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Causes of cardiac valve disease
Congenital​
Acquired​
Infectious or non-infectious endocarditis​
Degenerative
Classifications of valve disease
Stenosis
Regurgitation/Insufficiency
Stenosis
Problem of valve OPENING​
Narrowing of valve​
Chamber behind the diseased valve will HYPERTROPHY as it will have to work harder to pump blood through a narrowed opening
Regurgitation/Insufficiency
Problem of valve CLOSURE​
Blood is ejected backwards​
Chamber behind the diseased valve will eventually DILATE to accommodate for the extra blood
Symptoms associated with valve disease
Often asymptomatic as body will compensate ​
Eventually, signs of cardiac muscle dysfunction will begin to show ​
Dyspnea​
Heart palpitations​
Chest pain​
Fatigue​
Type and severity of symptoms will vary based on what valve(s) is(are) affected and how advanced the problem is
Diagnosis
Echocardiography ​
Non-invasive​
Real time​
Option for stress ECHO​
Allows for monitoring immediately post-exercise
Transesophageal ECHO (TEE)
Requires sedation​
Allows for better visualization​
Often used during/after surgery
Mitral Valve Stenosis
Mitral valve between L atria and L ventricle doesn’t open properly​
Commonly secondary to rheumatic heart disease​
Other causes​
calcifications, valve inflammation, can be congenital, autoimmune​
Women > men​
Can auscultate snap with opening and slowed closing causes murmur
Mitral Valve Stenosis
Let’s talk through what is going to happen:​
What chamber will we see a build-up of pressure?​
What will happen to End Diastolic Volume?​
What will happen to cardiac output?​
Will EF change?
L atrium
decrease
decrease
no
Complications of Mitral Valve Stenosis
Enlarged atrium beats irregularly → development of atrial fibrillation​
Increased risk for blood clots ​
Severe cases​
Significant reduction in cardiac output → dyspnea, fatigue​
Pulmonary venous congestion from back-up into pulmonary circulation ​
Difficulty laying flat
Medical Management
Severe cases: surgery​
Valve repair or replacement​
Pharmacology: to manage a-fib
Mitral Valve Regurgitation
Occurs secondary to ischemic heart disease, endocarditis, cardiomyopathy​
MV should be closed during systole​
Instead of all blood going through the aortic valve and into systemic circulation, some is pushed back through the still open MV​
Can be acute or chronic; with chronic cases we will see delayed symptoms like what we discussed with stenosis​
Can be treated with valve repair, but not common
What is going on at the left ventricle to maintain cardiac output as regurgitation worsens?
hypertrophy from attempting to pump harder
Mitral Valve Prolapse (MVP)
Cause unknown​
Structural abnormality in valve leaflets lead one or both to bulge back into atrium during ventricular systole​
Can causes mitral valve regurgitation​
Often a benign condition
Mitral Valve Prolapse
Symptoms include
Managed with drugs to decrease
Symptoms include fatigue, palpitations, and dyspnea (but many will be asymptomatic)​
Managed with drugs to decrease arrhythmias, decreasing caffeine and smoking, antibiotics prior to dental procedures due to increased risk of endocarditis
Aortic Valve Stenosis
Disease of aging​
Age 60-65 commonly start to become symptomatic​
Valvular calcification​
Risk factors are the same for ischemic heart disease and HTN
Complications from Aortic Valve Stenosis
Where will we see a build-up of pressure?​
What is going to happen to cardiac output?​
What about EF?​
How well is body being perfused?​
What will this mean for the patient? What symptoms do you think the patient will present with?​
What do you think about exercise and the patient with severe aortic stenosis?​
LV
decrease
will eventually decrease
perfusion will decrease
fatigue, dizziness, chest pain
contradicted
focus on functional mobility
What do you think vitals will look like in the patient with severe aortic stenosis?
Heart rate​
Blood pressure​
Respiratory rate​
Oxygen saturation
Heart rate​
increase
Blood pressure​
decrease at rest; will not rise with exercise
Respiratory rate​
increase
Oxygen saturation
decrease
Aortic Stenosis Medical Management
Can be difficult to assess​
Pharmacological intervention not primary management​
Valve replacement surgery​
Need to monitor for infective endocarditis
Aortic Valve Regurgitation/Insufficiency
Causes: infective endocarditis, congenital, HTN, rheumatic fever​
Aortic blood flow leaks back into LV​
Dilation and LVH to compensate to maintain cardiac output​
When this can no longer keep up, symptoms of fatigue, exertional dyspnea occur​
Treated with valve repair/replacement
Valvotomy
Like a PTCA for the valves​
Minimally invasive​
Dilates the valve
Annuloplasty
Used in mitral and tricuspid repair​
Replaces the annulus, or rim, of these valves
Valve Replacement
Mechanical
Tissue
Mechanical
Metal or synthetic material​
Highly durable​
Require lifelong anticoagulation therapy
bc body starts to attack it → blood clots
should last a good amount of time
increased risk of internal bleeding
Tissue
Bovine or porcine; or allograft​
Only last 10-20 years​
No need for lifelong coagulation therapy​
Ross procedure: replace aortic valve with pulmonary valve and replace pulmonary valve with homograft
New Lab Value: INR
International Normalized Ratio (INR) looks at time to clot​
Used to use prothrombin time, but there were differences when comparing results across laboratories and INR allows for values to be comparable no matter who runs the test
Increased INR (supertherapeutic)​
Causes​
ETOH​
Use of anticoagulants​
Liver disease​
Vitamin K deficiency ​
Presentation​
Increased bleeding risk​
Bruising​
Oozing from wounds​
Clinical Implications​
Screen for falls​
Apply prolonged pressure if injury does occur​
Manual BP (not automatic)​
Monitor cognition/alertness as changes may indicate intercranial bleed​
Patient education on safety; problems with contact sports​
Interprofessional communication for safe mobility and physical activity
Decreased INR (subtherapeutic)​
Increased risk for
Patient may need drug from another
Increased risk for clot development​
Patient may need drug from another anticoagulant class to bridge the gap while coumadin (warfarin) dose can be adjusted
More on INR
Preferred Adult Range according to indication for anticoagulation: ​
DVT prophylaxis: 1.5-2.0 ​
History of TIA or CVA and aortic valve replacement: 2.5-3.5 ​
Pulmonary embolism: 2.5-3.5 ​
DVT, atrial fibrillation, mitral or aortic valve replacement, orthopedic surgery 2.0-3.0​
what we need to know
Possible Critical Value: Greater than 5.5
Transcatheter Aortic Valve Replacement​
Transfemoral, transapical, or transaortic approaches​
This approach can only be done for tissue valves (not mechanical )
Pharmacology Associated with Valve Disease​
ACE inhibitors:
Antiarrhythmic meds:
Antibiotics:
Beta-blockers:
Anticoagulants:
ACE inhibitors: vasodilation, decrease cardiac workload​
Antiarrhythmic meds: maintain regular beat​
Antibiotics: if infection​
Beta-blockers: decrease myocardial oxygen demand​
Anticoagulants: prevention of blood clots
New Lab Value: White Blood Cells (WBC)
White blood cells play a role in immune response​
WBC is used to look for:​
Infection​
Inflammation​
Allergic reaction​
Cancers of blood and lymphatic system​​
Reference: 5,000-10,000 mm3​
Critical <2,500 or >30,000
White Blood Cells
trending upward
trending downward
trending upward
Leukocytosis
Causes: infection, inflammation, bone marrow disease, immune system disorder, severe stress/pain​
Presentation: fever, fatigue, bleeding, bruising, frequent infections​
Clinical implications: watch for signs of multisystem involvement; think about scheduling after early morning low and late afternoon high peak
trending downward
Leukopenia
Causes: chemo, radiation, infections, marrow infiltrate, autoimmune disease​
Presentation: frequent infections, ulcers in mouth, headache, stiff neck, sore throat, fever, chills, night sweats​
Clinical implications: refer to facility specific guidelines, watch for signs of infection, consider use of RPE scale, look at Absolute Neutrophil Count (ANC) and consider reverse precautions if <1,000
Infective Endocarditis
Infection of inner lining of the heart​
Mitral valve most commonly affected valve​
Multiple valves could be infected at once​
Can be acute or subacute​
Much more common in older adults ​
Men > women
Why does endocarditis occur?
Bacteria from another site (mouth, respiratory track, GI tract) travel to the heart and cause inflammation​
Enzymes try to come and fight off the infectious agents but end up further damaging cardiac connective tissue​
End result is vegetative growths which can break off (similar to an atherosclerotic plaque) and lead to an infection elsewhere in the body or a thrombus that could lead to infarction​
Typically, this is more common in those that have existing valve damage​
Also seen in those that use IV drugs (including patients with IV ports for long times)​
Can also include those after valve repair​
Those who are immunosuppressed​
Can occur after dental procedures ​
Also common to see hospital acquired endocarditis
Clinical Manifestations of infective endocarditis
Can develop over time or rapidly​
Systemic infection​
Fever, malaise, weight loss, etc. ​
Intravascular signs​
Chest pain, CHF, clubbing​
Immunologic signs ​
Joint pain, blood in the urine​
MSK signs​
Joint pain, muscle pain, low-back pain​
Neurologic signs ​
Confusion, meningitis, stroke
PT considerations with endocarditis
Early signs include joint pain ​
Proximal joints usually affected first​
Don’t c/o morning stiffness (differentiation from RA)​
Low back pain ​
Could our patient have a systemic disorder?​
Are they improving as anticipated?​
S/S of infection?​
Risk factors?​
For those with a known diagnosis of endocarditis​
Limited exercise capacity on antibiotics ​
Prioritize mobility over exercise
Rheumatic Fever
One cause of endocarditis ​
Typically starts as strep throat and then causes heart damage 50% of the time​
Use of specific antibiotics has decreased incidence in the US, but endemic in lower- and middle-income countries
Pericarditis
Inflammation of the outer lining of the heart​
Can be acute or chronic​
Typical causes:​
IV drug use​
Associated with autoimmune disorders (lupus, RA)​
After an MI or open-heart surgery​
After radiation therapy (lung/breast cancer)​
Can be associated with viruses and tumors
Pericarditis
What is happening here? ​
What kind of dysfunction (systolic vs. diastolic) will we likely see?​
What happens with stroke volume? ​
Cardiac output?​
Ejection fraction?
What is happening here? ​
inflammation
What kind of dysfunction (systolic vs. diastolic) will we likely see?​
filling problem
diastolic
What happens with stroke volume? ​
decreases
Cardiac output?
decreases​
Ejection fraction?
stays the same
Differential Diagnosis
Timeline​
Did the patient just have a heart attack?​
Recent radiation therapy? ​
Clinical exam​
Pericardial friction rub (lower left sternal border)​
CXR​
Lab values (WBC, erythrocyte sedimentation rate)​
Chest pain ​
Sharp, stabbing; not increased with activity​
Worsens with changes in breathing patterns (laughing, coughing, deep breathing, increased when laying down)​
Fever​
Fatigue​
Weakness
Treatment
Need to treat the underlying cause if bacterial​
Supportive​
Anti-inflammatory drugs​
Inotropes (enhance contraction)​
Pericardiocentesis to remove fluid from pericardial effusion ​
Surgery​
In the case of chronic, constrictive pericarditis​
Pericardium can be resected