Structural and heart disorders Flashcards
Infective endocarditis
aka bacterial endocarditis (can be caused by other organisms too)
infection of the heart valves or the endocardial (innermost layer of tissue that lines the chambers of the heart) surface of the heart
blood flow turbulence within heart allows causative organism to infect valves or endothelial surfaces
Endocardium
continuous with valves of the heart so IE effects the heart valves too
Two types of IE
acute (develops suddenly and becomes life threatening in a matter of days)
subacute (develops over weeks/months)
4 categories of IE
informed by site of infection, presence of device, mode of infection
1. L sided native valve IE
2. L sided prosthetic valve IE
3. R sided IE (includes IV drug use)
4. intracardiac and intravascular devices (pacemaker, defibrillator)
what are the risk factors of IE
prior endocarditis, prosthetic valves, acquired valvular diseases, congenital heart defects, cardiac lesions, pneumatic fever
How does IE happen?
vegetations (lesions which are fibrin, leukocytes, platelets, microbes) which form emboli in circulation (fallen off in circulation)
L sided heart vegetations (IE)
progress to the kidney, spleen, small peripheral veins of the arms and legs (causing infarction)
caused by bacterial infection, cocaine abuse
R sided heart vegetations (IE)
embolize in the lungs
Caused by IV use of illicit drugs
What does IE cause?
dysrhythmias, valvular incompetence, invasion in myocardium causing HF, sepsis and heart block
What is the most causative organism of IE?
staphylococcus aureus
When is the risk the greatest in IE?
within first few days of antimicrobial treatment
Manifestations of IE
non-specific: chills, weakness, night sweats, SOB, malaise, fatigue, anorexia, weight loss
LOW GRADE FEVER (may be absent in immunocompromised or older adults)
splinter hemorrhages
Osler’s nodes
Janeway’s lesions
Petechiae
Onset of a new or changing murmur is noted in most pts (aortic and mitral valves)
Splinter hemorrhages
longitudinal streaks in nail beds
Osler’s nodes
painful red or purple pea sized lesions that last 1-2 days
fingertips and toes
Janeway’s lesions
small, flat, painless, red spots on palms of hand
Petechiae
conjunctivae of the eyelids and whites of the eyes, buccal mucosa and sometimes in the extremities
Manifestations of IE secondary to embolization
spleen: sharp, LUQ pain, local tenderness
kidneys: pain in flank, hematuria and azotemia (increased BUN)
peripheral BV: gangrene
brain: hemiplegia, ataxia, aphasia, visual changes, LOC changes
Diagnosis of IE
health history (recent surgeries or dental work, valvular disease, rheumatic fever, congenital heart defects, IV drug use, intracardiac prosthetic device, resp/urinary infection, recent cardiac categorization)
lab data (BLOOD CULTURES)
Echocardiograms
ECG
CXR
possible cardiac catheterization to evaluate coronary artery patency and valvular function when surgery is considered
Management of IE
- prophylactic tx (abx for pts with specific cardiac conditions prior to certain surgical or dental procedures - prevents infection from even happening)
- Drug therapy (success of tx is dependent on identifying causative organism, abx tx should be started as soon as results of blood culture returns, long term tx is needed for removing dormant bacteria clustered within vegetation, vlave replacements are very likely to be needed)
Overall goal of IE management
- normal/baseline cardiac function
- ADL without fatigue
- prevent recurrence of endocarditis
Health promotion of IE
TEACHING IS CRITICAL
avoid ppl with infections, report early signs of infection, avoid fatigue, good oral hygiene, regular dental visits, inform providers of IE hx
prophylactic tx before procedure is important
if hx of IV drug use –> need drug tx program
ambulatory and home care (abx for 4-6 weeks, adequate physical and emotional rest at home, repeat blood culture to see effectiveness of abx)
Acute Pericarditis
the inflammation of the pericardial sac
pericardium
composed of inner serous membrane (visceral pericardium) which closely adheres to the epicardial surface of the heart and outer fibrous (parietal) layer
Pericardial space
the cavity between the 2 layers, contains 10-30 ml of serous fluid (protects heart)
What causes acute pericarditis?
- infectious: viral, bacterial, fungal
- non-infectious: acute MI, radiation, neoplasm (tissue growth - benign or malignant)
- hypersensitive (drug rxn) or autoimmune
2 syndromes in acute MI
acute pericarditis (within 48-72 hours)
Dressler’s syndrome (after 4-6 weeks)
Dressler’s syndrome
immune response after damage to the heart tissue/pericardium or inflammation of sacs surrounding heart (influx of neutrophils - causes shaggy fibrin heart)
Manifestations of acute pericarditis
most common = progressive, severe chest pain (sharp, pleuritic)
- worse with deep inspiration and on supine position, relieved in upright pos
- dyspnea (rapid shallow breaths to avoid chest pain)
HALLMARK - pericardial friction rub (scratching, grating sound - like walking on snow). Arises from roughened pericardial and epicardial surfaces rubbing against eachother - best heard in L sternal boarder with pt leaning forward
Complications of acute pericarditis
- pericardial effusions (accumulation of access fluid in pericardium)
- Cardiac tamponade (develops as fluid accumulates in the pericardial sac - causes increase in pressure and compresses the heart)
Manifestations of cardiac tamponade
heart sounds become muffled (heart pressure)
pt will c/o chest pain, confused, anxious, restless, tachypnea and tachycardia as pressure increases
management is pericariocentesis
Diagnosis and management of acute pericarditis
ECG, labs (leukocytosis, elevated CPR and ESR - inflammation markers)
treat underlying problem (abx for bacterial pericarditis)
pain and inflammation (NSAIDs or ASA)
Colchicine (used for gout) –> will decrease inflammation in the heart
pericardiocentesis –> if drainage necessary (removes build up of fluid in the pericardium)
bedrest and pain relief
HOB over 45 degrees
Rheumatic fever
an inflammatory disease that may affect several connective tissues (heart, brain, joints, skin)
causes scarring and deformity of heart valves
involves all layers of the heart (endo, myo, peri)
Acute rheumatic fever (ARF)
complication of A streptococcal pharyngitis (strep throat)
Rheumatic endocarditis
swelling and erosion of valve leaflets (where vegetations form - deposits of fibrin and blood)
- causes thickened and calcified, which causes stenosis (reduction of mobility and failure of valves)
Regurgitation
reduction of mobility and failure of valves
Manifestations of rheumatic fever
chest pain
excessive fatigue
heart palpitations
dyspnea
swollen ankles, wrists or stomach
Rheumatic fever criteria
MAJOR:
carditis
mono/poliarthritis
chorea (sydenham)
erythema margination
MINOR:
fever
lab findings (increased ESR, increased WBC, increased CRP)
ECG findings: prolonged PR interval)
the presence of 2 major criteria OORRR 1 major and 2 minor criteria + strep infection*
= high risk
What are the 2 atrial ventricular valves?
mitral and tricuspid
What are the 2 semilunar valves?
aortic and pulmonic
Valvular heart disease is defined according to…
- valve(s)
- functional alteration (stenosis or regurgitation)
Stenosis (VHD)
functional alteration
valve orifice restricted
forward blood flow impeded, causing change in pressure gradient across open valve (pressure increase b/c increase resistance to flow)
How should blood flow through vessel/across heart valve happen?
must be a force propelling the blood (a difference in pressure across valve)
for pressure gradient flow rate to be adequate, there must be resistance of flow
normal= very small resistance flow/small pressure gradient, valve opens easily
Regurgitation (VHD)
Functional alteration
aka valvular incompetence or insufficiency
complete closure of valve leaflets
results in backward flow of blood
Mitral Stenosis
valve doesn’t open all the way - not enough blood passing though
most causes of rheumatic mitral stenosis
rheumatic endocarditis causes scarring of valve leaflets and chordae tendineae (contractures and adhesions b/w commissures, structural deformities, obstruction of blood flow, results in pressure diff b/t LA and LV)
increased pressure increases volume of LA which increases pulmonary vascular pressure (as the LA tries to press harder on LA, high resistance causes blood to back up in LA and increase pressure (causing pulmonary HTN)
Manifestations of mitral stenosis
exertional dyspnea (decreased lung compliance)
atrial fib (fatigue, palpitations)
hemoptysis (coughing up blood) –> caused by pulmonary HTN
Mitral regurgitation
incomplete mitral valve closure
R/T defect form any heart structure
most cases by MI, rheumatic heart disease, mitral valve prolapse, ischemia or papillary muscles or infection carditis
blood flows backward from LV-LA during systole
LA and LV have to work harder to generate CO
eventual enlargement of LA, ventricular hypotrophy and dilation
What happens with acute mitral regurgitation?
LA and V cant dilate cause sudden increase in pressure and volume causing pulmonary edema and shock
Manifestations of mitral regurgitation
acute: thready pulse, cool, clammy ext.
chronic: may be asymptomatic
symptoms of LV failure: weakness and fatigue from decreased CO, dyspnea develops into orphognia (nocturnal), exertional dyspnea, increased CO
Aortic stenosis
causes thickening and narrowing of LV and aorta (causes smaller opening from blood to flow through)
blood flow to heart and body is decreased/blocked
congenital, childhood, adolescence or young adulthood
Aortic stenosis in older adults
results in rheumatic fever or degeneration
Aortic stenosis in rheumatic fever
fusion of commissures and calcification
causes valve leaflets to stiffen and retract
causing stenosis
mitral valve disease accompanies it
Aortic stenosis manifestations
symptoms develop when valve orifice decreases to 1/3 or normal size
classic triad:
1. angina
2. syncope
3. exertional dyspnea
What is NOT recommended with aortic stenosis?
use of nitro because it reduces preload and preload is necessary to open the stiffened aortic valve and can causes decreased BP
Aortic regurgitation
may be a result of primary disease or aortic valve leaflets or aortic root
backward blood flow from aorta, into LV when aortic V should be closed (results in volume overload)
Acute aortic regurgitation
from IE, trauma, aortic dissection
Chronic aortic regurgitation
generally results from rheumatic heart disease, congenital bicuspid aortic valve, syphilis
Systole
when heart sends blood out
Diastole
heart fills with blood
Clinical manifestations of aortic regurgitation
acute: sudden severe dyspnea, chest pain, shock
chronic: exertional dyspnea, fatigue, orthopnea, paroxysmal nocturnal dyspnea, normally asymptomatic until myocardial dysfunction has occurred, water hammer pulse (a strong, quick beat that collapses)
Conservative management of valvular heart diseases
prevention of recurrent rheumatic fever and IE
depends on valve involved and severity of disease
preventing exacerbation of HF, acute pulmonary edema, thrombo embolism and recurrent IE
If no signs of HF: may need vasodilators, pos inotropes (epinephrine) - makes heart contract more powerfully, beta blockers (slows and strengthens the heart), low sodium diet (fluid goes where salt is), diuretics
percutaneous aortic valve replacements
percutaneous transluminal balloon valvuloplasty
surgical
Percutaneous aortic valve replacement
for people who are at high risk for surgical tx
replacements via femoral artery
Percutaneous transluminal balloon valvuloplasty
splits open fused commissures
used for mitral, tricuspid, pulmonic (less often for aortic)
surgical for valvular heart disease
all types of valve surgery are palliative not curative and the pt will require life long health care
prosthetic valves
1. mechanical
- more durable and last longer, increased risk of thromboembolism, require long term anticoagulant therapy
2. Biologic (tissue)
- from animals
- foes not require anticoagulant therapy, less durable
Diagnosis of valvular heart disease
based on:
hx
physical exam
echocardiogram (valve structure, function, chamber size)
cardiac catheterization (especially for surgically option) - pressure changes in cardiac chambers, measures pressure gradients across valves, quantifies the size of valve openings
Nursing post op care in ICU (VHD)
hemodynamic monitoring (continuous VS q15min, 12 lead ECG)
resp: ventilation, routine ABGs, CXR
Pain control (IV morphine, start PO T3) - start oral intake post extubating
accurate I and O (managements of blood loss, chest tube output q1h, U/O CVP q1h)
N/G to intermittent low suction
wound: sternal incision (look for signs of infection)
mobility: post extubating, PT (can only turn pt with exubated)
Nursing post op care in step down unit (VHD)
head to toe physical assessment
pain control (PO)
titrate O2 to maintain SPo2>95% (with NP)
D/C CVP line, chest tubes, foley cath
get patient to sit up on edge of bed or in chair
electrolyte replacement (diuretics)
resume cardiac meds (beta blockers) and pre-op meds and SC heparin
DB and C q1h when awake and mobilize
daily BW and wieghts
