Transcript Cardiovascular Disorders

Cardiovascular Disorders
Chapter 18
Pgs 285-308
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
Homework
• Due Tuesday Oct 4
• Do the following Case Study questions on Pg. 306
– You do not have to type them; Put the answers in your own
words!
• Case Study A
– a, b, e, g, k, l, m
• Case Study B
– a-f
• You may work together
– If you work in a group, you can turn in one paper!
– You must be present in class to get credit!
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
Diagnostic Tests
• Cardiac
Catheterization
– Visualize inside of
heart, measure
pressure, assess valve
and heart function
– Determine blood flow
to and from heart
Diagnostic Tests
• Angiography
– Visualization of blood
flow in coronary artery
– Obstruction assessed
and treated
• Basic catheterization
• Balloon angioplasty
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
General Treatment Measures for
Cardiac Disorders
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Dietary modification
Regular exercise program
Quit smoking
Drug therapy
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
Drug Therapy
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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
– Pts 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, CHF, after MI
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
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
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
CAD—Atherosclerosis:
Pathophysiology
• Presence of
atheromas
– Plaques
• Consist of lipids, cells,
fibrin, cell debris
– Lipids usually
transported with
lipoproteins
Lipoproteins and Transport
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
Development of Atheroma
Consequences of Atherosclerosis
Atherosclerosis—Etiology
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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
Combo of BC pills and smoking
Atherosclerosis—Diagnostic Tests
• Serum lipid levels
• Exercise stress test
• Radioisotope
Atherosclerosis—Treatment
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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
CABG
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
Myocardial Infarction
MI—Pathophysiology
• Function of myocardium contraction and
conduction quickly lost
– Oxygen supplies depleted
• 1st 20 minutes critical
• 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
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
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
MI—Complications
• Arrhythmias
– 25% pts sudden death after MI
• Due to ventricular arrhythmias and fibrillation
– Heart block
– Premature ventricular contraction (PVCs)
• Cardiogenic shock
• CHF
MI—Treatment
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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
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
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
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
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
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
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
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
CHF—Pathophysiology
• 2nd effect when heart cannot maintain
pumping capability
– Decrease in CO or SV
• “forward effect”
– “backup” congestion
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
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
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
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
CHF—Diagnostic Tests
• Radiographs
• Catheterization
• Arterial blood gases
CHF—Treatment
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Underlying problem should be treated
Decrease work load on heart
Prophylactic measures
Other methods
– Diet
– Drugs
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
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:
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Chronic renal failure
Stroke
Loss of vision
CHF
Hypertension—Etiology
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Increases with age
Males more freq and severe
Genetic factors
High sodium ion intake
Excessive alcohol
Obesity
Prolonged, recurrent stress
Hypertension—Signs and
Symptoms
• Asymptomatic in early stages
• Initial signs vague, nonspecific
– Fatigue, malaise, morning headache
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
Shock (Hypotension)
• Results from decreased circulating blood
vol
– General hypoxia
– Low CO
Classification and Mechanisms of
Shock
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
Shock—Pathophysiology
• Bp decreases when blood vol, heart contraction,
or periph resistance fails
• Low CO, microcirculation
– = decreased oxygen, nutrients for cells
• Compensation mechanism
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SNS, adrenal medulla stimulated
Renin secreted
Increased secretion of ADH
Secretion of glucocorticoids
Acidosis stimulates respiration
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
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
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
Shock—Treatment
• Primary problem must be treated
• Hypovolemic shock
– Whole blood, plasma, electrolytes, bicarbonate required
• Anaphylactic shock
– Antihistamines, corticosteroids
• Septic
– Antimicrobials, glucocorticoids
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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