Structural and Heart Disorders Flashcards
-Distinguish the difference between
inflammatory and structural heart
diseases in terms of etiology,
pathophysiology and clinical
manifestations.
*Identify collaborative care and
nursing management of
inflammatory and structural heart
diseases.
- Describe etiology, pathophysiology
and clinical manifestations of
valvular heart diseases. - Identify collaborative care and
nursing management of valvular
heart diseases.
Infective Endocarditis (IE)(aka) bacterial endocarditis
def: infection of the heart valves, or the endocardial surface of heart.
Blood flow turbulence within heart allows causative organism to infect valves or endothelial surfaces
Acute vs. Subacute (or chronic)
-an Acute infective endocarditis develops suddenly and may become life-threatening within days
-subacute develops over weeks-months
4 categories of IE (informs site of infection, presence of device, mode of infection)
-Left-sided native valve IE
-Left-sided prosthetic valve IE
-Right-sided IE (includes IV drug use)
-Intracardiac & intravascular devices (e.g., pacemaker, defibrillator)
IE Etiology & Pathophysiology
Gram Positive organisms are responsible for over 80% of IE
gram pos easier to kill than neg
Most common causative organism : staphylococcus aureus
Vegetations: primary lesions of IE- fibrin, leukocytes, platelets, microbes
Vegetations can form emboli when they fall off into circulation
emboli → portion of vegetation falls off into circulation (22-50%)
Left to the __brain, kidneys, spleen, small peripheral veins in the arms and legs____________and Rt to the __lungs________
Risk is greatest within the first few days of starting antibiotic therapy
Left – most common with bacterial infections
Right sided: most common with the use of illicit drugs
infective endocarditis
S/s
Nonspecific:
-Low-grade fever in >90%, may be absent in immunocompromised pts or older adults
-Chills
-Weakness
-Night sweat
-SOB
-Malaise, Fatigue
-Anorexia, Weightloss
-Splinter hemorrhages: longitudinal dark streaks in nail bed
-Osler’s nodes: Painful tender, red or purple pea-sized lesions that last 1-2 days
-Janeway’s lesions: flat painless small red spots on plams/soles of hand
-Petechiae: found in the conjunctiva of inside of the eyelid, whites of the eyes, and buccal mucosa, sometimes extremities
Embolism manifestations-
in the spleen:
-sharp left UQ pain, enlarged spleen
In the kidneys:
-Pain in the flank, blood in urine, increased BUN
Diagnosis:
Health hx: need to know any recent sx or dental work, hx of valvular disease, rheumatic fever, or congenital heart defects, IV drug use, intracardiac prosthetic devices, resp or urinary infections, recent cardiac catheterization
Lab data especially blood cultures
Echocardiograms
ECG
Chest X-ray
Possible cardiac catheterization to evaluate coronary artery patency and valvular function when surgery is being considered
Prophylactic treatment
-Abx prophylaxis for pts with specific cardiac conditions (ex. prosthetic heart valves, hx of congenital HD) prior to certain _surgical__ or _dental_procedures – to prevent infection
Drug therapy
-dependant on identifying the causative organism
-abx treatment should be started as soon as results of blood culture returns or if IE highly likely
-Long term tx needed for eradicating dormant bacteria clustered within vegetation. Complete eradication takes weeks to achieve.
-Valve replacements needed in more then 25% of cases.
-Fungal infections respond poorly to abx and need surgical debridement
Nursing interventions:
goals:
-Normal or baseline cardiac function
-ADL without fatigue
-Prevent recurrence of endocarditis
Health promotion:
-Avoid people with infections
-report any early signs of infection
-avoid fatigue
-good oral hygiene
-regular dental visits
-inform provider of hx of IE before any procedure so they can receive prophylactic therapy
-if they have hx of IV drug use they need a drug tx program
-Ambulatory & Home Care
Abx treatment for _4-6___ week
Adequate physical and emotional rest at home
Repeat blood culture – assess effectiveness of abx
therapy
Acute Pericarditis
Inflammation of pericardial sac (pericardium)
-Double-walled sac containing the heart and roots of the great vessels
-It has 2 layers: strong+ineleastic connective tissue outer ’fibrous pericardium” and inner layer of serous membrane “serous pericardium”
-serous pericardium encloses the pericardial cavity and contains ~10-30 ml serous fluid
Etiologies:
1. Infectious (viral, bacterial, fungal)
2. Non-infectious (acute MI, radiation, neoplasm)
Neoplasm: tissue growth that can be benign or
malignant
3. Hypersensitive (drug reaction) or Autoimmune
Pericarditis in acute MI
-2 distinct syndromes
1. acute pericarditis ( within 48 - 72 hrs)
2. Dressler’s syndrome (after 4 - 6 wks)
Dressler’s syndrome: Immune system response
after damage to heart tissue or the
pericardium due to inflammation
Shaggy coat of fibrin
inflammatory response: influx of neutrophils → characteristics of acute pericarditis
S/s:
-Most common symptom: progressive, severe chest pain→ sharp, pleuritic in nature
-worse with deep inspiration and in supine position, relieved in upright position.
-dyspnea – rapid shallow breaths, to avoid chest pain
-Hallmark of acute pericarditis → pericardial friction rub (scratching, grating sound, like walking on snow)
heard in Left sternal border of the chest with pt
leaning forward
Complications:
-Pericardial effusion - Accumulation of excess fluid in the pericardium
-Cardiac tamponade – develops as fluid accumulates in pericardial sac, causes increase in pericardial pressure = compresses the heart = heart sounds are muffled, chest pain, confusion, restlessness, anxious, tachycardia, tachypnea,
triad: hypotension, JVD, muffled heart sounds
Diagnosis:
-ECG, labs- Leukocytosis, elevated CRP and ESR (inflammation)
tx:
-treat underlying problem, e.g., abx for bacterial pericarditis
-pericardiocentesis → if drainage necessary to relieve pressure usually in cardiac tamponade
-Colchicine – used to tx gout but can reduce inflammation in the heart
Nursing interventions:
-pain and inflammation → NSAIDS or high-dose ASA
-bedrest & pain relief
-HOB ↑ 45º
Rheumatic Fever and Heart Disease
An inflammatory disease that may affect several connective tissues, such as heart, brain, joints or skin
Result of rheumatic fever → characterized by scarring & deformity of heart valves
Involves all layers of the heart (endo-, myo-, and pericardium)
Acute rheumatic fever (ARF) is a complication of A streptococcal pharyngitis (strept throat)
40% of ARF episodes are marked by carditis
Rheumatic endocarditis→ swelling & erosion of valve leaflets, on which vegetations form (deposits of fibrin & blood)→ thickening of valves and fusion of commissures and chordae tendineae →valves becomes thickened and calcified →stenosis
reduction of mobility with failure of valves →
regurgitation
S/s:
minor criteria:
-Chest pain
-Excessive fatigue
-Heart palpitations
-Dyspnea
-Swollen ankles, wrists, or stomach
Major criteria:
-Carditis
-Mono- or polyarthritis
-Chorea (Sydenham chorea)
-Erythema marginatum
Chorea- involuntary movement disorder caused by overactivity of the neurotransmitter dopamine
erythema: inflammatory skin rash caused by injured/inflamed blood capillaries
(2 minor, 1 major) OR (2 major) + a streptococcal infection = high probability of ARF (acute rheumatic fever)
Valvular Heart Disease
2 AV valves: mitral & tricuspid
2 semilunar valves:
aortic & pulmonic
defined according to:
-which Valve (s)
-Functional alteration:
Stenosis
or
Regurgitation
Functional alteration
stenosis
vs
regurgitation
Stenosis: pressure across the open valve increaeses
Valve orifice restricted
Forward blood flow impeded
valve narrowed
Regurgitation: (aka) valvular incompetence or insufficiency
Incomplete closure of valve leaflets
Results in backward flow of blood
Mitral stenosis
Most cases: dt rheumatic heart disease
rheumatic mitral stenosis → most prevalent in developing countries
Rheumatic endocarditis causes scarring of valve leaflets & chordae tendineae
contractures & adhesions between
commissures → structural deformities →
obstruction of blood flow → results in pressure
difference (pressure difference between LA
(left atrium) & LV
increase volume and pressure in LA -> backs up into pulmonary vasculature -> pulmonary hypertension
S/s:
-Exertional dyspnea
d/t ↓ lung compliance
-Atrial fibrillation
-Fatigue, palpitation
-Hemoptysis
-Pulmonary hypertension
Mitral regurgitation
Incomplete mitral valve closure
R/T defect from any of:
Mitral leaflet, mitral annulus, chordae tendineae, papillary muscles, LA & LV
Most cases by MI, chronic rheumatic heart disease, MVP (mitral valve prolapse), ischemia of papillary muscles, or Infective Carditis
Blood flows backward from LV→ LA (during systole)
LA and LV have to work harder to generate adequate CO
Eventual enlargement of LA, ventricular hypertrophy and dilatation
Acute mitral valve regurgitation: the LA and LV can’t dilate= sudden increase in volume and pressure =pulm edema and shock
S/s:
Acute MR:
Thready pulses, cool, clammy extremities
Chronic MR:
May be asymptomatic for years
Symptoms of LV failure
LV failure:
-weakness, fatigue dt decreased CO.
-dyspnea gradually progressing to orthopnea,
-nocturnal resp distress that awakens pt from sleep
-exertional dyspnea (high CO is needed but unable to provide dt mitral stenosis)
Normal:
Valve opens fully and blood flows thru
Valve closes tightly, no back flow
Stenosis: valve doesn’t open all the way = not enough blood passes through
Regurgitation: valve doesn’t close all the way = blood leaks backward
Aortic valve
Aortic Valve Stenosis
causes:
Congenital aortic stenosis (AS)
-Usually discovered in childhood, adolescence, or
young adulthood
-Usually the aortic is tricuspid = has three cusps.
Some people are born with 2 cusps (congential
bicuspid aortic valve)
In older adults
Result of rheumatic fever or degeneration.
In rheumatic fever: fusion of commissures and secondary calcification → causes valve leaflets to stiffen and retract→ results in stenosis.
If AS is from rheumatic fever, mitral valve disease accompanies it.
Causes obstruction of blood flow from LV to aorta during systole → LV hypertrophy and ↑ myocardial O2 consumption
AVS: Causes thickening and narrowing of valve between main pumping chamber (LV) and main the main artery (aorta). The narrow opening creates a smaller opening. Flow to body is reduced.
Symptoms develop when valve orifice ↓ to 1/3 of its normal size.
Classic triad:
1. angina
2. syncope
3. exertional dyspnea
Use of nitro not recommended because it reduces preload and preload is necessary to open the stiffened aortic valve and Nitro can also cause significant decrease in BP.
Preload- amount of stretch the heart has at its most full, right before it empties. Preload requires enough blood to fill the chambers and requires the muscle to stretch enough (this is why nitro should not be used – because it reduces preload)
