Clin med- cardio cumulative

What are common pharmacologic causes of secondary hypertension?

chronic NSAID use

corticosteroids

decongestants

stimulants

weight loss medications

What are signs of end-organ damage from hypertension?

headaches, loss of visual acuity, transient weakness/blindness, chest pain, dyspnea, claudication

What are some signs and symptoms of hypertension?

xanthelasma

diminished peripheral pulses

unequal BPs in arms

bruits

CHF signs (LE edema, ascites, crackles and rales)

How to diagnose hypertension?

must have at least 3 readings at 3 different times with elevated BP to diagnose HTN

every patient 18+ should have their BP checked at least once a year in clinic

measure BP at home AND in clinic for white coat HTN or masked HTN

What is the gold standard for hypertension diagnosis?

ambulatory BP monitoring- outside clinic with automatic cuff preset to 3-4x/hour during day and 1-2x/hour during sleep

What are factors in calculating 10-year risk for first occurrence of non-fatal MI, CHD death, or fatal/non-fatal CVA? (ACC/AHA 2013)

race, sex, age, total cholesterol, HDL, SBP, anti-HTN meds, diabetes, smoking

When should pharmacologic therapy be initiated for hypertension?

stage 1 HTN: do when lifestyle modification fails

stage 1 and comorbid condition (established CVD, diabetes, CKD, >65, estimated 10 year risk of CVD ≥10%): need treatment

stage 2, hypertensive urgency, or hypertensive emergency: need treatment

What is the BP goal for hypertensive patients on pharmacologic therapy?

<130/<80

What is atrial flutter typically caused by?

macroreentrant circuit within the right atrium

How may a patient with atrial flutter present?

same as Afib but usually more poorly tolerated due to faster ventricular rate

What type of heartbeat are re-entry circuits responsible for?

tachycardia

What constitutes a diagnosis of ventricular tachycardia?

3 or more consecutive PVCs with rate >100bpm

How to determine which statin to prescribe for dyslipidemia?

10 year CVD risk <5%- don't start statin

LDL >100 and 10 year CVD risk 5-10%- shared decision making

LDL >100 and 10 year CVD risk ≥10%- moderate dose statin

LDL ≥190 OR 10 year CVD risk >20%- high dose statin

What is the criteria for diagnosing metabolic syndrome?

need 3+ of the following:

abdominal obesity

TRIG ≥150

HDL <40 in men or <50 in women

HTN with BP ≥130/85

Fasting glucose ≥100

What can increase a person's risk of developing atherosclerosis?

increased levels of LDL and VLDL

leads to subendothelial retention of extra LDL and formation of atherosclerotic plaques

oxidized LDL is bad player= promotes cytokine release from macrophages and antibody production= increased inflammation

Symptoms of sick sinus syndrome? Tx?

Sx: palpitations, dizziness, lightheadedness, angina, dyspnea on exertion, presyncope or syncope

Tx:

stable- none

unstable- atropine

chronic- pacemaker

What are key problems with Afib?

loss of atrial kick= lose 30% of cardiac output b/c atria not producing coordinated contractions

rapid ventricular response

risk of thrombosis due to impaired left atrial appendage emptying

If a younger patient presents with Afib, what is it most likely caused by?

binge drinking (glug glug)

What are heart diseases associated with Afib?

hypertension, valvular heart disease (especially mitral valve), coronary artery disease, heart failure, post-surgical

What is considered "valvular" Afib?

if patient has mitral stenosis or mechanical valve

How to determine need for anticoagulation in Afib patients?

CHA2DS2-VASc score of 2 or greater

Treatment for Afib?

rate control- beta blockers, NDCCB, +/- digoxin, ablation

rhythm control- cardioversion, antiarrhythmics (amiodarone), ablation

anticoagulation (CHA2DS2-VASc score of 2 or greater)

rate control is usually preferred over rhythm control for long-term management

Treatment for atrial flutter?

elective electrical cardioversion is preferred management for stable patients

should also start on anticoagulation if CHA2DS2-VASc score of 2 or greater

If you are going to use cardioversion on a patient in Afib, what must you do first?

get an echo to ensure there are no atrial clots or else they will be dislodged and could cause a stroke

What is AV block?

interruption of the normal impulse from the SA node to the AV node (AV node dysfunction)

What are common causes of AV block?

beta blockers, NDCCB, digoxin, Lyme disease

Where do the 2 types of 2nd degree AV block occur in the electrical pathway?

Type 1- occurs ABOVE the level of the bundle branches

Type 2- occurs AT the level of the bundle branches

Which types of AV block are typically symptomatic and higher risk?

2nd degree type 2

3rd degree

Treatment of AV block?

1st degree: atropine ONLY if symptomatic

2nd degree type 1: atropine, pacemaker ONLY if symptomatic

2nd degree type 2: pacemaker, NO atropine

3rd degree: pacemaker

True or false: carotid massage can be used to treat acute PSVT

FALSE- increases risk of stroke from plaque dislodgement or syncope

How will a patient in SVT present? Treatment?

can be asymptomatic but can have palpitations, dizzy/lightheaded, shortness of breath

Acute tx: Valsalva maneuver, adenosine, IV beta blocker or CCB

Chronic tx: CCB or beta blockers, catheter ablation

Characteristics of SVT?

sporadic, sudden onset and termination, regular ventricular response

What are premature atrial complexes caused by? Do they require treatment?

premature atrial activation from an atrial site other than the sinus node

can be provoked with caffeine- clinically benign, just annoying for patient

What are junctional premature complexes caused by?

early ectopic activation from the AV node or His bundle- originates below atrium so no P wave seen, less commonly seen than other premature beats

Treatment for APCs and JPCs?

generally don't require treatment, attempt reassurance and limitation of provoking factors

if severe- try beta blockers, antiarrythmics, ablation (rare)

How will a hemodynamically unstable patient present? How do you treat them?

hypotension, acute heart failure, crushing chest pain, shock, altered mental status

Tx: need electrical shock to get out of abnormal rhythm

What is multifocal atrial tachycardia highly associated with? Treatment?

pulmonary disease

Tx: put down those cigs BOYYYYY (aka treat underlying condition)

Treatment for PVCs?

if symptomatic= minimize triggers, beta blockers, antiarrhythmics, ablation

Difference between sustained and nonsustained Vtach?

sustained= longer than 30 seconds or causes hemodynamic compromise- *can lead to Vfib*

nonsustained= spontaneous termination under 30 sec

Treatment for Vtach?

Acute tx:

1. antiarrhythmics- amiodarone, lidocaine, or procainamide

2. cardioversion

Chronic tx: beta blockers and ICD implantation

Difference between synchronized cardioversion and defibrillation?

synchronized cardioversion- shock delivered on peak of R wave, prevents Vfib, for patients WITH pulse

defibrillation- shock delivered regardless of timing in cardiac cycle, for patients WITHOUT pulse, used for heart rhythms too chaotic for monitor to recognize R wave (Vfib and Torsades)

How to treat Torsades de pointes?

if stable= IV magnesium sulfate, beta blockers, further cardiac workup

if unstable= defibrillation and IV magnesium

What are some causes of Torsades de pointes?

prolonged QT interval

drugs- antiarrhythmics, macrolides, digoxin, antipsychotics

hypokalemia, hypomagnesemia

Common causes of Vtach?

underlying heart disease (ischemic heart disease most common- post MI)

prolonged QT interval

hypomagnesemia, hypokalemia, hypocalcemia, digoxin toxicity

Complications of an MI?

Arrhythmias (Vfib), ventricular aneurysm/rupture, cardiogenic shock, HF

Dressler syndrome: post-MI pericarditis + fever + pulmonary infiltrates

Pathophysiology of plaque formation?

hypercholesteremia leads to accumulation of LDL in artery wall

LDL and its components elicit vascular inflammation that drives the build-up of lipid-laden atherosclerotic plaques by oxidation and aggregation

propagation leads to xanthoma= fatty streak

xanthomas can progress and develop into atherosclerotic lesions of artery

plaques have fibrous cap, if they rupture= thrombus

Pathophysiology of angina?

due to atherosclerosis- inadequate tissue perfusion due to imbalance between increased demand and decreased coronary artery blood supply

symptoms usually occur with occlusion ≥70%

Symptoms of acute coronary syndrome?

severe chest pain that is prolonged compared to stable angina may not be relieved with rest or nitroglycerin

dyspnea, nausea, vomiting, diaphoresis, epigastric or shoulder pain

Levine's sign- clenched fist over heart with associated clenched teeth

How to distinguish between unstable angina and NSTEMI/STEMI?

unstable angina- cardiac enzymes negative

NSTEMI/STEMI- cardiac enzymes positive

Sx of Prinzmetal (vasospastic) angina? How to diagnose? Tx?

Sx: chest pain at rest, not exertional and not relieved by rest (typically occurs between midnight and 8AM due to decreased vagal tone)

Diagnosis:

EKG: transient ST elevations that resolve with symptom resolution

CTA- rule out CAD, may show evidence of vasospasm

Tx:

1. CCB 2. nitroglycerin

What is the most common etiology of acute coronary syndrome?

atherosclerosis= plaque rupture= acute coronary artery occlusion with platelet adhesion/activation/aggregation along with fibrin formation= vasculitis, embolism

Who is most likely to have a silent MI?

women, elderly, diabetic and obese patients

How to manage ACS?

EKG within 10 min

MONA B- morphine, oxygen, nitrates, aspirin, beta blockers

Unstable angina or NSTEMI: MONA B + heparin

STEMI: MONA B, heparin, reperfusion (need emergent cardiac cath or fibrinolytics if cath lab not available)

Long-term therapy following MI?

ASA (dual if stent)- 81 mg daily

beta blocker

high intensity statin

What EKG finding is considered a STEMI equivalent?

a new left bundle branch block

need to use Sgarbossa criteria to diagnose

Female patient presents with headache, jaw claudication with mastication, visual changes, scalp tenderness, and a fever. Labs show increased ESR and CRP, normocytic and normochromic anemia. Dx? Tx?

Giant cell arteritis

Dx with temporal artery biopsy- gold standard

Tx: HD steroids- blindness is most common complication

What is superficial thrombophlebitis most commonly associated with?

IV catheterization, preggers, varicose veins, venous stasis, Factor V Leiden

Trousseau sign- migratory thrombophlebitis associated with malignancy

Patient presents with tenderness, pain, induration, edema and erythema along the course of a vein under the skin. They report they can feel a palpable cord in the area. Dx? Tx?

Superficial thrombophlebitis- inflammation and/or thrombosis of a superficial vein

Tx: NSAIDs, extremity elevation, warm compresses

What is postphlebitic syndrome?

symptoms and signs of chronic venous insufficiency that develop following DVT

Risk factors: preexisting primary venous insufficiency, older age, obesity, varicose veins

What are the risk factors for DVT?

Virchow's triad:

1. intimal damage- trauma, infection, inflammation

2. stasis

3. hypercoaguability- protein C or S deficiency, oral contraceptives, malignancy, preggers, smoking

Patient presents with edema of one of their calves. They report their calf is painful and tender. Dx? Tx?

Deep venous thrombosis

Tx: anticoagulation- apixaban, dabigatran, rivaroxaban or LMWH or warfarin

How to diagnose a DVT?

Well's criteria

D-dimer: elevated but not specific

Venous duplex US: very accurate in proximal vein but not for calf

Venography w/ contrast: most accurate but invasive

What are some risk factors of varicose veins? Tx?

family hx, female, age, standing for long periods, obesity, OCP use, preggers, chronic venous insufficiency

Tx: compression stockings, leg elevation, pain control

Pathophysiology of pulmonary hypertension?

when the pressure in the blood vessels leading from the heart to the lungs is too high. this slows blood flow through the lungs, heart must work harder to pump blood through the lungs

extra effort eventually causes the heart muscle to become weak and fail

Definitive diagnosis for pulmonary hypertension?

R heart catheterization- elevated pulmonary artery pressure, RV pressure, and increased pulmonary vascular resistance

EKG findings for cor pulmonale?

RVH, R axis deviation, R atrial enlargement, RBBB

Causes of cor pulmonale?

lung function declines → hypoxia → pulmonary arteries constrict → widespread vasoconstriction → pulmonary hypertension → more work for R side of heart → R side of heart enlarges → cor pulmonale (R sided heart failure)

What is lymphangitis? What can it lead to?

red streak from wound or cellulitis toward regional lymph nodes, which are usually enlarged and tender

can lead to bacteremia if untreated, which can cause endocarditis

What is lymphedema?

lymph vessels are injured or obstructed= lymph fluid can't drain and accumulates in tissues= swelling

Patient presents with leg pain (burning, aching, throbbing, cramping) that worsens with prolonged standing, but improves with walking and leg elevation. They report their feet often turn blue while they are standing. Physical exam reveals medial malleolus ulcers, dependent pitting leg edema, itchy eczematous rash and brownish/dark purple hyperpigmentation of the lower extremity skin. Dx? Tx?

Chronic venous insufficiency

Tx: leg elevation, compression stockings, exercise, weight management, tx underlying cause

Pathophysiology of chronic venous insufficiency?

occurs when the valves in the leg veins don't shut properly during blood's return to the heart

Patient presents with leg pain that gets worse when they walk but improves with rest, decreased peripheral pulses, thin/shiny skin and loss of hair on their lower extremities. They also report that when they are on their legs, their feet turn red, but when they elevate them, their feet turn blue. Dx? Tx?

Peripheral artery disease

Dx with ankle-branchial index (PAD= ABI <0.90)

Tx: exercise, smoking cessation, tx hyperlipidemia, cilostazol

What are the most common arteries involves in peripheral artery disease and how do they manifest clinically?

femoral artery- thigh and upper calf claudication

popliteal artery- lower calf, ankle and foot claudication

Patient presents with paresthesia, pain, pallor, pulselessness, poikilothermia (skin feels cool to the touch), and paralysis of their leg. Dx? Tx?

Acute arterial occlusion- medical emergency!

Need beside arterial doppler to assess for pulses, CTA

Tx: immediate reperfusion- surgical bypass, surgical or catheter thromboembolectomy

What are the most common causes of acute pericarditis?

Coxsackie, COVID, adenovirus, flu

can also be caused by Dressler syndrome

Gold standard for diagnosing pericarditis?

EKG- will show diffuse ST elevation with PR depression that doesn't follow coronary distribution, may be present in all leads

A patient presents with a sudden onset of pleuritic chest pain (sharp, worse with inspiration) that is persistent and worse when they are supine but better when they sit forward. Physical exam reveals pericardial friction rub, ECG shows diffuse ST elevations and PR depressions in the precordial leads. Dx? Tx?

Acute pericarditis

Tx: 1. NSAIDs or aspirin 2. colchicine

activity restriction until sx resolution and normalization of biomarkers

If Dressler syndrome- avoid NSAIDs b/c can interfere with myocardial scar formation

What is cardiac tamponade?

when intra-pericardial pressure exceeds R atrial pressure- around 8mmHg

significant pressure on the heart= decreased cardiac filling= decreased SV= decreased CO= hypotension and eventually shock

medical emergency!!

Symptoms of cardiac tamponade?

Beck's Triad: distant (muffled) heart sounds, increased JVP, systemic hypotension

pulsus paradoxus- >10mmHg decrease in systolic BP with inspiration

tachycardia

dyspnea, fatigue, shock, cool extremities

Diagnostic findings for cardiac tamponade? Tx?

requires dynamic imaging b/c functional diagnosis

Echo: pericardial effusion and diastolic collapse of cardiac chambers, ↓ valve velocity w/ inspiration

ECG: low voltage QRS, electrical alternans

Tx: immediate pericardiocentesis

Very ill-appearing patient presents with dyspnea on exertion, hypoxia, hypotension, and cool extremities. Physical exam reveals a rise in JVP with inspiration, ascites, and peripheral edema. Dx? Tx?

constrictive pericarditis

Tx: anti-inflammatory drugs and steroids if early, surgery if late

How to differentiate between constrictive pericarditis and restrictive cardiomyopathy?

constrictive pericarditis: hx of pericarditis or TB, thickened and/or calcified pericardium on imaging

restrictive cardiomyopathy: hx of predisposing systemic diseases, thickened myocardium, abnormal myocardial texture on imaging

What is constrictive pericarditis?

chronic process- scarring, calcification and loss of elasticity of pericardium= ↓ cardiac filling

Most common causes of pericardial effusion?

inflammation

post cardiotomy syndrome

cancer

trauma/bleeding

cirrhosis

iatrogenic

What is the cutoff for distinguishing between chronic and acute pericardial effusion?

3 months

Symptoms of pericardial effusion? Diagnostic findings? Tx?

Sx: chest pain, dyspnea, fatigue, decreased (muffled) heart sounds on exam

Diagnosis: echo is test of choice- PLAX view

ECG- low QRS voltage, electrical alternans

Tx: underlying cause, pericardiocentesis if big

What is the etiology of aortic stenosis?

98-99% are from degenerative calcification

1-2% are congenital

What is the most common cause of congenital aortic stenosis?

bicuspid aortic valve

What are the cardinal symptoms of aortic stenosis?

angina, syncope, HF

Differences between drug eluting stent and bare metal stent?

Drug eluting- less risk of restenosis but more risk of stent thrombosis, requires 1 year min of dual antiplatelet therapy

BMS- less risk of stent thrombosis but more risk of restenosis, requires 1 month min of dual antiplatelet therapy

Indications for coronary artery bypass graft?

3 vessel coronary artery disease

left main coronary artery stenosis

coronary lesions not amenable to stent (heavily calcified coronaries, some lesions at bifurcation of vessels)

How to differentiate between stable and unstable angina?

both may present with ST depressions on EKG or normal EKG

stable: exertional chest pain relieved with rest

unstable: chest pain that happens anytime, not relieved with rest

What is the gold standard for diagnosis of aortic stenosis?

echocardiogram

if patient is being referred for surgery, should get coronary angiogram to look for plaques

Indications for valve replacement in aortic stenosis? What meds should these patients avoid?

symptomatic and severe (decreased EF or area <0.6 cm2)

no medical treatment is truly effective

avoid: beta blockers, calcium channel blockers (negative inotropes) and venodilators (nitrates)

Etiology of aortic regurgitation?

endocarditis, hypertension, aortic dissection, thoracic trauma

What should be high on your differential for all regurgitant valves?

endocarditis

How do patients with acute aortic regurgitation present? Treatment?

patients are very sick- usually results in hemodynamic instability and cardiogenic shock

immediate management= IV vasodilator therapy

often requires urgent surgical intervention

How do patients with chronic aortic regurgitation present? Treatment?

mild-moderate disease can be managed with long-term vasodilator therapy, severe disease is an indication for surgery

What are some features of mechanical valves?

more durable, preferred for younger patients

requires lifelong anticoagulation with warfarin (cannot use DOACs)

What are some features of bioprosthetic valves?

made from pig or cow pericardium

shorter lifespan- may require repeat surgery

anticoagulation not required unless other indications present (can use DOACs if needed)