Cardiovascular System

DANGER SIGNALS

Acute Myocardial Infarction (MI)

Also known as ST elevation myocardial infarction (STEMI) and acute coronary syndrome (ACS). A middle-aged or older man complains of gradual onset of intense and steady chest discomfort or pain that is described as squeezing, tightness, crushing, heavy pressure (“an elephant sitting on my chest”), or band-like. The pain is provoked by physical exertion or eating a heavy meal. The pain or discomfort may radiate to the left side of the neck, jaw, and left arm (or both arms). Continues to have pain or discomfort at rest (angina relieved by rest and nitroglycerin). The patient may be diaphoretic with cool, clammy skin. Women and those who are elderly with MIs are more likely to present with nonspecific symptoms such as shortness of breath or dyspnea, weakness, nausea and vomiting, fatigue, and syncope. May complain of back pain instead of anterior chest pain.

Congestive Heart Failure (CHF)

Older patient complains of an acute (or gradual) onset of dyspnea, fatigue, dry cough, and swollen feet and ankles. The patient has a sudden (or gradual) increase in weight. Lung exam will reveal crackles on both the lung bases (bibasilar crackles) along with an S3 heart sound. History of preexisting coronary artery disease (CAD), angina, prior MI, or previous episode of CHF. Usually is taking diuretics and other antihypertensive medications.

Infective Endocarditis (IE)

Also known as bacterial endocarditis. Patient presents with fever, chills, and malaise that is associated with onset of a new murmur. Associated skin findings are found mostly on the fingers/hands and toes/feet. These are subungual hemorrhages (splinter hemorrhages on the nail bed), petechiae on the palate, painful violet-colored nodes on the fingers or feet (Osler nodes), and nontender red spots on the palms/soles (Janeway lesions). Funduscopic exam may show Roth spots or retinal hemorrhages. Usually fatal if not treated.

Dissecting Abdominal Aortic Aneurysm (AAA)

Elderly white male complains of sudden onset of severe, sharp, excruciating pain located in the abdomen, flank, and/or back. Accompanied by a distended abdomen and abnormal vital signs (hypotension). Older male patients who are smokers with hypertension (HTN) are at higher risk. Incidental finding on chest x-ray may show widened mediastinum, tracheal deviation, and obliteration of aortic knob (thoracic aortic dissection).

Anatomy

Position of the Heart

The right ventricle is the chamber of the heart that lies closest to the sternum. The lower border of the left ventricle is where the apical impulse is generated. The heart is roughly the size of a large adult fist. The apex beat is caused by the left ventricle.

Apical impulse: Located at the fifth intercostal space (ICS) by the midclavicular line on the left side of the chest

Displacement of the Point of Maximal Impulse (PMI)

Severe left ventricular hypertrophy (LVH) and cardiomyopathy: The PMI is displaced laterally on the chest, is larger (more than 3 cm) in size, and is more prominent.

Pregnancy, third trimester: As the uterus grows larger, it pushes up against the diaphragm and causes the heart to shift to the left of the chest anteriorly. The result is a displaced PMI that is located slightly upward on the left side of the chest. May hear S3 heart sound during pregnancy.

Deoxygenated Blood

Enters the heart through the superior vena cava and inferior vena cava

Right atrium → tricuspid valve → right ventricle → pulmonic valve → pulmonary artery → the lungs → alveoli (RBCs pick up oxygen and release carbon dioxide)

Oxygenated Blood

Exits the lungs through the pulmonary veins and enters the heart

Left atrium → mitral valve → left ventricle → aortic valve → aorta → general circulation

Systole and Diastole

The mnemonic to use is “motivated apples.” These two words give you several clues. They will remind you of the names of the valves (which produce the sound) and the type of valve (atrioventricular [AV] or semilunar valve).

Heart Sounds

S1 (Systole): “Motivated” (M = mitral and T = tricuspid and AV = AV valves)

The “lub” sound (of “lub-dub”)

Closure of the mitral and tricuspid valves AV valves

S2 (Diastole): “Apples” (A = aortic and P = pulmonic and S = semilunar valves)

The “dub” sound (of “lub-dub”)

Closure of the aortic and pulmonic valves Semilunar valves

S3 Heart Sound

Usually indicative of heart failure or CHF

Occurs during early diastole (also called a “ventricular gallop” or an “S3 gallop”)

Sounds like “Kentucky”

Always considered abnormal if it occurs after the age of 35 to 40 years

This can be a normal finding in children, pregnant women, and some athletes (older than 35 years of age).

S4 Heart Sound

Cause: Increased resistance due to a stiff left ventricle; usually indicates LVH Considered a normal finding in some elderly (slight stiffness of left ventricle) Occurs during late diastole (also called an “atrial gallop” or “atrial kick”) Sounds like “Tennessee”

Best heard at the apex or apical area (mitral area) using the bell of the stethoscope

Stethoscope Skills

Bell of Stethoscope

Low tones such as the extra heart sounds (S3 or S4) Mitral stenosis\

Diaphragm of the Stethoscope

Mid- to high-pitched tones such as lung sounds Mitral regurgitation

Aortic stenosis

Benign Variants

Pysiologic S2

Best heard over the pulmonic area (or second ICS on the upper left side of sternum); due to splitting of the aortic and pulmonic components. A normal finding if it appears during inspiration and disappears at expiration.

S4 in the Elderly

Some healthy elderly patients have an S4 (late diastole) heart sound; also known as the “atrial kick” (the atria have to squeeze harder to overcome resistance of a stiff left ventricle). If there are no signs or symptoms of heart/valvular disease, it is considered a normal variant. Pathological S4 is associated with LVH due to increased resistance from the left ventricle.

SOLVING QUESTIONS: HEART MURMURS

To solve a murmur question correctly, only two pieces of information are needed.

Look for the timing of the murmur (systole or diastole).

Look for the location of the murmur (aortic, Erb’s Point, or mitral area).

All the murmurs seen on the exams will fit into the following two mnemonics.

Timing

Systolic Murmurs

Use the “MR. ASS” (Mitral regurgitation/aortic stenosis = systolic) mnemonic.

Diastolic Murmurs

Use the “MS. ARD” (Mitral stenosis/aortic regurgitation = diastolic) mnemonic.

Location

Auscultatory Areas

It is necessary to memorize the locations of the auscultatory areas in order to correctly identify a heart murmur.

Mitral Area

The mitral area is also known as the apex or the apical area of the heart.

Fifth left ICS is about 8 to 9 cm from the midsternal line and slightly medial to the midclavicular line.

PMI or the apical pulse is located in this area.

Aortic Area

The aortic area is the second ICS to the right side of the upper border of the sternum. The location of the aortic area can also be described as the “second ICS by the right side of the sternum at the base of the heart.” It can also be described as a murmur that is located on the right side of the upper sternum.

Erb’s Point

Erb’s Point is located at the third to fourth ICS on the left sternal border.

Heart Murmurs: Mnemonics
  1. ASS (Use for Systolic Murmurs)

Systolic murmurs are also described as occurring during S1, or as holosystolic, pansystolic, early systolic, late systolic, or midsystolic murmurs.

Compared with diastolic murmurs, these murmurs are louder and can radiate to the neck or axillae.

MR (Mitral Regurgitation)

A pansystolic (or holosystolic) murmur:

Heard best at the apex of the heart or the apical area Radiates to axilla

Loud blowing and high-pitched murmur (use the diaphragm of the stethoscope)

AS (Aortic Stenosis)

A midsystolic ejection murmur:

This murmur is best heard at the second ICS at the right side of the sternum. It radiates to the neck.

A harsh and noisy murmur (use diaphragm of stethoscope). Patients with aortic stenosis should avoid physical overexertion, because there is increased risk of sudden death.

Refer to cardiologist.

Aortic stenosis is monitored by serial cardiac sonograms with Doppler flow studies. Surgical valve replacement needed if it worsens.

  1. ARD (Use for Diastolic Murmurs)

Diastole is also known as the S2 heart sound, early diastole, late diastole, or middiastole.

Diastolic murmurs are always indicative of heart disease (unlike systolic murmurs).

MS (Mitral Stenosis)

A low-pitched diastolic rumbling murmur:

Heard best at the apex (or apical area) of the heart

Also called an opening snap (use bell of the stethoscope)

AR (Aortic Regurgitation)

A high-pitched diastolic murmur (use diaphragm of the stethoscope):

If AR is due to a diseased aortic valve, the murmur is located at the third ICS by the left sternal border (Erb’s Point).

If AR is due to an abnormal aortic root, the murmur is best heard at the right upper sternal border (aortic area).

Heart Murmurs: Grading System

Grade I: A very soft murmur heard only under optimal conditions.

Grade II: This is a mild to moderately loud murmur.

Grade III: Loud murmur that is easily heard once the stethoscope is placed on the chest.

Grade IV: A louder murmur. First time that a thrill is present. A thrill is like a “palpable murmur.”

Grade V: Very loud murmur heard with edge of stethoscope off chest. Thrill is more obvious.

Grade VI: The murmur is so loud that it can be heard even with the stethoscope off the chest. The thrill is easily palpated.

ABNORMAL FINDINGS

Pathological Murmurs

All diastolic murmurs are abnormal.

All benign murmurs occur during systole (S2).

Benign murmurs do not have a thrill; only very loud murmurs will produce a thrill.

EXAM TIPS

There are usually two questions regarding heart murmurs on the exam. Learn to use the mnemonics “MR. ASS” and “MS. ARD.”

Memorize the locations of the mitral area as well as the aortic area.

All murmurs with “mitral” in their names are only described as located:

  • On the apex of the heart or the apical area or
  • On the fifth ICS on the left side of the sternum medial to the midclavicular line If an apical/apex murmur occurs during S1, it is mitral regurgitation (MR. ASS). If an apical/apex murmur occurs during S2, it is mitral stenosis (MS. ARD).

On the exam, only the systolic murmurs radiate (to the axilla in mitral regurgitation and to the neck with aortic stenosis).

S3 is a sign of CHF; S4 is a sign of LVH.

A split S2 is best heard at the pulmonic area (upper left sternum).

Memorize the mnemonic “motivated apples” to help you remember the names of the valves that are responsible for producing S1 and S2.

Grading murmurs: Be aware that the first time a thrill is palpated is at grade IV. If you forget on which side of the sternum the aortic or pulmonic area lies (left or right?):

Rule out AAA in an older male who has a pulsatile abdominal mass that is more than 3 cm in width. The next step is to order an abdominal ultrasound and CT. Learn the signs/symptoms of infective endocarditis (bacterial endocarditis).

Cardiac Arrhythmias

Atrial Fibrillation (AF) and Atrial Flutter

AF is the most common cardiac arrhythmia in the United States. It is a major cause of stroke and classified as a supraventricular tachyarrhythmia. AF may be asymptomatic. If patient is hemodynamically unstable (chest pain/angina, hypotension, heart failure, cold clammy skin, acute kidney failure) with new onset of AF with severe symptoms, call 911. Risk of stroke/death is higher in elderly patients.

Risk Factors

HTN, CAD, ACS, caffeine, nicotine, hyperthyroidism, alcohol intake (“holiday heart”), heart failure, LVH, pulmonary embolism (PE), chronic obstructive pulmonary disease (COPD), sleep apnea, other

Paroxysmal AF (intermittent or self-terminating): Episodes terminate with 7 days or less (usually in less than 24 hours); it is usually asymptomatic

Classic Case

Patient reports the sudden onset of heart palpitations accompanied by feelings of weakness, dizziness, dyspnea/dyspnea on exertion, and reduction in exercise capacity. May complain of chest pain and feeling like passing out (presyncope to syncope). Rapid and irregular pulse may be more than 110 beats/min with hypotension. AF can be paroxysmal and stop spontaneously (within 7 days) or be persistent or long-standing.

Treatment Plan

Search for underlying cause. Treatment depends on patient type and risk factors for stroke. Newer tool is the CHA2DS2-VASc score.

  • CHA2DS2-VASc scoring system (score of 0 is low risk): Score of 2 or more requires C (CHF), H (HTN), A (age >75 years), D (diabetes), S2

(stroke/TIA), V (vascular disease), A (age 65–74 years), S (sex: female gender is higher risk).

Diagnostic test is the 12-lead EKG (does not show discrete P waves, irregularly irregular rhythm).

New onset: Test EKG, TSH, electrolytes (calcium, potassium, magnesium, sodium), renal function, B-type natriuretic peptide (rule out heart failure), troponin.

Consider 24-hour Holter monitor if paroxysmal AF. Digoxin level (if on digoxin). Order echocardiogram (rule out valvular pathology, which increases risk of stroke). Lifestyle: Avoid stimulants (caffeine, nicotine, decongestants) and alcohol (some patients).

Medications

Patients are referred to cardiologists for medical management. An option for new-onset AF with stable patients is cardioversion (first 48 hours) or rate control.

Management varies based on AF severity and symptoms.

Rate control: Use beta-blockers, calcium channel blockers (CCBS), digoxin. Antiarrhythmics such as amiodarone (Cordarone). Amiodarone has a Food and Drug Administration (FDA) Black Box Warning of pulmonary and liver damage.

Simvastatin with amiodarone can cause rhabdomyolysis.

Warfarin (Coumadin; vitamin K antagonist) for anticoagulation remains the most prescribed therapy and the only recommended option for patients with severe or end- stage chronic kidney disease. Baseline INR, aPTT, CBC (check platelets), creatinine,

LFTs.

  • Initial daily dose equal to or less than 5 mg, but frail, sensitive, or elderly patients older than 70 years of age should take lower dose (2.5 mg).
  • Full effect takes from 2 to 3 days. Check INR every 2 to 3 days until therapeutic for two consecutive checks; then recheck weekly and so on until INR is stable at 2 to 3. Check every 4 weeks when stable.
  • You may wish to check the institutional protocols or refer to anticoagulation If you do not have experience with anticoagulation, best to refer to cardiologist.

If suspect a bleeding episode, check the INR with the PT and the PTT.

Antidote for warfarin is vitamin K.

For nonvalvular AF, direct thrombin inhibitor dabigatran (Pradaxa) or the Factor Xa inhibitors rivaroxaban (Xarelto) and apixaban (Eliquis) do not require INR monitoring, have no major dietary restrictions, and have fewer drug interactions.

Platelet inhibitors, such as clopidogrel (Plavix), either alone or in combination with other anticoagulants, may be better tolerated but less effective than warfarin.

Complications

Death caused by thromboembolic event (i.e., stroke, pulmonary embolism), CHF, angina, etc.

Warfarin-associated intracerebral hemorrhage has very high mortality and causes 90% of warfarin deaths. It is a medical emergency. Call 911. Stop all anticoagulants, acetylsalicylic acid (ASA), nonsteroidal anti-inflammatory drugs (NSAIDs). Initiate vitamin K to reverse.

Warfarin can be reversed, as can Pradaxa (Praxbind [reversal agent] is available in all 50 states)

Anticoagulation Guidelines

Atrial Fibrillation

INR: 2.0 to 3.0

Synthetic/Prosthetic Valves

INR: 2.5 to 3.5

Patient Education: Dietary Sources of Vitamin K

Advise patients to be consistent with their day-to-day consumption of vitamin K foods. Give patient a list of foods with high levels of vitamin K (“greens” such as kale, collard, mustard, spinach, iceberg or romaine lettuce, brussels sprouts, potatoes).

Only one serving per day is recommended for very high vitamin K foods.

Hold one or two doses; with or without administration of low- dosed vitamin K (1 to 2.5 mg). Monitor INR every 2 to 3 days until it is stable. Decrease the Coumadin maintenance dose.

Paroxysmal Supraventricular Tachycardia (PSVT)

EKG shows tachycardia with peaked QRS complex with P waves present. May be seen in Wolff–Parkinson–White (WPW) syndrome, which is more common in children. Causes include digitalis toxicity, alcohol, hyperthyroidism, caffeine intake, alcohol, illegal drug use, etc.

Classic Case

Patient complains of the abrupt onset of palpitations, rapid pulse, lightheadedness, shortness of breath, and anxiety. Rapid heart rate can range from 150 to 250 beats/min.

Treatment Plan

Check EKG. If shows WPW syndrome or is symptomatic, refer to cardiologist. If hemodynamically unstable, may require electrical cardioversion. Call 911.

Vagal maneuvers: Carotid sinus massage (patient supine, monitor vital signs). Monitor with EKG. If a carotid sinus massage is needed, refer to a cardiologist. Contraindicated if history of transient ischemic attack or stroke in past 3 months or has carotid bruits. Holding one’s breath and straining hard, or splashing ice cold water on the face may interrupt and stop this arrhythmia but is rarely used (elicits the diving reflex).

Pulsus Paradoxus

Also known as a paradoxical pulse. The paradox is that the apical pulse can still be heard even though the radial pulse is no longer palpable. It is measured by using the blood pressure cuff (sphygmomanometer) and a stethoscope. Certain pulmonary and cardiac conditions that compress the chambers of the heart (impair diastolic filling) can cause an exaggerated decrease of the systolic pressure of more than 10 mmHg (a drop of <10 mmHg is not pulsus paradoxus).

Pulmonary Cause

Asthma, emphysema (increased positive pressure)

Cardiac Cause

Tamponade, pericarditis, cardiac effusion (decreases movement of left ventricle)

EKG Interpretation

Because family nurse practitioners (NPs) function in the primary care area (not the CCU), they very well may be expected to diagnose complex rhythms. The important ones to memorize (EKG appearance) are AF (irregularly irregular rhythm with no p waves), ventricular tachycardia (jagged irregular QRS), and the norms such as sinus rhythm and sinus arrhythmia.

Anterior wall MI or an anterior STEMI is the most common and serious type of MI. EKG changes include ST segment elevation (leads V2 to V4) and Q waves. Wide QRS complex resembles a “tombstone.”

EXAM TIPS

One EKG strip may show up in the FNP or AGNP exam (ANCC or AANP exam). Memorize appearance of EKG with AF and anterior wall MI (tombstone-like pattern).

AF: Goal is INR of 2 to 3.

AF have many causes, such as alcohol intoxication; CAD, CHF, history of MI, older age, hypertension; stimulants (caffeine, decongestants, cocaine, amphetamines, etc.).

Learn the proper procedure to check for pulsus paradoxus.

If INR is between 4.01 to 4.99, hold one dose. Do not give vitamin K.

Major bleeding episodes can occur even with a normal INR. Order an INR with the PT and the PTT if you suspect bleeding.

It may take up to 3 days after changing the warfarin dose to see a change in the INR.

Coumadin is an FDA category X drug.

Hypertension

Correct BP Measurement

Avoid smoking or caffeine intake 30 minutes before measurement. Instruct patient not to cross their legs (increases SBP).

Begin BP measurement after at least 5 minutes of rest (mercury sphygmomanometer preferred over digital machines).

Two or more readings separated by 2 minutes should be averaged per visit.

Higher number determines BP stage (BP 140/100 is stage II instead of stage I)

Primary HTN

Previously known as essential hypertension. It is usually asymptomatic. Both the American Nurses Credentialing Center (ANCC) and the American Academy of Nurse Practitioners Certification Board (AANPCB) exams are now based on the JNC 8 Hypertension Guidelines (2014). The American College of Cardiology/American Heart Association 2017 guideline for high BP in adults has changed the BP classification and goals (BP <130/80). But as of May 2018, the JNC 8 is still the guideline that is followed on the exams.

Peripheral Vascular Resistance × Cardiac Output

Any change in the PVR or CO results in a change in BP (increase/decrease). Examples:

Na+ (Sodium):

  • Water retention increases vascular volume, increased CO (BP increases)

Angiotensin I to Angiotensin II:

  • Increased vasoconstriction will increase PVR (BP increases).
  • Younger patients have higher renin levels compared with the

Sympathetic System Stimulation:

  • Epinephrine secretion causes tachycardia and vasoconstriction (BP increases).

Alpha-Blockers, Beta-Blockers, Calcium-Channel Blockers:

  • Drugs decrease peripheral vascular resistance from vasodilation (BP decreases).

Pregnancy:

  • Systemic vascular resistance is lowered due to hormones (systolic and diastolic BP decreases during the first and second trimesters).

Labs

Kidneys: Creatinine, urinalysis

Endocrine: TSH, fasting blood glucose

Electrolyte: Potassium (K+), sodium (Na+), calcium (Ca2+)

Heart: Cholesterol, HDL, LDL, triglycerides (complete lipid panel)

Anemia: CBC

Baseline EKG and chest x-ray (to rule out cardiomegaly)

Rule Out Target Organ Damage

Look for the following clinical findings:

Microvascular Damage

Eyes

  • Silver and/or copper wire arterioles
  • Arteriovenous junction nicking (caused when an arteriole crosses on top of a vein)
  • Flame-shaped hemorrhages, papilledema Kidneys
  • Microalbuminuria and proteinuria
  • Elevated serum creatinine and abnormal eGFR (rule out kidney disease)
  • Peripheral or generalized edema

Macrovascular damage Heart

  • S3 (CHF)
  • S4 (LVH)
  • Carotid bruits (narrowing due to plaque, increased risk of CAD)
  • CAD and acute MI
  • Decreased or absent peripheral pulses (pulmonary artery disease [PAD])

Brain

  • Transient ischemic attacks (TIAS) with ischemic brain damage
  • Hemorrhagic strokes (cerebrovascular accident [CVA])
Secondary HTN

The causes of secondary HTN can be classified into three major groups:

  1. Renal (renal artery stenosis, polycystic kidneys, chronic kidney disease)
  2. Endocrine (hyperthyroidism, hyperaldosteronism, pheochromocytoma)
  3. Other causes (obstructive sleep apnea, coarctation of the aorta)

Renal artery stenosis is more common in younger adults. Middle-aged adults are more likely to have endocrine-related disorders. Chronic kidney disease is more common in elderly patients.

Rule out secondary cause and maintain a high index of suspicion if the following: Age younger than 30 years

Severe HTN or acute rise in BP (previously stable patient)

Resistant HTN despite treatment with at least three antihypertensive agents Malignant HTN (severe HTN with end-organ damage such as retinal hemorrhages, papilledema, acute renal failure, and severe headache

Other causes include:

Coarctation of the aorta

  • BP of the arms is higher than BP of the legs
  • Delayed or diminished femoral pulses (check both radial and femoral pulse at the same time)

Sleep apnea

  • Sleep partner will report severe snoring with apneic episodes during sleep
  • Marked hypoxic episodes during sleep increases BP

Clinical Findings Kidneys

Bruit epigastric or flank area (renal artery stenosis); avoid angiotensin-converting enzyme inhibitors (ACEIS) and angiotensin receptor blockers (ARBS) Enlarged kidneys with cystic renal masses (polycystic kidney)

Increased creatinine and decreased GFR (renal insufficiency to renal failure)

Endocrine

Primary hyperaldosteronism

  • HTN with hypokalemia (low K+)
  • Normal to elevated sodium levels (high/normal Na+) Hyperthyroidism
  • Weight loss, tachycardia, fine tremor, moist skin, anxiety
  • New onset of AF (check EKG)
  • Check TSH Pheochromocytoma
  • Excessive secretion of catecholamines (causes severe HTN, arrhythmias)
  • Labile increase in BP accompanied by palpitations
  • Sudden onset of anxiety, sweating, severe headache
How to Diagnose HTN

Check BP (serial BP) and confirm diagnosis at another subsequent visit from 1 to 4 weeks (after initial visit). Check BP at home and keep diary. Does office BP correlate with home BP monitoring results? If home BP numbers lower, rule out white-coat hypertension.

JNC 8 treatment goals have been grouped by age, race, and disease (chronic kidney disease [CKD] and diabetes mellitus [DM]). In a nutshell, the goal is BP less than 140/90 mmHg for everyone. The exception is older patients (60 years of age or older) who do not have CKD and/or DM; the systolic BP can go up by 10 mmHg (<150/90 mmHg).

“White Coat” Hypertension

Office BP readings are consistently elevated compared with home BP measurements. To rule out, have patient check his or her BP outside of the clinic a few times and compare with office BP.

Hypertensive Emergency

Diastolic BP greater than 120 mmHg (severe hypertension) with clinical findings of target organ damage such as nausea and vomiting (increased intracranial pressure [ICP]), CVA/TIA, subarachnoid hemorrhage, MI, acute PE, acute renal failure, retinopathy (flame-shaped hemorrhages), papilledema, acute severe low-back pain (dissecting aorta).

Isolated Systolic Hypertension in the Elderly

Caused by loss of recoil in the arteries (atherosclerosis), which increases PVR. Pulse pressure (systolic BP – diastolic BP) increases in this disorder.

For frail patients with severe orthostatic hypotension (falls, syncope) or if older than age 60 (without CKD or DM), it is now acceptable to have a systolic BP of up to 150 mmHg.

Treatment Plan

Thiazide diuretics at low dose (chlorthalidone 12.5 to 25 mg/d)

And/or can start with long-acting dihydropyridine CCB (amlodipine/Norvasc, nifedipine/Procardia XL) and/or ACEI or ARB

Orthostatic Hypotension

Elderly are at higher risk for orthostatic hypotension due to a less active autonomic nervous system and slower metabolism of drugs by the liver (prolongs half-life of drugs).

To Evaluate for Orthostatic Hypotension

Check BP in both supine and standing positions, especially in the elderly, before and after treatment for HTN.

Ask patient if dizzy or lightheaded with changes in position.

Lifestyle Recommendations

This is the first-line therapy for HTN, hyperlipidemia, and type 2 DM:

Lose weight if overweight (body mass index [BMI] 25–29.9) or obese (BMI 30 or higher).

Normal weight is a BMI of 18.5 to 24.9. Stop smoking. Reduce stress level.

Reduce dietary sodium:

  • Less than 4 g per day (2,400 mg/d)

Maintain adequate intake of potassium, calcium, and magnesium. Limit alcohol intake:

  • 1 ounce (30 mL) or less per day for men
  • 5 ounce or less per day for women

Eat fatty cold-water fish (salmon, anchovy) three times a week.

DASH Diet (Dietary Approaches to Stop HTN)

Recommended for prehypertension, HTN, weight loss. Goal is to eat foods rich in potassium, magnesium, and calcium. Reduce red meat and processed foods. Eat more whole grains, legumes. Eat more fish and poultry.

Grains: Seven to eight daily servings

Fruits and vegetables: Four to five daily servings

Nuts, seeds, and dry beans: Four to five servings per week

Fats, oils, or fat-free dairy products: Two to three daily servings

Meat, poultry, and fish: Two or fewer daily servings Sweets: Try to limit to fewer than five servings per week Avoid high-sodium foods:

  • Cold cuts, ready-made foods, any pickled foods (cucumbers, eggs, pork parts)
Dietary Sources of Minerals

Calcium (low-fat dairy)

Potassium (most fruits and vegetables) Magnesium (dried beans, whole grains, nuts) Omega-3 oils (anchovy, krill, salmon, flaxseed)

Exercise

Advise that aerobic physical activity will reduce LDL cholesterol and BP. Frequency: Three to four sessions per week

Intensity: Moderate to vigorous (50%–80% of exercise capacity) Duration: 40 minutes average

Modalities: Walking, treadmill, cycling, rowing, stair-climbing; include resistance exercises for 2 to 3 days (e.g., elastic bands, weight machines, dumbbells)

Medications

Under JNC 8, can initiate treatment with one to two antihypertensive medications (combination drug or two separate agents)

Diuretics: General

All diuretics will decrease blood volume, venous pressure, and preload (cardiac filling). Effect is antagonized by NSAIDS. Monitor electrolytes, especially K+.

Thiazide Diuretics

Action: Change the way that the kidney handles sodium, which increases urine output.

Have a favorable effect with osteopenia/osteoporosis (slows down demineralization). All thiazides contain sulfa compounds. Avoid if patient has a sulfa allergy.

Side Effects

“Hyper”

  • Hyperglycemia (be careful with diabetics)
  • Hyperuricemia (can precipitate a gout attack)
  • Hypertriglyceridemia and hypercholesteremia (check lipid profile) “Hypo”
  • Hypokalemia (potentiates digoxin toxicity, increases risk of arrhythmias)
  • Hyponatremia (hold diuretic, restrict water intake, replace K+ loss)
  • Hypomagnesemia

Contraindications

Sensitivity to sulfa drugs and thiazides

Examples

Hydrochlorothiazide 12.5 to 25 mg PO daily Chlorthalidone (Hygroton) 12.5 to 25 mg PO daily Indapamide (Lozol) PO daily

Loop Diuretics

Action: Inhibit the sodium–potassium–chloride pump of the kidney in the loop of Henle.

Side Effects

Hypokalemia (potentiates digoxin toxicity, increases risk of arrhythmias) Hyponatremia (hold diuretic, restrict water intake, replace K+ loss) Hypomagnesemia

Possibly altered excretion of lithium and salicylates

Contraindications

Sensitivity to loop diuretics

Furosemide (Lasix) PO BID Bumetanide (Bumex) PO BID

Sulfa Allergy and Diuretics

If people are allergic to sulfa, they may have cross-sensitivity to thiazides and loop diuretics. Other drugs with sulfa are sulfonylureas, sulfa antibiotics, sulfasalazine, some protease inhibitors (darunavir, fosamprenavir). May also be sensitive to topical sulfas (ophthalmic drops) or topical silver sulfadiazine (Silvadene).

Aldosterone Receptor Antagonist Diuretics

Action: Antagonizes the action of aldosterone. Increases elimination of water in the kidneys and conserves potassium. Drug class also known as mineralocorticoid receptor antagonists or antimineralcorticoid.

Indications: Administer for HTN, heart failure, hirsutism, precocious puberty.

Avoid combining with potassium-sparing diuretics, ACEIS, or potassium supplements.

Side Effects

Gynecomastia, galactorrhea Hyperkalemia

GI (vomiting, diarrhea, stomach cramps), postmenopausal bleeding, erectile dysfunction

Contraindications

Hyperkalemia (serum potassium greater than 5.5 mEq/L)

Renal insufficiency (serum creatinine greater than 2.0 mg/dL in men or greater than 1.8 mg/dL for women)

DM type 2 with microalbuminuria

Examples

Spironolactone (Aldactone) daily Eplerenone (Inspra) daily

Beta-Blockers

Avoid abrupt discontinuation after chronic use. Wean slowly. May precipitate severe rebound hypertension.

Action: Decreases vasomotor activity, CO, inhibits renin and norepinephrine release. Blocks beta receptors on the heart and the peripheral vasculature. There are two types of beta-blocker receptors in the body: B1 (cardiac effects) and B2 (lungs and peripheral vasculature).

Contraindications

Asthma, COPD, chronic bronchitis, emphysema (chronic lung disease) Second- and third-degree heart block (fine to use with first-degree block) Sinus bradycardia

Acute MI: Reduces mortality during acute MI and post-MI

Migraine headache: For prophylaxis only (not for acute attacks)

Glaucoma: Reduces intraocular pressure (Betimol ophthalmic drops for open-angle glaucoma)

Resting tachycardia (target heart rate <100 beats/min)

Angina pectoris: Treats symptoms

Post-MI: Decreases mortality

Hyperthyroidism and pheochromocytoma: To control symptoms until primary disease treated

Beta-blockers: Ends with “-olol”:

  • Metoprolol (Lopressor) 100 mg QD to BID
  • Atenolol (Tenormin) 50 mg daily
  • Propranolol (long-acting Inderal) 40 mg BID

Do not use propranolol (plain Inderal) to treat HTN (shorter half-life)

Calcium Channel Blockers (CCBS)

Action: Blocks voltage-gated calcium channels in cardiac smooth muscle and the blood vessels. Results in systemic vasodilation. The nondihydropyridines depress the muscles of the heart (inotropic effect). The dihydropyridines slow down heart rate (chronotropic effect).

Side Effects

Headaches (due to vasodilation)

Ankle edema (caused by vasodilation and considered benign)

Heart block or bradycardia (depresses cardiac muscle and AV node) Reflex tachycardia (seen with dihydropyridines such as nifedipine)

Contraindications

Second- and third-degree heart block (fine to use with first-degree block) Bradycardia

CHF

Examples

Dihydropyridine CCBs (“-pine” ending): Nifedipine (Procardia XL) daily Amlodipine (Norvasc) daily Felodipine (Plendil) daily

Nondihydropyridine CCBs: Verapamil (Calan SR) daily to BID Diltiazem (Cardizem CD) daily

ACEIs and ARBs

Blocks conversion of angiotensin I to II (more potent vasoconstrictor) DM and/or CKD: Drugs of choice (protect kidneys)

Fetal kidney malformations and fetal hypotension

Side Effects

Dry hacking cough (up to 10% with ACEIs; less with ARBs) Hyperkalemia, angioedema (rare but may be life-threatening)

Contraindications

Moderate to severe kidney disease Renal artery stenosis

  • Precipitates acute renal failure if given ACEI or ARB
  • Hyperkalemia (this is also a side effect of ACEIs and ARBs; will have additive effect)

Examples

ACEIs

  • Ramipril (Altace) once a day in one to two divided doses
  • Benazepril (Lotensin) once a day initially
  • Enalapril (Vasotec) once a day in one to two divided doses

ARBs

  • Losartan (Cozaar) once a day in one to two divided doses
  • Candesartan (Atacand) once a day in one to two divided doses
  • Olmesartan (Benicar) once a day in one to two divided doses

Alpha-1 Blockers/Antagonists

Also known as alpha-adrenergic blockers. Suffix of “zosin.” Potent vasodilators. Common side effects are dizziness and hypotension. Give at bedtime at very low doses and slowly titrate up.

Side Effects

“First-dose orthostatic hypotension” is common (warn patient).

Side effects are dizziness and postural hypotension (common side effect). May cause severe hypotension and reflex tachycardia.

Give at bedtime. Start at very low doses and titrate up slowly until good BP control. Advise patient to get out of bed slowly to prevent postural hypotension.

Not a first-line choice for HTN except for men with both HTN and benign prostatic hyperplasia (BPH). Alpha-blockers relax smooth muscle found on the bladder neck and the prostate gland and relieves obstructive voiding symptoms such as weak urinary stream, urgency, and nocturia.

Examples

Terazosin (Hytrin): Used for both HTN and BPH (starting dose 1 mg PO at bedtime) Doxazosin (Cardura): Used for both HTN and BPH

Tamsulosin (Flomax): Used for BPH only

Sample Case Scenarios (JNC 8)*

Can initiate with one to two antihypertensive medications (combined or two separate agents).

Heart failure: ACEI or ARB as first line, plus BB plus diuretic and others

DM: ACEI or ARB as first line; if African American, can start with CCB or thiazide

CKD: ARB or ACEI as first line; can add CCB or thiazides

Stroke history: ACEI or ARB as first-line drugs; add CCB or thiazide as second-line drugs

African Americans (including people with DM): Thiazides or CCBs

EXAM TIPS

Follow JNC 8 guidelines for both ANCC and AANPCB exams.

Eye findings: Learn to distinguish the findings in hypertensive retinopathy (copper and silver wire arterioles, arteriovenous nicking) from those in diabetic retinopathy (neovascularization, cotton wall spots, microaneurysms). Arteriovenous nicking occurs when a retinal vein is compressed by an arteriole that causes the venule to collapse.

Isolated systolic HTN in the elderly: Preferred medications are low-dose thiazide diuretic or CCB (long-acting dihydropyridine).

To assess orthostatic hypotension, measure both, the supine first, then standing BP. Memorize the side effects of thiazide diuretics.

Side effect of spironolactone is gynecomastia Spironolactone is side effect of gynecomastia.

Memorize the numbers for a normal BP and for stages I and II HTN.

ACEIs or ARBs: Use for DM, CKD, and heart failure. It may cause a dry cough (10%).

Careful when combining ACEIs with potassium-sparing diuretics (i.e., triamterene, spironolactone) because of increased risk of hyperkalemia.

Bilateral renal artery stenosis: ACEIs or ARBs will precipitate acute renal failure. Alpha-blockers are not first-line drugs for HTN except if patient has preexisting BPH.

Women with HTN and osteopenia/osteoporosis should receive thiazides. Thiazides help bone loss by slowing down calcium loss (from the bone) and stimulating osteoclasts.

CLINICAL PEARLS

Hypertensive patients who are less than 20/10 mmHg above goal can initially be treated with monotherapy (Mann, 2017).

Per JNC 8, consider chlorthalidone or indapamide (instead of hydrochlorothiazide); better evidence and longer half-life.

Heart Failure

Numerous causes and precipitating factors such as an acute MI, CAD, HTN, fluid retention, valvular abnormalities, arrhythmias, and so on. Ejection fraction (EF) less than 40% is also known as systolic heart failure (or heart failure with reduced ejection fraction/HFrEF). If EF more than 40%, also known as diastolic failure (or heart failure with preserved ejection fraction/HFpEF). Heart failure patients are best managed by cardiologists or heart clinics.

Left Ventricular Failure

Crackles, bibasilar rales (rales on lower lobes of the lungs), cough, dyspnea, decreased breath sounds, dullness to percussion

Paroxysmal nocturnal dyspnea, orthopnea, nocturnal nonproductive cough, wheezing (cardiac asthma), hypertension, and fatigue are symptoms of both left and right heart failure

Right Ventricular Failure

Jugular venous distention (JVD): Normal JVD is 4 cm or less

Enlarged spleen, enlarged liver causes anorexia, nausea, and abdominal pain Lower extremity edema with cool skin

Other PE Findings

Presence of S3 gallop, which can be accompanied by anasarca (severe generalized edema due to effusion of fluid into the extracellular space)

Labs

Chest x-ray result will show increased heart size, interstitial and alveolar edema, Kerley B lines, and other signs of pulmonary edema

EKG, CPK, cardiac troponins, B-type natriuretic peptide BUN and creatinine, electrolytes, CBC, liver function tests Echocardiogram with Doppler flow study

Weight should be checked daily to detect fluid accumulation

Treatment Plan

If acute decompensated heart failure: Refer to ED (IV furosemide, oxygen, vasodilators, others).

Stable HF (HFrEF) with hypertension: Start on ACEI or ARB, then add a beta-blocker, aldosterone-receptor antagonist (spironolactone), and other medications as needed (Colucci, 2018; Ferri, 2016).

Limit sodium intake.

Patients with HF are best managed by cardiologists or at a heart clinic.

Use beta-blocker if heart failure with reduced EF (carvedilol, bisoprolol, extended- release metoprolol succinate); start with very low dose; careful with initial dosing, can worsen; consult or refer to experienced heart clinic

Use New York Heart Association (NYHA) system to classify patient’s degree of cardiac disability

Refer to cardiologist; if in distress, refer to ED

Lifestyle Modification for Heart Failure

Restrict or abstain from alcohol. Smoking cessation if smoker; weight loss Restrict sodium to 2 to 3 g/d

Fluid restriction (1.5–2 L/d) may help some patients

Deep Vein Thrombosis (DVT)

Thrombi develop inside the deep venous system of the legs or pelvis secondary to stasis, trauma to vessel walls, inflammation, or increased coagulation. Pulmonary embolus is considered another manifestation of this thromboembolic disorder.

Etiology (three categories):

  1. Stasis: Prolonged travel/inactivity (more than 3 hours), bed rest, CHF
  2. Inherited coagulation disorders: Factor C deficiency, Leiden, and so forth
  3. Increased coagulation due to external factors: Oral contraceptive use, pregnancy, bone fractures especially of the long bones, trauma, recent surgery, malignancy
Classic Case

A patient with risk factors for DVT complains of gradual onset of swelling on a lower extremity after a history of travel (more than 3 hours) or prolonged sitting. The patient complains of a painful and swollen lower extremity that is red and warm. If patient has PE, it may be accompanied by abrupt onset of chest pain, dyspnea, dizziness, or syncope. Many patients are asymptomatic.

Treatment Plan

Homan’s sign: Lower leg pain on dorsiflexion of the foot (low sensitivity)

CBC, platelets, clotting time (PT/PTT, INR), D-dimer level, chest x-ray, EKG Ultrasonography (whole leg or proximal leg)

Hospital admission, heparin IV then warfarin PO (Coumadin) for 3 to 6 months (first episode) or longer

For recurrent DVT or elderly, antithrombotic treatment may last a lifetime

Complications

Pulmonary emboli

Stroke and other embolic episodes

EXAM TIPS

Memorize goal for atrial fibrillation is an INR of 2.0 to 3.0. Learn how to manage elevated INR

Memorize presentation of a patient with NYHA class II heart disease. First line medication for stable HF is an ACEI or ARB.

The S3 heart sound is a sign of HF, although it can also be heard in pregnant women and children/young adults.

Learn DVT risk factors.

Superficial Thrombophlebitis

Inflammation of a superficial vein due to local trauma. Higher risk if indwelling catheters, intravenous drugs (e.g., potassium), secondary bacterial infection (S. aureus). Some patients may have coexistent DVT.

Classic Case

Adult patient complains of an acute onset of an indurated vein (localized redness, swelling, and tenderness). Usually located on the extremities. The patient is afebrile with normal vital signs.

Objective Findings

Indurated cord-like vein that is warm and tender to touch with a surrounding area of erythema.

There should be no swelling or edema of the entire limb (think of DVT).

Treatment Plan

Administer NSAIDs, such as ibuprofen or naproxen sodium (Anaprox DS), BID. Warm compresses. Elevate limb.

If septic cause, admit to hospital.

Peripheral Arterial Disease (PAD)

Gradual (decades) narrowing and/or occlusion of medium to large arteries in the lower extremities. Blood flow to the extremities gradually decreases over time, resulting in permanent ischemic damage (gangrene of the toes/foot). Higher risk with HTN, smoking, diabetes, and hyperlipidemia. Previously known as peripheral vascular disease.

Classic Case

Older patient who has a history of smoking and hyperlipidemia complains of worsening pain on ambulation (intermittent claudication) that is instantly relieved by rest. Over time, symptoms worsen until the patient’s walking distance is greatly limited. Atrophic skin changes. Some have gangrene on one or more toes.

Ankle-Brachial Index (ABI)

ABI score equal or less than 0.9 is diagnostic for PAD. ABI score of 0.91 to 1.3 is normal.

Procedure

Systolic BP of the ankle and the arm (brachial) is checked after in a supine position for 10 minutes by using a BP cuff and ultrasound probe.

An ABI score is done for each leg.

To calculate ABI, the SBP of each foot is divided by the SBP of both arms.

Objective Findings

Skin: Atrophic changes (shiny and hyperpigmented ankles that are hairless and cool to touch); gangrene of the toe(s)

Cardiovascular: Decreased to absent dorsal pedal pulse (may include popliteal and posterior tibial pulse), increased capillary refill time (less than 2 seconds), and bruits over partially blocked arteries

Treatment Plan

Initial method (low tech): Check pedal and posterior tibial pulses.

Ankle-Brachial index (ABI) Score: Used to evaluate severity of PAD; done by checking systolic BP of ankles and upper arm; score of 0.9 or less is diagnostic of PAD. Encourage smoking cessation (smoking causes vasoconstriction) and daily ambulation exercises

Pentoxifylline (Trental) if indicated, but effect is marginal (compared with cilostazol) Cilostazol (Pletal) is a phosphodiesterase inhibitor (direct vasodilator); can be taken with aspirin or clopidogrel. Grapefruit juice, diltiazem, and omeprazole can increase serum concentration if taken together. Percutaneous angioplasty or surgery for severe cases

Complications

Gangrene of foot and/or lower limb with amputation Increased risk of CAD

Increased risk of carotid plaquing (check for carotid bruits)

Raynaud’s Phenomenon

Reversible vasospasm of the peripheral arterioles on the fingers and toes. Cause is unknown. Associated with an increased risk of autoimmune disorders (e.g., thyroid disorder, pernicious anemia, rheumatoid arthritis). Most patients are females (60% to 90%), with a gender ratio of 8:1. Patients with no underlying disease have “primary” Raynaud’s phenomenon. Up to 95% of patients with scleroderma have “secondary” Raynaud’s phenomenon.

Classic Case

A middle-aged woman complains of chronic and recurrent episodes of color changes on her fingertips in a symmetric pattern (both hands and both feet). The colors range from white (pallor) and blue (cyanosis) to red (reperfusion). Complains of numbness and tingling. Attacks last for several hours. Hands and feet become numb with very cold temperatures. Ischemic changes may be present after a severe episode such as shallow ulcers (that eventually heal) on some of the fingertips.

Treatment Plan

Avoid touching cold objects, cold weather; avoid stimulants (e.g., caffeine) Smoking cessation is important; nifedipine (Adalat) or amlodipine (Norvasc) Evaluate: Check distal pulses, ischemic signs (ischemic ulcers at the fingers/toes) Do not use any vasoconstricting drugs (e.g., Imitrex, ergots, pseudoephedrine/decongestants, amphetamines); avoid nonselective beta-blockers

Complications

Small ulcers in the fingertips and toes

EXAM TIPS

Raynaud’s phenomenon: Think of the colors of the American flag as a reminder for this disorder.

Medicines for Raynaud’s phenomenon include CCBs (nifedipine, amlodipine)

Bacterial Endocarditis

Presentation ranges from full-blown disease to subacute endocarditis. Bacterial pathogens are gram positive (i.e., viridans streptococcus, S. aureus, etc.). Also known as IE.

Classic Case

A middle-aged male presents with fever, chills, and malaise that are associated with subungual hemorrhages (splinter hemorrhages on nail bed) and tender violet-colored nodules on the fingers and/or on the toes (Osler’s nodes). Palms and soles may have tender red spots on the skin (Janeway lesions). Some patients may have a heart murmur.

Treatment Plan

Refer to cardiologist or ED for hospitalization and intravenous antibiotics Blood cultures × three (first 24 hours)

CBC (elevated WBCs) and sedimentation rate greater than 20 mm per hour (elevated)

Complications

Valvular destruction, myocardial abscess, emboli, etc.

Endocarditis Prophylaxis

Antibiotic prophylaxis is no longer recommended for:

  • Mitral valve prolapse
  • Genitourinary or GI incisions/invasive procedures (except if there is an existing infection present such as a urinary tract infection [UTI] before a cystoscopy)

Standard regimen: Give 1 hour before procedure:

  • Amoxicillin 2 g PO × 1 dose (adults)
  • Amoxicillin 50 mg/kg 1 hour before procedure × one dose (children)
Penicillin Allergy

Clindamycin 600 mg or clarithromycin (Biaxin) 500 mg or cephalexin (Keflex) 2 g

Mitral Valve Prolapse (MVP)

The classic finding is an S2 “click” followed by a systolic murmur. Some patients with

MVP are at higher risk of thromboemboli, TIAs, AF, and ruptured chordae tendineae. Diagnosed by cardiac echocardiogram with Doppler flow study.

Classic Case

Tall and thin adult female patient complains of fatigue, palpitations, and lightheadedness (orthostatic hypotension) that is aggravated by heavy exertion. May be asymptomatic. Associated with pectus excavatum, hypermobility of the joints, arm span greater than height (rule out Marfan’s syndrome).

Treatment Plan

Asymptomatic MVP does not need treatment.

MVP with palpitations is treated with beta-blockers, avoidance of caffeine, alcohol, and cigarettes.

Holter monitoring is useful in detecting significant arrhythmias.

Hyperlipidemia

The treatment guidelines and type of statin and intensity (low, moderate, or high dose) are from the 2014 updated American College of Cardiology (ACC) and American Heart Association (AHA) Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Disease Risk. See the ACC web address for tool (http://tools.acc.org/ascvd-risk-estimator).

To determine the risk of atherosclerotic cardiovascular disease (ASCVD), use the ACC’s new “ASCVD Risk Estimator” tool (or the Pooled Cohort Equations for ASCVD risk prediction). The free app is available and can be accessed directly online (see previous paragraph).

Screening Guidelines

Complete lipid profile (fasting) starting at age 20 (then every 5 years) Older than age 40 years, screen every 2 to 3 years

Preexisting hyperlipidemia: Screen annually or more frequently

Total Cholesterol

Normal: Less than 200 mg/dL Borderline: Between 200 and 239 mg/dL High: Greater than 240 mg/dL

HDL Cholesterol (HDL-C) Men: Greater than 40 mg/dL Women: Greater than 50 mg/dL

If less than 40 mg/dL, associated with increased risk of CAD even if normal LDL or cholesterol

High carbohydrate and low-fat diets and smoking are associated with low HDL Lifestyle modifications: Do regular moderate cardiovascular/aerobic exercises most days of the week, lose weight, eat healthy fats (salmon, tuna, nuts), eliminate trans fats, stop smoking

LDL cholesterol (LDL-C)

Optimal: Less than 100 mg/dL

LDL: Less than 130 mg/dL for low-risk patients with fewer than two risk factors

Very high: Greater than 190 mg/dL

Heart disease or diabetes: Less than 100 mg/dL

Triglycerides

Normal: Less than 150 mg/dL

High risk of acute pancreatitis: 1000 mg/dL or higher If triglycerides >500 mg/dL or higher:

  • Treat triglycerides Give fibrate such as fenofibrate (Tricor), niacin (Niaspan), OTC niacin, or high-dose fish oil (EPA/DHA). Prescription fish oil: Lovaza 4 g/d; when triglycerides are under control, switch target to lowering LDL

Possible causes: Metabolic syndrome, DM, familial hypertriglyceridemia, alcohol abuse, hyperthyroidism, kidney disease, medications (anabolic steroids, Accutane, etc.)

Lifestyle modifications: Decrease sugar and simple carbohydrates (junk food), avoid alcoholic drinks, follow low-fat diet, eat fish with omega-3 (salmon, sardines) twice a week, lose weight and increase aerobic type physical activity.

Risk Factors: Heart Disease

HTN

Family history of premature heart disease (women with MI before age 65 years or men with MI before age 55 years)

DM (considered a CHD risk equivalent even if patient has no history of preexisting heart disease)

Dyslipidemia

Low HDL-C (<40 mg/dL)

Age (men older than 45 or women older than 55) Cigarette smoking

Obesity (BMI ≥30 kg/m2) Microalbuminuria Carotid artery disease PVD

Treatment Plan: Hyperlipidemia

First-line treatment is lifestyle changes (weight loss, exercise most days of the week, better diet low in saturated fat, smoking cessation), but the presence of ASCVD and other factors, initiate statin therapy with lifestyle changes.

Reduce dietary salt intake and learn about the DASH diet (low salt, low saturated fat <30%).

Encourage use of soluble fiber in diet (e.g., inulin, guar gum, fruit, vegetables) to enhance lowering of LDL (lowers LDL by blocking absorption in GI tract up to 10%). Target goal is to lower LDL first (except if very high triglyceride levels). If high triglycerides (500 mg/dL or higher), treat hypertriglyceridemia first because patients are at high risk for acute pancreatitis.

Low HDL alone (even if normal LDL and cholesterol) is a risk factor for heart disease.

ACC and AHA Updated Guidelines

The 2013 ACC and AHA updated guidelines have no recommendations for or against specific target levels for LDL or HDL in the primary or secondary prevention of ASCVD. The expert panel did not find evidence to support use of specific LDL-C or HDL-C target levels. Previously, the goal for secondary prevention was LDL of 70 mg/dL and for primary prevention LDL of less than 100 mg/dL.

The ACC and AHA Guideline on the Treatment of Blood Cholesterol to Reduce ASCVD Risk (2014) list four statin benefit groups, which are discussed in terms of type of prevention (secondary or primary). These are outlined here and summarized in Table 7.8. Table 7.9 categorizes statin drugs by level of intensity of treatment.

  1. Secondary Prevention (ASCVD):
    1. Patients with any form of ASCVD (history of MI, CAD, angina, stroke/TIA, PAD, coronary revascularization)

Younger than 75 years: High-intensity statin

Older than 75 years (or not candidate for high-intensity statin): Moderate- intensity statin

  1. Primary Prevention (No ASCVD)
  2. LDL-C 190 mg/dL or higher: High-intensity statin
  3. DM (aged 40–75 years) with LDL 70 to 189 mg/dL: Moderate-intensity statin
  4. Without DM or ASCVD (aged 40–75 years) with an estimated 10-year ASCVD risk of 7.5% or higher: Moderate-intensity to high-intensity statin
Lipid-Lowering  Medications

HMG CoA reductase inhibitors (statins) are best at lowering LDL, and some can moderately increase HDL. Under 2014 ACC/AHA guidelines, only two high-intensity statins are recommended: atorvastatin (Lipitor; 40–80 mg/d) and rosuvastatin (Crestor; 20–40 mg/d; see Table 7.9.) But in “real life,” start at lower doses and titrate dose slowly until correct dose reached.

If high-intensity statin candidate, start at lower doses and titrate up slowly. Some patients may not tolerate high-intensity statins (muscle pains, weakness, etc.) but can tolerate moderate-intensity statins. If not effective after a few months, consider low- to moderate-intensity statin dosing.

Pravastatin (Pravachol), lovastatin (Mevacor), simvastatin (Zocor) Simvastatin and lovastatin drug interactions (high risk of rhabdomyolysis):

  • Avoid grapefruit juice
  • Fibrates
  • Antifungals (itraconazole, ketoconazole)
  • Macrolides (erythromycin, clarithromycin, telithromycin)
  • Amiodarone (Cordarone), some CCBs (diltiazem, amlodipine, verapamil) Combination regimens (especially in high doses) of statins, fibrates, niacin, and/or ezetimibe increase the risk of rhabdomyolysis and drug-induced hepatitis and are now discouraged
Nicotinic Acid and Fibrates

Nicotinic acid: Niacin (OTC) daily to TID, Niaspan (slow-release niacin) daily. Avoid combining niacin with statins (higher risk of liver damage).

Fibrates: Gemfibrozil (Lopid), fenofibrate (Tricor). Do not use with severe renal disease. Action: Reduces production of triglycerides by the liver and increases production of HDL.

Very good agents for lowering triglycerides and elevating HDL level. Less effective at lowering LDLs compared with the statins.

Side effects of niacin: Flushing, itching, tingling, hepatotoxicity; GI effects. Take ASA (aspirin) with niacin after a meal. Divide niacin and take half (or less) of the tablet until higher dose tolerated.

Side effects of fibrates: Dyspepsia, gallstones, are side effects; myopathy

Bile Acid Sequestrants

Cholestyramine (Questran Light), colestipol (Colestid), colesevelam (Welchol)

  • Action: Work locally in the small intestine; interfere with fat absorption, including fat-soluble vitamins (vitamins A, D, E, and K)

Alternative drug for patients who cannot tolerate statins, fibrates, and niacin Used alone, it is not as effective as statins in lowering LDL; no hepatotoxicity

  • Side effects: Bloating, flatulence, abdominal pain; start at low doses and titrate up slowly
  • Side effects mainly from the GI tract; advise patient to take multivitamin tablets daily
Other Lipid-Lowering Drugs

Ezetimibe (Zetia) and combination of simvastatin and ezetimibe (Vytorin)

  • Can be taken alone or combined with a statin; can also cause rhabdomyolysis (rare)
  • Side effects: Diarrhea, joint pains, tiredness

Prescribe fish oil omega-3 DHA/EPA Lovaza 4 g/d (for high triglycerides)

Lab Tests

Avoid combination regimen (especially in high doses) of statins, fibrates, niacin, ezetimibe, and drugs that affect the CYP450 system; increases risk of rhabdomyolysis and drug-induced hepatitis.

Test baseline LFTs and periodic testing as clinically indicated.

Rhabdomyolysis

Acute breakdown of skeletal muscle (myoglobins) will cause acute renal failure. Triad of muscle pain, weakness, and dark urine. Look for muscle pain and aches that persist (not associated with muscular exertion). Higher doses or combination therapy have higher risk.

Labs: Order creatine kinase if markedly elevated (at least five times the upper limit of normal from 1,500 to >100,000 IU/L).

Urine: Reddish-brown color (myoglobinuria) and proteinuria in up to 45% LFTs (will be elevated). Other labs are UA, BUN, creatinine, potassium/electrolytes, EKG, others.

Acute Drug-Induced Hepatitis

Anorexia, nausea, dark-colored urine, jaundice, fatigue, flu-like symptoms

Labs: Elevated ALT and AST

Patient Education

Minimize alcohol intake or other hepatotoxic substances while on statins. Avoid prescribing to alcoholics.

Advise patient to report symptoms of hepatitis or rhabdomyolysis. If present, tell patient to stop the drug and to call or go to ED.

First-line treatment for hypertension (or prehypertension) is lifestyle and dietary changes.

First-line treatment for hyperlipidemia is lifestyle, but presence of ASCVD or equivalents, need drug therapy, too.

You must memorize some values. These are (list is not all inclusive):

  • An adult (21–75 years) with any type of ASCVD (CAD, PAD, stroke, TIA, etc.) is given high-intensity statins such as atorvastatin 40 to 80 mg or rosuvastatin 20 to 40 mg (considered as secondary prevention).
  • An adult with LDL greater than 190 mg/dL (without ASCVD or DM) is a candidate for high-intensity statin dosing.
  • If 10-year estimated ASCVD risk (for up to 75 years of age) is 5% or higher, high-intensity statin dosing is recommended. But if risk is less (5%–7.5%), try lifestyle first.

If patient has markedly high triglycerides (500 mg/dL or higher), lower triglyceride first (niacin or fibrate) before treating the high cholesterol and LDL levels. High triglycerides increase risk of acute pancreatitis.

  • Educate to avoid alcohol, acetaminophen (hepatotoxic)
  • Obese patients: Encourage weight loss and reduce simple carbohydrates, sugars, junk foods. Treat first before treating high LDL.
  • Advise patient to reduce intake of simple carbohydrates, “junk” foods, and fried

Niacin and fibrates are best agents for lowering triglycerides.

Become familiar with dietary sources of magnesium, potassium, and calcium. Bacterial endocarditis prophylaxis drug and dose, splinter hemorrhages on nails, Janeway lesions (red macules palms/soles not painful), Osler’s nodes (painful violaceous nodes found mostly on pads of the fingers and toes, thenar eminence).

Statins may cause memory loss, confusion, etc. (cognitive effects), which are reversible upon discontinuation of statin therapy.

Patients on simvastatin and lovastatin should avoid grapefruit juice. Also, they should not mix these two statins with macrolides.

Muscle pain (mild to severe) from rhabdomyolysis is usually located on the calves, thighs, lower back, and/or shoulders. Urine will be darker than normal (reddish- brown color). Rule out rhabdomyolysis if patient on a statin complains of muscular pain with dark-colored urine.

Obesity

All obese and overweight patients should have their BMI and abdominal obesity calculated (Table 7.10). Evaluate for metabolic syndrome and DM type 2. In the United States, more than one third (36.5%) of adults are obese (Centers for Disease Control and Prevention, 2016). Non-Hispanic Blacks have the highest rates of obesity (48.1%), followed by Hispanics (42.5%) and non-Hispanic Whites (34.5%). Among the obese, 40.2% are middle-aged adults (age 40–59 years).

Abdominal Obesity

The “apple-shaped” body type is considered more dangerous for health compared with the “pear-shaped” body type.

Waist Circumference

Males: Greater than 40 inches or 102 cm

Females: Greater than 35 inches or 88 cm

Waist-to-Hip Ratio

Waist-to-hip ratio: 1.0 or higher (males) Waist-to-hip ratio: 0.8 or higher (females)

Metabolic Syndrome

Metabolic syndrome is a metabolic disorder with a cluster of symptoms. These patients are at higher risk for type 2 DM and cardiovascular disease.

Criteria for Metabolic Syndrome (Adult Treatment Panel III)

At least three characteristics must be present to diagnose metabolic syndrome:

  1. Abdominal obesity (greater than 40 inches in men and greater than 35 inches in women)
  2. HTN
  3. Hyperlipidemia
    • Fasting plasma glucose (>100 mg/dL)
    • Elevated triglycerides (>150 mg/dL)
    • Decreased HDL (<40 mg/dL)
Labs

Fasting (from 9 to 12 hours) lipid profile (especially triglycerides and HDL) Fasting blood glucose

Nonalcoholic Fatty Liver Disease (NAFLD)

Nonalcoholic fatty liver disease (NAFLD) is caused by triglyceride fat deposits in the hepatocytes of the liver. Most are asymptomatic.

Risk factors: Obesity, diabetes, metabolic syndrome, HTN, certain drugs

Classic Case

Usually asymptomatic. Some patients may have hepatomegaly. Annual physical exam labs will show mild to moderate elevations of ALT and AST. If symptomatic, complains of fatigue and malaise with vague right upper quadrant pain. Associated with obesity, metabolic syndrome, DM, and hyperlipidemia.

Labs

Liver function tests. ALT and AST may be slightly elevated. Order hepatitis A, B, and C profile.

Refer to GI specialist for management and a liver biopsy (gold standard).

Treatment Plan

Lose weight. Exercise and watch diet. Discontinue alcohol intake permanently.

Avoid hepatotoxic drugs (i.e., acetaminophen, isoniazid, statins).

Recommend vaccination for hepatitis A and B. Recommend annual flu vaccine. Refer to GI specialist for liver biopsy.

Calculating BMI

The BMI is a measure of the ratio of weight to height. Muscular patients can have falsely elevated BMIs (higher muscle mass).

Formula for BMI calculation: Weight (kilograms)/Height (meters)2

Patient Education

All obese and overweight patients should be advised to lose weight (especially diabetics). Lifestyle changes are important (diet, nutrition, exercise, portion control).

Daily aerobic exercise (walking, swimming, biking, etc.) for 30 to 45 minutes is recommended.

  • Weight Watchers: Some patients like the support and education (tertiary prevention).

EXAM TIPS

Expect about two questions about murmurs. Memorize mnemonics: MR. ASS (systolic murmurs) and MS. ARD (diastolic murmurs) and learn how to use them. Look for the timing (S1 or S2) and then the location.

Know metabolic syndrome criteria (abdominal obesity, HTN, hyperlipidemia or elevated triglycerides and low HDL, elevated fasting glucose >100 mg/dL) caused by hyperinsulinemia and peripheral insulin resistance.

Nonalcoholic fatty liver disease (NAFLD) is associated with metabolic syndrome and/or obesity. Look for slight elevation of ALT and AST (not related to alcohol or medications) and negative hepatitis A, B, and C.

Abdominal obesity in males (>40 inches), females (>35 inches).

Do not confuse BMI formula with the PEF (peak expiratory flow). PEF is calculated using the height, age, gender (mnemonic is “HAG”).

A person with a BMI of 27 is overweight (initiate lifestyle education).

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