, and fused leaflets with a narrow orifice, creating the
characteristic “fish mouth” appearance of the rheumatic mitral stenosis.

16. D. Cardiomyopathy
 Group of diseases that affect myocardium
structure and function
 Can be primary or secondary
 Caused by many things
 Cardiotoxic agents
 HTN
 Endomyocardial fibrosis
 Not necessarily related to CAD

17. 1. Consequences of Cardiomyopathy
 3 different types
 Each type has own pathogenesis, clinical
presentation, and treatment protocols
 Regardless of type - often leads to heart
failure and death

18. 2. Types of Cardiomyopathy
a. Dilated - most common form.
 Cardiomegaly w/ventricular dilation
 Impaired systolic function
 Atrial enlargement
 Stasis of blood in LV.
 Heart: globular shape

19. 2. Types of Cardiomyopathy
b. Hypertrophic - 4 main characteristics:
 Massive ventricular hypertrophy
 Rapid, forceful contraction of LV
 Impaired relaxation
 as ventricles become noncompliant
 Obstruction of aortic outflow (not always)
 Growth is asymmetric
 No dilation of ventricles

20. 2. Types of Cardiomyopathy
c. Restrictive - least frequent.
Impairs diastolic filling & stretch.
Systolic function remains unaffected.
Heart becomes infiltrated by various substances,
resulting in severe fibrosis – can’t stretch.
(Amyloidosis: protein deposits)

21. II. Angina Pectoris
A. Definition/description
 Pain (angina) in chest (pectoris)
 Ischemia related to supply and demand
 Usually transient - about 3 to 5 minutes
 Subsides when precipitating factor relieved
 If blood flow restored, no permanent damage

22. B. Causes of myocardial ischemia:
Supply: decreased O2 supply
 Develops if flow of O2 content of coronary
blood insufficient to meet metabolic needs
of myocardial cells or conditions exist that
increase hearts O2 demands
 Usually caused by atherosclerosis and
almost always by obstruction of major
coronary artery

23. B. Causes of myocardial ischemia:
Demand – increased O2 need
 High systolic BP
 Increased ventricular volume
 Increased thickness of myocardium
 Increased HR

24. Angina Pectoris: Risk Factors
Modifiable Unmodifiable
Cigarette smoking Age
Hypertension Sex
Abnormal lipid profile Heredity
Obesity Race and ethnicity
Hyperglycemia
Physical inactivity
Stress

25. C. Types of Angina Pectoris
 Chronic stable angina
 Unstable angina
(pre-infarction)
 Printzmetal’s angina
(variant)
 Silent ischemia

26. Types of Coronary Heart Disease

27. 1. Stable angina
1. Stable angina
 Caused by narrowing & hardening of
arterial walls – the 4 E’s
 Exertion
 Extremes in temperature – vasoconstriction
 Emotions – SNS stimulation
 Excessive eating – blood diverted to GI tract
 Affected vessels can’t dilate
 Pain usually relieved by rest & nitrates

28. 2. Variant or Prinzmental’s angina
 Chest pain caused by transmural ischemia of
myocardium
 Occurs unpredictably & almost exclusively at rest
 Pain caused by vasospasm of one or more
coronary arteries
 Pain frequent during rest and at night
 Rare type of angina, not precipitated by exertion,
etc.
 Treated with nitrates and Ca++ channel blockers

29. 3. Unstable angina (Pre-infarction)
 Angina that is new in onset, occurs at rest, or
has a worsening pattern
 Seldom predictable
 Often associated with deterioration of stable
atherosclerotic plaque
 May mean impending infarction

30. 4. Silent Ischemia
 May only be detected on routine EKG
 Lack of pain or discomfort
 Increases risk of myocardial infarction
 May precede a sudden & severe MI without
warning
 Largely associated with HTN

31. D. Clinical manifestations & related
pathogenesis
 Substernal chest discomfort
 May radiate to neck, lower jaw, left arm, left
shoulder, or back
 LT arm most common
 But may also radiate to RT arm
 Often mistaken for indigestion
 May be accompanied by severe apprehension &
feeling of impending death
Myocardial cells are viable for 20 minutes
Eventually revert to anaerobic metabolism  lactic acid  pain

32. Locations of Chest Pain During Angina or MI

33. Angina Pain Areas

34. E. Potential medical complications
1. Myocardial infarction
 Worst case scenario
2. Arrhythmias/Dysrhythmias
 Affects myocardial cell’s sensitivity to nerve
impulses
Initially, BP rises, then eventually as heart stops pumping
effectively & F/F response wears off, CO drops & BP
drops

35. Tissue Destruction After MI

36. Acute MI
X-section of ventricles of a man who died a few days after onset of severe chest pain.
Transmural infarct & septal regions of the left ventricle.
The necrotic/infarcted myocardium is soft, yellowish, and sharply demarcated.

37. F. Management
Primary aim – Reduce myocardial O2 consumption
1. Diagnostic studies
a. EKG/ECG – Electrocardiography
 May have normal EKG when no pain, so requires
EKG during attack
 Can indicate which coronary artery is involved
 Treatment:
 A.
 B.
 C.
 D. diet & diabetes management
 E. education & exercise

38. b. Serum enzyme level tests
Creatine Kinase (CK) – 3 isoenzymes
 CK-MB: present in heart muscle
 CK-MM: present in skeletal muscle
 CK-BB: present in brain tissue
 CK-MB found only in cardiac cells - rises only
when damage to cells
 Always increases in MI:
 Rises 4-6 hours after onset
 Peaks at 18-24
 Returns to normal in 3-4 days (0-6%)

39. Troponin
myocardial protein released into circulation after injury
 Greater specificity:
specific MI indicator
 Rises 2-12 hours
after MI
 Peaks at 24-48
hours
 Returns to normal in
5-14 days (remain
elevated for 2
weeks)

40. Myoglobin
 O2 carrying protein present in cardiac and
skeletal muscle
 Released quickly from infarcted myocardial
tissue
 Not cardiac specific
 Rapidly excreted from urine

41. Albumin Colbalt-binding test
 Measures how much cobalt is bound to
albumin
 Changes in structure of albumin occur with MI
 Used in conjunction with EKG & troponin test

42. c. Serum lipid level tests
 Triglycerides
 Total Cholesterol
 Cholesterol fractionation
 Not used for MI diagnostic purposes, but reveals if
high-risk

43. c. Serum lipid level tests
 C-Reactive Protein (CRP)
 Appears in blood 6-10 hours after acute
inflammatory process and tissue destruction
 Peaks at 48-72 hours after MI
 N High Sensitivity C- Reactive Protein (hs
CRP) - highly sensitive test for detecting risk
of cardiovascular and peripheral vascular
diseases. Frequently done with cholesterol
screening

44. d. Exercise stress test
 Reveals heart function
during exercise
 Attach patient to EKG
& BP cuff
 Useful to differentiate
angina from other
types of chest pain
 Can be done with a scan as well
 Patients who can’t walk may use
a bike

45. e. Nuclear Cardiology Imaging
 Several tests use
radionuclides to
visualize distribution of:
 Blood flow
 Ventricular structures
 “cold spots” in infarcted
zone – no accumulation
of radionuclides
 Perfusion or metabolism
of myocardium

46. f. Coronary angiography
 Diagnostic radiography
of heart & blood
vessels using
radiopaque contrast
media
 Used to evaluate
coronary arteries and
collateral circulation
 Helps determine
anatomic extent of
CAD

47. Non-pharmacologic Treatment
Education
 R – Rest
 E – Exercise
 S – Stop smoking
 C – Count cholesterol & calories
 U – Unwind  reduce stress
 E – Education

48. Nitrate Therapy
 First line of defense –
prevention/prophylaxis and treatment
 Relax smooth muscles in the blood vessel
walls
 Improve blood delivery to the heart by
dilating blood vessels
 Improve blood delivery to the heart by
decreasing the workload of the heart
 Ineffective in sclerosed vessels, effective if
collateral vessels in place

49. 2. Pharmacologic therapy
a. In acute attacks
i) Nitroglycerine SL
Actions - increases coronary blood flow by
dilating coronary arteries & improving
collateral flow
Destruction by GI tract
Must dissolve sublingually, patient shouldn’t swallow saliva
while dissolving

50. i) Nitroglycerine SL
NI: Give sublingually. Teach patient:
 keep tongue still
 keep med with you at all times
 very unstable - capped, dark, glass bottle
 inactivated by heat, moisture, air, light,
time. Should have burning sensation
 Replace every 6months
 Not fixed dose - patient regulates usage

51. Nitroglycerine SL - continued
 maximum of 3 tablets in 15 minutes - 5 minutes
apart
 transient side effects – hypotension, headache,
facial flushing
 lie down to prevent falling
 carry medic-alert information
 journal all attacks
 precipitating factors, duration, pills taken, etc.

52. b. For chronic anginal prophylaxis
i) Nitroglyercin ointment - topical
- rotate sites to prevent skin irritation
- remove old patch/paper
- dose may be increased to highest does that
doesn’t cause hypotension
- apply only with measuring applicator
- don’t allow contact with your skin
DON’T SHAVE an area. This will create small abrasions. Clip hair

53. ii) Transdermal nitrates
Transderm-Nitro, Nitro-Dur, Nitrodisc
 apply to hairless site
 remove all previous patches
 apply firm pressure
 waterproof - not affected by bathing
 do not cut or trim patches
 remove before cardioversion or
defibrillation to prevent burns

54. iii) Long-acting nitrates
 Extended release capsules
 Nitrocap T.D., Nitrogly, Nitrolin, Nitrospan
 Extended release tablets
 Nitrong
 Taken every 8 to 12 hours

55. iv) SL nitroglycerine prior to activity
 Can be used to prevent or minimize anginal
attacks before stressful events
 Will increase tolerance for exercise & stress
 Best to take before pain develops

56. Case Study
 A 60 year old male was shoveling snow
after a heavy snowstorm and experienced
chest pain. He has a history of angina
and has SL nitroglycerin in the house. He
keeps it on his windowsill in a clear plastic
pillbox.

57. Questions:
 What type of angina is he experiencing?
 What should he do to treat this episode?
 After taking the maximum tablets, his pain has
not subsided. What should he do?
 What patient teaching is indicated in this
situation?

58. v) Beta-adrenergic blockers
Propanolol (Inderal)
Action:
 Decreases CO and reduces sympathetic
vasoconstrictor tone.
 Decreases renin secretion by kidney.
 Decreases HR, BP, & myocardial
contractility.

59. vi) Calcium channel blockers
Action - inhibits transport of calcium into
myocardial & vascular smooth muscle
cells, resulting in inhibition of excitation-
contraction coupling & subsequent
contraction
Nifedipine (Procardia), verapamil (Calan)

60. Calcium Movement
Ca2+ channel blocker:
mechanism of action
A.During muscle relaxation,
K+ inside muscle cell, Ca++ &
Na+ outside muscle cell.
A.For muscle contraction to
occur, K+ efflux, Na+ & Ca2+
influx through open
membrane channels.
A.When Ca2+ channels are
blocked by drug molecules,
muscle contraction decreases
because Ca2+ can’t move
through cell membrane into
muscle cell.

61. vii) Antithrombotic therapy . . .
Aspirin (ASA)
Action - in low doses, appears to impede
clotting by blocking prostaglandin
synthesis, which prevents formation of
platelet-aggregation
81 mg
(325 mg Rx)

62. 3. Invasive & surgical treatments
a. Percutaneous transluminal coronary
angioplasty (PTCA)
 Improve blood flow - crack plaque or
atheroma that has built up & interfering
with circulation
Done more frequently than CABG

63. b. Intracoronary stents
 PTCA with
intravascular stent
over balloon
 When balloon is
deflated, stent
remains in artery &
holds it open.
Eventually
endothelium covers
stent & incorporates
into wall

64. c. Laser angioplasty
 Catheter with small laser introduced into
peripheral artery then diseased coronary
artery
 Vaporizes plaque

65. d. Atherectomy
 Plaque is shaved off
using rotational blade
 Removes atheromas

66. e. Coronary artery bypass grafting
(CABG)
 Blood vessel from another part of body
(saphenous vein, left internal mammary
artery) is grafted distal to coronary artery
lesion - “bypassing” obstruction
 MIDCABG – newer procedure; limited use

67. Coronary Artery Revascularization

68. 4. Prehospital emergency care
of chest pain (from AHA)
For person with unknown CHD:
 recognize symptoms - chest pain,
sweating, nausea, SOB, weakness
 stop activity and sit or lie down
 if pain persists for 5 minutes or more,
activate the EMS

69. 4. Prehospital emergency care
of chest pain (From AHA)
For person with known CHD:
 recognize symptoms - chest pain,
sweating, nausea, SOB, weakness
 stop activity - sit or lie down
 place one NTG tablet under tongue.
Repeat at 5 minute intervals up to 3 times
 if symptoms persist, activate the EMS

70. III. Congestive Heart Failure
A. Definition
Abnormal condition
involving impaired
cardiac pumping
Associated with
numerous types of
heart disease - esp.
long-standing HTN
and CAD

71. Characterized by:
 ventricular
dysfunction
 reduced exercise
tolerance
 diminished quality of
life
 shortened life
expectancy

72. Can be:
Systolic Failure
 Results from inability of heart to pump
blood. Caused by:
 impaired contractile function
 increased afterload
 Cardiomyopathy
 mechanical abnormalities
 Decreased CO

73. Can be:
Diastolic Failure
 Impaired ability of ventricles to fill
 Results in decreased stroke volume
 Decreased CO
Mixed systolic and diastolic failure

74. B. Compensatory Mechanisms
Overloaded heart tries to compensate to
maintain adequate CO
1. Ventricular dilation
 Chambers enlarge when pressure
elevated over time
 Muscle fibers stretch and increase
contractile force

75. 2. Ventricular hypertrophy
 Heart hypertrophies in response to
overwork
 Will lead to increased CO

76. 3. Sympathetic nervous system
activation
 Inadequate stroke volume and CO caused
sympathetic nerve activation
 Results in increased HR, myocardial
contractility, and peripheral vascular
constriction
 Initially increase in HR and contractility
improve CO, but detrimental over time

77. 4. Neurohormonal responses
 Decrease blood flow to kidneys causes
release of renin
 Renin caused conversion of angiotension I
to II – which caused adrenal cortex to
release aldosterone (increased sodium
retention & ↑ peripheral vasoconstriction
 Posterior pituitary secretes ADH – ↑ water
reabsorption in renal tubels

78. C. Types of CHF
1. Left-sided heart failure
a. Pathogenesis
 Left ventricle fails - unable to pump
adequate blood coming to it from lungs
 Increases pressure in pulmonary
circulation - causes fluid to be forced into
pulmonary tissues

79. Left-Sided Heart Failure

80. 2. Right-sided failure
a. Pathogenesis
Venous congestion in systemic circulation
results in:
 peripheral edema
 hepatomegaly
 splenomegaly
 vascular congestion of GI tract
 jugular venous distention

81. Right-Sided Heart Failure

82. 3. Clinical manifestations
a. Fluid retention and
edema
 Edema
 Nocturia

83. b. Respiratory manifestations
 Pulmonary edema
 Dyspnea
 Orthopnea
 Paroxysmal nocturnal dyspnea
 Cough

84. c. Fatigue & limited exercise tolerance
 Fatigue
 Tachycardia
 Anxiety and
restlessness

85. d. Cachexia
 Weight loss
 Malnutrition

86. e. Cyanosis
 Skin changes

88. 4. Complications
a. Pleural effusions
b. Arrhythmias
c. Left ventricular thrombus
d. Hepatomegaly

89. E. Management
1. Diagnostic studies
a. CXR
b. EKG
c. Echocardiogram
d. Radionuclide angiography
e. Labs

90. Normal EKG

91. 2. Pharmacologic Therapy
a. ACE inhibitors (Angiotension Converting
Vasotec
 Prevents production of Angiotension II by
blocking it’s conversion to the active form -
results in systemic vasodilation
 Decreases preload & afterload in patients
with CHF

92. Angiotensin Conversion

93. b. Inotropics
Digoxin
Increases force of myocardial contraction,
decreases conduction through SA and AV
nodes, slows heart rate and increases
diastolic filing time
Increases CO, slows heart rate
NI - Take AP for one minute. Hold & notify
MD if below 60

94. c. Diuretics
Promotes excretion of edema fluid and
helps sustain cardiac output and tissue
perfusion by reducing preload
Review notes on Thiazides, loop diuretics,
and K+ sparing diuretics

95. d. Vasodilator drugs
Nitrates
 Reduces circulating volume by decreasing
preload and also increases coronary
artery circulation by dilating coronary
arteries

96. e. Beta adrenergic blockers
 Becoming more important in management
of CHF
 Block sympathetic nervous system’s
negative effects on the failing heart - such
as increased heart rate

97. 3. Supportive
a. Supplemental oxygen
b. Rest
c. Daily weights
c. Sodium restricted diet