4. Diagnostic Tests
• Angiography
– Visualization of blood
flow in coronary artery
– Obstruction assessed
and treated
• Basic catheterization
• Balloon angioplasty
5. Diagnostic Tests
• Doppler Studies
– Assessment of blood flow in peripheral vessels
– Microphone records sounds of blood flow
• Can detect obstruction
• Blood tests
– Assess triglyceride and cholesterol levels
– Electrolytes
– Hb, hematocrit, cbcs
• Arterial Blood Gas Determination
– Essential for pts with shock, MI
– Check current oxygen levels, acid-base balance
6. General Treatment Measures for
Cardiac Disorders
• Dietary modification
• Regular exercise program
• Quit smoking
• Drug therapy
7. 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
8. Drug Therapy
• Calcium ion channel blockers
– 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
9. 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
10. 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
21. 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
23. 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
24.
25. 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 i.e. cardiac output)
• Low grade fever
26. 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
27. MI—Complications
• Arrhythmias
– 25% pts sudden death after MI
• Due to ventricular arrhythmias and fibrillation
– Heart block
– Premature ventricular contraction (PVCs)
• Cardiogenic shock
• CHF
28. 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
29. 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
30.
31. 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
32.
33. 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
• *Atrial flutter (AFL) is a type of
abnormal heart rate, or arrhythmia.
It occurs when the upper chambers
of your heart beat too fast. When the
chambers in the top of your heart (atria)
beat faster than the bottom ones (ventricles),
it causes your heart rhythm to be out of sync.
34. 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
35.
36. 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
37. 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
38. 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
39.
40. CHF—Pathophysiology
• 2nd effect when heart cannot maintain
pumping capability
– Decrease in CO or SV
• “forward effect”
– “backup” congestion
41.
42. 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
43. 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
– Ex: Pulmonary disease
– Damages lung caps, increases pulm resistance
– Increase work load to R vent
44.
45. 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
46. CHF—Signs and Symptoms
• Systemic backup effects of R-sided failure
– Edema in feet, legs
– Hepatomegaly, splenomegaly
– Ascites
– Acute R-sided failure
• Increased pressure on SVC
– Flushed face, distended neck veins, headaches, vision
problems
48. CHF—Treatment
• Underlying problem should be treated
• Decrease work load on heart
• Prophylactic measures
• Other methods
– Diet
– Drugs
49. 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
50.
51. 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
52. Hypertension—Etiology
• Increases with age
• Males more freq and severe
• Genetic factors
• High sodium ion intake
• Excessive alcohol
• Obesity
• Prolonged, recurrent stress
54. 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
56. 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 vasomotor
tone
57.
58. 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
59.
60. 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