Cardiovascular Disorders

Cardiovascular Disorders


الدكتور عبد المهدي عبد الرضا حسن الشحماني
كلية التمريض / جامعة بابل
PhD, pediatric & Mental Health Nursing
• 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
• 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
• 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 à cells
– Dangerous component
• HDL
– “good”
– Low cholesterol content
– Transports cholesterol cells à 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
• 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
– 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
• 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
– 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
• 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
• 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