Cardiovascular Disorders
‫الدكتور عبد المهدي عبد الرضا حسن الشحماني‬
‫ جامعة بابل‬/ ‫كلية التمريض‬
PhD, pediatric & Mental Health Nursing
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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
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
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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
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
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
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
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• 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
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
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– “good”
– Low cholesterol content
– Transports cholesterol cells  liver
– Development of Atheroma
Consequences of Atherosclerosis
Atherosclerosis—Etiology
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
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
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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
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
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
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– 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
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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
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Radiographs
Catheterization
Arterial blood gases
CHF—Treatment
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:
– Chronic renal failure
– Stroke
– Loss of vision
– CHF
Hypertension—Etiology
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
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– 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
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
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
nd
2 signs
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– 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
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
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