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
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
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
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
30.
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
36.
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
38.
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
41.
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
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
50.
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
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
56.
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
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
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
63.
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
65.
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
