Cardiac disorders Flashcards

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1
Q

How to calculate ASCVD risk (different factors)

A

Non modifiable factors: age, gender, ethnicity

Modifiable factors: cholesterol level, blood pressure

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2
Q

Making the hypertension diagnosis

A

Two or more BP measurements performed at least 1-2 minutes apart

  • If elevated, BP reading should be checked again in office in 1-4 weeks to confirm diagnosis
    • Can be diagnosed in single visit if evidence of HTN TOD
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3
Q

Symptoms of hypertensive emergency

A
  • Headache
  • SOB
  • Epistaxis
  • Flushing
  • Dizziness
  • Chest pain
  • Hematuria
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4
Q

Important considerations before prescribing ACE inhibitors or ARBs to patients

A
  • Monitor potassium levels (hyperkalemia risk)
  • Contraindicated with bilateral renal artery stenosis (risk of acute renal failure)
  • Avoid in pregnancy
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5
Q

Dihydropyridine CCB (nifedipine, amlodipine) contraindications

A

HFrEF

  • Monitor for LE and pedal edema
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6
Q

ACC/AHA and JNC-8 target BPs for adults and elderly

A

Adults

  • ACC/AHA - <130/80
  • JNC-8 - <140/90

Elderly

  • ACC/AHA - <130 systolic in adults 65+ years
  • JNC-8 - <150/90 in adults 60+ years
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7
Q

How is postural hypotension defined?

A
  • Fall in BP less than or equal to 20 mmHg systolic
  • Less than or equal to 10 mmHg diastolic
  • Or both within 3 minutes of standing upright
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8
Q

What is considered a hypertensive emergency?

A

BP exceeding 180/120 mmHg also associated with new or worsening TOD

  • Evidence of new or worsening TOD prompts immediate admittance to ICU and IV antihypertensive medications
  • Goal: reduce MAP by no more than 25% within first few minutes to an hour
    • Once stable, attain BP of 160/100 within next 2-6 hours
    • Normal BP achieved within 24-48 hours
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9
Q

What is acute coronary syndrome (ACS)?

A

Caused by atherosclerosis; results from imbalance in ability to supply myocardium with sufficient oxygen to meet demands

  • Umbrella term for: STEMI, NSTEMI, unstable angina
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10
Q

STEMI vs NSTEMI

A

STEMI → transmural MI (full thickness necrosis of myocardium in region of MI), Q waves, total occlusion of coronary artery

NSTEMI → non transmural MI, no Q wave, subtotal occlusion

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11
Q

How is myocardial ischemia (MI) commonly described?

A
  • Substernal compression or crush, pressure, tightness, heaviness, cramping, aching sensation, unexplained digestion, belching, epigastric pain
  • Radiating pain to neck, jaw, shoulders, back, or one or both arms
  • Dyspnea, N/V, diaphoresis
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12
Q

How does a MI present in women?

A
  • Unusual fatigue
  • Sleep disturbance
  • SOB
  • Indigestion
  • Anxiety
  • Diaphoresis
  • Dizziness
  • Chest pain or pressure
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13
Q

How would a MI present in geriatric patients (80+ years)?

A
  • Confusion
  • Dyspnea
  • Cognitive impairment
  • Chest pain
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14
Q

MI/ACS diagnostic testing (imaging and labs)

A

Imaging → ECG; others include chest x-ray, echo, nuclear scan, CT angiogram, coronary angiogram

Labs → troponin (increases rapidly within first 12 hours; remains elevated for 1-2 weeks), CK-MB, BNP

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15
Q

Initial therapy plans for patients presenting with ACS symptoms

A
  • Administer NTG
  • Provide supplemental oxygen (determine if adequate SpO2)
  • Adequate analgesia with morphine sulfate (if not relieved by NTG)
  • Beta blocker
  • Aspirin (162 or 325) then maintenance with 81
  • 12 lead ECG, collect cardiac marker labs, history
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16
Q

True/false: Clinical significant ST segment elevation dictates reperfusion therapy with the use of thrombolytic therapy, PCI, etc.

A

True - ST segment elevation >1 mm in contiguous leads

  • Indicates acute coronary artery occlusion from thrombosis
  • Best effect is therapies used within 6 hours of chest pain onset
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17
Q

How soon with a suspected STEMI or patient presenting with ischemic symptoms should PCI be performed? How long should they be on antiplatelet therapy for?

A

PCI recommended in presence of STEMI and ischemic symptoms of <12 hours

  • After PCI, antiplatelet therapy (aspirin and clopidogrel) should be given for at least 12 months
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18
Q

Absolute contraindications for tPA therapy

A
  • Prior intracranial hemorrhage
  • Known structural cerebral vascular lesion (AV malformation)
  • Known malignant intracranial neoplasm
  • Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 4.5 hours
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis (including menses)
  • Closed head or facial trauma within 3 months
  • Intracranial or intraspinal surgery within 2 months
  • Severe uncontrolled HTN (unresponsive to therapy)
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19
Q

Management and treatment of ACS after stabilization

A
  • Beta blockers → reduce myocardial workload, lower SV, lower HR
  • ACE inhibitors
  • ASA and clopidogrel for at least 12 months
  • CCB → non-DHP (verapamil, diltiazem)
  • NTG
  • Statin therapy
  • Before discharge, undergo exercise stress test
20
Q

What are the two types of HF?

A

HFrEF: ejection fraction <40%

  • Common risk factors: ACS with antecedent MI

HFpEF: ejection fraction >50%

  • Common cause: HTN (others include obesity, CAD, DM, AF, HLD)
21
Q

Clinical presentation of stable vs acute HF

A

Stable → DOE, unexplained fatigue, LE edema

Acute exacerbation → unexplained weight gain, worsening dyspnea from baseline

22
Q

What do the two classification systems used to determine severity of HF (ACCF/AHA vs NYHA)?

A

ACCF/AHA → emphasize development and progression of disease (stages A-D)

NYHA → focused on exercise capacity and symptomatic status (I-IV)

23
Q

True/false: Patients who reach stage B HF require expert consultation with cardiology while those at stage C or D are co-managed with cardiology specialists

A

True

24
Q

HF diagnostic testing

A

Labs: CBC, UA, electrolytes, BUN, creatinine, glucose, fasting lipid profile, LFT, TSH, BNP

  • Amount of circulating BNP proportional to ventricular volume expansion and pressure overload

Imaging: echocardiogram

25
Q

ACCF/AHA stages of HF (A through D)

A

A: high risk for HF but without structural heart disease or symptoms

B: structural heart disease but without s/s of HF

C: structural heart disease with prior or current symptoms

D: refectory HF requiring specialized interventions

26
Q

NYHA functional classification of HF (I through IV)

A

I: no limitation of physical activity, ordinary physical activity does not cause symptoms

II: slight limitation of physical activity, comfortable at rest but ordinary physical activity results in symptoms

III: marked limitation of physical activity, comfortable at rest but less than ordinary activity causes symptoms

IV: unable to carry on any physical activity without symptoms of HF or symptoms of HF at rest

27
Q

Lifestyle modifications for HFpEF

A
  • Low sodium diet
  • Restricted fluid intake
  • Daily weight measurement
  • Exercise
  • Weight loss
28
Q

What are the three goals of HF pharmacotherapy?

A
  • Reduce preload
  • Reduce systemic vascular resistance (after load reduction)
  • Inhibit renin and sympathetic nervous system
29
Q

HF pharmacotherapy treatment options

A
  • ACE inhibitors and ARBs → start low and go slow to reduce hypotension
  • Beta blockers
  • Diuretics (potassium sparing - spironolactone)
  • Warfarin for those with afib (monitor TI)
30
Q

Drugs that interact with digoxin that can lead to toxicity

A
  • Amiodarone
  • Diltiazem
  • Macrolides (clarithromycin, erythromycin)
  • Oral azole antifungals
  • Cyclosporine
  • Verapamil
  • Diuretics (cause potassium depletion)
31
Q

Examination findings of a physiologic murmur (innocent, functional)

A
  • Grade 1 to 3 out of 6 murmur
  • Early to midsystolic murmur
  • Best at left sternal border or also over precordium
  • Disappears with standing; increases with activity, fever, anemia
32
Q

Examination findings of aortic stenosis murmur

A
  • Grade 1 to 4 out of 6 murmur
  • Harsh systolic (crescendo-decrescendo)
  • Second right intercostal space, apex
  • Softens with standing; worse with squatting
33
Q

Examination findings of mitral regurgitation

A
  • Grade 1 to 4 out of 6 murmur
  • High pitched blowing systolic (long “haaa, hooo”)
  • Right lower scapular border
34
Q

Examination findings of mitral valve prolapse (MVP)

A
  • Grade 1 to 3 out of 6 murmur
  • Late systolic crescendo, honking quality, mid systolic “click”
  • Apex
35
Q

Aortic stenosis history findings and characteristics

A
  • Long symptom-free period with rapid clinical deterioration
  • Symptoms: dyspnea, syncope, chest pain, HF
  • Cause in older adults usually calcification
36
Q

Mitral regurgitation history findings and characteristics

A
  • Causes: rheumatic fever, endocarditis, calcific annulus, ruptured chord, papillary muscle dysfunction
  • Once symptomatic, disease progresses in downhill course leading to HF in next 10 years
37
Q

Mitral valve prolapse history findings and characteristics

A
  • One leaflet of valve is longer than others
  • Common in patients with connective tissue disease (Marfan syndrome)
  • Risk of bacterial endocarditis
  • Predominant abnormality in patients under 35 years that lead to sudden cardiac death in sports
38
Q

What is hypertrophic cardiomyopathy?

A

Disease of cardiac muscle → ventricular septum is thick, asymmetric leading to potential blockage of outflow tract

  • Symptoms: chest pain, post exertion syncope
  • PE: systolic murmur that gets louder with position change from supine to standing
39
Q

Murmurs and abnormal heart sounds diagnostic testing

A
  • ECG
  • Transthoracic or transesophageal echocardiogram
  • Cardiac CT or MRI
  • Genetic testing for hypertrophic cardiomyopathy
40
Q

MVP management and treatment

A
  • If asymptomatic, no further evaluation/treatment needed
  • Able to follow program of aerobic activity okay
  • Maintain high level of fluid intake
  • Consider beta blockers only when symptomatic with tachycardia or palpitations
41
Q

Hypertrophic cardiomyopathy treatment and management

A
  • Goal: minimize risk of outflow track and sudden cardiac death
  • Beta blocker to lower HR, inotropic effect
  • Septum myomectomy, septal ablation
  • Implantable cardioverter-defibrillator
42
Q

AS and MR treatment and management

A

AS: If asymptomatic, continue to monitor with ECG, echocardiogram, exercise stress test, CT scan, MRI

MR: management of underlying condition

43
Q

Questions to ask during a preparticipation sports screening examination

A
  • Prior occurrence of exertion chest pain/discomfort or syncope/near syncope
  • Excessive, unexpected, and unexplained SOB or fatigue associated with exercise
  • Past detection of a heart murmur or high BP
  • Family history of:
    • Premature death, significant disability from CVD, specific knowledge of occurrence of certain conditions (hypertrophic cardiomyopathy, dilated cardiomyopathy, long QT syndrome, Marfan syndrome, dysrhythmias)
44
Q

Physical examination components during a preparticipation sports screening

A
  • Precordial auscultation in supine and standing positions
  • Assessment of femoral artery pulses (exclude coarctation of the aorta)
  • Recognition of physical stigmata of Marfan syndrome
  • BP measurement in sitting and standing position
45
Q

Infective endocarditis clinical presentation

A
  • Fever, chills
  • New or altered heart murmur
  • Fatigue, SOB
  • aching joints and muscles
  • Edema
  • Persistent cough
  • Unexplained weight loss
  • Hematuria
  • Tenderness of the spleen
  • Osler’s nodes - painful, red, raised lesions on hands and feet
  • Petechiae
46
Q

Infective endocarditis diagnostic testing

A
  • Blood culture
  • Transesophageal echocardiogram - identify vegetations and infected tissue
  • ECG
  • Chest x-ray, CT scan, MRI
47
Q

Infective endocarditis treatment

A

Given 30-60 minutes before procedure (dental, oral, respiratory, esophageal)

  • Adults and children: amoxicillin
  • If PCN or ampicillin allergy → clindamycin, cephalexin, azithromycin