Cardiovascular disorders
-
Upload
cynthia-acosta -
Category
Health & Medicine
-
view
222 -
download
0
Transcript of Cardiovascular disorders
CARDIOVASCULAR DISORDERS
CYNTHIA R. ACOSTA, RN, MAN
LEARNING OBJECTIVES:LEARNING OBJECTIVES:
At the end of the lecture, the students will be able to:
1.Identify the major organs and structures of cardiovascular system
2.Discuss the risk factors associated in the development of cardiovascular disorder
3.Discuss the physical assessment that provide information about the functioning of the cardiovascular disorder
LEARNING OBJECTIVES:LEARNING OBJECTIVES:
At the end of the lecture, the students will be able to:
4.Describe common diagnostic tests and their nursing responsibilities
5.Discuss the pathophysiology of clients with cardiovascular disorder
6.Enumerate the different clinical manifestations associated with each illness of clients with cardiovascular disorder
LEARNING OBJECTIVES:LEARNING OBJECTIVES:
At the end of the lecture, the students will be able to:
7.Identify actual and at-risk nursing diagnosis8.Discuss medical and surgical interventions 9.Discuss the appropriate nursing
interventions with client/s and family for identified nursing interventions
10.Implement plan of care with clients and family
CARDIOVASCULAR SYSTEM
is a closed system consistingof the heart and blood vessels
- to supply body cells and tissues with
oxygen-rich blood and eliminate carbon
dioxide and cellular wastes
FUNCTIONFUNCTION
- a cone-shaped muscle with four
chambers; a double pump about the size
of a clenched fist
HEARTHEART
-pumps blood throughout circulatory system
RIGHT SIDERIGHT SIDE
- upper chamber of right heart- receives
unoxygenated blood from superior and inferior vena cava
RIGHT ATRIUM
RIGHT SIDERIGHT SIDE
-Right AV valve with three cusps (tricuspid)
-Valve between right atrium and right
ventricle
TRICUSPID VALVE
RIGHT SIDERIGHT SIDE
-lower chamber of right heart
-receives blood from right atrium and
pumps it into pulmonary circuit
RIGHT VENTRICLE
RIGHT SIDERIGHT SIDE
-composed of three cusps
-valve between right ventricle and main pulmonary artery
PULMONARY SEMILUNAR VALVE
RIGHT SIDERIGHT SIDE
-artery leading from right ventricle to lungs-divides into right and
left branches supplying respective lungs
-carries unoxygenated blood from right ventricle to lungs
MAIN PULMONARY ARTERY
RIGHT SIDERIGHT SIDE
-veins leading from lungs to left atrium-carry oxygenated blood to left atrium
PULMONARY VEINS
LEFT SIDELEFT SIDE
- upper chamber of left heart.- receives
oxygenated blood from lungs through pulmonary veins
LEFT ATRIUM
LEFT SIDELEFT SIDE
-AV valve with two cusps (bicuspid)
-valve between left atrium and left
ventricle
MITRAL VALVE
LEFT SIDELEFT SIDE
-lower chamber of left half of heart
- receives blood from left atrium and pumps
oxygenated blood through systemic
circulation
LEFT VENTRICLE
LEFT SIDELEFT SIDE
- composed of three cusps
- valve between left ventricle and aorta.
AORTIC VALVE
LEFT SIDELEFT SIDE
- wall between left and right ventricles.- vertically separates left and right sides of
heart
INTERVENTRICULAR SEPTUM
LAYERS OF THE HEARTLAYERS OF THE HEART
- inner layer of heart; a smooth,
thin layer of endothelium and
connective tissue. -smooth inner
lining of the heart
ENDOCARDIUM
LAYERS OF THE HEARTLAYERS OF THE HEART
- middle and thickest layer of heart; heart muscle.
-responsible for cardiac contraction
MYOCARDIUM
- the layer of serous pericardium on heart’s surface.
- contains main coronary blood vessels
EPICARDIUM
LAYERS OF THE HEARTLAYERS OF THE HEART
- Sac that surrounds the heart and roots of the great vessels.
-Composed of two layers: Fibrous pericardium (outer layer of
fibrous connective tissue) and serous pericardium
PERICARDIUM
SYSTEMIC AND SYSTEMIC AND PULMONARY PULMONARY CIRCULATIONCIRCULATION
LAYERS OF ARTERIES AND VEINSLAYERS OF ARTERIES AND VEINS
- blood vessels with three coats: tunica intima, tunica media, and tunica
adventitia.- carry oxygenated blood away from left heart and unoxygenated blood to
lungs via pulmonary arteries
ARTERIES
LAYERS OF ARTERIES AND VEINSLAYERS OF ARTERIES AND VEINS
- Smallest arteries; contain large amount of smooth muscle cells that
can dilate and constrict.- Carry blood to capillaries and control
blood flow to capillaries throughdilation/constriction
ARTERIOLES
LAYERS OF ARTERIES AND VEINSLAYERS OF ARTERIES AND VEINS
- Single layer of microscopic endothelial cells.
- Connect arterial and venous system for exchange of gases, fluids,
nutrients, and wastes.
CAPILLARIES
LAYERS OF ARTERIES AND VEINSLAYERS OF ARTERIES AND VEINS
- Contain same three layers as arteries, but are thinner with less
elastic and collagenous tissue and smooth muscle.
- BP in venous system is low; veins have valves to prevent backflow.
VEINS
- VEINS carry unoxygenated blood back to
right heart, except for pulmonary
veins, which carry oxygenated blood from lungs to left
heart.
- HEART RATE fluctuates according to
stimulation from autonomic nervous
system, baroreceptors, and chemoreceptors
REGULATION OF HEART RATE
- AUTONOMIC NERVOUS SYSTEM
affects heart rate through sympathetic and parasympathetic
nervous system innervation
- SYMPATHETIC NERVE FIBERS, adrenergic neurotransmitters
(norepinephrine, epinephrine) excite SA and AV nodes in the conduction system,
thus INCREASING HEART RATE
- The same neurotransmitters also stimulate
BETA ADRENERGIC RECEPTORS in the atria ventricles, increasing force of
myocardial contraction
- Heart rate slows when parasympathetic nerve fibers from the cardiac branches of
the vagus nerve release the CHOLINERGIC neurotransmitter
ACETYLCHOLINE
CARDIAC OUTPUT – is the amount of
blood pumped out of the left ventricle
each minute
PROPERTIES OF CARDIAC CYCLE
AUTOMATICITY: Generates electrical impulse independently,
without involving the nervous system
EXCITABILITY: Responds to electrical stimulation
PROPERTIES OF CARDIAC CYCLE
CONDUCTIVITY: Passes or propagates electrical impulses from cell to cell
CONTRACTILITY: Shortens in response to electrical stimulation
ELECTRICAL CONDUCTION SYSTEM OF
THE HEART
Conduction System Structures and
Functions
ELECTRICAL CONDUCTION SYSTEM OF THE HEART
SINOATRIAL (SA) NODE: Dominant pacemaker of the heart, located in
upper portion of right atrium. Intrinsic rate
60–100 bpm.
SA NODE
ELECTRICAL CONDUCTION SYSTEM OF THE HEART
INTERNODAL PATHWAYS: Direct electrical impulses
between SA and AVnodes.
INTERNODAL PATHWAYS
ELECTRICAL CONDUCTION SYSTEM OF THE HEART
ATRIO VENTRICULAR (AV) NODE: Part of AV junctional tissue. Slows conduction, creating a
slight delay before impulses reach
ventricles. Intrinsic rate 40–60 bpm
AV NODE
ELECTRICAL CONDUCTION SYSTEM OF THE HEART
BUNDLE OF HIS: Transmits impulses to
bundle branches.Located below AV
node
BUNDLE OF HIS
ELECTRICAL CONDUCTION SYSTEM OF THE HEART
LEFT BUNDLE BRANCH: Conducts impulses that lead to
left ventricle
LEFT BUNDLE BRANCH
ELECTRICAL CONDUCTION SYSTEM OF THE HEART
RIGHT BUNDLE BRANCH: Conducts impulses that lead to
right ventricle
RIGHT BUNDLE BRANCH
ELECTRICAL CONDUCTION SYSTEM OF THE HEART
PURKENJE SYSTEM: Network of fibers that
spreads impulsesrapidly throughout ventricular walls.
Located at terminals of bundle branches.
Intrinsic rate 20–40 bpmPURKENJE FIBERS
ELECTROPHYSIOLOGY
DEPOLARIZATION: The electrical charge of a cell is altered by a shift of electrolytes on either side of the cell membrane. This
change stimulates muscle fiber to contract
ELECTROPHYSIOLOGY
REPOLARIZATION: Chemical pumps re-establish an internal negative charge
as the cells return to their resting state
Mechanical and electrical functions of the heart are influenced by proper
electrolyte balance. Important components of this balance
are sodium, calcium, potassium, andmagnesium
ASSESSMENT
CARDIOVASCULAR
PAST MEDICAL HISTORY
REVIEW OF ALLERGIES
MEDICATION HISTORY
FAMILY HISTORY
PERSONAL AND SOCIAL HISTORY
COMMON MANIFESTATIONS OF
HEART DISEASE
CHEST PAIN
OTHER MANIFESTATIONS:
•shortness of breath
•palpitations•weakness
•fatigue•dizziness•syncope
•GI complaints
PHYSICAL EXAMINATION
GENERAL APPEARANCE-non-verbal behavior and body position
(anxious, depressed, pain, uncomfortable)
PAIN -classic sign of
ischemia
PHYSICAL EXAMINATION
VITAL SIGNS
TEMPERATURE-note presence of fever
PULSE RATE-note rate, rhythm and
quality
PHYSICAL EXAMINATION
VITAL SIGNS
RESPIRATORY RATE-note if patient has labored breathing
BLOOD PRESSURE-take BP lying, sitting, & standing positions
(orthostatic VS)
CARDIAC RHYTHM
-electrical activity can be observed continuously with bedside CARDIAC
MONITOR
-electrodes are attached to the chest & connected to a machine that displays the
cardiac rhythm
HEART SOUNDS
“LUBLUB” – first heart sound – referred to S1,
is the closing of the mitral and tricuspid
valves
“DUBDUB” – referred to S2, is the closing of the aortic and pulmonic valves
ABNORMAL HEART SOUNDS
S3 HEART SOUND – or a ventricular gallop“LUB-DUB-DEELUB-DUB-DEE” or
“KEN-TUCK-Y”
Normal in children, but indication of heart failure in an adult
ABNORMAL HEART SOUNDS
S4 HEART SOUND – or a atrial gallop, an extra heart sound
before S1“LUB-LUB-DUBLUB-LUB-DUB” or “TEN-NES-SEE” –
- often associated with hypertensive heart disease
PERIPHERAL PULSES
-palpate the radial arteries and the major arteries of the leg bilaterally
-record the presence or
absence of pulses and strength
SKIN
-note changes in skin color (cyanosis, pallor)
-note if the skin is warm or cold, dry
or clammy
PERIPHERAL EDEMA
EDEMA occurs when blood is not pumped efficiently or plasma protein
levels are inadequate to maintain osmotic pressure
AREA: feet and anklesOTHER AREAS: fingers, hands, over the
sacrum
Evaluated on a scale of 1-4
PERIPHERAL EDEMAPITTING EDEMA – marks of the
fingers remain
1+ PITTING EDEMA – slight indentation (2mm), normal contours
2+ PITTING EDEMA – deeper pit after pressing (4mm), lasts longer than 1+
PERIPHERAL EDEMA
3+ PITTING EDEMA – deep pit (6mm), remains several seconds after pressing
4+ PITTING EDEMA – dip pit (8mm), remains prolonged time after pressing,
possibly minutes
WEIGHT GAIN-can indicate edema
JUGULAR VEINS-distention of this vein usually indicates
increased fluid volume and pressure in the right side of the heart
MENTAL STATUS-note if patient is alert and oriented,
confused and disoriented
CONFUSION and DISORIENTATION can
result from a decrease in the oxygen supply to the brain (cerebral ischemia) as a result of poor circulation
DIAGNOSTIC DIAGNOSTIC TESTSTESTS
LABORATORY LABORATORY STUDIESSTUDIES
Enzyme,
Isoenzyme,
and Biochemical Markers
ENZYMES
CREATINE KINASE (CK) - 98% sensitivity for AMI 72 hours after
infarction
-present in heart muscles, skeletal muscles, and brain tissue
ENZYMES
CK ISOENZYMES - more specific than CK
CK-MM – skeletal musclesCK-BB – appears primarily in the brain
and nerve tissueCK-MB – heart muscles
-generally, CK-MB levels rise 4-8hrs after the onset of AMI, peak after 20hrs, & may
remain elevated for up to 72hrs
ENZYMES
TROPONIN I and TROPONIN T - is a protein found in the skeletal and
cardiac musclesTROPONIN T – may also be found in
the skeletal muscleTROPONIN I – found only in the myocardium, (more specific to
myocardial damage)
TROPONIN LEVELS rises within 3-6hrs after myocardial damage.
Troponin I peaks in 12-24hrs, with a return to baseline in 5-7days
Troponin T peaks in 24hrs , with a return to baseline in 10-15days
ENZYMES
MYOGLOBIN - is a small, oxygen-binding protein found in cardiac and
skeletal muscles and is rapidly released into the bloodstream
ENZYMES
C-REACTIVE PROTEIN (CRP) - is an inflammatory marker that may be
an important risk factor for atherosclerosis and ischemic heart
disease
Elevated CRP is associated with AMI, stroke, and the progression of peripheral vascular disease
ENZYMES
LIPOPROTEIN - a molecule that is similar to low-density lipoprotein
cholesterol (LDL-C)
It increases cholesterol deposits in the arterial wall, enhances oxidation of LDL-C, and inhibits fibrinolysis, resulting in the formation of atherosclerotic plaque
and thrombosis
ENZYMES
FACTOR I or FIBRINOGEN - is directly linked to increased
cardiovascular risk
It is involved in the coagulation cascade (converting fibrinogen to
fibrin by thrombin)
HEMATOLOGIC STUDIES
CBC - indication of the type and number of formed elements in the
blood
HEMATOLOGIC STUDIES
HEMATOCRIT – expresses the relationship of the formed elements in
the blood to the total volume
LOWERED when blood volume increases as in CHF
RISES when blood volume is lost as in bleeding, shock and burns
HEMATOLOGIC STUDIES
PROTHROMBIN TIME - measures how long it takes for prothrombin to become active in clotting process
PARTIAL THROMBOPLASTIN TIME - determine deficiencies in all
coagulation factors except factor VII
HEMATOLOGIC STUDIES
ERYTHROCYTE SEDIMENTATION RATE (ESR) - indicates the extent to which RBC settle to the bottom of the
test tube containing a sample of blood
ESR rises during the inflammatory processes such as rheumatic fever and MI
BLOOD CHEMISTRIES
SERUM CHOLESTEROL
SERUM TRIGLYCERIDES
GRAPHIC GRAPHIC RECORDING RECORDING
STUDIESSTUDIES
ECGHOLTER
MONITORING
GRAPHIC RECORDING STUDIES
ECG - graphically record electrical current generated by the heart
Helps identify primary conduction
abnormalities, arrhythmias, cardiac
hypertrophy, pericarditis, electrolyte imbalance,
and MI
GRAPHIC RECORDING STUDIES
EXERCISE ECG (Stress Test) - non invasive test that helps the doctor
assess cardiovascular response to an increased workload
Provides diagnostic information that can’t be obtained from a resting ECG
GRAPHIC RECORDING STUDIES
HOLTER MONITORING - records the heart’s electrical activity for 24 hours or longer as the patient performs his
usual activities and experiences normal physical and emotional stress
RADIOLOGY AND RADIOLOGY AND IMAGINGIMAGING
Chest X-rayMyocardial Imaging
RADIOLOGY AND IMAGING
CHEST X-RAY - a noninvasive tool used to visualize internal structures,
such as the heart, lungs, soft tissues, and bones
RADIOLOGY AND IMAGING
MYOCARDIAL IMAGING - with the use of radionuclides and scintillation cameras, radionuclide angiograms
can be used to assess left ventricular performance
RADIOLOGY AND IMAGING
ECHOCARDIOGRAPHY – a noninvasive imaging technique,
records the reflection of ultra-high frequency sound waves directed at
the patient’s heart
RADIOLOGY AND IMAGING
MRI (MAGNETIC RESONANCE IMAGING)– yields high-resolution,
tomographic, three dimensional images of body structures
Permits visualization of valve leaflets and structures, pericardial abnormalities and
processes, ventricular hypertrophy, cardiac neoplasm, infarcted tissue
RADIOLOGY AND IMAGING
ULTRAFAST CT SCAN – uses a scanner that takes images as fast speeds, resulting in high resolution
pictures
-can identify microcalcifications in the coronary arteries
RADIOLOGY AND IMAGING
ELECTRON BEAM COMPUTED TOMOGRAPHY – a radiologic test
that produces x-rays of the coronary arteries using electron beam
-can detect and quantify calcified plaque in the coronary arteries
RADIONUCLIDE RADIONUCLIDE IMAGING TESTSIMAGING TESTS
CARDIAC CATHETERIZATION
AND CORONARY ANGIOGRAPHY
RADIONUCLIDE IMAGING TESTS
CARDIAC CATHETERIZATION AND CORONARY ANGIOGRAPHY –
invasive tests, use a catheter threaded through an artery or vein into the heart
-to determine the size and location of a coronary lesion, evaluate ventricular
function, measure heart pressures and oxygen saturation
RADIONUCLIDE IMAGING TESTS
CORONARY FLOW AND PERFUSION EVALUATION – used to assess blood
flow through the coronary arteries, investigate myocardial anatomy and
perfusion, and determine the extent of lesions
RADIONUCLIDE IMAGING TESTS
DSA – combines angiography with computer processing to produce high-
resolution images of cardiovascular structures
-provides a clear view of arterial structures
RADIONUCLIDE IMAGING TESTS
VENOGRAM– Insertion of a dye into the vein for the purpose of outlining an
obstruction or lesion
TREATMENTSTREATMENTS
DRUG THERAPYDRUG THERAPY
ADRENERGICSANTIANGINALS
ANTIARRHYTHMICSANTIHYPERTENSIVES
ANTILIPEMICSANTIPLATELET AGENTS
DIURETICSINOTROPHIC AGENTS
THROMBOLYTICS
ANALGESIC
Antipyretic, Non-Steroidal Anti-inflammatory drugs, acetaminophen,
acetylsalicylic acid, ibuprofen
Relieves pain, fever, and inflammation
ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS
Captopril, Enalapril
Prevent angiotensin I from converting to angiotensin II, a potent
vasoconstrictor, thereby decreasinbg peripheral vascular resistance, blocks
the secretion of aldosterone from adrenal gland
ANGIOTENSIN II RECEPTOR ANTAGONISTS
LOSARTAN, VALSARTAN
Block angiotensin II at the receptor sites, thereby decreasing peripheral
vascular resistance
ANTIARRHYTHMICS
Lidocaine, propanolol, amiodarone
Reduce automaticity, slow conduction of electrical impulses through the heart,
and prolong the refractory period of myocardial cells
ANTIBIOTICS
Aminoglycocides (gentamycin, tobramycin), Amoxicillin, Erythromycin,
penicillin, tetracycline
Prevent or treat infections caused by pathogenic microorganism
ANTICHOLINERGICS
Atropine
Block effects of vagus nerve stimulation
ANTICOAGULANTS
IV Heparin, oral warfarin sodium
Prevent recurrence of emboli but have no effect on emboli that are
already present
ANTICOAGULANTS
Subcutaneous – low dose heparin (5,000 units)
Prophylactically prevent deep vein thrombosis, heparin activates
antithrombin III
ANTILIPEMIC AGENTS
Cholestyramine, clofibrate, colestipol, lovastatin
Lower the serum cholesterol level by binding bile salts in the bowel and
forming an insoluble complex that is excreted in the stool
ANTIPLATELET AGENTS
Aspirin, ticlopidine
Inhibit the aggregation of platelets to form a plug, platelets do not initiate thrombus formation as readily when
taking antiplatelets
BETA-ADRENERGIC BLOCKERS
Atenolol, metoprolol, propanolol
Decrease the heart rate and the force of contraction and reduce
vasoconstriction by antagonizing beta-receptors in the myocardium and
vasculature
BETA-ADRENERGICS
Beta only (dobutamine), beta or alpha plus beta – dopamine, epinephrine,
metaraminol
Increase myocardial contractility and heart rate, which in turn raises blood pressure, alpha plus beta-adrenergic
activity
CALCIUM CHANNEL BLOCKERS
Nifedipine, Verapamil
Inhibit calcium ions from crossing myocardial and vascular smooth
muscle, thereby producing vasodilation and decreased myocardial contractility
CARDIAC GLYCOSIDES
Digoxin
Increase the force of myocardial contractions and slow heart rate and
conduction through the atrioventricular node and bundle of His
CORTICOSTEROIDS
Oral hydrocortisone, oral methylprednisolone, oral prednisone
Strengthen the biologic membrane, which inhibits capillary permeability and
prevents leakage of fluid into the injured area and development of
edema
DIURETICS
Loop diuretics – furosemide, potassium sparing diuretic – spironolactone,
thiazide diuretic
Decrease blood volume, which decreases the workload of the heart
OPIOD ANALGESICS
Codeine, morpine, hydromorphone
Release moderate to severe pain by reducing pain sensation, producing
sedation, and decreasing the emotional upset often associated with pain
NITRATES
Isosorbide dinitrate, nitroglycerine – sublingual, topical, patch, tablet, IV
Reduce myocardial oxygen demand by promoting vasodilation and by
increasing oxygen supply to myocardial tissue
STOOL SOFTENERS
Docusate calcium, docusate sodium
Decrease the surface tension of the fecal mass to allow water to penetrate into the stool; prevents the client from
straining from defecation
THROMBOLYTIC AGENTS
Streptokinase, urokinase
Dissolve thrombus or emboli in the coronary arteries
VASODILATORS
Hydralazine, nitroprusside sodium
Decrease preload (venous dilators) and afterload (arterial dilators); act directly on blood vessels to cause dilation and decrease peripheral
vascular resistance
AUTONOMIC NERVOUS SYSTEM
DIVISIONS:
SYMPATHETIC NERVOUS SYSTEM
PARASYMPATHETIC NERVOUS SYSTEM
-generally function antagonistically toward each other
- critical to the stability of our internal environment (homeostasis)
SYMPATHETIC NERVOUS SYSTEM
- regulates the expenditure of energy
- Neurotransmitter are known as CATECHOLAMINES – epinephrine, norepinephrine, and dopamine
- controls “fight-or-flight responses”
SYMPATHETIC NERVOUS SYSTEM
ENZYMES: Monoamine oxidase (MAO) & Catechol-O-methyltransferase
(COMT)
4 TYPES OF RECEPTORS:alpha1, alpha2, beta1, beta2
PARASYMPATHETIC NERVOUS SYSTEM
-Works to conserve body energy and is partly responsible for slowing heart rate, digesting food, and eliminating
body wastes
- “rest and digest”
-Neurotransmitter: ACETYLCHOLINE
PARASYMPATHETIC NERVOUS SYSTEM
ENZYME: Acetylcholinesterase
2 TYPES OF RECEPTORS:Nicotinic, Muscarinic (both are
alkaloids)
CHOLINERGIC FIBERSCHOLINERGIC FIBERS – are NERVE ENDINGS that liberate
ACETYLCHOLINE
ADRENERGIC FIBERSADRENERGIC FIBERS – are NERVE ENDINGS that secrete
NOREPINEPHRINE
- They produce opposite responses
EXAMPLE:
HEART ADRENERGIC AGENTS
increase the heart rate
CHOLINERGIC AGENTS slow the heart rate
RESPONSES TO SYMPATHETIC
ACTIVATION
RESPONSES TO PARASYMPATHETIC
ACTIVATION
CARDIAC CARDIAC PACINGPACING
CARDIAC PACEMAKER
- is an electronic device that delivers direct
electrical stimulation to stimulate the
myocardium to depolarize, initiating a
mechanical contraction
The PACEMAKER initiates and maintains the heart rate when the
heart's natural pacemaker is unable to do so
PACEMAKERS can be used to correct bradycardias, tachycardias, sick sinus syndrome, and second-
and third-degree heart blocks, and for prophylaxis
Pacing may be accomplished through a permanent implantable
system, a temporary system with an external
pulse generator and percutaneously threaded
leads, or a transcutaneous external system with
electrode pads placed over the chest
CARDIAC PACEMAKER
INDICATIONSINDICATIONS
1. Symptomatic bradydysrhythmias2. Symptomatic heart block
a. Mobitz II second-degree heart blockb. Complete heart blockc. Bifascicular and trifascicular bundle
branch blocks
CARDIAC PACEMAKER
INDICATIONSINDICATIONS
3. Prophylaxisa. After acute MI: dysrhythmia and
conduction defectsb. Before or after cardiac surgeryc. During diagnostic testing
CARDIAC PACEMAKER
INDICATIONSINDICATIONS
4. Tachydysrhythmias; to break rapid rhythm disturbances
a. Supraventricular tachycardiab. Ventricular tachycardia
CARDIAC PACEMAKER
TYPESTYPES
PERMANENT PACEMAKERS•Used to treat chronic heart conditions; surgically placed, utilizing a local anesthetic, the leads are placed transvenously in the appropriate chamber of the heart and then anchored to the endocardium
CARDIAC PACEMAKER
TYPESTYPES
PERMANENT PACEMAKERS
• The pulse generator is placed in a surgically made pocket in subcutaneous tissue under the clavicle.
• Once placed and programmed it can be adjusted externally as needed.
CARDIAC PACEMAKER
TYPESTYPES
TEMPORARY PACEMAKERS
• are usually placed during an emergency, such as when a patient demonstrates signs of decreased CO until the temporary condition is resolved
CARDIAC PACEMAKER
TYPESTYPES
TEMPORARY PACEMAKERS
• Indicated for patients with high-grade AV blocks, bradycardia, or low CO
Temporary transvenous
pacer wire with external pulse
generator
SURGERYSURGERY
CORONARY ARTERY BYPASS GRAFTING
• CABG circumvents an occluded coronary artery with an autogenous
graft (usually a segment of saphenous vein or internal mammary artery, thereby restoring blood flow to
the myocardium
Coronary artery bypass graft
surgery is done primarily to
alleviate anginal symptoms as well
as improve survival
CORONARY ARTERY BYPASS GRAFTING
CANDIDATES FOR CABG- Severe angina from atherosclerosis
- CAD with high risk of MI
TRANSMYOCARDIAL REVASCULARIZATION
• TMR is a relatively new procedure.• Can provide relief for sever angina
when medical therapy fails or the patient isn’t a candidate for
angioplasty or by-pass surgery• Is performed through an incision on
the left side of the chest
TRANSMYOCARDIAL REVASCULARIZATION
POTENTIAL COMPLICATIONS:
- Arrhythmias, bleeding, damage to the great vessels, valves, and coronary
arteries
MINIMALLY INVASIVE CORONARY ARTERY BYPASS
• is CABG surgery done through a left anterior small thoracotomy (LAST)
• a short parasternal incision, or small incisions using port access and video-
assisted technology
Minimally invasive direct grafting of left
internal mammary
bypass graft to left anterior descending
coronary artery (LAD).
Surgery is performed on the beating heart. To allow suturing of the graft anastomosis
to the beating heart, pharmacologic measures such as adenosine and beta-blockers are used to slow or temporarily
stop the heart
PORT ACCESS CARDIAC SURGERY
• is another minimally invasive surgical technique that uses femorofemoral bypass through a small incision with
aid of videoscopes.• is performed using a small anterior thoracotomy and several small “port”
chest incisions
VASCULAR REPAIR
• may treat:- Vessels damaged by arteriosclerotic or
thromboembolic disorders (such as aortic aneurysm or arterial occlusive
disease), trauma, infections, or congenital defects
- Vascular obstructions that severely compromise circulation
VASCULAR REPAIR
• may treat:- Vascular disease that doesn’t repsond
to drug therapy- Life-threatening dissecting or ruptured
aortic aneurysm
VASCULAR REPAIR
• includes aneurysm resection, grafting, embolectomy, vena caval filtering, and
vein stripping
VASCULAR REPAIR
TYPES:
AORTIC ANEURYSM REPAIR- Removes an aneurysmal segment of the
aorta
VEIN STRIPPING- Removes the saphenous vein and it's branches to treat varicosities
VASCULAR REPAIR
TYPES:
VENA CAVAL FILTER INSERTION- Traps emboli in the vena cava,
preventing them from reaching the pulmonary vessels
EMBOLECTOMY- Removes an embolism from an artery
VASCULAR REPAIR
TYPES:
BYPASS GRAFTING- bypasses an arterial obstruction
resulting from arteriosclerosis
BALLOON CATHETER TREATMENTS
PERCUTANEOUS BALLOON VALVULOPLASTY
PERCUTANEOUS TRANSLUMINAL CORONARY
ANGIOPLASTY (PTCA)
PERCUTANEOUS BALLOON VALVULOPLASTY
-can be performed in the cardiac catheterization laboratory
- seeks to improve valvular function by enlarging the orifice of a stenotic heart
valve caused by congenital defect, calcification, rheumatic fever, or aging
PTCA
-offers a nonsurgical alternative to coronary artery bypass surgery
- uses a balloon-tipped catheter to dilate a coronary artery that has become
narrowed because of atherosclerotic plaque
-can open an occluded coronary artery without opening the chest
DISEASES OF DISEASES OF THE HEARTTHE HEART
Thrombus• A thrombus
– a blood clot that can develop anywhere in the vascular system
– causing the narrowing of a vessel.
– blood flow can be occluded (reduced or totally blocked)
Thrombus– develop from any injury to the vessel wall
• endothelial cell injury draws platelets and other mediators of inflammation to the area.
• substances stimulate clotting and activation of the coagulation cascade.
• formation can occur when blood flow through a vessel is sluggish,
• when blood flow is irregular or erratic
–during periods of irregular heartbeat or cardiac arrest
Thrombus
Embolus• Embolus
–a substance that travels in the bloodstream from a primary site to a secondary site
–becomes trapped in the vessels at the secondary site
–causes blood flow obstruction. –Most emboli are blood clots
(thromboemboli) • usually deep leg veins
–Other sources of emboli • fat
–released during the break of a long bone–produced in response to any physical
trauma, and amniotic fluid»which may enter maternal circulation
during the intense pressure gradients generated by labor contractions.
• Air and displaced tumor cells also may act as emboli to obstruct flow.
Embolus
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
-focal narrowing of the large and medium-sized coronary arteries
- due to deposition of atheromatous plaque in the vessel wall
- LIPID or FATTY Substance- FIBROUS TISSUE
ARTERIOSCLEROSIS – hardening of the arteries, which results in loss of
elasticity of intimal layer of the artery
ATHEROSCLEROSIS – accumulated fatty plaques made of lipids in the
arteries
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
RISK FACTORS
- Hereditary, including race- Age, Gender
- Cigarette Smoking- HTN- Elevated Serum Cholesterol Level- Diabetes Mellitus- Physical Inactivity- Obesity
- fatty, fibrous plaques
- occlude the coronary arteries
- reduce volume of blood flow leading to myocardial ischemia
Progression of atheromatous plaque from initial lesion to complex and ruptured plaque
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
SIGNS AND SYMPTOMS
ANGINAANGINA – classic symptom
occurs as burning, squeezing or crushing
tightness in the substernal or precordial chest
- may radiate to the left arm, neck, jaw or shoulder blade
4 MAJOR FORMS OF ANGINA
STABLE – pain that’s predictable in frequency and duration and can be
relieved with nitrates and rest
UNSTABLE – increased pain that’s easily induced
4 MAJOR FORMS OF ANGINA
PRINZMETAL’S or VARIANT – from unpredictable coronary artery spasm
MICROVASCULAR – impairment of vasodilator reserve, which causes
angina-like chest pain in a patient with normal coronary arteries
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
OTHER SIGNS AND SYMPTOMS
NauseaVomiting
WeaknessDiaphoresis
Cool extremities
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
DIAGNOSTICS
ECG – shows ischemiaExercise ECG – provoke chest pain
Coronary Angiography – reveals coronary artery stenosis or obstruction,
shows arteries beyond narrowing
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
DIAGNOSTICS
Laboratory evaluation– to eliminate a diagnosis of MI
Serum lipid studies – to detect hyperlipidemia
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
NURSING DIAGNOSIS
Acute PainDecreased Cardiac Output
Anxiety
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
TREATMENT
MEDICATIONS:Nitrates
AntiplateletsAntilipemics
Beta-adrenergic blockersCalcium channel blockers
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
NURSING MANAGEMENT
Provide care during an acute anginal attack
- Nitrates (SL)-stat 12-Lead ECG
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
NURSING MANAGEMENT
PROMOTE PAIN RELIEF-reduce activity to a point at which pain
does not occur-Position patient for comfort; Fowler's
position promotes ventilation-Administer oxygen if prescribed
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
NURSING MANAGEMENT
MAINTAIN CARDIAC OUTPUT-monitor vital signs, note changes in BP-note patient complaints of headache
(especially with use of nitrates)-evaluate for development of heart
failure
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
NURSING MANAGEMENT
DECREASING ANXIETY-Rule out physiologic etiologies for increasing or new onset of anxiety
-Explain to patient and family reasons for hospitalization
Encourage patient to verbalize fears and concerns
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
SURGERY
Obstructive lesions may necessitate CORONARY ARTERY BYPASS surgery
or PTCA
CORONARY ARTERY DISEASECORONARY ARTERY DISEASE
PREVENTION
Cessation of smokingControl of high BP
Diet low in saturated fat, cholesterolLimit alcohol intakePhysical exercise Weight control
Control of diabetes mellitus
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
refers to a dynamic process by which one or more regions of the heart
experience a severe and prolonged decrease in oxygen supply because of
insufficient coronary blood flow; subsequently, necrosis or death to the
myocardial tissue occurs
Obstruction in a coronary artery resulting in necrosis
Due to: Atherosclerotic plaque
ThrombusEmbolism
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
CLINICAL MANIFESTATIONS
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
CHEST PAIN
Typically, persistent and crushing, located
substernally with radiation to the arm,
neck, jaw and unrelieved by rest or nitrates
CLINICAL MANIFESTATIONS
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
CHEST PAIN
Occurs without cause, primarily early morning
NOT relieved by rest or nitroglycerinLasts 30 minutes or longer
CLINICAL MANIFESTATIONS
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
Diaphoresis, cool clammy skin, facial pallor
Hypertension or hypotensionBradycardia or tachycardia
Premature ventricular and/or atrial beats
Palpitations, severe anxiety, dyspnea
CLINICAL MANIFESTATIONS
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
Disorientation, confusion, restlessness
Fainting, marked weaknessNausea, vomiting, hiccups
Atypical symptoms: epigastric or abdominal distress, dull aching or
tingling sensations, shortness of breath, extreme fatigue
DIAGNOSTICS
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
•ST segment is ELEVATED.
T wave inversion, presence of Q
wave
- Elevated CK-MB, LDH and Troponin levelsCBC - Elevated WBC count
NURSING DIAGNOSIS
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
•Acute Pain•Anxiety related to chest pain, fear of
death, threatening environment•Decreased Cardiac Output related to
impaired contractility•Activity Intolerance
•Risk for Injury (bleeding) related to dissolution of protective clots
MANAGEMENT
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
M – Morphine sulfateO – O2 therapyN – NitratesA – Aspirin/Adequate rest
MANAGEMENT
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
O2 – to increase oxygenation of the bloodNITRATES – to relieve chestpainMORPHINE – for analgesiaASPIRIN – to inhibit platelet aggregation
MANAGEMENT
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
-Relieve pain-Stabilize heart rhythm -Revascularize the coronary artery-Reduce cardiac workload-PTCA
NURSING MANAGEMENT
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
Administer prescribed medications – morphine, nitrates, antilipemics,
thrombolytics, anticoagulants
Provide ongoing assessment-monitor cardiac enzymes
NURSING MANAGEMENT
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
Minimize anxiety
Minimize metabolic demands-institute a liquid diet, advance to a low
sodium, low cholesterol, low fat diet
NURSING MANAGEMENT
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
prepare the client for treatment, such as percutaneous transluminal coronary angioplasty and coronary artery bypass
grafting
HEART FAILUREHEART FAILURE
is a syndrome of pulmonary or systemic circulatory congestion caused by decreased myocardial contractility,
resulting in inadequate CO to meet oxygen requirements of tissues.
HEART FAILUREHEART FAILURE
CLASSIFICATION:
LEFT-SIDED (or left ventricular)
RIGHT-SIDED (or right ventricular)
HEART FAILUREHEART FAILURELEFT-SIDED - congestion occurs primarily in
the lungs from backup of blood into pulmonary veins and capillaries because of
left ventricular pump failure.
As blood backs up into the pulmonary bed, increased hydrostatic pressure causes fluid
accumulation in the lungs.
Blood flow is consequently decreased to the brain, kidneys, and other tissues
HEART FAILUREHEART FAILURERIGHT-SIDED - congestion in systemic
circulation results from right ventricular pump failure.
As blood backs up into the pulmonary bed, increased hydrostatic pressure produces peripheral and dependent pitting edema.
Venous congestion in the kidneys, liver, and GI tract also develops.
HEART FAILUREHEART FAILURECAUSES:
-atherosclerotic heart disease-MI
-hypertension-Rheumatic heart disease-congenital heart disease-ischemic heart disease
-Arrhythmias
HEART FAILUREHEART FAILUREDIAGNOSTICS:
ECHOCARDIOGRAPHY - depressed cardiac output, evidence of
cardiomegalyCHEST X-RAY-reveals cardiomegaly
ABG-decreased partial pressure of arterial O2
HEART FAILUREHEART FAILURECLINICAL MANIFESTATIONSLEFT SIDED HEART FAILURE
-dyspnea on exertion, paroxysmal nocturnal dyspnea, or orthopnea
-crackles on lung auscultation-frothy blood-tinged sputum
-tachycardia with S3 heart sound-pale, cool extremities
-peripheral and central cyanosis
HEART FAILUREHEART FAILURECLINICAL MANIFESTATIONSLEFT SIDED HEART FAILURE
-decreased peripheral pulses and capillary refill
Decreased urinary output easy fatigability
Insomnia and restlessness
HEART FAILUREHEART FAILURECLINICAL MANIFESTATIONSRIGHT SIDED HEART FAILURE
•dependent pitting edema (peripheral and sacral)
•Weight gain•Nausea and anorexia•Jugular vein distention
•Liver congestion, ascites, weakness
HEART FAILUREHEART FAILURENURSING DIAGNOSIS:
Decreased CO related to an ineffective ventricular pump
HEART FAILUREHEART FAILUREPHARMACOLOGIC TREATMENT:
VasodilatorsDiureticsDigoxin
DobutamineBeta-adrenergic blocking agents
(metoprolol, carvedilol)
HEART FAILUREHEART FAILURENURSING MANAGEMENT:
Administer medications as ordered Provide ongoing assessment
-Monitor hemodynamic parameters, HR, rhythm,
-weigh OD Prevent complications of immobility
HEART FAILUREHEART FAILURENURSING MANAGEMENT:
Provide a low-sodium diet, as prescribed
provide client and family teaching
HYPERTENSIONHYPERTENSION
refers to an intermittent or sustained elevation in diastolic or systolic blood
pressure
HYPERTENSIONHYPERTENSION
TYPES:TYPES:ESSENTIAL (IDIOPATHIC) – most
common formSECONDARY – results from a number of disorders that impair blood pressure
regulationMALIGNANT HYPERTENSION –
severe, fulminant form of hypertension common to both types
HYPERTENSIONHYPERTENSION
CAUSES:CAUSES:ESSENTIAL (IDIOPATHIC) –associated
with risk factors such as genetic predisposition, stress, obesity, and a
high-sodium diet
HYPERTENSIONHYPERTENSION
CAUSES:CAUSES:SECONDARY – results from underlying
disorders that impair blood pressure regulation, particularly renal, endocrine,
vascular, and neurological disorders; hypertensive disease of pregnancy
(formerly known as toxemia); and use of estrogen-containing oral contraceptives
HYPERTENSIONHYPERTENSION
CAUSES:CAUSES:
MALIGNANT HYPERTENSION – not known, but it may be associated with
dilation of cerebral arteries and generalized arteriolar fibrinoid necrosis,
which increases intracerebralblood flow, resulting in encephalopathy
Guidelines for Determining Hypertension
Category Systolic Pressure Diastolic Pressure
Normal <120 mm Hg <80 mm Hg
Prehypertension 120-139 mm Hg 80-89 mm Hg
Stage 1 hypertension
140-159 mm H g 90-99 mm Hg
Stage 2 hypertension
>160 mm Hg >100 mm Hg
HYPERTENSIONHYPERTENSION
RISK FACTORSRISK FACTORS
Family history of hypertensionRace (more common in blacks)
GenderDiabetes mellitus
Stress Obesity
HYPERTENSIONHYPERTENSION
RISK FACTORSRISK FACTORS
High dietary intake of saturated fats or sodium
Tobacco use Hormonal contraceptive use
Sedentary lifestyleaging
HYPERTENSIONHYPERTENSIONSYMPTOMS:SYMPTOMS:
blood pressure measurements of more than 140/90mmHg
Throbbing occipital headaches upon waking
DrowsinessConfusion
vision problemsnausea
HYPERTENSIONHYPERTENSION
DIAGNOSTICS:DIAGNOSTICS:
BUN - May be elevatedSERUM CREATININE - determines if
renal dysfunction is present as a complication of hypertension
Total cholesterol, TriglyceridesElectrocardiogram
HYPERTENSIONHYPERTENSION
TREATMENT:TREATMENT:
SECONDARY HPN - correcting the underlying cause and controlling
hypertensive effects
LIFESTYLE MODIFICATIONS: change in diet, relaxation techniques,
exercise, smoking cessation, limited intake of alcohol
HYPERTENSIONHYPERTENSION
TREATMENT:TREATMENT:
DRUG THERAPY
THIAZIDE – for uncomplicated HPNACE INHIBITOR
BETA-ADRENERGIC BLOCKER
HYPERTENSIONHYPERTENSION
TREATMENT:TREATMENT:
DRUG THERAPY
Angiotensin II receptor blockersAlpha-receptor blockers
Calcium channel blockers
HYPERTENSIONHYPERTENSION
NURSING DIAGNOSIS:NURSING DIAGNOSIS:
Knowledge deficit related to chronic disease management
INTERVENTIONS: Health education; Teaching: Diet, Disease process, Health
behaviors, Medication, Prescribed activity, Treatment regimen
INFLAMMATORY INFLAMMATORY DISORDERS OF THE DISORDERS OF THE PERIPHERAL BLOOD PERIPHERAL BLOOD
VESSELSVESSELS
VARICOSE VEINS
• Permanently distended veins that develop from
loss of valvular competency
• Faulty valves elevate venous pressure
• Causes distension and tortuosity
Predisposing Factors
•Pregnancy
•Obesity
•Heart disease
Assessment Findings
•Aching, a feeling of heaviness in the legs
• Itching, moderate swelling
•Superficial inflammation
•Dilated tortuous skin veins
Diagnostic test
• Trendelenberg test:
• Doppler ultrasound– Decrease or no blood flow
heard after calf or thigh compression
Medical Management
THROMBOPHLEBITISTHROMBOPHLEBITIS
-is an inflammation of a vein accompanied by clot or thrombus
formation
DEEP VEIN THROMBOSIS –
veins that are deep in the lower
extremeties
THROMBOPHLEBITISTHROMBOPHLEBITIS
-when inner lining of a vein is irritated or injured, platelets clump together, forming
a clot
Clot interferes with blood flow, causing congestion of venous blood
THROMBOPHLEBITISTHROMBOPHLEBITIS
SIGNS AND SYMPTOMS
-complaints of discomfort in the affected extremity
-Calf pain (+Homan’s sign)-heat, redness, swelling on the affected
vein
THROMBOPHLEBITISTHROMBOPHLEBITIS
DIAGNOSTICS
VENOGRAPHY – indicates a filling defect in the area
of the clot
THROMBOPHLEBITISTHROMBOPHLEBITIS
MANAGEMENT
Complete rest of the affected partanticoagulant therapy (heparin)Continues warm, wet packs – to
improve circulation, ease pain, decrease inflammation
THROMBECTOMY- surgical removal of the clot
THROMBOANGITIS OBLITERANS THROMBOANGITIS OBLITERANS (BUERGER’S DISEASE)(BUERGER’S DISEASE)
Inflammatory, nonatheromatous occlusive condition that causes
segmental lesions and subsequent thrombus formation
- affects small arteries and veins of the legs
THROMBOANGITIS OBLITERANS THROMBOANGITIS OBLITERANS (BUERGER’S DISEASE)(BUERGER’S DISEASE)
CAUSE: -unknown but definite link to smoking
CLINICAL MANIFESTATIONS:-Intermittent Claudication
THROMBOANGITIS OBLITERANS THROMBOANGITIS OBLITERANS (BUERGER’S DISEASE)(BUERGER’S DISEASE)
- No specific treatment exist, except smoking cessation
- Amputation maybe necessary for patients with
gangrene formation
INFECTIOUS AND INFECTIOUS AND INFLAMMATORY INFLAMMATORY
DISORDERS OF THE DISORDERS OF THE HEARTHEART
RHEUMATIC FEVERRHEUMATIC FEVERis a systemic inflammatory disease
that sometimes follows a group A streptococcal infection of the throat
RHEUMATIC CARDITISRHEUMATIC CARDITISrefers to the inflammatory cardiac
manifestations of Rheumatic Fever in either the acute or later stage
RHEUMATIC FEVERRHEUMATIC FEVER
STRUCTURES AFFECTED:
heart valves, praticularly mitral valveendocardiummyocardiumpericardium
RHEUMATIC FEVERRHEUMATIC FEVERSTREPTOCOCCAL INFECTION
Antistreptococcal antibodies attack normal heart cells
� � � � � � � � � � � � � � � � � � � � � � � � � � � �
� � � � � �
Rheumatic carditis develops
RHEUMATIC FEVERRHEUMATIC FEVER
SIGNS AND SYMPTOMS:
most common in children 2-3 weeks after a streptococcal infection
CARDITIS – inflammation of the layers of the heart
RHEUMATIC FEVERRHEUMATIC FEVER
POLYARTHRITIS – inflammation of more than 1 joint
rash, subcutaneous nodules, chorea (characterized by involuntary
grimacing & an inability to use skeletal muscles in coordinated manner
RHEUMATIC FEVERRHEUMATIC FEVERSIGNS AND SYMPTOMS:
mild feverHeart rate (rapid, rhythm abnormal)Red, spotty rash (trunk, disappears
rapidly)Swollen, warm, red & painful joints
RHEUMATIC FEVERRHEUMATIC FEVER
DIAGNOSTICS:
no specific laboratory testsASO titer
ESR, C-reactive protein – elevated,ECG, ECHOCARDIOGRAPHY – structural changes in the heart
RHEUMATIC FEVERRHEUMATIC FEVERMEDICAL MANAGEMENT:
IV ANTIBIOTICS:PENICILLIN – drug of choice
Others: AZYTHROMYCIN (ZYTHROMAX), CLINDAMYCIN,
VANCOMYCINCEPHALOSPORINS: Cephalexin, Cefadroxil
RHEUMATIC FEVERRHEUMATIC FEVER
MEDICAL MANAGEMENT:
ASPIRIN – to control the formation of blood clots around heart valvesSTEROIDS – to suppress the
inflammatory responseBED REST
RHEUMATIC FEVERRHEUMATIC FEVER
MEDICAL MANAGEMENT:
SURGERY may be required to treat constrictive pericarditis and damage to
heart valves
RHEUMATIC FEVERRHEUMATIC FEVER
NURSING MANAGEMENT:
Administer prescribed drug therapy and monitor
for therapeutic and adverse effects
Plan diversional activities that require minimal activity
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
formerly called BACTERIAL ENDOCARDITIS
is inflammation of the inner layer of heart tissue as a result of an infectious
microorganism
MICROORGANISM – bacteria and fungiBACTERIA: Streptococcus viridans,
Staphylococcus aureus
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
SIGNS AND SYMPTOMS:
-can have an acute onset – less than one week
-fever, chills, muscle aches in the lower back and thighs, joint pain
ADVANCE: OSLER NODES - purplish, painful nodules, appear on the pads of the
fingers & toes
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
SIGNS AND SYMPTOMS:
-SPLINTER HEMORRHAGES – black longitudinal lines can be seen in the nails
-JANEWAY LESIONS – small, painless, red-blue macular lesions on the palms
and soles of the feet
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
SIGNS AND SYMPTOMS:
-ROTH’S SPOT – white areas in the retina surrounded by areas of
hemorrhage
-HEART MURMUR – may be present from malfunctioning valves
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
SIGNS AND SYMPTOMS:
-PETECHIAE – tiny red-dish hemorrhagic spots on the skin and
mucous membranes
-weakness, anorexia, weight loss
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
DIAGNOSTICS
-BLOOD CULTURE – to determine microorganism circulating in the blood
-ECG
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
MEDICAL MANAGEMENT
High doses of IV Antibiotics Antibiotic Therapy extends at least 2-
6 weeksBed rest
SURGERY – valve replacement if heart valve is severely damaged
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITISNURSING MANAGEMENTRemind client to limit activity
Assess for changes in weight and pulse rate and rhythm
Administer prescribed antibiotics Inform client that periodic antibiotic
therapy is a lifelong necessity because they will be vulnerable to the disease for
the rest of their lives
MYOCARDITISMYOCARDITIS
is an inflammation of the myocardium (the muscle layer
of the heart)
CAUSES: Viral, bacterial, fungal, or parasitic infections
VIRAL AGENTS: coxsackie virus A & B, influenza A & B, measles, adenovirus,
mumps, rubeola, rubella
MYOCARDITISMYOCARDITIS
Inflammatory response causes the cardiac muscle to swell
Interferes with the myocardium’s ability to stretch and recoil
Cardiac output is reduced and blood
circulation is impaired, predisposing the client to CHF
MYOCARDITISMYOCARDITIS
CLINICAL MANIFESTATIONS:
-sharp stabbing pain or squeezing chest discomfort that resembles a MI (pain is
relieved by sitting up)-Low-grade fever, tachycardia,
dysrhythmias-Dyspnea, malaise, fatigue, anorexia
-Skin is pale and cyanotic
MYOCARDITISMYOCARDITIS
CLINICAL MANIFESTATIONS:
IF THERE’S IMPAIRED HEART’S PUMPING ACTIVITY:
-Neck vein distention, ascites, -Peripheral edema,
-crackles
MYOCARDITISMYOCARDITIS
DIAGNOSTICS:
-WBC – elevated-C-Reactive protein – elevated,
inflammatory conditions-CARDIAC ISOENZYMES-elevated
-CHEST X-RAY – heart enlargement, fluid infiltration in the lungs
MYOCARDITISMYOCARDITIS
MANAGEMENT
Treat underlying cause and prevent complications
ANTIBIOTICS if bacterialBed Rest
Sodium-restricted dietCardiotonic drugs – digitalis to prevent or
treat heart failure
MYOCARDITISMYOCARDITIS
MANAGEMENT
Heart transplant is necessary in severe cases of cardiomyopathy
MYOCARDITISMYOCARDITISNURSING MANAGEMENT
Monitor client’s cardiopulmonary status (daily weights, vital signs, I & O, heart &
lung sounds, edema)Maintain bed rest
Administer antipyretics if patient has feverElevate head of the bed for maximal
breathing potential
CARDIOMYOPATHYCARDIOMYOPATHY
is a chronic condition characterized by structural changes in the heart muscle
TYPES:DILATED CARDIOMYOPATHY
HYPERTROPHIC CARDIOMYOPATHYRESTRICTIVE CARDIOMYOPATHY
CARDIOMYOPATHYCARDIOMYOPATHYDILATED CARDIOMYOPATHY
-dyspnea on exertion & when lying down, fatigue, edema, palpitations, chestpain
HYPERTROPHIC CARDIOMYOPATHY
-syncope, fatigue, shortness of breath, chestpain
-some are asymptomatic
CARDIOMYOPATHYCARDIOMYOPATHYRESTRICTIVE CARDIOMYOPATHY
-exertional dyspnea, dependent edema in the legs, ascites, hepatomegaly
CARDIOMYOPATHYCARDIOMYOPATHYDILATED CARDIOMYOPATHY
-the cavity of the heart is stretched (dilated)
CAUSES: Viral myocarditis, Autoimmune response, chemicals (chronic alcohol ingestion)
TREATMENT: Drug Therapy to minimize symptoms & prevent complications,
abstinence from alcohol, salt restriction, weight loss, possible heart transplantation
CARDIOMYOPATHYCARDIOMYOPATHYHYPERTROPHIC CARDIOMYOPATHY
-the muscle of the left ventricle & septum thickens, causing heart enlargement)
CAUSES: hereditary, unknown
TREATMENT: Drug Therapy to reduce heart rate & force of contraction, antidysrhythmic
drugs, artificial pacemaker
CARDIOMYOPATHYCARDIOMYOPATHYRESTRICTIVE CARDIOMYOPATHY-heart muscle stiffens, which interferes with
its ability to stretch & fill with blood
CAUSES: deposits of amyloid, scleroderma,
TREATMENT: no specific treatment, drugs such as diuretics & antihypertensives used to
control symptoms
CARDIOMYOPATHYCARDIOMYOPATHYTREATMENT:
-DIURETICS-CARDIAC GLYCOSIDES
-ANTIHYPERTENSIVE
PERICARDITISPERICARDITIS
inflammation of the pericardium
PRIMARY – develops independently of any
other condition
SECONDARY – develops because of another condition
PERICARDITISPERICARDITIS
Usually secondary to endocarditis, myocarditis, chest trauma or MI
OTHER CAUSES: tuberculosis, malignant tumors, uremia
PERICARDITISPERICARDITIS
SIGNS AND SYMPTOMSFever and malaise
Dyspnea, or complaints of chest heaviness
PRECORDIAL PAIN (relieved by upright or leaning forward)
PERICARDITISPERICARDITIS
DIAGNOSTICSECG – ST segment elevation (cardiac
isoenzymes normal)ECHOCARDIOGRAPHYWBC & ESR - elevated
PERICARDITISPERICARDITIS
MANAGEMENTRest
DRUGS: Analgesics, antipyretics, NSAIDs, corticosteroids
PERICARDIOCENTESIS – needle aspiration of fluid from between the visceral and parietal pericardium