Cardiac disorders Flashcards
How to calculate ASCVD risk (different factors)
Non modifiable factors: age, gender, ethnicity
Modifiable factors: cholesterol level, blood pressure
Making the hypertension diagnosis
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
Symptoms of hypertensive emergency
- Headache
- SOB
- Epistaxis
- Flushing
- Dizziness
- Chest pain
- Hematuria
Important considerations before prescribing ACE inhibitors or ARBs to patients
- Monitor potassium levels (hyperkalemia risk)
- Contraindicated with bilateral renal artery stenosis (risk of acute renal failure)
- Avoid in pregnancy
Dihydropyridine CCB (nifedipine, amlodipine) contraindications
HFrEF
- Monitor for LE and pedal edema
ACC/AHA and JNC-8 target BPs for adults and elderly
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
How is postural hypotension defined?
- 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
What is considered a hypertensive emergency?
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
What is acute coronary syndrome (ACS)?
Caused by atherosclerosis; results from imbalance in ability to supply myocardium with sufficient oxygen to meet demands
- Umbrella term for: STEMI, NSTEMI, unstable angina
STEMI vs NSTEMI
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
How is myocardial ischemia (MI) commonly described?
- 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
How does a MI present in women?
- Unusual fatigue
- Sleep disturbance
- SOB
- Indigestion
- Anxiety
- Diaphoresis
- Dizziness
- Chest pain or pressure
How would a MI present in geriatric patients (80+ years)?
- Confusion
- Dyspnea
- Cognitive impairment
- Chest pain
MI/ACS diagnostic testing (imaging and labs)
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
Initial therapy plans for patients presenting with ACS symptoms
- 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
True/false: Clinical significant ST segment elevation dictates reperfusion therapy with the use of thrombolytic therapy, PCI, etc.
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
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?
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
Absolute contraindications for tPA therapy
- 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)
Management and treatment of ACS after stabilization
- 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
What are the two types of HF?
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)
Clinical presentation of stable vs acute HF
Stable → DOE, unexplained fatigue, LE edema
Acute exacerbation → unexplained weight gain, worsening dyspnea from baseline
What do the two classification systems used to determine severity of HF (ACCF/AHA vs NYHA)?
ACCF/AHA → emphasize development and progression of disease (stages A-D)
NYHA → focused on exercise capacity and symptomatic status (I-IV)
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
True
HF diagnostic testing
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
ACCF/AHA stages of HF (A through D)
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
NYHA functional classification of HF (I through IV)
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
Lifestyle modifications for HFpEF
- Low sodium diet
- Restricted fluid intake
- Daily weight measurement
- Exercise
- Weight loss
What are the three goals of HF pharmacotherapy?
- Reduce preload
- Reduce systemic vascular resistance (after load reduction)
- Inhibit renin and sympathetic nervous system
HF pharmacotherapy treatment options
- 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)
Drugs that interact with digoxin that can lead to toxicity
- Amiodarone
- Diltiazem
- Macrolides (clarithromycin, erythromycin)
- Oral azole antifungals
- Cyclosporine
- Verapamil
- Diuretics (cause potassium depletion)
Examination findings of a physiologic murmur (innocent, functional)
- 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
Examination findings of aortic stenosis murmur
- Grade 1 to 4 out of 6 murmur
- Harsh systolic (crescendo-decrescendo)
- Second right intercostal space, apex
- Softens with standing; worse with squatting
Examination findings of mitral regurgitation
- Grade 1 to 4 out of 6 murmur
- High pitched blowing systolic (long “haaa, hooo”)
- Right lower scapular border
Examination findings of mitral valve prolapse (MVP)
- Grade 1 to 3 out of 6 murmur
- Late systolic crescendo, honking quality, mid systolic “click”
- Apex
Aortic stenosis history findings and characteristics
- Long symptom-free period with rapid clinical deterioration
- Symptoms: dyspnea, syncope, chest pain, HF
- Cause in older adults usually calcification
Mitral regurgitation history findings and characteristics
- 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
Mitral valve prolapse history findings and characteristics
- 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
What is hypertrophic cardiomyopathy?
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
Murmurs and abnormal heart sounds diagnostic testing
- ECG
- Transthoracic or transesophageal echocardiogram
- Cardiac CT or MRI
- Genetic testing for hypertrophic cardiomyopathy
MVP management and treatment
- 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
Hypertrophic cardiomyopathy treatment and management
- Goal: minimize risk of outflow track and sudden cardiac death
- Beta blocker to lower HR, inotropic effect
- Septum myomectomy, septal ablation
- Implantable cardioverter-defibrillator
AS and MR treatment and management
AS: If asymptomatic, continue to monitor with ECG, echocardiogram, exercise stress test, CT scan, MRI
MR: management of underlying condition
Questions to ask during a preparticipation sports screening examination
- 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)
Physical examination components during a preparticipation sports screening
- 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
Infective endocarditis clinical presentation
- 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
Infective endocarditis diagnostic testing
- Blood culture
- Transesophageal echocardiogram - identify vegetations and infected tissue
- ECG
- Chest x-ray, CT scan, MRI
Infective endocarditis treatment
Given 30-60 minutes before procedure (dental, oral, respiratory, esophageal)
- Adults and children: amoxicillin
- If PCN or ampicillin allergy → clindamycin, cephalexin, azithromycin
