Mr. Tsigaridis
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Diagnostic Tests for
Cardiovascular
Function
General Treatment
Measures for Cardiac
Disorders
Coronary Artery
Disease (CAD)
◦ Arteriosclerosis
◦ Atherosclerosis
◦ Myocardial Infarction (MI)
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Cardiac Arrhythmias
◦ Sinus node abnormalities
◦ Atrial conduction
abnormalities
◦ Cardiac arrest
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Congestive Heart
Failure (CHF)
Arterial Diseases
◦ Hypertension
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Shock
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ECG
◦ Monitors arrhythmias, MI, infection, pericarditis
◦ Studies conduction activation and systemic abnormalities
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Auscultation
◦ Studies heart sounds using stethoscope
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Exercise stress test
◦ Assess general cardiovascular function
◦ Checks for exercise-induced problems
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Chest X-ray Film
◦ Shows shape, size of heart
◦ Evidence of pulmonary congestion associated with heart
failure
◦ Nuclear imaging
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Cardiac
Catheterization
◦ Visualize inside of
heart, measure
pressure, assess
valve and heart
function
◦ Determine blood flow
to and from heart
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Angiography
◦ Visualization of
blood flow in
coronary artery
◦ Obstruction assessed
and treated
 Basic catheterization
 Balloon angioplasty
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Dietary modification
Regular exercise program
Quit smoking
Drug therapy
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Vasodilators (Nitroglycerin)
◦ Provide better balance of oxygen supply and
demand in heart muscle
◦ May cause low bp
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Beta-blockers (Metoprolol or Atenolol)
◦ Treats angina, hypertension, arrhythmias
◦ Blocks beta1-adrenergic receptors in heart
 Prevent epine from increasing heart activity
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Calcium ion channel blockers
◦ Block movement of calcium
◦ Decrease heart contraction
 Antiarrhytmatic for excessive atrial activity
 Antihypertension and vasodilator
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Digoxin
◦ Treats heart failure
◦ Increases efficiency of heart
 Decreases conduction of impulses and HR
 Increases contraction of heart
◦ Patients must be checked for toxicity
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Antihypertensive drugs
◦ Decrease bp to normal levels
◦ Include:
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Adrenergic blocking agents
Calcium ion blockers
Diuretics
Angiotensin-converting enzyme (ACE) inhibitors
◦ Used to treat hypertension, Congestive Heart Failure, after MI
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Adrenergic Blocking drugs
◦ Act on SNS, block arteriole alpha adrenergic
receptors, or act directly as vasodilator
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ACE Inhibitors
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Diuretics
◦ Treat hypertension, Congestive Heart Failure
◦ Remove excess water, sodium ions
◦ Block resorption in kidneys
◦ Treat high bp, Congestive Heart Failure
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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
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Presence of
atheromas
◦ Plaques
 Consist of lipids, cells,
fibrin, cell debris
◦ Lipids usually
transported with
lipoproteins
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Analysis of serum lipids:
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LDL
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HDL
◦ Total cholesterol, triglycerides, LDL, HDL
◦ High cholesterol content
◦ Transports cholesterol liver  cells
◦ Dangerous component
◦ “good”
◦ Low cholesterol content
◦ Transports cholesterol cells  liver
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Age
Gender
Genetic factors
Obesity, diet high in cholesterol, animal fats
Cigarette smoking
Sedentary life style
Diabetes mellitus
Poorly controlled hypertension
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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
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Coronary artery completely obstructed
◦ Prolonged ischemia and cell death of myocardium
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Most common cause is atherosclerosis with
thrombus
3 ways it may develop:
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Majority involve L ventricle
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◦ Thrombus obstructs artery
◦ Vasospasm due to partial occlusion
◦ Embolus blocks small branch of coronary artery
◦ Size and location of infarction determine severity
of damage
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Function of myocardium contraction and
conduction quickly lost
◦ Oxygen supplies depleted
 1st 20 minutes critical
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Time Line
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1st 20 min critical
48 hrs inflammation begins to subside
7th day necrosis area replaced by fibrous tissue
6-8 weeks scar forms
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Pain
◦ Sudden, substernal area
◦ Radiates to L arm and neck
◦ Less severe in females
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Sweating, nausea, dizziness
Anxiety and fear
Hypotension, rapid and weak pulse (low
Cardiac Output)
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Arrhythmias
◦ 25% patients sudden death after Myocardial
Infarction
 Due to ventricular arrhythmias and fibrillation
◦ Heart block
◦ Premature ventricular contraction (PVCs)
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Cardiogenic shock
Congestive Heart Failure
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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
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Alteration in HR or rhythm
ECG monitors
◦ Holter monitors
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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
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Irregular contraction inefficient
◦ Interferes with normal filling/emptying cycle
Cardiac Arrhythmias
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Brachycardia
◦ Regular but slow HR
 Less than 60 beats/min
◦ Results from vagus nerve stimulation or PNS
stimulation
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Tachycardia
◦ Regular rapid HR
 100-160 beats/min
◦ SNS stimulation, exercise, fever, compensation for
low blood volume
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Premature Atrial Contractions (PAC)
◦ Extra contraction or ectopic beats of atria
◦ Irritable atrial muscle cells outside conduction
pathway
 Interfere with timing of next beat
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Atrial flutter
◦ HR 160-350 beats/min
◦ AV node delays conduction
 Slower ventricular rate
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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
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Cessation of all activity in the heart
No conduction of impulses (flat line)
May occur b/c:
◦ Excessive vagal nerve stimulation (decreases heart
rate)
◦ Drug toxicity
◦ Insufficient oxygen to maintain heart tissue
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Blood flow to heart and brain must be
maintained to resuscitate
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Heart unable to pump sufficient blood to
meet metabolic needs of body
Acute or chronic
Results from
◦ Problem in heart itself
◦ Increased demands placed on heart
◦ Combo
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One side usually fails 1st
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Causes of failure on affected side:
◦ Infarction that impairs pumping ability or efficiency
of conduction system
◦ Valve defects
◦ Congenital heart defects
◦ Coronary artery disease
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Increased demands on heart cause failure
◦ Depends on ventricle most adversely affected
◦ Ex: Hypertension increases diastolic bp
 Requires Left ventricle to contract more forcibly to open
aortic valve
◦ Ex: Pulmonary disease
 Damages lung caps, increases pulmonary resistance
 Increase work load to Right ventricle
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Forward effects
◦ Similar with failure on either side
◦ Decrease blood supply to tissue and general
hypoxia
◦ Fatigue, weakness, dyspnea (breathlessness), cold
intolerance, dizziness
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Compensation mechanism
◦ Indicated by tachycardia
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Systemic backup effects of Right-sided failure
◦ Edema in feet, legs
◦ Hepatomegaly, splenomegaly
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Underlying problem should be treated
Decrease work load on heart
Prophylactic measures
Other methods
◦ Diet
◦ Drugs
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Increased bp
Insidious onset, mild symptoms and signs
3 major categories
◦ Essential (primary)
◦ Secondary
◦ Malignant
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Can be classified as diastolic or systolic
Develops when bp consistently over 140/90
Diastolic more important
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Over long time, high bp damages arterial
walls
◦ Sclerosis, decreased lumen
◦ Wall may dilate, tear
 Aneurysm
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Areas most frequently damaged:
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End result of poorly controlled
hypertension:
◦ Kidneys, brain, retina
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Chronic renal failure
Stroke
Loss of vision
CHF
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Increases with age
Males more freq and severe
Genetic factors
High sodium ion intake
Excessive alcohol
Obesity
Prolonged, recurrent stress
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Asymptomatic in early stages
Initial signs vague, nonspecific
◦ Fatigue, malaise, morning headache
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Treated in sequence of steps
◦ Life style changes
◦ Mild diuretics, ACE inhibitors
◦ One or more drugs added
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Patient compliance is an issue
Prognosis depends on treating underlying
problems and maintaining constant control of
bp
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Results from decreased circulating blood
volume
◦ General hypoxia
◦ Low Cardiac Output
Type
Hypovolemic
Cardiogenic
Anaphylactic
Septic
Neurogenic
Mechanism
loss of blood or plasma
Decreased pumping
capability of heart
Systemic vasodilation
due to severe allergic
reaction
Vasodilation due to
severe infection
Vasodilation due to loss
of SNS and vaso-motor
tone
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Bp decreases when blood volume, heart
contraction, or peripheral resistance fails
Low CO, microcirculation
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Compensation mechanism
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◦ = decreased oxygen, nutrients for cells
◦ Sympathetic Nervous System, adrenal medulla
stimulated
◦ Renin secreted
◦ Increased secretion of ADH
◦ Secretion of glucocorticoids
◦ Acidosis stimulates respiration
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Complications of shock
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Acute renal failure
Adult respiratory distress syndrome (ARDS)
Hepatic failures
Hemorrhagic ulcers
Infection of septicemia
Decreased cardiac function
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Hypovolemic shock
◦ Loss of blood, plasma
 Burn pts, dehydration
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Cardiogenic shock
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Distributive shock
◦ Assoc w/ cardiac impairment
◦ Blood relocated b/c vasodilation
 Anaphylactic shock
 Neurogenic shock
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Septic shock
◦ Severe infection
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1st signs
◦ Shock, thirst, agitation,
restlessness
◦ Often missed
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2nd signs
◦ Cool, moist, pale skin;
tachycardia; oliguria
◦ Compensation
◦ Vasoconstriction
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Direct effects
◦ Decrease bp and blood
flow
◦ Acidosis
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Prolonged
◦ Decreased
responsiveness in body
◦ Compensated metabolic
acidosis progresses to
decompensated
◦ Acute renal failure
◦ Monitoring
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Primary problem must be treated
Hypovolemic shock
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Anaphylactic shock
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Septic
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◦ Whole blood, plasma, electrolytes, bicarbonate required
◦ Antihistamines, corticosteroids
◦ 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