cardiology

1. Addis Ababa Medical University
College

2. What is Cardiovascular Disease (CVD)?
“ Cardiovascular Disease is an
abnormal function of the heart
involving the narrowing or
blocking of blood vessels.”
- Cardiovascular Disease
2

3. 3

4. Symptoms of CVD
• Chest Pain/ Chest
Discomfort
• Pain in one or both
arms, left shoulder,
neck jaw, or back.
• Shortness of breath
• Dizziness
• Faster heart beats
• Nausea
• Abnormal heart beats
• Fatigue
4

5. 5

6. 6

7. Overview
• Diagnostic Tests for
Cardiovascular Function
• General Treatment
Measures for Cardiac
Disorders
• Coronary Artery Disease
(CAD)
– Arteriosclerosis
– Atherosclerosis
– Myocardial Infarction (MI)
• Cardiac Arrhythmias
– Sinus node abnormalities
– Atrial conduction
abnormalities
– Cardiac arrest
• Congestive Heart Failure
(CHF)
• Arterial Diseases
– Hypertension
• Shock

8. Diagnostic Tests for Cardiovascular
Function
• ECG
– Monitors arrhythmias, MI, infection, pericarditis
– Studies conduction activation and systemic abnormalities
• Ausculation
– Studies heart sounds using stethoscope
• Exercise stress test
– Assess general cardiovascular function
– Checks for exercise-induced problems
• Chest X-ray Film
– Shows shape, size of heart
– Evidence of pulmonary congestion associated with heart failure
– Nuclear imaging

9. Diagnostic Tests
• Cardiac
Catheterization
– Visualize inside of
heart, measure
pressure, assess valve
and heart function
– Determine blood flow
to and from heart

10. Diagnostic Tests
• Angiography
– Visualization of blood
flow in coronary artery
– Obstruction assessed
and treated
• Basic catheterization
• Balloon angioplasty

11. General Treatment Measures for
Cardiac Disorders
• Dietary modification
• Regular exercise program
• Quit smoking
• Drug therapy

12. Drug Therapy
• Vasodilators (Nitroglycerin)
– Provide better balance of oxygen supply and
demand in heart muscle
– May cause low bp
• Beta-blockers (Metoprolol or Atenolol)
– Treats angina, hypertension, arrhythmias
– Blocks beta1-adrenergic receptors in heart
• Prevent epine from increasing heart activity

13. Drug Therapy
• Calcium ion channel blockers( amlodipine,aranidipine}
– Block movement of calcium
– Decrease heart contraction
• Antiarrhytmatic for excessive atrial activity
• Antihypertension and vasodilator
• Digoxin
– Treats heart failure
– Increases efficiency of heart
• Decreases conduction of impulses and HR
• Increases contraction of heart
– Pts must be checked for toxicity
• Antihypertensive drugs
– Decrease bp to normal levels
– Include:
• Adrenergic blocking agents
• Calcium ion blockers
• Diuretics
• Angiotensin-converting enzyme (ACE) inhibitors
– Used to treat hypertension, CHF, after MI

14. Drug Therapy
• Adrenergic Blocking drugs
– Act on SNS, block arteriole alpha adrenergic
receptors, or act directly as vasodilator
• ACE Inhibitors
– Treat hypertension, CHF
• Diuretics
– Remove excess water, sodium ions
– Block resorption in kidneys
– Treat high bp, CHF

15. Drug Therapy
• Anticoagulant
– Decrease risk of blood clot formation
– ASA decreases platelet adhesion
– Block coagulation process
• Cholesterol or lipid reducing drugs
– When diet and exercise fail
– Decrease LDL and cholesterol

16. Common Blood Vessel
Disorders
Figure 15.6

17. CAD—Arteriosclerosis:
Pathophysiology
• General term for all
types of arterial
changes
• Best for degeneration
in small arteries and
arterioles
• Loss of elasticity,
walls thick and hard,
lumen narrows

18. CAD—Atherosclerosis:
Pathophysiology
• Presence of
*atheroma
– Plaques
• Consist of lipids, cells,
fibrin, cell debris
– Lipids usually
transported with
lipoproteins

19. Lipoproteins and Transport

20. Atherosclerosis--Pathophysiology
• Analysis of serum lipids:
– Total cholesterol, triglycerides, LDL, HDL
• LDL
– High cholesterol content
– Transports cholesterol liver  cells
– Dangerous component
• HDL
– “good”
– Low cholesterol content
– Transports cholesterol cells  liver

21. Development of Atheroma

22. Consequences of Atherosclerosis

23. Atherosclerosis—Etiology
• Age
• Gender
• Genetic factors
• Obesity, diet high in cholesterol, animal fats
• Cigarette smoking
• Sedentary life style
• Diabetes mellitus
• Poorly controlled hypertension
• Combo of BC pills and smoking

24. Atherosclerosis—Diagnostic Tests
• Serum lipid levels
• Exercise stress test
• Radioisotope

25. Atherosclerosis—Treatment
• Decrease cholesterol and LDL
• Decrease sodium ion intake
• Control primary disorders
• Quit smoking
• Oral anticoagulant
• Surgical intervention
– Percutaneous transluminal coronary angioplasty
(PTCA)
– Cardiac catheterization
– Laser beam technology
– Coronary artery bypass grafting

26. CABG

27. CAD: Myocardial Infarction—
Pathophysiology
• Coronary artery completely obstructed
– Prolonged ischemia and cell death of myocardium
• Most common cause is atherosclerosis with
thrombus
• 3 ways it may develop:
– Thrombus obstructs artery
– Vasospasm due to partial occlusion
– Embolus blocks small branch of coronary artery
• Majority involve L ventricle
– Size and location of infarction determine severity of
damage

28. Myocardial Infarction

29. MI—Pathophysiology
• Function of myocardium contraction and
conduction quickly lost
– Oxygen supplies depleted
• 1st
20 minutes critical
• Time Line
– 1st
20 min critical
– 48 hrs inflammation begins to subside
– 7th
day necrosis area replaced by fibrous tissue
– 6-8 weeks scar forms

31. MI—Signs and Symptoms
• Pain
– Sudden, substernal area
– Radiates to L arm and neck
– Less severe in females
• Pallor, sweating, nausea, dizziness
• Anxiety and fear
• Hypotension, rapid and weak pulse (low
CO)
• Low grade fever

32. MI—Diagnostic Tests
• ECG
• Serum enzyme and
isoenzyme test
• High serum levels of
myosin and troponin
• Abnormal electrolytes
• Leukocytosis
• Arterial blood gases
• Pulmonary artery
pressure measure
– Determines ventricular
function

33. MI—Complications
• Arrhythmias
– 25% pts sudden death after MI
• Due to ventricular arrhythmias and fibrillation
– Heart block
– Premature ventricular contraction (PVCs)
• Cardiogenic shock
• CHF

34. MI—Treatment
• Rest, oxygen therapy, morphine
• Anticoagulant
• Drugs
• Cardiac rehabilitation
• Prognosis depends on site/size of infarct,
presence of collateral circulation, time elapsed
before treatment
• Mortality rate in 1st
year
– 30-40% due to complications, recurrences

35. Cardiac Arrhythmias
• Alteration in HR or rhythm
• ECG monitors
– Holter monitors
• decreases efficiency of heart’s pumping cycle
– Slight increase in HR increases CO
– Very rapid HR prevents adequate filling in diastole
– Very slow HR reduces output to tissues
• Irregular contraction inefficient
– Interferes with normal filling/emptying cycle

37. CA: Sinus Node Abnormalities
• Brachycardia
– Regular but slow HR
• Less than 60 beats/min
– Results from vagus nerve stimulation or PNS
stimulation
• Tachycardia
– Regular rapid HR
• 100-160 beats/min
– SNS stimulation, exercise, fever,
compensation for low blood volume

39. CA: Atrial Conduction
Abnormalities
• Premature Atrial Contractions (PAC)
– Extra contraction or ectopic beats of atria
– Irritable atrial muscle cells outside conduction
pathway
• Interfere with timing of next beat
• Atrial flutter
– HR 160-350 beats/min
– AV node delays conduction
• Slower ventricular rate

40. Treatment of CA
• Cause should be determined and treated
• Easiest to treat are those due to meds
• SA node problems may require a
pacemaker
• Some may require defibrillators

42. Cardiac Arrest
• Cessation of all activity in the heart
• No conduction of impulses (flat line)
• May occur b/c:
– Excessive vagal nerve stimulation (decreases
heart)
– Drug toxicity
– Insufficient oxygen to maintain heart tissue
• Blood flow to heart and brain must be
maintained to resuscitate

43. CHF—Pathophysiology
• Heart unable to pump sufficient blood to
meet metabolic needs of body
• Complication
• Acute or chronic
• Results from
– Problem in heart itself
– Increased demands placed on heart
– Combo
• One side usually fails 1st

44. CHF—Pathophysiology
• 1st
compensation mechanism to maintain CO
– Often aggravates instead of assists
– Decreased flow to systemic circ
• Kidneys increase renin, aldosterone secretion
• Vasoconstriction (increase afterload) and increased blood vol
(increased preload) = increased work load for heart
– SNS increases HF and periph resistance
– Dilatation of heart chambers, myocardium,
hypertrophies

46. CHF—Pathophysiology
• 2nd
effect when heart cannot maintain
pumping capability
– Decrease in CO or SV
• “forward effect”
– “backup” congestion

48. CHF—Etiology
• Causes of failure on affected side:
– Infarction that impairs pumping ability or
efficiency of conduction system
– Valve defects
– Congenital heart defects
– Coronary artery disease

49. CHF—Etiology
• Increased demands on heart cause failure
– Depends on ventricle most adversely affected
– Ex: Hypertension increases diastolic bp
– Requires L ventricle to contract more forcibly to open
aortic valve

51. CHF—Signs and Symptoms
• Forward effects
– Similar with failure on either side
– Decrease blood supply to tissue and general
hypoxia
– Fatigue, weakness, dyspnea
(breathlessness), cold intolerance, dizziness
• Compensation mechanism
– Indicated by tachycardia, pallor, daytime
oliguira

52. CHF—Signs and Symptoms
• Systemic backup effects of R-sided failure
– Edema in feet, legs
– Hepatomegaly, splenomegaly
– Ascites
– Acute R-sided failure
– Flushed face, distended neck veins, headaches, vision
problems

53. CHF—Diagnostic Tests
• Radiographs
• Catheterization
• Arterial blood gases

54. CHF—Treatment
• Underlying problem should be treated
• Decrease work load on heart
• Prophylactic measures
• Other methods
– Diet
– Drugs

55. Arterial Diseases: Hypertension—
Pathophysiology
• Increased bp
• Insidious onset, mild symptoms and signs
• 3 major categories
– Essential (primary)
– Secondary
– Malignant
• Can be classified as diastolic or systolic
• Develops when bp consistently over 140/90
• Diastolic more important

57. Hypertension—Pathophysiology
• Over long time, high bp damages arterial walls
– *Sclerosis, decreased lumen
– Wall may dilate, tear
• Aneurysm
• Areas most frequently damaged:
– Kidneys, brain, retina
• End result of poorly controlled hypertension:
– Chronic renal failure
– Stroke
– Loss of vision
– CHF

58. Hypertension—Etiology
• Increases with age
• Males more freq and severe
• Genetic factors
• High sodium ion intake
• Excessive alcohol
• Obesity
• Prolonged, recurrent stress

59. Hypertension—Signs and
Symptoms
• Asymptomatic in early stages
• Initial signs vague, nonspecific
– Fatigue, malaise, morning headache

60. Hypertension—Treatment
• Treated in sequence of steps
– Life style changes
– Mild diuretics, ACE inhibitors
– One or more drugs added
• Pt compliance is an issue
• Prognosis depends on treating underlying
problems and maintaining constant control
of bp

61. Shock (Hypotension)
• Results from decreased circulating blood
vol
– General hypoxia
– Low CO

62. Classification and Mechanisms of
Shock
Type Mechanism
Hypovolemic loss of blood or plasma
Cardiogenic Decreased pumping
capability of heart
Anaphylactic Systemic vasodilation
due to severe allergic
reaction
Septic Vasodilation due to
severe infection
Neurogenic Vasodilation due to loss
of SNS and vaso-motor
tone

64. Shock—Pathophysiology
• Bp decreases when blood vol, heart contraction,
or periph resistance fails
• Low CO, microcirculation
– = decreased oxygen, nutrients for cells
• Compensation mechanism
– SNS, adrenal medulla stimulated
– Renin secreted
– Increased secretion of ADH
– Secretion of glucocorticoids
– Acidosis stimulates respiration

66. Shock—Pathophysiology
• Complications of decompensation of
shock
– Acute renal failure
– Adult respiratory distress syndrome (ARDS)
– Hepatic failures
– Hemorrhagic ulcers
– Infection of septicemia
– Decreased cardiac function

67. Shock—Etiology
• Hypovolemic shock
– Loss of blood, plasma
• Burn pts, dehydration
• Cardiogenic shock
– Assoc w/ cardiac impairment
• Distributive shock
– Blood relocated b/c vasodilation
• Anaphylactic shock
• Neurogenic shock
• Septic shock
– Severe infection

68. Shock—Signs and Symptoms
• 1st
signs
– Shock, thirst, agitation,
restlessness
– Often missed
• 2nd
signs
– Cool, moist, pale skin;
tachycardia; oliguria
– Compensation
– Vasoconstriction
• Direct effects
– Decrease bp and blood
flow
– Acidosis
• Prolonged
– Decreased responsiveness
in body
– Compensated metabolic
acidosis progresses to
decompensated
– Acute renal failure
– Monitoring

69. Shock—Treatment
• Primary problem must be treated
• Hypovolemic shock
– Whole blood, plasma, electrolytes, bicarbonate required
• Anaphylactic shock
– Antihistamines, corticosteroids
• Septic
– Antimicrobials, glucocorticoids
• Maximize oxygen supply
• Epine reinforces heart action and vasoconstriction
• Dopamine, dubutamine increase heart function
• Good prognosis in early stages
• Mortality increases as irreversible shock develops