Chronic Cardiac Disease

1. Has the patient's level of activity decreased since last visit?

• Beta blockers, diltiazem, or verapamil.
• Endocarditis prophylaxis only for those with frank mitral regurg on echo.

• Mid-systolic click, and late systolic murmur.
• Frequently in young, healthy and asymptomatic women.
• However, some is associated with palpitations, chest pain, or postural syncope.

• Acute mitral regurg is a medical emergency requiring vasodilators or intraaortic ballon counterpulsation to improve forward cardiac output. Surgical valve correction is standard therapy for mitral regurg.
• Asymptomatic individuals may be followed until left ventricular ejection fraction falls below 60% or end systolic dimension exceeds 45 mm.
• Endocarditis prophylaxis

• Signs of left heart failure,
• Holosystolic apical murmur that radiates to axilla.

myxomatous valve degeneration, ischemic heart dz, endocarditis, or chordal rupture.

• Diastolic rumble that follows an opening snap.
• Medical tx includes diuretics and ABX prophylaxis.

DOE, orthopnea, PND. As pulmonary HTN develops->hemoptysis.

typically sequela of rheumatic heart dz

• water-hammer bounding pulse, systolic HTN, blowing murmur at left sternal border. Patient often presents with signs of left heart failure (dyspnea, orthopnea, PND).
• Tx: dihydropyridine CCB's or an ACE with endocarditis prophylaxis.

Age-associated changes in aortic root or injury to valve leaflets that is most often produced by infective endocarditis or rheumatic fever.

• Systolic crescendo-decrescendo (diamond shaped) cardiac murmur heard in aortic area that radiates to neck.
• Need prophylaxis against endocarditis!

• Assume the following are pathologic until proven otherwise:
• 1. Diastolic or continuous murmurs
• 2. holosystolic or late systolic murmurs
• 3. Grade 3 or higher murmurs
• 4. Grade 1 and 2 murmurs with other cardiac signs and symptoms.

• 1. is this murmur significant to patient's health?
• 2. Is therapeutic intervention warranted?
• 3. When is medical or surgical therapy indicated?

• Patients with intermittent, stable, but symptomatic episodes of SVT.
• Non-dihydropyridine CCB's
• Beta blockers
• Digoxin
• For long term suppression.

A combination of bradycardia and tachycardia most often fount in elderly patients., caused by sinus node dysfunction secondary to ischemia, inflammation, or scarring. Significant SSS that is accompanied by syncope or other symptoms may require placement of a pacemaker.

• Look for underlying causes: serum electrolytes, oxygenation, acid-base status, med related effects, hyperthyroidism, cocaine, caffeine, alcohol etc.
• Symptomatic patients with underlying cardiac disease should be referred to cardiologist for electrophysiologic testing and possibly arrythmia suppression therapy or defibrillator

• Risk factors:
• Congestive heart failure: 1 pt
• HTN: 1pt
• Age older than 75: 1pt
• DM: 1 pt
• Stroke or TIA: 2 pts
• High: 3 or more points
• Moderate: 1-2 pts
• Low: 0

• High risk: History of stroke or TIA, HTN, heart failure, age older than 75 years, or at least 2 moderate risk factors.
• Moderate risk: Age 65 to 75 years, DM or coronary artery dz; not high risk.
• Low risk: not moderate or high risk.
• If high risk->coumadin,
• Low risk->aspirin

Rate control with chronic anticoagulation.

• New onset a-fib in patients who are unstable, or have difficult to control symptoms.
• Meds used to convert:class Ia(procainamide), class Ic (flecainide), and class III (amiodarone) antiarrythmic drugs.
• Warfarin therapy for 3 weeks before and 4 weeks after cardioversion is crucial!

• Ventricular rate control to between 60-80 bpm, using:
• 1. Digoxin (mainly for co-existing heart failure)
• 2. B-blockers (effective and rapid onset, but relative contraindication in COPD, asthma and must initiate slowly in pts with systolic HF)
• 3. CCB (non-dihydropyridine-verapamil, diltiazem)-may be safest and most effective in pts without co-morbidities.

• 1. Detect underlying causes for a-fib (COPD, CAD, HF, thyroid dz, valvular dz) and coexisting cardiovascular disease.
• 2. Determinine whether to attempt cardioversion to sinus rhythm.
• 3. Control ventricular rate for patients with chronic a-fib
• 4. Determine plan for anticoagulation to prevent stroke.

paroxysmal, persistent or chronic

palpitations, dizziness, angina, dyspnea, or heart failure.

• 1. Alleviate pulmonary congestion with cautious diuresis or nitrates.
• 2. Drug therapy: consider CCB(non-dihydropyridines), beta-blockers, or ACE inhibitors.

Ventricles are stiff, can't fill without high end diastolic pressures. Impaired capacity to change filling with varying activity levels. Clinical diagnosis is made when patients have typical HF symptoms, only mildly reduced or normal LVEF, and changes in echocardiography suggestive of poor diastolic filling of left ventricle.

• To control ventricular response rate in patients with a-fib. They alleviate symptoms and reduce hospitalizations, but don't effect mortality, and may increase mortality in women.
• Initial dose: 0.125 to 0.25 mg QD with optimal serum range 0.5-0.8 ng/mL.Important to monitor serum levels to detect toxicity.
• Risks include: arrythmias, GI symptoms, and neuro complaints.

They block aldosterone receptors, reducing risk of morbidity and mortality in class III and IV HF patients.

By using 2 diuretics (furosemide and metazolone)

measureing daily body weight.

hydralazine and isosorbide dinitrate either as an addition to ACE or an alternative.

II and III

All HF patients without contraindication (pregnancy, bilateral renal artery stenosis, hypotension-systolic <90, worsening renal, potassium retention (K+ >5.5), angioedema, and chronic cough. Treatment should be initiated at low doses and increased by doubling dose every 3-7 days until recommended target dose. Check BUN, Cr, potassium and BP before initiating and again at 2 weeks and with each dose change.

• 1. Prevention of coronary insufficiency and MI by smoking cessation, weight reduction, control of HTN, hyperlipidemia and diabetes.
• 2. Fluid retention should be monitored by measuring daily body weight and controlled by restricting daily salt intake to less than 2g.
• 3. A-fib with rapid ventricular response should be controlled to avoid cardiac decompensation.
• 4. Certain meds should be avoided in HF. Nsaids inhibit effects of diuretics and ACE inhibitors. Antiarrythmic agents generally not recommended.
• 5. All HF patients should have regular clinic follow up.

Exercise or dipyridamole stress test with follow up angiography as indicated.

• It can be helpful in ruing out HF in a dyspneic patient.
• A BNP level >100 pcg/dl 90% sensitive and 76% specific for dx of systolic HF in acutely dyspneic patients presenting to ED.

CBC, UA, CMP (including serum Magnesium, phosphorus, and calcium), TSH, chest radiograph, and ECG.

A transthoracic 2 dimensional echocardiogram with Doppler flow studies, because it defines the type and severity of LV impairment. It allows measurement of ejection fraction, ventricular mass, chamber dimensions, and wall motion in addition to eval of valvular, pericardial, and vascular structures. It also allows measurement of flow across the mitral valve, categorizing patients into normal (E>A), delayed relaxation (E<A), and restrictive (E>>A) filling patterns. An abnormal E:A ratio is associated with diastolic HF.

• 1. Gallop rhythm
• 2. Displaced point of maximal impulse
• 3. JVD
• Other useful signs and symptoms: DOE or at night (PND), unexpected weight gain, wheezing or rales, and presacral or leg edema. Tachycardia may be a compensatory response for a low cardiac output.

• 1. Establish HF as the patient's diagnosis
• 2. determine the type of HF (systolic or diastolic)
• 3. Assess presence of fluid retention (euvolemic, hypervolemic)
• 4. Determine severity of patient's functional limitation.

Reduced renal perfusion activates the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system, which leads to myocardial toxicity, peripheral vasoconstriction and renal salt and water retention.

hypertension, valvular disease, alcohol abuse, congenital abnormality, viral infections, idiopathic cardiomyopathy.

• Systolic function normal (ejection fraction >40%)
• Left ventricle is stiff, fails to relax, does not fill adequately at normal diastolic pressures.
• Causes: aging, HTN, CAD most common causes.

<40%

• Patients with:
• 1, 2 or 3 vessel disease who have anatomy suitable for catheter therapy and who have normal left ventricular function.

• 1. Significant left main coronary dz
• 2. Significant stenosis of proximal LAD and left circumflex arteries.
• 3. Presence of 3 vessel coronary artery dz
• 4. Disabling angina despite maximal medical therapy
• 5. Significant CAD in presence of left ventricular dysfunction (ejection fraction <50%).

• 1. Has the patient's level of physical activity decreased since last visit?
• 2. Have anginal symptoms increased in frequency or become more severe since last visit?
• 3. How well is patient tolerating therapy?
• 4. How successfull has pt been in modifying risk factors and improving knowledge about ischemic heart disease?
• 5. Has patient developed any new co-morbid illness or has the severity of tx of known comorbid illness worsened the patient's angina?

When there is a change in anginal pattern, symptoms of dysrhythmia or syncope. Cardiac stress imaging should be considered for any CAD patient with a change in patern of angina symptoms.

• Verapamil and diltiazem. They moderately reduce peripheral resistance, decrease heart rate, reduce contractility, and slow electrical conduction.
• A potentially unsafe combo is diltiazem or verapamil combined with a B-blocker which can cause significant bradycardia or conduction defects.

• nifedipine, amlodipine. Produce significant peripheral vasodilation and may produce reflex tachycardia.
• *A potentially unsafe combo is dihydropyridine with a nitrate-> may produce profound hypotension.

non-dihydropyridines and dihydropyridines.

• 1. decrease venous return
• 2. reduce left ventricular wall stress,
• 3. dilate stenotic coronary arteries.
• Hypotension and headache are common side effects of nitrates.

• Nitrates
• Calcium channel blockers

• reduce risk of:
• Cardiovascular death, MI and stroke.

• LDL: <100 mg/dL
• HDL: >35
• Trigs: < 200
• Recent studies suggest even lower LDL levels are beneficial for pts with multiple risk factors or an acute cardiac event, especially DM. (<70)

• 1. Non-selective B-blockers such as propranolol may induce bronchospasm in patients with asthma or COPD. Use cardiac selective such as metoprolol or atenolol.
• 2. bradycardia
• 3. impaired glucose control in diabetes
• 4. exercise intolerance
• 5. depression
• 6. impotence

• 1. Decrease myocardial contractile force
• 2. reduce heart rate
• 3. block deleterious sympathetic tone on coronary arteries.

• 1. When patients don't tolerate aspirin
• 2. Pts who have experienced worsening CAD while taking aspirin.
• 3. Patients who have had recent angioplasty with stenting

• 1. Antiplatelet meds
• 2. B-blockers
• 3. lipid-lowering agents
• 4. ACE inhibitors

Age, male sex, family hx of early CAD, smoking, HTN, hyperlipidemia, DM, obesity, sedentary lifestyle, being post menopausal in women.

• - High pretest probability of left main or 3 vessel CAD
• - Patients who can't undergo noninvasive testing due to disability, illness or morbid obesity
• -Uncertain dx after noninvasive testing where the benefits of dx outweighs risks of angiography.
• -Occupational requirement for definitive dx (pilots, police, etc)
• -Coronary artery spasm is suspected and provocative testing may be necessary.

CAD patients who are unable to exercise, have left bundle branch block, or who have an electronically paced ventricular rhythm on baseline ECG.

For any pt with known CAD- to be completed before and after stressing the myocardium with exercise. Echo before and after cardiac stress is another imaging option.

Inability to carry out physical activity w/o symptoms. Fatigue, palpitation, dyspnea, or anginal pain at rest. Increased symptoms or discomfort with even minor physical activity.

Marked limitation of physical activity. Pt comfortable at rest, but less than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain.

Slight limitations of physical activity.Patient comfortable at rest. Ordinary activity results in fatigue, palpitation, dyspnea, or anginal pain.

No limitation of activity. Ordinary activity does not cause undue fatigue, palpitation, dyspnea or anginal pain.

abnormal fundi, decreased peripheral pulses, bruits

JVD, ascites, pedal edema

3rd heart sound, displaced apical pulse, basilar rales.

• 1) Substernal chest discomfort or pressure
• 2) discomfort/pressure that is provoked by exertion
• 3) discomfort/pressure that is releived by rest or nitro