Barkley Cardiology

Blood flow through the heart

Superior vena cava→Right atrium→Tricuspid valve→Right ventricle→Pulmonic valve→Pulmonary artery→Lungs→Pulmonary veins→Left atrium→Mitral valve→Left ventricle→Aortic valve→Aorta→Body

S1

Mitral tricuspid (AV) valves closure; aortic pulmonic (semilunar) valves open

S2

Aortic/pulmonic (semilunar) valves closure; mitral/tricuspid (AV) valves open

Systole

Period between S1 and S2

Diastole

Period between S2 and S1

S3

“Ken-tuck-y”; increased fluid states (e.g., HF, pregnancy, etc.)

S4

“Ten-ne-ssee”; stiff ventricular wall (e.g., MI, left ventricular hypertrophy, chronic hypertension, etc.)

Murmurs

Grade:

I/VI: Barely audible

II/VI: Audible but faint

III/VI: Moderately loud; easily heard

IV/VI: Loud; associated with a thrill

V/VI: Very loud; heard with one corner of stethoscope off the chest wall.

VI/VI: Loudest

Mitral stenosis

Loud S1 murmur

Low pitched

Mid-diastolic

Apical “crescendo” rumble

Mitral regurgitation

Systolic murmur at the 5th intercostal space, midclavicular line (apex)

May radiate to base or left axilla

Musical, blowing, or high pitched

May follow an S3

Aortic stenosis

Systolic, “blowing,” rough harsh murmur at 2nd right ICS usually radiating to the neck

Aortic regurgitation

Diastolic, “blowing” murmur at 2nd ICS

Mitral stenosis and aortic regurgitation = diastolic

Mitral regurgitation and aortic stenosis = systolic

Ms. Ard and Mr. Ass

Throughout

“Holo” and “pan”

Mitral

5th ICS = Apex

Aortic

2nd or 3rd ICS = Base

Heart failure

A syndrome that results when the cardiac output is insufficient to meet the metabolic needs of the body.

Heart failure with reduced ejection fraction (HFrEF)

Systolic failure

Inability to contract; results in decreased cardiac output

Subcategories:

1. HFrEF: Left ventricular ejection fraction (LVEF) <40%

2. Hf with mildly improved EF (HFimpEF): previous LVEF <40%, but >40% on follow up

3. HF with mildly reduced EF (HFmrEF): LVEF 41%-49%

Heart failure with preserved ejection fraction (HFpEF)

Diastolic failure

Inability to relax and fill; results in decreased cardiac output

LVEF >50%

Acute heart failure

Abrupt onset

Usually follows acute myocardial infarction or valve rupture

L sided heart failure

Chronic heart failure

Develops as a result of inadequate compensatory mechanisms that have been employed over time to improve cardiac output

Right sided heart failure

Left heart failure

Signs/Symptoms: (Acute/Lungs)*

1. Dyspnea at rest

2. Coarse rales over all lung fields

3. Wheezing, frothy cough

4. Appears generally healthy except for the acute event

5. S3 gallop

6. Murmur of mitral regurgitation (systolic murmur loudest at apex)

Right heart failure

Signs/Symptoms: (Chronic)

1. Jugular vein distention (JVD)

2. Hepatomegaly, splenomegaly

3. Dependent edema: As a result of increased capillary hydrostatic pressure

4. Paroxysmal nocturnal dyspnea (PND)

5. Appears chronically ill

6. Diffuse chest wall heave

7. Displaced point of maximal impulse (PMI)

8. Abdominal fullness

9. Fatigue on exertion

10. S3 and/or S4

New York Heart Association (NYHA) Functional Classification of Heart Failure

I: No limitations of physical activity (i.e., normal activity causing no signs/symptoms)

II: Slight limitations of physical activity but comfortable at rest (i.e., physical activity results in fatigue, palpitations, dyspnea, or angina.

III: Marked limitations of physical activity but comfortable at rest.

IV: Severe; inability to carry out any physical activity but comfortable at rest.

Heart failure

Labs/Diagnostics:

1. Hypoxemia and hypocapnia on ABG

2. BMP usually normal unless chronic failure is present

3. B-type natriuretic peptide (BNP) or N-terminal proBNP (NT-proBNP)

4. UA

5. CXR: Pulmonary edema, Kerley B lines, effusions

6. Echocardiogram shows contraction/relaxation, valve function, wall motion, ejection fraction; 2-D echo to assess left ventricular function

7. ECG may show deviation or underlying problem: Acute MI, dysrhythmia

8. Pulmonary function tests for wheezing

Heart Failure

Management:

Non-Pharmacologic:

1. Sodium restriction

2. Rest/activity balance

3. Weight reduction

4. Others

Heart failure

Pharmacologic management:

HFrEF:

1. First-line agents:

   1. ACE inhibitors: Captopril (Capoten), enalapril (Vasotec), fosinopril (Monopril), lisinopril (Zestril), perindopril (Aceon), quinapril (Accupril), ramipril (Altace), trandolapril (Mavik)

   2. ARBs: Losarten (Cozier), valsartan (Diovan), candesartan (Atecand), irbesartan (Avapro), azilsartan (Edarbi)

   3. Angiotensin-receptor/neprilysin inhibitors (ARNIs): Sacubitril/valsartan (entreats)

2. Other recommended agents:

   1. SGLT2 inhibitors: Empagliflozin (Jardiance), dapagliflozin (Farxiga)

   2. For patients with DM: Canagliflozin (Invoking), sotagliflozin (Inpefa)

   3. Beta blockers: Bisoprolol (Zebeta), metoprolol (Lopressor), carvedilol (Coreg)

   4. Mineralocorticoid receptor antagonists (MRA): Spironolactone (Aldactone), eplerenone (inspire)

HFimpEF:

1. Treat as if HFrEF

HFmrEF:

1. Next-line agents:

   1. SGLT2 inhibitors

2. Other options:

   1. ACE inhibitors

   2. ARBs

   3. ARNIs

   4. MRAs

   5. Beta blockers

HFpEF:

1. Next-line agents:

   1. SGLT2 inhibitors

2. Other options:

   1. ARBs

   2. ARNIs

   3. MRAs

3. ACE inhibitors not strongly recommended.

Cardiomyopathies

Any disorder that affects the heart muscle.

Dilated cardiomyopathy

Dilation of the heart muscle

The most common type

Hypertrophic cardiomyopathy

Hypertrophy of the left, and occasionally the right, ventricle

Restrictive cardiomyopathy

Scarring/stiffening of the heart muscle

The least common type

Arrythmogenic right ventricular dysplasia

Irregular heart rhythm caused by the dying of the muscle tissue in the right ventricle that is replaced by scar or fat tissue

Transthyretin amyloid cardiomyopathy (ATTR-CM)

Abnormal protein buildup (deposits of amyloid protein fibrils) in the walls of the heart’s left ventricle.

Cardiomyopathies

Signs/Symptoms:

Same symptoms as heart failure

Cardiomyopathy

Management:

1. Acute management of heart failure

   1. ABCs

   2. Symptomatic relief

      1. Preload and after load reduction with vasodilators (nitrates, hydralazine, nitride, nesiritide, ACEIs/ARBs, and diuretics)

      2. Inhibition of neurohormonal activation (RAAS and sympathetic nervous system): ACEIs/ARBs, beta-blockers, and aldosterone antagonists

   3. Routine management after stabilization:

      1. Beta-blockers started in the hospital once euvolemic status is achieved.

      2. Three-drug combination for most patients with HF:

         1. Diuretic

         2. ACEIs or an ARB

         3. Beta blocker

2. Long-term management

   1. Lifestyle changes: Diet, exercise, sleep patterns, avoidance of alcohol and other drugs

   2. Stress reduction

   3. Maintaining treatment of comorbidities (e.g., HTN, DM)

3. Other medications as needed (e.g., anticoagulants, antiarrhythmics, etc.)

4. Surgical/nonsurgical therapies and procedures

Acute pulmonary edema

Inpatient management:

1. O2 at 1-2 L/min while awaiting ABGs

2. Place patient in sitting or semi-Fowler’s position

3. Morphine 2-4 mg IVP; repeat 20-30 min PRN; stop if hypercapnia occurs.

4. Furosemide 40 mg IVP; repeat in 10 minutes if no response.

5. If a severe bronchospasm presents, give inhaled sympathomimetics

6. If severe, after load and preload reduction with nitroprusside, hydralazine, or others

7. If cardiac index remains low, dobutamine 2.5-20 ug/kg/min; if systolic blood pressure <100 mmHg, dopamine 5-20 ug/kg/min is preferred.

Hypertension

Two types:

1. Primary/essential: 95% of all cases; onset usually < 55 years of age.

2. Secondary: 5% of all cases; secondary to other known causes such as estrogen use, renal disease, pregnancy, endocrine disorders, renal artery stenosis (RAS), etc.

Exacerbating factors: Smoking, obesity, excessive alcohol intake, use of NSAIDs, and others.

Hypertension

Signs/Symptoms:

1. Often none: “Silent killer”

2. Elevated BP

3. With severe this: suboccipital pulsating headache, occurring early in the morning and resolving throughout the day

4. Epistaxis

5. Dizziness/lightheadedness

6. S4 related to left ventricular hypertrophy

7. Arteriovenous (AV) nicking

8. Tearing chest pain may indicate aortic dissection

Hypertension

Labs/Diagnostics

1. In uncomplicated this, laboratory findings are usually normal.

2. Other tests to rule out particular cause:

   1. Renovascular disease studies

   2. CXR if cardiomegaly is suspected

   3. Plasma aldosterone level to rule out aldosteronism

   4. AM/PM cortisol levels to rule out Cushing’s syndrome

3. UA, CBC, BMP, calcium, phosphorus, uric acid, cholesterol, triglycerides

4. ECG

5. PA and lateral CXR

ACC/AHA Guidelines

Normal: <120 AND <80

Elevated: 120-129 AND <80

HTN Stage 1: 130-139 OR 80-89

HTN Stage 2: >140 OR > 90

Hypertension

Nonpharmacologic management:

1. Restrict dietary sodium

2. Weight loss, if overweight

3. DASH (Dietary Approaches to Stop Hypertension) diet (rich in fruits, vegetables, and low-fat dairy products, with reduced saturated and total fat).

4. Exercise (aerobic exercise 30-40 minutes each day on most days of the week.

5. Stress management planning

6. Reduction or elimination of alcohol (no more than 2 drinks daily for men, or one drink daily for women and lighter weight persons)

7. Smoking cessation

8. Maintenance of adequate potassium, calcium, and magnesium intake.

Hypertension

Pharmacologic management:

Non-African American:

1. Thiazide diuretic

2. ACEI

3. ARB

4. CCB

African American:

1. Thiazide diuretics

2. CCBs?

Diabetic:

1. ACEI (or ARB)

Adults >18 with CKD:

1. ACEI

Hypertension

Treatment goal for initial treatment is 1 month; then (1) increase dose, followed by (2) adding a second drug.

Continue to assess monthly until goal is reached.

Do not use an ACEI and ARB together.

Refer to hypertensive specialist if having difficulty reaching the goal (e.g., three or more drugs are needed).

Goal of therapy: Prescribe the least number of medications possible at the lowest dosage to attain successful BP.

Hypertension

Neither age nor gender usually affects agent responsiveness.

Thiazide-type diuretics are usually recommended for first-line treatment; may also protect against osteoporosis by reducing the amount of calcium expelled in the urine.

ACE inhibitors, adrenergic receptor blockers, and CCBs are also useful alone or in combination therapy.

Hypertensive urgencies

>180/110

May or may not be associated with severe headache, shortness of breath, epistaxis, or severe anxiety.

Management:

1. Oral therapies such as clonidine (Catapres)—alpha agonist

2. Parenteral therapy is rarely required.

Hypertensive emergencies

>180/120

Requires immediate (within 1 hour) BP reduction to prevent or limit target organ damage.

BP may be <180/120 with any of the following:

1. Malignant hypertension

2. Hypertensive encephalopathy

3. Intracranial hemorrhage

4. Unstable angina

5. Acute MI

6. Acute heart failure

7. Dissecting aortic aneurysm

8. Eclampsia

Management:

1. ICU admission for continuous monitoring of BP and target organ damage and for parenteral administration of an appropriate agent (e.g., nicardipine—Cardene, sodium nitroprusside—Nitride, or others).

2. For compelling conditions (e.g., aortic dissection, severe preeclampsia or eclampsia, or pheochromocytoma crisis), SBP should be reduced to <140 mmHg during the first hour and to <120 mmHg in aortic dissection.

3. For adults without a compelling condition, SBP should be reduced by no more than 25% within the first hour; then, if stable, to 160/100 mmHg within the next 2-6 hours; and then cautiously to normal during the following 24-48 hours.

Angina

Decreased blood flow through the vessel→tissue ischemia

Types:

1. Stable (classic or chronic): Exertional (most common)

2. Prinzmetal’s angina (variant/vasospastic): Occurs at various times, including rest—Patient takes CCB; ST elevations common.

3. Unstable (pre-infarction, rest or crescendo, coronary syndromes)

4. Microvascular (metabolic syndrome)

Angina

Signs/Symptoms:

1. Characteristic chest discomfort lasting several minutes.

2. Exertional is usually precipitated by physical activity; subsides with rest.

3. Nitroglycerin shortens or prevents attacks.

Physical exam findings:

1. May see signs of peripheral arterial disease

2. Levine’s sign = “clenched fist sign”—more than 90% diagnostic

3. Transient S4 not uncommon during angina.

Angina

Labs/Diagnostics:

1. ECG may be normal, with down sloping of ST segment, or T-wave peak or inversion during attack. (ST depression)

2. Exercise ECG

3. Serum lipid levels should be evaluated.

   1. Total cholesterol: Desirable = <200 mg/dl

   2. Very low-density lipoproteins (VLDLs) (triglycerides): Normal = <150 mg/dl

   3. Low-density lipoproteins (LDLs): Optimal = < 100 mg/dl

   4. High-density lipoproteins (HDLs): Low = < 40 mg/dl; high = >60 mg/dl

4. Historically, goals for patients with diabetes or documented coronary artery disease:

   1. LDL < 70 mg/dl

   2. HDL > 40 mg/dl

   3. Triglycerides (TG) , 150 mg/dl

5. Coronary angiography is the definitive diagnostic procedure but not indicated solely for diagnosis.

Angina

Management

1. Reduction of risk factors when possible.

2. Manage diet: Decreased saturated fats, then decreased unsaturated fats, and then consider plant sterols (e.g., nuts, vegetable oils, etc.)

3. Low dose enteric coated acetylsalicylic acid (ASA) (81 mg daily)

4. Common pharmacotherapy for this:

   1. Nitrates

   2. Beta blockers

   3. CCBs

5. Commonly used agents other than 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMH-CoA) reductase inhibitors (statins)

   1. Bile acide séquestrants: Mostly decreased LDL; may increase triglycerides

      1. Cholestyramine (Questran)

      2. Colesevalam (Wechol)

      3. Colestipol (Colestid)

   2. Fibrates: Decrease triglycerides, slightly decrease LDL and possible increase HDL

      1. Gemfibrozil (Lopid)

      2. Fenofibrate (Tricor)

      3. Fenofibric acid (Trilipix)

   3. Cholesterol absorption inhibitor: Used in combination with a statin to decrease LDL

      1. Ezetimibe (Zetia)

   4. Niacin: Decrease LDL and triglycerides and increase HDL

      1. Immediate and extended-release preparations

      2. High doses of niacin may cause “flushing” sensation.

Myocardial Infarction/Acute Coronary Syndromes

Contributing to the leading cause of death in adults in the US (i.e., heart disease); about 790,000 Americans each year have an MI each year; “clot on plaque”

Sudden cardiac death: (1) coronary artery disease, and (2) cardiomyopathies

Myocardial Infarction/Acute Coronary Syndromes

Signs/Symptoms:

One third of patients give a history of alteration in typical anginal pain.

Most infarctions occur at rest: Pain similar to angina but more severe.

Nitroglycerin has little effect.

1. Cold sweat; weakness

2. Impending doom

3. Apprehension

4. Light-headedness

5. Syncope

6. Dyspnea

7. Cough

8. Nausea and vomiting

Physical exam findings:

1. Dysrhythmia common

2. S4 very common

3. Wheezing

4. Pulmonary crackles

5. Low grade fever during first 48 hours

6. Tachycardia

Myocardial Infarction/Acute Coronary Syndromes

Labs/Diagnostics:

1. ECG changes almost always; About 30% of patients have no initial ECG changes.

2. Peaked T waves, ST elevations, Q wave development (Q waves do not develop in 30%-50% of MIs)

   1. I, aVL: Lateral

   2. II, III, aVF: Inferior

   3. V leads (precordial leads) or V3 and V4: Anterior

3. Cardiac enzyme elevations above normal within 4-6 hours (Troponin T, Troponin I—only elevates with true myocardial damage, CK-MB—100% cardio-selective) and remain high for several days (3 days to 3 weeks)

4. Echocardiography for bed-side assessment of wall motion, EF, etc.

5. Leukocytosis 10,000-20,000 uL on the second day.

Myocardial Infarction/Acute Coronary Syndromes

Management:

1. ASA 325 mg tablet to chew

2. Nitroglycerin sublingual (NTG SL) every 5 minutes x 3

3. Begin O2 therapy; IV access

4. 12 Lead ECG and cardiac monitor

5. Morphine 2-4 mg IVP

6. Furosemide if pulmonary edema present: 40 mg IVP

7. If not contraindicated, consider 5 mg metoprolol IV x 3 doses at 2-minute intervals, then 50 mg PO Q6H starting 15 minutes after the last IV dose.

8. ACEI are most beneficial when patient has failure or a large infarction.

9. Heparin vs. low molecular weight heparin (Lovenox 1 mg/kg Q12H)

10. Monitor therapeutic coagulation values.

First-degree atrioventricular (AV) block

PR interval > 0.20 seconds

Type 1 second-degree AV block (Wenckebach or Mobitz type 1)

The PR interval gradually gets longer until a QRS complex is dropped.

Type 2 second-degree AV block (Mobitz type II)

The atrial rhythm is regular, the PR interval is constant, but the ventricular rhythm is irregular; dropped QRS complexes occur.

Third-degree AV block (complete heart block)

The atrial and ventricular rhythms are regular, PR interval varies with no regularity, the P and R waves can be walked across the strip in rhythm, some P waves may be buried in QRS complexes or T waves; no relationship between P wave and QRS complex.

Atrial fibrillation

Anticoagulation vs. cardioversion x 2, then ablation for third episode; monitor patients in this for risk of stroke: CHAD2DS2-VASc (congestive heart failure, hypertension, age > 75 [doubled], diabetes, stroke [doubled'], vascular disease, age 65-74, and sex category [female]).

International normalized ration (INR)

Normal: 0.8-1.2 seconds

MI: 2.5-3.5 x normal

Coumadin: 2-3 mg/dl

Activated coagulation time (ACT)

Normal: 70-120 seconds

Therapeutic value: 150-190 or > 300 seconds post PTCA/stent

Activated partial thromboplastin time (APTT)

Normal: 28-38 seconds

Therapeutic value: 1.5-2.5 x normal

Prothrombin time (PT)

Normal: 11-16 seconds

Therapeutic value: 1.5-2.5 x normal

Partial thromboplastin time (PTT)

Normal: 60-90 seconds

Therapeutic value: 1.5-2.5 x normal

Traditional anticoagulants

Warfarin:

Depletes functional vitamin K reserves to impair clotting.

Reversal: Vitamin K, FFP, prothrombin complex concentrate (PCC, Kcentra)

Enoxaparin (Lovenox), Dalteparin (Fragmin):

Inhibits factor Xa and factor IIa

Reversal: Protamine

Direct oral anticoagulants

Apixaban (Eliquis), Rivaroxaban (Xarelto), Edoxaban (Savaysa):

Selective inhibition of factor Xa

Reversal: Andexanet alfa (Andexxa), PCC (KCentra)

Dabigatran (Pradaxa):

Thrombin inhibition

Reversal: Idarucizumab (Praxhind)

Reversible P2Y12 inhibitors

Ticagrelor (Brilinta):

Reversibly blocks P2Y12 receptors, reducing platelet aggregation

Reversal: Bentracimab

Irreversible P2Y12 inhibitors

Clopidogrel (Plavix), Prasugrel (Effient):

Irreversibly blocks P2Y12 receptors

Reversal: None

Injectables

Fondaparinux (Arixta):

Selective inhibition of factor Xa

Reversal: Recombinant factor VIIIa

DVT

Risk factors:

1. Liver disease

2. Obesity

3. Protein S deficiency

4. Hypertension

5. Diabetes

6. Smoking

7. Female gender

8. Immobility/sedentary lifestyle

9. Tamoxifen (breast cancer)

10. Others

Pharmacologic revascularization

Indications:

1. Unrelieved chest pain (>30 minutes and <6 hours) WITH:

2. ST segment elevation >0.1 mV in two or more contiguous leads

Pharmacologic revascularization

Contraindications:

1. Prior ICH

2. Structural cerebral vascular lesion or malignant intracranial neoplasm

3. Ischemic stroke within 3 months

4. Suspected aortic dissection

5. Active bleeding or bleeding diathesis

6. Significant closed head trauma or facial trauma within 3 months

7. Intracranial or intraspinal surgery within 2 months

8. Severe uncontrolled hypertension (>185/110)

9. Active bleeding or risk thereof, including abnormal coagulation values

Peripheral vascular disease (PVD)

Pathology:

1. Arteriosclerotic narrowing of the lumen of arteries resulting in decreased blood supply to the extremities.

Causes/Incidence:

1. Usually caused by atherosclerosis

2. Similar risk factors for coronary artery disease

3. Peak incidence: 40-70 years of age

4. Hyperlipidemia

5. Smoking

6. DM

Peripheral vascular disease (PVD)

Signs/Symptoms:

1. Usually first symptom: Complaint of calf pain (claudication)

2. Cold/numbness to extremities

3. Progresses to pain at rest

Physical findings:

1. Shiny/hairless skin

2. Dependent rubor

3. Pallor

4. Cyanosis

5. Ulcerations

6. Reduced pulses

Peripheral vascular disease (PVD)

Labs/Diagnostics:

1. Doppler US to evaluate flow

2. Ankle-brachial index (ABI)*

3. X-rays may show calcifications

4. Arteriography: Most definitive test

Management:

1. Stop smoking and all tobacco use.

2. Exercise: Walk 1 hour/day; stopping during pain and resuming when pain subsides to develop collateral circulation.

3. Cilostazol (Pletal)

4. Weight reduction, as needed.

5. Manage diabetes and HLD

6. Angioplasty

7. Bypass surgery

8. Amputation

Chronic venous insufficiency (CVI)

Pathology:

Impaired venous return due to either destruction of valves, changes due to deep thrombophlebitis, leg trauma, or sustained elevation of venous pressure (HF)

Causes/Incidence:

1. More common in women than men

2. May be genetic predisposition

3. History of leg trauma; may be associated with varicose veins

Chronic venous insufficiency (CVI)

Signs/Symptoms:

1. Aching of the lower extremities relieved by elevation

2. Edema after prolonged standing

3. Night cramps of the lower extremities

Physical findings:

1. Trophic changes with brownish discoloration

2. Stasis leg ulcers

3. Edema of lower extremities

4. Dermatitis may be common

5. Cool to touch

Chronic venous insufficiency (CVI)

Labs/Diagnostics:

1. Nonspecifically diagnostic of this

2. R/O edema due to HF and other causes (e.g., May-Thurner syndrome: Compression of left common iliac vein by overlying right common iliac artery = LLE DVT)

Management:

1. Bed rest with legs elevated on pillows to diminish chronic edema.

2. Use of heavy-duty elastic support stockings

3. Weight reduction in the obese

4. Treat dermatitis or ulcers as indicated.

5. Acute weeping dermatitis

   1. Tap water compresses

   2. Hydrocolloid dressings

   3. For less acute dermatitis, hydrocortisone cream

Pericarditis

Inflammation of the pericardium. A thorough history is essential to making an accurate diagnosis.

Causes/Incidence:

1. Viruses: most common cause

2. Post myocardial infarction

3. Renal failure

4. Neoplastic, tuberculosis, septicemia

5. Endocarditis

6. Collagen diseases

7. Drug/trauma induced

8. Viral infection

9. Idiopathic (probably viral)

Pericarditis

Signs/Symptoms:

1. Very localized retrosternal/precordial chest pain, pleuritic in nature

2. Pain increased by deep inspiration, coughing, swallowing or recumbent

3. Pain relieved by sitting forward

4. Shortness of breath secondary to pain with inspiration

Physical findings:

1. Pericardial friction rub characteristically present

2. Pleural friction rub may also be present

3. Fever may be present depending on underlying cause

Pericarditis

Labs/Diagnostics:

1. ST segment elevation in all leads

2. Return of ST segment to normal in a few days followed by temporary T wave inversion

3. Depression of PR segment highly indicative of this.

4. Erythrocyte sedimentation rate (ESR) elevation

5. Blood cultures if bacterial cause suspected

6. CBC to rule out infection

7. Echocardiogram to confirm presence of pericardial fluid or other abnormalities

8. Baseline BMP

Pericarditis

Management:

1. NSAIDs are mainstay of treatment

   1. Indomethacin (Indocin)

   2. Ketorolac (Toradol)

   3. Ibuprofen

2. Corticosteroids are indicated only when there is total failure of high-dose NSAIDs over several weeks and with relapsing pericarditis. Can increase viral replication.

3. Antibiotics in cases of bacterial infection

4. Monitor for tamponade (hypotension, JVC [increased central venous pressure], muffled/distant heart sounds, pulsus paradoxus).

Endocarditis

Infection of the endothelial surface of the heart. Usually affects the valves. A diagnosis of infective this must be considered an excluded in all patients with a heart murmur and fever of unknown origin.

Causes/Incidence:

1. Usually caused by bacteria.

2. Known valvular heart disease; especially in rheumatic, bicuspid aortic valve/mitral valve prolapse, with significant regurgitation.

3. Recent dental/oropharyngeal surgery.

4. Genitourinary instrumentation/surgery of the respiratory tract

5. Congenital heart disease

6. Prolonged use of IV catheters or total parenteral nutrition (TPN)

7. Patients with burns

8. Hemodialysis

Endocarditis

Signs/Symptoms:

1. Fever and malaise

2. Night sweats and weight loss

3. General “sick” feeling

Physical findings:

1. Murmur often present but may be absent in up to 30% of patients, especially those with right sided this.

2. Medium to high fever

3. Osler’s nodes: Painful, red nodules in the distal phalanges

4. Petechiae, purpura, pallor

5. Splinter hemorrhages: Linear, subungal splinter-appearing

6. Splenomegaly observed in 50% of patients.

7. Janeway lesions: Rarely observed, small and not painful macule on the palms and soles

8. Roth spots: Small retinal infarcts, white in color, encircled by areas of hemorrhage.

Endocarditis

Labs/Diagnostics:

1. WBC may be normal or elevated, but there is always a left shift with bands

2. Echocardiogram for valvular damage

3. Blood culture for causative organism

   1. Three separate cultures at three separate sites in 1 hour

4. ESR virtually always elevated.

Management:

1. For suspected cases of subacute endocarditis, empiric therapy is generally not started until blood culture results identify the pathogen.

2. Acute this: Usually due to staphylococcus aureus (both MRSA and MSSA), streptococci, and enterococci; empiric therapy; vancomycin until culture results are available.

Cardiovascular gerontology considerations

Physiologic:

1. Arterial walls thicken and stiffen, resulting in decreased compliance.

2. The heart becomes slightly stiffer and may increase in size, related to left ventricular and atrial hypertrophy.

3. Sclerosis of valves.

4. Intrinsic and maximum heart rates decrease; resting heart rate and cardiac output are unaffected.

5. Baroreceptors that monitor blood pressure become less sensitive.

6. Circulatory changes with diminished blood flow.

7. Loss of pacemaker cells with increased AV conduction time.

8. Arteriosclerosis and atherosclerosis.

Cardiovascular gerontology considerations

Possible findings and/or results:

1. Hypertension: Increased risk for CVA, MI, and renal failure

2. Heart murmurs common

3. Decreased cardiac reserve (may lead to orthostatic hypotension or syncope)

4. Overall, diminished peripheral pulses and cool extremities

5. Dysrhythmias