Clin Med- Cardiology

Dyslipidemia

Abnormal levels of lipids (fats) in the blood that are divided on the basis of density

• HDL: good, more the better, (transport; most dense)

• LDL: bad, want less (less dense; triglyceride component)

• VLDL: bad, want less (least dense; triglyceride transport)

• Total cholesterol: HDL+LDL+VLDL

• Lipoprotein (a): key role in development of atherosclerosis (LDL-C)

Niacin

dyslipidemia medication that should be discontinued in all patients

HDL

• Good cholesterol 

• >40 mg/dL in men, >50 mg/dL in women

• Low HDL: insulin resistance, obesity, smoking, high carbs, drugs, decreased physical activity

• High HDL, low risk of coronary heart disease

LDL

• bad cholesterol

• Low LDL will decrease rate of MI, stroke, angina and need for CABG

• Primary prevention: decrease risk with reduction of LDL-C

• Secondary prevention: prevents future additional occurrences 

Triglycerides in the blood should be

<150 mg/dL

• diet and exercise (lifestyle) are key

Secondary causes of dyslipidemia

Alcohol use, diabetes, pancreatic and liver disease, hyper/hypothyroidism, drugs

Signs and symptoms of dyslipidemia 

• Most are non-specific and caught on routine lab screening

• >1000 mg/dL in triglyceride/VLDL- eruptive xanthomas (red-yellow papules on buttocks)

• High LDL- tendinous xanthomas (Achilles, patella, back of hand)

• Lipidemia retinalis (cream colored blood vessels in the fundus)

Screening for dyslipidemia should start

at 20 years old and continue once a year

Dyslipidemia Dx

Labs (lipid panel/profile)

Dyslipidemia Tx

1. Raise HDLs, improve diet, increase exercise (lifestyle changes)

2. If does not improve, go med route

   1. Statins (atorvastatin, fluvastatin), Ezetimibe (Zetia), PCSK9 inhibitors (Repatha, Praluent), Omega-3-fatty acids, Bempedoic acid (nexletol)

Pericarditis

Inflammation of the pericardial lining

• Acute: 2/4 criteria (chest pain, pericardial friction rub, ST changes, new or worsening effusion) and symptoms less than 4-6 weeks

• Incessant: Longer than 4-6 weeks, none at 3 months, no interruption

• Recurrent: longer than 4-6 weeks, has interruptions

• Chronic: lasting longer than 3 months, no breaks

Acute pericarditis

less than 2 weeks, inflammation of the pericardium

• Risks: idiopathic, infection, surgery, CT disease, radiation, pericardial injury. myxedema

• Infectious

  • Viral: coxsackie, echo, influenza, EBV, varicella, hepatitis, mumps, HIV, COVID

• Males <50 yo

• Bacterial: rare (TB)

• Uremic, neoplastic, post MI (Dressler syndrome), radiation, CT disease, drug induced

S/S of Acute Pericarditis 

chest pain (significant, continuous, sharp), dyspnea, fever, pericardial friction rub

• TB: TB symptoms

• Bacteria: inflammatory, toxic, critically ill (septic)

• Uremic: w/ or w/o symptoms, absent fever

• Neoplastic: Often painless, increase risk of pericardial effusion

Dx of acute pericarditis

• Viral: clinical diagnosis based on criteria, leukocytosis, echo is normal

• TB: TB testing

• Bacterial: pericardiocentesis

• Uremic: “shaggy pericardium”- irregular and thickened pericardium on ECHO or CT

• ECG: shows ST waves elevated in all ECG leads

• CXR: cardiac enlargement, masses (neoplastic)

• Neoplastic: cytologic examination

• Post MI: increased ESR, large pericardial effusion

• Myxedema: hypothyroidism, cholesterol crystals 

Acute Pericarditis Tx

• Tx of underlying cause

• NSAIDs

• Colchicine

Cardiac Tamponade 

Pressure that affects pericardial filling, cardiac perfusion, and cardiac output

• Triad

1. Jugular venous distention (JVD)

2. Hypertension

3. Muffled heart sounds

DO NOT CONFUSE WITH TENSION PNEUMO

Tx of Cardiac Tamponade

• Restriction in activity (3 mo)

• ASA, NSAID

• Colchicine + NSAID (3 mo) for prevention (cyclophosphamide or azathioprine if not tolerated)

• Underlying cause

  • TB: TB drug therapy

  • Radiation: symptomatic tx

  • Uremic: dialysis (tamponade common)

  • Neoplastic (poor prognosis): drain effusion, chemo, tetracycline

Dressler Syndrome (post MI pericarditis)

recurrence of pain with pleural-pericardial features, the rub is audible and repolarization changes on ECG may be confused with ischemia

• prior MI (weeks or months ago), large effusions (uncommon) 

• S/S: pain, fever, malaise, leukocytosis 

• DX: S/S and Hx

• TX: spontaneous resolution 

  • Post MI: ASA and colchicine for 3 months, no NSAIDS or Steroids

  • Refractory: colchicine (6 mo), Indomethacin doses, corticosteroids

Pericardial Effusion

accumulation of fluid in the pericardial sac 

• gradual= stretch and accommodate

• quickly= cardiac tamponade 

• Transudate= L heart failure, overhydration, hypoproteinemia

• Exudate= renal failure, malignancies, infection

• 1st affected= right atrium and ventricle

Pericardial Effusion S/S

underlying cause, dull chest pain, dyspnea, muffled heart sounds, poorly palpated apical pulse, pulsus paradoxus

Pericardial Effusion Dx

CXR: “water bottle heart”- enlarged flask shaped cardiac silhouette 

Echo: visualize fluid around heart 

Pericardial effusion tx

• Underlying cause

• NSAIDs (pain relief)

• Large effusion/cardiac tamponade (pericardiocentesis)

• Recurrent/Refractory effusion (pericardial window)

Pericardial tamponade + Constrictive pericarditis

Effusive-Constrictive pericarditis

Constrictive pericarditis (over time)

leads to thickened, fibrotic, adjacent pericardium that restricts diastolic filling and produces chronically elevated venous pressure 

• Risks: immune mediated/neoplastic pericarditis (increases risk after bacterial pericarditis)

Constrictive pericarditis S/S

S/S: dyspnea, fatigue, weakness (principle)

chronic edema, increase JV pressure, Kussmaul sign, pericardial knock, pulsus paradoxus, A-fib

Constrictive pericarditis Dx and Tx

• X-ray: normal, some cardiomegaly or peripheral calcification

• ECHO: septal bounce (best test choice)

• CT/MRI": pericardial thickening

• Cardiac cath: confirmatory but invasive and expensive 

Tx: aimed at specific etiology, anti-inflammatories, diuretics, pericardiectomy if dieuresis fails   

Metabolic syndrome

cluster of conditions that increase risk of heart disease, stroke, and type 2 diabetes

Metabolic syndrome criteria (must have at least 3)

1. Waist line: >40 inch for men, >35 inch in women

2. Hypertension: >130/85 or on anti-hypertensive medications

3. High blood sugar: >100 or on meds to control blood sugar

4. High triglycerides: >150 or on meds to control

5. Low HDL: <40 for men, <50 for women

Risk factor of metabolic syndrome

Insulin resistance, obesity (abdominal fat), physical inactivity, poor diet, aging, genetics 

Consequence of metabolic syndrome

increased cardiovascular disease risk, increased risk for type 2 diabetes, sleep apnea and osteoarthritis

Prevention and treatment of metabolic syndrome

• Lifestyle change: diet, physical activity, weight loss, quit smoking/alcohol, stress and sleep management

Treatment for metabolic syndrome

Medication for blood pressure, cholesterol, and blood sugar 

Claudication

cramping discomfort, weakness, tired sensation caused by lower extremity exercise and relieved with rest

Severely stenotic

pain continuous and severe from constant inadequate tissue perfusion

Peripheral artery disease (PAD) is also known as

Peripheral vascular disease (PVD), peripheral vascular occlusive (PVOD), peripheral arterial occlusive disease

Peripheral artery disease (PAD)

Most commonly atherosclerotic disease of the arteries that perfuse the limbs an occlusion can reduce or completely obstruct blood flow to distal tissues (arterial insufficiency) it chronic or acute

• occlusion of 50% of arterial lumen (75% of vessel diameter), produces significant reduction in blood flow

• Decreases blood flow causes tissue hypoxia and ischemia (severe: tissue necrosis w/ gangrene)

• Plaques develop @ bifurcations, lower extremities affected more

• Atherosclerosis: chronic, slow process

Risks for peripheral artery disease

Smoking, hypercholesterolemia, diabetes mellitus, hypertension, family hx, male sex

S/S and PE findings for peripheral artery disease

• Intermittent claudication: calves MC, thighs and buttocks, severing claudication (in worsening cases)

• SEVERE: rest pain, severely stenotic artery (foot) (pain at rest requires surgical intervention)

  • Aortic iliac: Leriche’s Syndrome- erectile dysfunction

  • Intestinal Angina: visceral artery insufficiency- postprandial pain (fear of eating and weight loss), pain out of proportion to PE

  • Amaurosis Fugax: transient monocular blindness (ophthalmic branch of ICA)

• PE: diminished/absent peripheral pulses, bruits (severely stenotic- absent), pallor on elevation, erythema on dependency, poor capillary refill, digital cyanosis, tropic changes (hair loss), painful ischemic changes (gangrenous ulcers)

DX of Peripheral Artery Disease

• Ankle-Brachial Ratio/Index (ABI/AAI)- normal is 1.0-1.1, <0.9 is PAD, <0.5 is critical PAD

  • Most common first thing done (non-invasive)

• USN: arterial duplex scanning

  • Done 1st after ABI

• CTA/MRA: precise location and extent of vascular occlusion with contrast

  • Gold standard test

TX of peripheral artery disease (PAD)

• Reduce cardiovascular risk (smoking cessation, lipid/BP control, weight loss, antiplatelet)

• Exercise program (daily walking and tracking point of claudication)

• Meds (after initial lifestyle changes)

  • Aspirin

  • High dose statin (atorvastatin)

  • ± Rivaroxaban (DOAC)

  • ± Cliostazol (symptom relief of claudication)

• SEVERE: vascular reconstruction or angioplasty and stenting, arterial grafts, thromboendarectomy (repairing diseased arteries), amputation in the case of gangrene

• F/U 3-6 months with stable disease and consult vascular surgery

• Complications: secondary infection (cellulitis, tissue necrosis, ischemic ulcers

Aneurysm

Localized dilation or out pouching of a vessel wall or cardiac chamber

• aorta is susceptible

• Atherosclerosis contributes

• Genetic conditions predispose to aneurysm

Acute arterial insufficiency

Usually occurs acutely as a result of thrombosis or embolism (MCC- emboli from heart)

• emboli from A-fib/flutter, mitral stenosis, transmural infarction

• 10x more likely in lower extremity than upper (most common superficial femoral artery)

• Acute occlusion= severe ischemia (no collateral circulation)

• Must catch within 4-6 hours to minimize the risks of limb loss

Acute arterial insufficiency S/S

Acute onset of severe pain, loss of pulses, ischemic changes (cool limbs and cyanosis), unilateral, can present as stroke

• 5 P’s

  • Pain: constant and aggravated by movement

  • Pallor: occurs initially, followed by cyanosis

  • Pulselessness: w/ cold limb

  • Paresthesia: caused by anoxia to peripheral nerves

  • Paralysis: necrosis of muscles and nerves

Dx of acute arterial insufficiency

• Hx (time of onset, previous heart disease, atherosclerotic PVD, hypotension)

• 5 P’s (HALLMARK)

• Finding distal to occlusion

• Paresthesia and paralysis are late findings

• MRA/CTA: GOLD STANDARD, if no time straight to OR

Tx of acute arterial insufficiency

• Consult vascular surgery for operative intervention

• Immediate anticoagulation with heparin

• Cardiac embolism: PERMANENT oral anticoagulation

Complications if not treated: limb loss, organ failure, compartment syndrome, reperfusion syndrome

Abdominal aortic aneurysms (AAA)

Localized dilation or out pouching of abdominal aorta, can be apart of aging, 90% are below renal artery

• Healthy young man 2 cm

• Aneurysm present when diameter exceeds 3 cm

• Rarely rupture until >5 cm

• Male to female ration 4:1, occurs in 2% of men over 55 yo

• Involve the aortic bifurcation and often the common iliac arteries

AAA S/S

• Asymptomatic: found incidentally on CT/ultrasound or palpated

• Symptomatic: mild/severe mid-abdominal discomfort often radiating to the lower back

• RUPTURE- SURGICAL EMERGENCY

  • Rupture causes severe pain, palpable abdominal mass, hypotension

  • Free rupture into peritoneal sac: death

AAA DX and TX

Dx: abdominal ultrasounds, aneurysm around 5 cm perform a CT

• F/U every 2 yrs< 4cm, 6 mo if 5 cm Aneurysm present

• Screen 65-74 yo men who were previous or current smokers, no enlargement do not repeat

Tx: Elective repair if >5.5cm or rapid expansion >0.5 cm in 6 mo

• Pain, tenderness, impending rupture= urgent repair

• Open Sx repair= ruptured

• Endovascular repair = noncomplicated, unruptured

Thoracic aortic aneurysms

Happens due to atherosclerosis, CT disorders (Marfan), less than 10% are thoracic

S/S: most asymptomatic, may have substernal or neck pain, can cause SVC syndrome

Dx: CTA scan (SCAN OF CHOICE), could be followed by cardiac catheter and ECHO to see where arteries are

Tx: > 6cm consider repair

• Ascending aorta/proximal aortic arch: open procedure

• Descending thoracic aorta: endovascular grafting

Aortic dissection

Spontaneous initimal tear develops, blood dissects into the media of the aorta and blood flows into the lining and not the lumen, HTN is a key finding, often confused for an MI

If there is an absence of HTN, abnormalities of smooth muscle, elastic tissue, or collagen are present

• Type A: arch proximal to the left subclavian artery

• Type B: proximal descending thoracic aorta beyond the left subclavian artery

Aortic dissection risks and S/S

• Risks: pregnancy, bicuspid aortic valve or coarctation

• Occludes major aortic branches: cause ischemia of brain, intestine, kidney, and extremities

• S/S: severe sudden onset of chest pain, radiates down back-anterior chest-and neck, HTN, syncope or paralysis of lower extremities, new murmur, peripheral pulses diminisheD

Aortic Dissection Dx and Tx

Dx

• EKG (to eliminate MI confusion)- can show LVH might be clear

• CT Chest and Abdomen (TEST OF CHOICE): line (dissection)

Tx

• Bring down BP: Beta blockers (labetelol or Esmolol), CCB if doesn’t work (nicardipine or nitroprusside IV)

  • Prior to definitive Dx even being known

Sx

• Type A: URGENT Sx repair

• Type B: early thoracic stent repair if signs of malperfusion

• Uncomplicated B: BP control, urgent Sx not required, monitor with yearly CT

Varicose veins

Dilated tortuous superficial veins in the legs due to high venous pressure

• Risks: prolonged standing, pregnancy, heavy lifting, hereditary

• S/S: dull aching heaviness of legs, worse w/ standing, itching over the ankles or large varicosities

  • older patients bleed with minimal trauma

• Dx: Hx and PE

• Tx:

  • Non-surgical: medical grade compression stockings

  • Scleortherapy: sclerosing agents to veins

  • Surgical: thermal ablation or vein stripping

Superficial Venous Thrombophlebitis

Red, painful in duration along a superficial veins, MC @ the site of an IV Line

• Risks: Pregnancy, trauma, varicose veins, systemic hyper-coagulable states, IV lines

  • Monitor site for SEPTIC phlebitis (erythema, fever, fatigue, leukocytosis)

• Dx: Hx and PE

• Tx:

  • Symptomatic: analgesics (Tylenol) and warm compresses

  • Septic thrombophlebitis: remove lines/catheters, IV abx (VANC and CEFTRIAXONE)

Chronic venous insufficiency

Inadequate venous return over a long period of time

• Risks: prior DVT, leg trauma/surgery, obesity

• S/S: progressive pitting edema, itching-dull-aching after standing, taut shiny skin at ankle, brownish discoloration of the skin, ulcerations above the ankles, frequent cellulitis

• Dx: Hx and PE

• Tx: prevention of primary causes, graduated compression stockings, meticulous wound care in cellulitis

Superior Vena Cava Syndrome (SVCS)

Occlusion of the superior vena cava leading to venous distention in the upper extremities and head (“swollen head”)

• Risks: MCC is malignancy, histoplasmosis, TB, CF, benign masses, invasive procedures

• S/S: headache, fuzziness, dizziness, dilated facial veins, facial flushing, edema of face-neck-arms, cyanotic appearance of skin

  • Bending over and lying down exacerbates the symptoms

  • Dx: PE signs, CT of the chest (BEST IMAGING)- shows site of occlusion

  • Tx: elevate the head, balloon angioplasty/stent of the occlusion, Tx of the underlying cause, treatment of the neoplasm

Lymphedema

Progressive disease that results in accumulation of interstitial fluid and fibroadipose tissue

• Primary form: congenital abnormalities of distal lymphatics (often unilateral)

• Secondary form: inflammatory or traumatic lymphatic obstruction

  • Trauma, external beam radiation tx, lymph node removal, inflammatory disorders, obesity, FILARISIS (WORM)

Lymphedema S/S, Dx, and Tx

• S/S: insidious onset of symptoms, limb hypertrophy, thickened and fibrotic skin, pitting edema initially- slowly becomes less pitting overtime, complain of limb pain, decrease ROM

• DX: clinical, USN Doppler

• TX: underlying cause, refer to specialty wound care, elastic compression stockings or lymphedema wraps, meticulous skin care to avoid cellulitis

  • Infection= use CEPHALEXIN

Lymphangitis (Lymph/fluid vessels infection)/ Lyphadenitis (lymph node infection)

Bacterial infection (hemolytic strep or staph aureus) that feeds bacteria into lymphatics

• Red streak extending towards involved nodes

• Infection can progress rapidly, may lead to septicemia and death

S/S: throbbing pain and warmth in areas of cellulitis, indurated cellulitis with spreading streaks, malaise, fever, chills, sweating, tachycardia

• streaking can be faint and easily missed in people of color

Dx: Labs (leukocytosis), blood cultures (+ if septicemia)

Tx: heat, elevation, immobilization, analgesia (Tylenol), meticulous wound care

• ABX: Staph and strep CEPHALEXIN, AUGMENTIN (MRSA: BACTRIM)

Raynaud’s Phenomenon

Vasospastic attacks of small arteries of the fingers (sometimes the toes too)- vasoconstrict and decrease blood flow

1. Primary: young women, course is more benign

2. More severe, causing digital ulceration or gangrene

• S/S: change in skin color and sensation, attacks precipitated by cold-stress-vibrations, pallor-cold sensation- numbness, sluggish blood flow and ischemia (cyanosis), chronic attacks (thin/brittle nails and skin), asymptomatic between attacks

• Dx: Hx and S/S

• Tx: Avoid cold to the extremities, keep body warm, NO SMOKING, avoid sympathomietric drugs

  • Meds: CCB- nifedipine, amlodipine

  • Sx: only in refractory cases

Thromboangitis Obliterans (Buerger Disease)

Segmental, inflammatory and thrombitic disease, occurs in distal arteries (sometimes veins) of extremities, usually plantar and digital vessels of the foot and lower leg (It is arteritis, inflammation of the arterial wall)

• Risks: male smokers, middle-aged

• S/S: lesions on toes and patient <40 yo, rest pain is frequent, progresses to tissue loss and amputation

• MRA/CTA: distal tree obliteration

• TX: Stop smoking (curative), if pt doesn’t stop smoking amputation to the extremities will be the outcome

Giant cell arteritis (GCA) or Temporal arteritis

Chronic-inflammatory disease involving large and medium sized arteries, can be widespread causing stenosis and aneurysm of affected vessels

• Risks: Age (almost never before 50, usually 70-79), MC in women, caucasians (Scandinavian), Polymyalgia Rheumatica

• S/S: fever, fatigue, weight-loss, headache (scalp tenderness), jaw claudication, ocular involvement (amaruosis fugax)

• Dx: Labs- increased ESR, CRP, TEMPORAL ARTERY BIOPSY

• Tx: 1 mo prednisone (do steroid taper)

Supraventricular arrhythmias

Originate ABOVE the cardiac ventricles

• narrow QRS complex, less serious because ventricle activity is preserved

• S/S

  • Fast heart rate: palpitations, chest pain, nausea, diaphoresis

  • Slow heart rate: dizziness, syncope

Sinus Bradycardia

Sinus rhythm w/ HR <60 bpm, regular rhythm slow-rate, P-waves followed by narrow QRS complexes, Can be a normal finding in healthy individuals, athletes, or during sleep

• Risks: Medications (Beta-blockers, CCB, Digoxin), athletes/healthy individual, sleep (benign)

• S/S: dizziness, weakness, fatigue, SOB, chest pain, syncope (fainting)

• Dx: confirm and exclude other causes of bradycardia, ELECTROLYTES and THYROID FXN TESTS

• Tx: not always needed

  • Symptomatic: Atropine (acute and symptomatic), pacemaker (chronic)

Sinus tachycardia

Heart rate >100 bpm, typically between 100-160 bpm originating from SA nodes, normal rhythm-fast rate

• Risks: exercise/exertion, stress-anxiety, fever, hyperthermia, hypoxia, anemia, stimulants

• Tx: Underlying conditions (pain, fever dehydration), avoid stimulants, address stress and anxiety problems, adequate hydration and sleep

  • Meds: Beta-Blockers (metoprolol, labetolol), or CCB (verapamil, diltiazem) to control heart rate

Premature atrial contractions (PACs)

Early beat originating from an ectopic pacemaker site in the atria, early beat interrupts the regularity of sinus rhythm, increase automacity of pacemaker cells

• Same ectopic site= regular irregular rhythm

• Different ectopic site= irregular, regular rhythm

• Risks: caffeine, nicotine, cocaine, amphetamines, thyroid disease, post-MI, stress/anxiety, hypoxia, CHF, Pulm dz

• Tx

  • Infrequent: no treatment

  • Frequent: underlying cause

Multifocal atrial tachycardia and wandering atrial pacemaker (WAP)

Occurs when the pacemaker site shifts back and forth b/t sinus node and ectopic atrial sites; P-waves vary in size, shape or direction across the rhythm strip as the pacemaker “wanders” b/t multiple sites

• 3 different P-wave morphologies

  • MAT: HR>100

  • WAP: HR<100

Supraventricular Tachycardia (SVT)

Often occurs in patients without structural heart disease, episodes start and end abruptly (seconds to hours)

• Rate 140-240 bpm, regular rhythm (not sinus)

• Loss of normal contour, P-wave differs in contour from sinus beats and is often buried in the T-wave (no sinus)

• Normal QRS complex

• S/S: palpitations and anxiety

• Tx: depends on pt stability

  • Unstable (hypotension, AMS, HF): cardioversion (synchronized electric shock)

  • Stable (least to most invasive)

    • Vagal maneuvers (carotid massage, Valsalva)

    • Bolus of adenosine IV →If that doesn’t work do another bolus of adenosine→ If ineffective do another bolus of adenosine

Wolff-Parkinson White (WPW)

Accessory pathway between atria and ventricles causes tachycardia

• short PR interval, HALLMARK DELTA WAVE

• Risks: sudden cardiac death

• S/S: palpitations, dizziness, dyspnea, chest pain, episodes of syncope

• Tx: Accessory pathway ablation (radio frequency energy)

Atrial flutter

Originates in ectopic pacemaker site in the atria discharging atria impulses at a rate of 250-400 bpm; ventricular contraction rate typically regular and ranges from 75-150 bpm, blood pools and the atria cannot drain

• rapid atrial impulses create a V-shaped waveform with a sawtooth pattern

• TX:

  • Unstable: Cardioversion (synchronized electric shock)

  • Stable: Rate control (B-blocker or CCB) or Rhythm control (amiodarone or cardioversion with med failure), catheter ablation (PREFERRED LONG TERM MANAGEMENT)

• Anticoagulation (decrease stroke incidence)

  • Onset <48 hrs can convert rhythm

  • Onset >48 hrs begin anticoag or schedule TEE for clot evaluation before cardiovert

  • Long term anticoag with a DOAC

Atrial Fibrillation (A-Fib)

MC arrhythmia requiring treatment and can be secondary to many medical conditions; atria contracts 300-500 contractions in a minute

• atrial pathology: increase atrial pressure, atrial dilation (disrupts underlying conduction path)

• Atrial rate >300 bpm, irregular rhythm, variable ventricular rate, absence of P-waves, irregularly regular, varying R-R interval

• Risks: enveloping blood clots, stroke, 60 and older

• S/S: dizziness, palpitations, fatigue, mild dyspnea, chest pain

• Tx: rate control, rhythm control, stroke prevention (anticoagulation)

  • Unstable: Cardioversion (synchronized cardioversion)→ TEE or anticoag first

    • DO a CHADS-VAS risk score (stroke risk >2 in men, >3 in women)

  • Stable: 1ST LINE- Rate control and anticoag for long term maintenance

    • Rate: Beta blocker (metoprolol, atenolol), CCBs (diltiazemn, verapamil), amiodarone

    • Anticoag: DOAC (apixaban, rivaroxaban)

Junctional escape rhythm

Junctional arrhythmia the heart rate is low at 40-60 bpm, SA node fails to initiate impulse so a secondary pacemaker within AV junction takes over

• P-waves typically absent/buried

• Bradycardia

Premature ventricular contractions (PVCs)

Early ectopic impulse that originates in ventricular tissue either in the right or left ventricle, premature wide morphology

• QRS complex is wide and morphology is different b/c of underlying rhythm

• Pause follows the PVC, usually compensatory

• Risks: MC in those w/ heart disease

• Tx: not indicated if asymptomatic

Ventricular Tachycardia (V-tachycardia) aka monomorphic tachycardia

Originates from an ectopic site in the ventricles discharging impulses at a rate of 140-250 beats per minute (complication of MI or cardiomyopathy)

• 3 or more premature beats

• Tombstone appearance

• Tx

  • Unstable: cardioversion (w/pulse)→ if recurs give amiodarone and shock again

  • Stable: amiodarone, if unsuccessful sedate patient and perform cardioversion as indicated

  • Long term: B-blocker or CCB

Torsades De Pointes→ Polymorphic Vtach

Prolonged QT interval, “twisting of the points”- twist around isometric line, QRS complexes are wide and have varying heights, widths, and shapes; seen anywheres from 200-300 bpm

• Risks: severe hypokalemia, severe HYPOMAGNESEMIA or prolonged QT interval

• Tx: O2 therapy, UNSYNCHRONIZED CARDIOVERSION and magnesium maintenance infusion (1st line)

  • Also correct electrolyte inbalance and d/c QT prolonging drugs

Ventricular fibrillation

No regularity, no complexes or waves present are able to be analyzed (no pulse), death is imminent unless rhythm is treated immediately

1. Defibrilate at highest energy level (unsuccessful do IV lines and intubate)

2. Administer epinephrine and perform 5 cycles of CPR

3. Continue drug therapy, CPR and defibrillation attempts

• Once pt is revived, tx the underlying cause

Heart Block

Rhythms where there is a delay or block in the conduction of impulses from the atria to the ventricles, 3 classes

1. First degree AV block: all conducted just delayed

2. Second Degree AV block

A. Mobitz I: Progressive PR interval with a dropped beat

B: Mobitz II: Fixed PR interval with a dropped beat

3. Third degree AV block: non conducted, firing completely on their own

First degree AV block

Electrical impulse leaves the sinus node and travels normally to AV node where it is delayed longer than normal before conducted to the ventricles

• prolonged QR interval (longer than 0.2 seconds)

• Mildest form, typically requires no specific treatment

Second degree heart block Mobitz Type I (Wenckebach)

Initial impulse leaves the sinus nose and travels through the AV node, is conducted through the ventricles but each successive impulse has increasing difficulty passing through the AV node until finally an impulse does conduct to the ventricles

• PR intervals longer and longer until dropped QRS

Second Degree Heart block Mobitz Type II

More than one P-wave to each QRS complex

• PR is normal or prolonged but will be consistent

• Can progress suddenly to 3rd degree

• TX: PERMANENT PACING if it does not resolve

Third Degree Heart Block

Impulses fail from atria to ventricles, complete heart block, beat totally separate of eachother

• TX: permanent pacemaker

Non-modifiable risk of HTN

• Age

• Family hx/genetics

• Male sex

Modifiable risks of HTN

• Obesity

• Diet

• High sodium

• Smoking

• Alcohol

• Sleep apnea

• Metabolic disorders

• Emphasis on lifestyle factors (sodium, alcohol, stress, weight, heart healthy habits)

Essential/Primary HTN

HTN without an identifiable secondary cause

Secondary HTN

Due to a specific underlying disease

Hypertension measurements and risks

• Goal: <130/80 mmHg

• Normal: less than 120/80

• Elevated 120-129 mmHg and <80 mmHg

• Stage I Hypertension: 130-139 mmHg or 80-89 mmHg

• Stage II: >140 mmHg or >90 mmHg

• Risks: Coronary artery disease, heart failure, A-Fib, stroke, dementia, CKD, heart attack

Hypertension S/S

Often asymptomatic, if present can present as

• Headache

• Dizziness

• Visual disturbances

• Palpitations/chest discomfort

• Nosebleeds

Hypertension Dx

Dx

• PREVENTTM risk calculator to evaluate risk for heart attack, stroke, and heart failure

• Ratio of urine albumin/creatine (recommended for all pts with HTN)

• Screening for primary aldosteronism (plasma aldosterone/renin)→ secondary causes

• Confirmed with 2+ readings on >2 visits and home BP monitoring

Hypertension Tx

1. First line: lifestyle modification

2. Medication- initiate if

• Stage 1 HTN with CVD, CKD, diabetes, Prevent risk >7.5%

• BP >130/80 mmHg after 3-6 mo of lifestyle change

• Stage 2 HTN (>140/90 mmHg): start 2 drugs (single pill combo preferred)

  • ACE/ARB+CCB (MC)

Tx of HTN with medications (after lifestyle modification ineffective or other indication)

First Line Medications

• Thiazide diuretics (HCTZ, chlorthalidione)- Mild HTN

• DHP-CCBs (amlodipine, nifedipine)

• ACE/ARBs (protects CKD)

Second Line Medications

• Beta-blockers

• Vasodilators (hydralazine)

• Central Alpha agonists (Clonidine)

ACE in HTN

First line in pts with HTN with a comorbidity such as diabetes and chronic kidney disease (CKD)

• ACE and ARB are kidney protective

CCB in HTN (DHPs)- amlodipine, nifedipine, nicardipine

Black patients with uncomplicated HTN (first line)

• Could also use HCTZ which is a thiazide diuretic

Alpha blocker in HTN (prazosin terazosin, doxazosin)

HTN and benign prosthetic hyperplasia, smooth muscle relaxer (tx both conditions)

• Tx hypertension and relaxes smooth muscle

Beta-Blocker for Pt with recent MI and HTN

Patients discharged for MI, all patients with recent MI, and also treats HTN (decreases O2 demand to the heart)

Thiazide diuretics in HTN

Tx mild, uncomplicated HTN

• Decreases urinary Ca++ excretion (GOOD for use in kidney stones)

Hypertensive Urgency

Chronic uncontrolled HTN or medication nonadherence, slow vascular adaptation, NO ORGAN DAMAGE

• >180 or >120 without organ damage

• Risk: non-compliance with meds, abrupt withdrawal of B-blocker or clonidine, pain/anxiety/stress

• Dx: BP measurement and evaluation for organ damage

• Tx: Outpatient or observation unit

  • Usually always a PO med- ACE/ARB, CCB (DHP), BB

  • Med adherence, diet, and at home BP monitoring

Hypertensive emergency

Sudden rise in systemic vascular resistance, endothelial injury, fibrinoid necrosis of arterioles, ischemia, organ dysfunction

• usually >180, >120 WITH ORGAN DAMAGE

• Risks: med non-adherence, renal disease, drugs, post-op, aortic dissection

• S/S: organ damage, headaches, confusion, HF, aortic dissection, acute kidney injury, retinal hemorrhages, stroke symptoms

• DX: confirm BP, Labs, Imaging (for signs of organ damage)

• TX: Need ICU and continuous monitoring

  • IV Meds (sodium nitroprusside, B-Blocker, CCB), NO ACE

Cardiovascular disease, heart disease, coronary heart disease

1. Cardiovascular disease- The Big Umbrella: all types of diseases that affect the heart or blood vessels

• Coronary Heart Disease: CAD and other conditions that affect coronary arteries like spasms and inflammation

• Coronary Artery Disease: Narrowing or blocking of coronary arteries caused by build-up of plaque, MC coronary heart disease and presents a MI

Coronary heart disease

• Risks:

  • Nonmodifiable: age (Men >45, women >55), family hx, Males, Race (Hispanic, south asain, Indian)

  • Modifiable: Hyperlipidemia (hypercholesterolemia), HTN, smoking, DM, obesity, sedentary, diet/alc, psychosocial, METABOLIC SYNDROME

• S/S: Always in a state of inflammation (high-sensitivity CRP inflammatory marker)

  • Atherosclerosis: CHD results from endothelial cell dysfunction, dyslipidemia and inflammation

1. Stage 1: endothelial dys leads to formation of a fatty streak

2. Stage 2: LDL enters the intima and becomes oxidized, attracts macrophages

3. Stage 3: plaque matures to fibrous cap, vessel of lumen narrows

• Plaques can remain stable or progressive or narrowing of arteries or can rupture

  • Risks for rupture: high lipid content, high concentration of macropahage, thin fibrous cap (signs of young, immature plaques)

• Can be asymptomatic; angina, arrhythmia, MI, possible sudden death

Myocardial ischemia pain

Dull, achin pressure, heaviness, tightness, squeezing

• Location: retrosternal or left precordial

• Referred: jaw, shoulder, arm, upper abdomen, back

• Ischemic S/S first felt with exercise and stress, progresses to at rest and unstable angina

• S/S: SOB, dizziness, nausea, diaphoresis, doom

• NOT reproduced with palpation, DEPRESSION in women, 1/3 will have no chest pain