1000-2000 5 ьшò

2 to 3 months postinitiation of all methods to assess tolerance

Check for IUD strings 1 month after insertion; spontaneous expulsion rate highest in the 1st month

BPcheck within 3 months of initiation in patients on estrogen-containing methods

DIET

St. John’s wort may alter estrogen levels, reducing efficacy or causing breakthrough bleeding.

PATIENT EDUCATION

Diaphragm: device inspected prior to each use, 1 tablespoon of spermicide in hollow of the dome, diaphragm is inserted into the vagina, additional applicator of spermicide placed in vagina. If placed >6 hours prior to intercourse need additional applicator of spermicide. Position needs to be checked post intercourse, and additional spermicide applied prior to each new episode of intercourse. Diaphragm should remain in place for at least 6 hours after the last episode of intercourse to maximize effectiveness.

Male condoms: New condom is placed on the penis before genital contact, remains intact until the penis is withdrawn; new condom needs to be used with every act of intercourse.

IUD: Patient should monitor presence of the string monthly following menses.

OCP: Pill should be taken at approximately the same time each day. Backup birth control method is needed for the first 7 days with quick start and Sunday start methods.

COMPLICATIONS

Estrogen-progestin contraceptives:

–Serious (requires discontinuation): stroke, thromboembolism, hypertension, myocardial infarction, and cholestatic jaundice

–Overall 5-fold increased risk of venous thrombosis compared to nonusers,

comparable to the 4-fold increased risk of venous thrombosis during pregnancy (4)[B], but absolute risk is low

Injectable contraceptive:

–Potential for decreased bone mineral density (BMD) if used for ≥2 years. Mostly recovers after discontinuation. Consider calcium/vitamin D supplementation if prolonged use.

Nexplanon: insertion site reaction including pain, bleeding, paresthesias, and

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infection

IUDs:

–PID: Treat without removal unless serious infection or failure to respond to therapy.

–Uterine perforation

–Absolute risk of ectopic pregnancy is reduced with IUD, but if pregnancy

does occur, there is a higher risk that it will be ectopic.

Sponge and diaphragm: rarely associated with toxic shock syndrome

REFERENCES

1.Daniels K, Daugherty J, Jones J. Current Contraceptive Status among Women Aged 15–44: United States, 2011–2013. Hyattsville, MD: National Center for Health Statistics; 2014. NCHS Data Brief, No 173.

2.Centers for Disease Control and Prevention. US Medical Eligibility Criteria (US MEC) for Contraceptive Use. https://www.cdc.gov/reproductivehealth/contraception/mmwr/mec/summary.h Accessed October 2, 2017.

3.American College of Obstetricians and Gynecologists. Practice Bulletin No. 152: emergency contraception. Obstet Gynecol. 2015;126(3):e1–e11.

4.van Hylckama Vlieg A, Helmerhorst FM, Vandenbroucke JP, et al. The venous thrombotic risk of oral contraceptives, effects of oestrogen dose and progestogen type: results of the MEGAcase-control study. BMJ. 2009;339:b2921.

ADDITIONALREADING

“CDC Contraception” Available as chart and app for smartphone “Chart comparing contraceptive methods: ARHPMethod Match at http://www.arhp.org/methodmatch/

CODES

ICD10

Z30.9 Encounter for contraceptive management, unspecified

Z30.41 Encounter for surveillance of contraceptive pills

Z30.431 Encounter for routine checking of intrauterine contracep dev

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CLINICALPEARLS

Hormonal and IUD contraceptives may be initiated immediately if the likelihood of preexisting pregnancy is low “Quick start” and improves adherence compared with traditional start.

LARC methods provide high efficacy and convenience for patients. All patients should be counseled on emergency contraception options.

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COR PULMONALE

Marissa Lombardo, MD Parag Goyal, MD, MSc

BASICS

DESCRIPTION

The term “cor pulmonale” derives from the Latin cor: heart and pulmonale: lungs. Hence, cor pulmonale is a cardiac complication of primary pulmonary disease.

Acute or chronic pulmonary processes can lead to increased right-sided cardiac pressures. Resultant pulmonary hypertension (PH) subsequently induces structural alterations and/or impairs right ventricle (RV) function.

PH may be secondary to abnormalities of the pulmonary system including disorders of the lung parenchyma, pulmonary circulation, chest wall, and/or ventilatory mechanisms. The pathophysiologic mechanisms of pulmonary arterial hypertension (WHO Group I) and PH secondary to pulmonary processes are biologically and clinically distinct. Therefore, for the purposes of this review, pulmonary arterial hypertension (WHO Group I) will not be considered as a cause of cor pulmonale.

Cor pulmonale may occur in acute or chronic setting.

–Acute: rapid increase of pulmonary arterial pressure resulting in RV overload, dysfunction, and potential cardiovascular collapse

–Chronic: progressive hypertrophy and dilation of the RV over months to years, leading to dysfunction, and potentially failure

EPIDEMIOLOGY

~6–7% of all types of adult heart disease in United States

Estimated 10–30% of heart failure admissions in the United States are the result of cor pulmonale, most commonly related to chronic obstructive pulmonary disease (COPD).

Incidence

Difficult to assess: Best estimate is 1/10,000 to 3/10,000/year.

Prevalence

Difficult to assess: Best estimate is 2/1,000 to 6/1,000.

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ETIOLOGYAND PATHOPHYSIOLOGY

Acute: Asudden event, such as large pulmonary embolism (PE), increases resistance to blood flow in the pulmonary vasculature, causing a quick and significant increase of pressure proximal to the right ventricular outflow tract. The RV may not be able to generate adequate force to overcome this pressure, leading to low RV cardiac output, which ultimately leads to a decreased left ventricle (LV) cardiac output. Increased RV pressures in conjunction with a low cardiac output may cause coronary ischemia, further impairing cardiac output and potentially causing complete cardiovascular collapse.

Chronic: Adisorder of the pulmonary system leading to chronic hypoxia results in progressive vasoconstriction of the pulmonary vasculature. Over time, the pulmonary arterial system hypertrophies and intrinsic vasoactive mechanisms (mediated by nitric oxide, cyclooxygenase, and endothelin) become dysregulated, leading to an increase in pulmonary vasculature resistance.

Increased pulmonary vascular resistance yields PH. PH transmits increased pressures and volumes to the thin-walled, low-pressure RV causing maladaptive remodeling (concentric hypertrophy, followed by eccentric dilation and frequently associated tricuspid regurgitation) and subsequent impairment in RV systolic and diastolic function.

Indicators for the presence of PH in these patients may include a disproportionally low diffusion capacity of the lungs for carbon monoxide (DLCO) and a low pCO2.

Pulmonary disorders

–Lung parenchymal disease: COPD (most common), interstitial lung disease (ILD), and pulmonary fibrosis

–Pulmonary circulation: thromboembolic disease (associated with WHO Group IV PH)

–Chest wall: severe obesity, kyphoscoliosis

–Ventilation: obstructive sleep apnea (OSA) and obesity hypoventilatory syndrome, neuromuscular diseases such as Guillain-Barré syndrome, muscular dystrophy, myasthenia gravis, spinal cord injuries

Left ventricular failure is not considered a cause of cor pulmonale.

RISK FACTORS

Acute cor pulmonale (most commonly caused by PE)

Chronic cor pulmonale (most commonly caused by underlying pulmonary disorder)

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–Risk factors associated with pulmonary disorders

Tobacco use (COPD)

Occupational exposures (ILD)

Hypercoagulable state (chronic thromboembolic disease)

Obesity, age (chest wall abnormalities)

GENERALPREVENTION

Management of underlying pulmonary disorders, including aggressive correction of hypoxia and acidosis, which may contribute to worsening PH

COMMONLYASSOCIATED CONDITIONS

PH, defined as the presence of a resting mean pulmonary artery pressure (PAP) >25 mm Hg

DIAGNOSIS

HISTORY

Dyspnea is the most common symptom, although nonspecific; may be present at rest, with exertion, or occur as paroxysmal nocturnal dyspnea

Other pulmonary symptoms: pleuritic chest pain, cough, hemoptysis

General heart failure symptoms: fatigue, lethargy, syncope; exertional angina less likely

Right-sided heart failure symptoms: anorexia, early satiety, digital cyanosis, clubbing, right upper quadrant discomfort (hepatic congestion), lower extremity edema

Hoarseness secondary to compression of the left recurrent laryngeal nerve by enlarged pulmonary vessels

Cardiovascular collapse, shock, and/or cardiac arrest may occur in acute or advanced chronic setting.

PHYSICALEXAM

Peripheral edema is the most common sign of right-sided heart failure, although it is nonspecific.

General: pallor, diaphoresis, clubbing, cyanosis, tachypnea

Neck: jugular venous distension, with prominent a-wave

Lungs: tachypnea, wheezing Heart

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–Increased intensity of pulmonic component of second heart sound (P2)

–Splitting of S2 over the cardiac apex with inspiration

–Audible right-sided S3 or S4

–RV heave

–Pansystolic murmur heard best at right midsternal border increasing with

inspiration, consistent with tricuspid regurgitation (typically a late sign) Abdomen: hepatomegaly

Extremities: clubbing, cyanosis, bilateral lower extremity edema, may also signs of deep vein thrombosis (DVT) such as tenderness or unilateral swelling

DIFFERENTIALDIAGNOSIS

Other causes of right-sided failure:

Left-sided heart failure

WHO Groups I, II, and V PH

Right-sided intrinsic cardiomyopathy

DIAGNOSTIC TESTS & INTERPRETATION

2D echocardiogram (1)[C]

–Initial diagnostic test of choice

–Elevated pulmonary arterial pressures

–Right ventricular hypertrophy

–Bulging of the interventricular septum into the LV with systole

–Flattening of the interventricular or interatrial septum

–Dilation and hypokinesis of the RV

–Tricuspid regurgitation

–Dilation of the right atrium

–Acute thromboembolic pulmonary disease as evidenced by right ventricular hypokinesis with sparing of the apex (McConnell sign)

–Echocardiography can overor underestimate the pulmonary arterial

pressures depending on image quality or operator. Pulmonary arterial pressures should therefore be verified by right heart catheterization.

MRI

–If echocardiography is inconclusive or as a substitute

–Most accurate modality for diagnosing emphysema and ILD

–Can assess cardiac pressures, size, function, myocardial mass, and viability

Right heart catheterization (1)[C]

–Gold standard for diagnosis of PH and therefore critical for diagnosis of cor pulmonale

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–Elevated central venous pressure (CVP)

–Mean PAP≥25 mm Hg at rest

Initial Tests (lab, imaging)

CBC may show signs of polycythemia due to chronic hypoxia.

Basic metabolic panel (BMP) may demonstrate elevated creatinine secondary to poor cardiac output.

Liver function tests (LFTs) may be abnormal due to proximal hepatic congestion or poor distal cardiac output secondary to RV failure.

Brain natriuretic peptide (BNP) and cardiac troponin can be elevated secondary to right ventricular strain.

D-dimer may be positive as evidence of underlying thromboembolic pulmonary disease.

Arterial blood gas may show hypercapnia due to COPD or hypoxemia due to ILD.

Arterial blood gases of COPD patients show a decreased PaO2 with normal or increased PaCO2.

ECG often shows signs of right-sided enlargement.

–Right axis deviation

–An R/S wave ratio >1 in V1

–Right ventricular hypertrophy (R wave in V1 and V2 with S waves in V5 and V6)

–Right atrial enlargement as evidenced by Ppulmonale (increased amplitude of Pwave in lead II)

–Incomplete or complete right bundle branch block

–S1S2S3 pattern or S1Q3T3 inverted pattern

Chest x-ray

–Cardiomegaly

–Enlargement of the central pulmonary arteries and reduced size of peripheral vessels (oligemia)

–Reduced retrosternal space due to right ventricular enlargement on lateral views

–Enlargement of the right atrium resulting in prominence of the right heart border

–Evidence of COPD, ILD, and structural disease (i.e., kyphosis)

–Evidence of PE (Westermark sign, Fleischner sign, and Hampton hump)

Spiral CT scan of chest

– Diagnosis of acute PE

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– Diagnosis of COPD and ILD

Ventilation/perfusion scan (V/Q)

–High specificity and sensitivity for acute and chronic thromboembolic disease

–Screening method of choice for chronic thromboembolic PH because of its higher sensitivity compared with computed tomography pulmonary angiogram

–May be used for diagnosis of acute thromboembolic disease if contraindication to chest spiral CT

–Diagnosis of chronic thromboembolic disease (WHO Group IV PH) may

warrant confirmation by pulmonary angiography. Pulmonary angiography

– Gold standard in diagnosis of chronic thromboembolic pulmonary disease Polysomnography

– Gold standard for diagnosis of OSA Pulmonary function tests (PFTs)

–DLCO: Adecrease in lung volume combined with decreased diffusion capacity for carbon monoxide may indicate ILD. COPD is associated with a decreased DLCO.

–Obstructive or restrictive ventilatory defects (ILD, chest wall abnormalities, and COPD)

TREATMENT

Reduce symptoms, improve quality of life, and increase survival. Reduce disease burden via oxygenation, preservation of cardiac function, and attenuation of PH.

GENERALMEASURES

Treat underlying disease (2)[A].

–For underlying pulmonary disease, bronchodilators and/or steroids may be beneficial.

–For underlying chronic thromboembolic disease, anticoagulation may be

indicated.

Supportive therapy as necessary

–Continuous positive airway pressure/bilevel positive airway pressure may be used for hypoxia/sleep disorders.

–Ventilation using positive-pressure masks, negative-pressure body suits, or mechanical ventilation is suggested for patients with neuromuscular

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disease.

–Phlebotomy may be indicated for severe polycythemia or signs and symptoms of hyperviscosity (hematocrit >55%).

MEDICATION

Oxygen (3)[A]

–Long-term continuous oxygen therapy improves the survival of hypoxemic patients with COPD and cor pulmonale.

–All patients with PH whose PaO2 is consistently <55 mm Hg or saturation ≤88% at rest, during sleep, or with ambulation should be prescribed oxygen to keep O2 >92 mm Hg.

–Exposure to high altitude should be avoided. Supplemental oxygen should be used during altitude exposure or air travel as needed to maintain oxygen

saturations >91%.

Preservation of cardiac function (4)[B]

–Inotropes: Dobutamine and milrinone may improve cardiac output.

–Diuretics: decrease RV filling pressures and reduces peripheral edema secondary to RHF

Excessive volume depletion should be avoided.

Monitor closely for metabolic alkalosis, as this may suppress ventilatory drive and contribute to hypoxia.

Ameliorate PH (1,4)[C]

–Treatment of underlying disease is hallmark of management.

–When refractory to traditional medical treatment, advanced therapies may be beneficial, although evidence is lacking.

–For chronic thromboembolic associated PH (WHO Group IV), riociguat and macitentan may be used.

ISSUES FOR REFERRAL

Patients with cor pulmonale should be referred to a specialized center for expert consultation.

SURGERY/OTHER PROCEDURES

Endarterectomy for chronic thromboembolic disease (WHO Group IV) Moderate to severe disease refractory to medication may require lung and/or heart transplantation.

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