Cardiovascular%20Disorders

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Cardiovascular Disorders

• Mr. Tsigaridis

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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

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Diagnostic Tests for Cardiovascular Function

• ECG
• Monitors arrhythmias, MI, infection, pericarditis
• Studies conduction activation and systemic
  abnormalities
• Auscultation
• 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

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Diagnostic Tests

• Cardiac Catheterization
• Visualize inside of heart, measure pressure,
  assess valve and heart function
• Determine blood flow to and from heart

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Diagnostic Tests

• Angiography
• Visualization of blood flow in coronary artery
• Obstruction assessed and treated
• Basic catheterization
• Balloon angioplasty

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General Treatment Measures for Cardiac Disorders

• Dietary modification
• Regular exercise program
• Quit smoking
• Drug therapy

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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

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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
• Patients 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, Congestive Heart
  Failure, after MI

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Drug Therapy

• Adrenergic Blocking drugs
• Act on SNS, block arteriole alpha adrenergic
  receptors, or act directly as vasodilator
• ACE Inhibitors
• Treat hypertension, Congestive Heart Failure
• Diuretics
• Remove excess water, sodium ions
• Block resorption in kidneys
• Treat high bp, Congestive Heart Failure

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CADArteriosclerosis 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

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CADAtherosclerosis Pathophysiology

• Presence of atheromas
• Plaques
• Consist of lipids, cells, fibrin, cell debris
• Lipids usually transported with lipoproteins

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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

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Development of Atheroma
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AtherosclerosisEtiology

• 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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AtherosclerosisTreatment

• 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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CABG
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Coronary Artery Disease 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

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Myocardial Infarction 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

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Myocardial Infarction - Signs and Symptoms

• Pain
• Sudden, substernal area
• Radiates to L arm and neck
• Less severe in females
• Sweating, nausea, dizziness
• Anxiety and fear
• Hypotension, rapid and weak pulse (low Cardiac
  Output)

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Myocardial Infarction - Complications

• Arrhythmias
• 25 patients sudden death after Myocardial
  Infarction
• Due to ventricular arrhythmias and fibrillation
• Heart block
• Premature ventricular contraction (PVCs)
• Cardiogenic shock
• Congestive Heart Failure

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Myocardial InfarctionTreatment

• 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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Cardiac Arrhythmias

• Alteration in HR or rhythm
• ECG monitors
• Holter monitors
• decreases efficiency of hearts 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

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Cardiac Arrhythmias
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Cardiac Arrhythmias 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

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Cardiac Arrhythmias 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

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Treatment of Cardiac Arrhythmias

• 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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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 rate)
• Drug toxicity
• Insufficient oxygen to maintain heart tissue
• Blood flow to heart and brain must be maintained
  to resuscitate

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Congestive Heart Failure - Pathophysiology

• 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
• One side usually fails 1st

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Congestive Heart Failure - 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

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Congestive Heart Failure - Etiology

• 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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Congestive Heart Failure - 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

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Congestive Heart Failure - Signs and Symptoms

• Systemic backup effects of Right-sided failure
• Edema in feet, legs
• Hepatomegaly, splenomegaly

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Congestive Heart Failure - Treatment

• Underlying problem should be treated
• Decrease work load on heart
• Prophylactic measures
• Other methods
• Diet
• Drugs

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Arterial Diseases HypertensionPathophysiology

• 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

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HypertensionPathophysiology

• 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

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HypertensionEtiology

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

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HypertensionSigns and Symptoms

• Asymptomatic in early stages
• Initial signs vague, nonspecific
• Fatigue, malaise, morning headache

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HypertensionTreatment

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

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Shock (Hypotension)

• Results from decreased circulating blood volume
• General hypoxia
• Low Cardiac Output

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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
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ShockPathophysiology

• Bp decreases when blood volume, heart
  contraction, or peripheral resistance fails
• Low CO, microcirculation
• decreased oxygen, nutrients for cells
• Compensation mechanism
• Sympathetic Nervous System, adrenal medulla
  stimulated
• Renin secreted
• Increased secretion of ADH
• Secretion of glucocorticoids
• Acidosis stimulates respiration

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ShockPathophysiology

• Complications of shock
• Acute renal failure
• Adult respiratory distress syndrome (ARDS)
• Hepatic failures
• Hemorrhagic ulcers
• Infection of septicemia
• Decreased cardiac function

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ShockEtiology

• 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

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ShockSigns 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

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ShockTreatment

• 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