Cardio 2 Flashcards
Typical angina of MI
crushing chest pain and feeling of impending doom!
midsternal pain which radiates to jaw, neck, shoulder and down left arm
stable vs unstable angina
stable - brought on with physical activity and relieved with rest, usually within 30 min
unstable - increasing chest pain at rest or with exercise
Prinzmetal’s angina
(aka variant angina)
spontaneous vasospasm of coronary arteries
typically lasts longer than 30 min
Levine’s sign
clenched fist held over the heart
ECG findings of ischemia
ST depression
Downsloping ST
What lab is done to rule out MI in patient with ischemia?
troponins
Quick acting, emergency treatment of ischemia
sublingual nitroglycerin
Side effects of vasodilator/nitrate medications
hypotension
headaches
N/V
Medications for angina
sublingual nitroglycerin long-acting nitrates BBs CCBs Aspirin
First line therapy for chronic angina
beta blockers
MOA of beta blockers to treat angina
lessen heart’s sympathetic response to epi and norepinephrine
MOA of calcium channel blockers to treat angina
decrease heart contractility
decrease peripheral vascular resistance
Surgical revascularization procedures for ischemia
Balloon angioplasty and stents
CABG = coronary artery bypass grafting
Possible cause of MI in young healthy individual
cocaine use
Atypical presentation of MI without chest pain most likely in what patients?
women and diabetics
Difference in clinical definition of angina vs MI
crushing chest pain in MI lasts longer than 30 min, whereas angina pain resolves within 30 min
Dressler Syndrome
post-MI syndrome; 1-2 weeks after MI patient experiences pericarditis, leukocytosis, pericardial effusion, pleural effusion
Changes in serial cardiac enzymes after MI (when do they elevate, peak, and normalize)?
Myoglobin: elevates in first 1-3 hrs, peaks at 6-7 hours, and normal by 24 hrs
Cardiac troponins I and K: elevate within 2-12 hrs, peak around 24 hrs, and normal by 2 weeks
CK-MB: elevate within 3-12 hrs, peaks around 24 hrs, and normal by 72 hrs
Progression of ECG findings with MI
peaked T waves -> ST segment elevation -> Q waves -> T wave inversion
ST elevation defined as > 0.1mv (one small box)
Using 12 lead how can you determine location of MI?
Inferior – II, III, aVF Posterior/septal – V1 and V2 Anterior – V3, V4 Anterolateral – V4, V5, V6 Lateral – I, aVL, V5, V6
Treatment of MI
“MONA”
Aspirin immediately Nitroglycerin Supplemental oxygen Morphine for pain Thromobytic
Contraindications of fibrinolytic therapy for STEMI (tPA)
Absolute: Ischemic stroke or head trauma within 3 months Intracranial neoplasm Active bleeding (excludes menses) Any prior intracranial hemorrhage Suspected aortic dissection
Relative: BP > 180/110 or h/o chronic severe HTN Past ischemic stroke +3 months Major surgery, prolonged CPR (>10 min), or internal bleeding within 3 wks Pregnant Active peptic ulcer Current use of anti-coags
Thrombolytic therapy (t-PA) for acute MI most effective within _____ hours, but can be used within _____ hours.
first 3 hrs
12 hrs
What is given to patient allergic to Aspirin?
Clopidogrel (Plavix)
Location of 2 valves between atria and ventricle
mitral = Left tricuspid = right
Symptoms of mitral valve stenosis and regurgitation
exertional dyspnea
orthopnea
paroxysmal nocturnal dyspnea secondary to pulmonary congestion
Way to definitively diagnose valve disorders?
Echo with Doppler
Valve disorders have close association with what other pathology?
rheumatic fever
Causes of mitral valve regurgitation
Mitral valve prolapse most common cause (thin females)
MI
Endocarditis
Ruptured chordae tendineae (d/t MI or endocarditis)
Which murmurs will have rales secondary to pulmonary congestion?
mitral stenosis
mitral regurg
opening snap following S2 best heard at apex =
mitral valve stenosis
pansystolic blowing murmur with loud S3
mitral valve regurg
Hallmark of mitral valve prolapse seen in mitral regurgitation
midsystolic click
Most common valvular disease in U.S.
mitral regurg
ECG findings of mitral regurg
LVH
A-fib
Mitral regurgitation and mitral valve stenosis treatment
Treat Afib – cardiovert, warfarin
Pulmonary congestion – diuretics and vasodilators
Surgical – Valve repair for prolapse, Valve replacement
Congenital and acquired causes of aortic stenosis
congenital bicuspid or unicuspid valve (middle aged)
acquired degeneration or calcification (over 65)
Symptoms of aortic stenosis
exertional dyspnea
syncope
angina - poor profusion of coronary arteries
Characteristics of aortic stenosis murmur
harsh crescendo-decrescendo systolic murmur
along right sternal border
Aortic stenosis treatment
VALVE REPLACEMENT
prosthetic - long lifespan but require anticoags
pericardial and porcine - shorter lifespan but don’t require anticoags
Ross Procedure - replace with patient’s pulm valve and cadaver to replace pulm valve
Patient with Marfan Syndrome likely has which valvular disorder?
Aortic regurgitation
Aortic regurgitation treatment
Control BP
Valve replacement if needed
Murmur with chest pain and swelling of feet and ankles?
Tricuspid regurg
Causes of pulmonary regurgitation
Pulmonary HTN Endocarditis MI Plaque Iatrogenic
Valve disorder that causes enlarged right atrium? How does this present on ECG?
tricuspid regurg
abnormal p wave
widely split S2 =
pulmonary regurg
holosystolic blowing murmur and radiates to right sternum
tricuspid regurg
tricuspid regurg treatment
Diuretics and salt restriction to decrease fluid volume
Surgical valve repair or replacement
If pulmonary HTN, treat with arterial vasodilators
With mitral valve stenosis it is presumed that the patient has had ________ even if there is no obvious history.
rheumatic fever
Pulmonary regurgitation treatment
By itself is well tolerated and typically doesn’t require treatment
Valve may be replaced or repaired and underlying causes should be addressed
Upon chest auscultation you here an opening snap following S2. You immediately think of what?
Mitral valve stenosis
Harsh systolic murmur along left sternal border and it may radiate to the neck
aortic stenosis
Low pitched murmur at the apex
mitral stenosis
Pansystolic blowing murmur at the apex and radiating to the axilla
mitral regurgitation
Where is the SA node and what does it do?
located in right atrium
pacemaker of the heart
Where is the AV node and what does it do?
electrically connects atria with ventricles
Firing rates of SA node, AV node
SA = 60-100 AV = 40-60
Pathway of heart’s electrical conduction system
SA node -> AV node -> bundle of His -> L and R bundles -> Purkinje fibers
What is rate of sinus bradycardia?
under 60 bpm
What is rate of sinus tachycardia?
> 100 bpm
The most common chronic arrhythmia?
Atrial fib
EKG of A-fib
irregularly irregular rhythm
disorganized electrical activity where p waves should be
Treatment of atrial fibrillation and atrial flutter
Rate control: BBs or CCBs, Digoxin (A-fib)
Anti-thrombotics: Heparin short term, Warfarin long term
Cardioversion: electrical or chemical (AMIODORONE)
Radiofrequency ablation
INR goal of A-fib and A-flutter anti-thrombolytic treatment
2.0 - 3.0
ECG with sawtooth pattern
Atrial flutter
A vague diagnosis encompassing chronic bradycardia, sinus arrest, and AV node exit block that occurs in elderly patients and is often brought on or exacerbated by drug therapy. Patients may have heart block or A-fib.
Sick sinus syndrome
Treatment of sick sinus syndrome
permanent pacemaker
Differences in ECG findings of supraventricular and ventricular arrhythmias?
supraventricular - narrow QRS
ventricular - wide QRS
Patient comes in with “skipped heart beats.” What is likely arrhythmia?
PVC
Bigeminy, trigeminy, unifocal, and multifocal PVCs
Bigeminy – PVC every other beat
Trigeminy – PVC every third beat (2 normal beats followed by a PVC)
Unifocal – all PVCs originate at same place within the ventricles and therefore all PVC QRS complexes look the same
Multifocal PVC – PVCs originate at different places and therefore QRS complexes appear different
ECG findings of premature ventricular contractions
beat without a p wave that has wide QRS and a compensatory pause before the next beat
PVC treatment
No treatment if asx
Beta blockers if sx
A run of 3 or more PVCs is considered _______.
V-tach
ECG of V-tach
Rate of 160-240
Several wide QRS waves with no p waves
Treatment of V-tach
Cardioversion:
Defibrillation for pulseless V-tach
Synchronized if pulse present
Medications:
BBs for sustained V-tach to reduce incidence of sudden death
Lidocaine for stable sustained V-tach
What is Torsades de Pointes?
deadly form of V tach where QRS complexes appear twist around isoelectric line
How is Torsades de Pointes treated?
Bolus of Magnesium
Cardioversion prn
Treatment of Ventricular Fibrillation
Immediate intervention to prevent sudden death
Defibrillation and lidocaine
Pathophysiology and ECG findings of 1st degree AV block
All SA node signals get through AV node to ventricles but are a little delayed
PR interval greater than 0.20 seconds (1 box)
Pathophysiology of 2nd degree AV block
Only some signals from SA node get to ventricles
What are the two types of 2nd degree AV blocks and what do they appear like on ECG?
Mobitz Type 1: longer and longer PR intervals until one impulse (QRS complex) is dropped
Mobitz Type 2: intermittent dropped ventricle impulses without lengthened PR intervals
What does 2:1 AV block mean?
two p waves for every QRS complex
How are 2nd degree AV blocks treated?
Type 1 may be benign
Type 2 requires pacemaker
- may use ACLS guidelines if symptomatic (Atropine or transcutaneous pacing)
Pathophysiology of 3rd degrees AV block? Tx?
No impulses reach ventricles = complete heart block
Requires pacemaker
Pathophysiology and ECG findings of Bundle Branch Block?
damaged bundle of His; AV node must propagate through muscle itself which is slower
ECG shows wide QRS wave as ventricles depolarize
Predisposing factors to endocarditis
Most commonly bacterial infection with damaged or prosthetic heart valves - strep viridian’s, staph aureus, enterococci
Post op valve replacement (infection w/i 2 mon) - staph aureus, fungi, G-
Dental work, IV drug use, central line, surgeries/procedures
PE findings of endocarditis
New or changed murmur Splinter hemorrhages Janeway lesions Osler nodes Roth spots Petechia
Difference between Janeway lesion and Osler nodes?
both found on palms and soles but Osler nodes are painful and Janeway lesions aren’t
“Jane is nice”
Duke Criteria for endocarditis
2 major, 1 major + 3 minor, 5 minor
Major Criteria
2 positive blood cultures that grow organism that typically causes endocarditis
Positive echo findings - New regurge, Abscess, Oscillating mass
Minor Criteria
Predisposing factor (eg. prosthetic heart valve, post op)
Fever
Embolic events - Janeway lesions, Petechia, Splinter hemorrhages
Immunologic events - Glomerulonephritis, Osler nodes
Positive blood culture not satisfying major criteria
Endocarditis treatment
Prophylactic antibiotic use for patients with predisposing cardiac issues undergoing higher risk surgical procedures
4-6 weeks of IV antibiotics
Surgical: Valve replacement or Debridement of abscess or infected material
Causes of pericarditis
Viral infection is the most common cause – echovirus, coxsackie, flu, HIV
Bacterial is more rare and typically follows respiratory infection
Post MI – Dressler Syndrome
Post cardiac surgery
Radiation
Autoimmune
Kidney failure
Patient came in because of dyspnea, diaphoresis, and looks extremely ill. There is a pericardial friction rub heard in on lung exam and WBC’s are elevated. Likely dx?
Pericarditis
ECG findings of pericarditis
ST-T wave changes
It begins with ST elevation. There is a return to baseline, and then a T wave inversion
Treatment of pericarditis
Treat underlying issue
High doses of NSAIDS to reduce inflammation (eg. Colchicine)
Corticosteroids if NSAIDS not effective
Diuretics
Pericardiocentesis
Pericardiotomy
___________ is when the pressure from a pericardial effusion constricts the heart to a point where it begins to affect cardiac output.
Cardiac tamponade
Pathognomonic ECG finding of cardiac tamponade?
Electrical alternans = QRS amplitudes fluctuate beat to beat
CXR of cardiac tamponade
water bottle heart
How is cause of pericarditis definitively dx’d?
Pericardiocentesis for culture and cytology
Treatment of cardiac tamponade
Small, stable effusions may be watched carefully
Treat underlying cause
Pericardiocentesis may be required
Pericardiectomy
How is endocarditis cause confirmed?
blood cultures
What is jaw claudication? What is it a hallmark sign of?
pain in jaw muscle or ear while chewing
Giant Cell Arteritis (aka temporal arteritis)
What is an aneurysm? Where is it most common?
abnormal widening or ballooning of an artery due to weakness in the vessel wall
abdominal aorta
Likely causes of aneurysm
Secondary to atherosclerosis - CAD, smoking, HTN, hyperlipidemia, etc.
What congenital conditions are risk factors for aneurysms?
Marfan’s Syndrome
Ehler’s Danlos type IV
Best diagnostic study for abdominal aneurysms?
Abdominal U/S
Blood work of temporal arteritis or Giant Cell arteritis
LFT with elevated Alk phos
Elevated C-reactive protein
Elevated Sed rate
Treatment of temporal arteritis or Giant Cell arteritis
High dose prednisone 40-60 mg po daily for 1-2 months followed by tapering over the period of 1-2 years
Aspirin 81 mg may help reduce risk of stroke and blindness etc.
Gold standard for diagnosis for temporal arteritis
Biopsy of temporal artery
List the six P’s of arterial occlusion.
pain pallor pulselessness paresthesias poikilothermia (cold) paralysis
I came in to see my physician assistant because of…
Claudication – pain with exertion
Ischemia in lower extremities - numbness, tingling, +/- ulcers
Erectile dysfunction
PVD
Diagnostic imaging of PVD
Doppler U/S flow studies
Ankle brachial index
Arteriography
CT/MRI angiography
What is a normal ankle brachial index? What does lower value indicate?
Normal ABI is 1.0-1.4
Peripheral arterial disease (PAD) is less than 0.9
Treatment of peripheral vascular disease
Lifestyle modifications to reduce atherosclerosis
Aspirin 81mg daily
Surgical intervention - Endovascular stenting and angioplasty, Bypass grafting
___________ is venous inflammation as a result of a blood clot. This tends to be superficial following trauma.
Thrombophlebitis
Causes and risk factors of DVT
Trauma Major surgery Prolonged bed rest or immobilization Smoking on oral contraception Cancer Pregnancy Genetic clotting issues/ FHX
Homan’s sign
pain and tenderness in the calf with a straight knee and dorsiflexion of foot
Gold standard for DVT and varicose vein diagnosis
U/S doppler
How to prevent DVTs?
Leg exercises Compression stockings Sequential compression devices Freq ambulation Anticoag therapy: Warfarin, Lovenox, Heparin
DVT treatment
Anticoags: Heparin, Warfarin
Filter for inferior vena cava
Thrombolysis
Thromboectomy
Risk factors of varicose veins
Pregnancy Genetic predisposing factors Valvular incompetence Increased abdominal pressure Long periods of standing
Treatment of varicose veins
Behavioral changes - avoid long periods of standing, elevate legs when possible
Graduated elastic stockings
Vein stripping
Sclerotherapy
I came in to see my physician assistant because of…
Progressive edema beginning at the ankles and moving up Skin changes – Hyperpigmentation Shiny Atrophic Dermatitis Painful ulcerations
Chronic Venous Insufficiency
Treatment of Chronic Venous Insufficiency
Behavioral changes - avoid long periods of standing, elevate legs when possible
Graduated elastic stockings
Heat
Ambulatory exercise
When can fibrinolytic therapy be done for chest pain?
ST elevation MI (STEMI) on ECG
Onset of angina
