Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
224 Cards in this Set
- Front
- Back
|
Angina (classic, effort, stable, atherosclerotic angina)
|
Symptom: cardiac pain due to ischemia. Acidic metabolites stimulate chemoreceptors.
Atherosclerotic plaques = most common cause |
|
|
Vasospastic angina, Prinzmetal Angina
|
Reversible / transient. Defect in endothelial cells imbalancing vasoconstriction / dilation factors.
|
|
|
Unstable angina
|
most risky, high risk of MI, emergency
|
|
|
Angina Therapeutic strategy
|
NBC, Nitrates, beta-blockers, Calcium channel blockers
Decrease O2 consumption or increase O2 supply |
|
|
Nitrate MOA
|
Dilation of veins, allows pooling of blood, decreasing preload / O2 consumption
|
|
|
Beta-Blockers MOA
|
Decrease heart rate, negatively inotropic, decrease AV conduction. Decreasing workload & O2 consumption.
|
|
|
Calcium channel blockers effects
|
dilate arteries, reducing afterload. O2 consumption decreased.
Coronary arteries also dilate, increased O2 delivery All used for chronic stable angina, or vasospastic angina |
|
|
Calcium Channel blockers MOA
|
Antagonize L type calcium channels (T type = antiseizure).
Contractile cells = decreased contractility (slight) Slow response cells (SA & AV node) = L channels slowed for phase 4/0, decreased HR. Smooth muscle cells = relaxation, vasodilation |
|
|
Verapamil
|
Cardioselective calcium channel blocker
treat supraventricular tachycardia SE: flushing, hypotension, constipation |
|
|
Diltiazem
|
Cardiac and vascular selective calcium channel blocker
treat supraventricular tachycardia SE: flushing, hypotension, dizziness, constipation |
|
|
Nifedipine
|
-dipines
vascular selective calcium channel blockers, coronary arteries and peripheral arteries treat angina (not acute cases) and hypertension SE: hypotension, reflex tachycardia, constipation, flushing, gum hyperplasia |
|
|
Verapamil and diltiazem contraindication
|
Not for anyone with AV block, decreases AV conductance even further
|
|
|
Gum hyperplasia
|
nifedipine, phenytoin, cyclosporin
|
|
|
Beta-blockers MoA
|
norepinephrine normally binds beta-1 receptors in heart, G protein coupled receptor activates adenylate cyclase, increased cAMP, activates PKA, increases activity of L-calcium channels. Increases calcium release from SR, increased contractility, and activity of slow response cells.
Competitively inhibit NE causes decrease in contractility, decrease in heart rate, decreased AV conductance. |
|
|
Selective Betablockers
|
Atenolol, metoprolol, acebutalol
selective for b1, possibly useful for COPD patients, but rarely used for them |
|
|
Non-selective beta blockers
|
propranolol, pindolol
never use with COPD patients |
|
|
Intrinsic Sympathomimetic Activity
|
Pindolol and acebutalol are partial agonists, less agonist than NE or epinephrine but cause some activity. Don't use with vasospasm
Could be used for patients with bradycardia from BB therapy |
|
|
Contraindications of Betablockers
|
Asthma, bradycardia, AV block.
Not really helpful in vasospastic angina because no effect on coronary arteries. |
|
|
Nitrate MoA
|
converted into NO, stimulating guanylyl cyclase, more cGMP, activating myosin light chain phosphatase, dephosphorylating them allowing relaxation.
Mostly venous smooth muscle, but dose dependent. Some effect on arterial. |
|
|
Nitrate types
|
Nitroglycerin: for acute angina abortion, or prophylaxis, fastest onset
isosorbide mononitrate: slower onset of action, prophylaxis Isosorbide dinitrate: also slower onset of action |
|
|
Nitrate side effects
|
Headaches (vasodilation), hypotension, reflex tachycardia (give with BB or CCb)
Overdose = methemoglobinemia (oxidize ferrous iron in hemoglobin). Methylene blue to cure |
|
|
Contraindications
|
Don't use with phosphodiesterase 5 inhibitors (PDE-5, -fil). Sildenafil, vardenafil, etc. erectile dysfunction drugs can increase hypotensive effects of nitrates
|
|
|
Nitrate tolerance
|
antianginal efficacy is lost with continuous delivery, possibly due to depletion of factors in nitrate metabolism. Must have drug free intervals, such as overnight
|
|
|
Stable angina treatment
|
Acute relief: nitroglycerin sublingual
Prophylaxis: BB = first line, no use if bradycardia, AV block, COPD Slow release nitrate: alongside betablockers, don't use with PDE-5 -fil CCb: verapamil / diltiazem instead of BB to slow heart rate, can use -dipines with BB. |
|
|
Vasospastic angina treatment
|
acute: nitroglycerin
prophylaxis: CCb and slow release nitrates. No beta-blockers, don't have an effect on vasoconstriction |
|
Digoxin MoA / ECG appearance
|
from digitalis plant, inhibits Na/K ATPase by keeping it phosphorylated. This causes a buildup of sodium within the cell, instead exchanged with extracellular calcium. Increased calcium causes calcium release from SR, causing positive inotropic effect.
Seen on ECG like a Dahli mustache |
|
|
Digoxin unpopularity
|
Narrow therapeutic range, unpredictable pharmacokinetic properties, increased toxicity with hypokalemia (happens with concurrent diuretics), causes acute hyperkalemia
|
|
|
Digoxin toxicity
|
amiodarone (antiarrhythmic class 3), verapamil (class 4 cardioselective), quinidine (class 1)
|
|
|
Other methods of Digoxin toxicity
|
inhibition of P-glycoprotein transporter in kidney (no excretion)
eradication of gut bacteria which metabolize digitalis(-mycins) inhibition of CYP3A displacement from tissue binding sites |
|
|
Symptoms of digoxin toxicity
|
Visual disturbances, hallucinations, lethargy, nausea, diarrhea, severe headache, dysrhythmia (more often bradycardia)
Van Gogh may have painted starry night with digoxin toxicity |
|
|
Two ways of treating cardiac insufficiency
|
Chronic: oral positive inotropic agent (digoxin)
Acute: IV vasopressors & positive inotropic agents |
|
|
Phenyelphrine
|
alpha-1 adrenergic receptor agonist, selective. Works only as a vasopressor no inotropic effect.
Can also be used as nasal decongestant, priapism (painful long erection), and induces mydriasis Can cause reflex bradycardia |
|
|
Phenyelphrine breakdown
|
pressor effect potentiated by MAO inhibitors (same breakdown pathway as dopamine, norepinephrine, epinephrine)
isocarboxazid, isoniazid, phenelzine, tranylcypromine, moclobemide, rasagiline, selegiline, linezolid = all MOA inhibitors |
|
|
Dopamine
|
endogenous catecholamine with dose dependent effect
Low = D1 receptors of Kidney (naturesis) / GI (decreased motility) medium = b1 = increased HR high = alpha = vasopressor |
|
|
Dobutamine
|
synthetic catecholamine, racemic, gives the effect of a b1 agonist (increased HR)
|
|
|
Fenoldopam
|
D1 selective, vasodilation
|
|
|
isoproterenol, isoprenaline
|
synthetic catecholamines, b1/2 selective agonists
Increased cardiac output (b1), vasorelaxant (b2) decreasing systemic resistance |
|
|
Phosphodiesterase-3 inhibitors PDE-3
|
-rinone
increase cAMP, increasing activity of calcium channels in heart. Also cause vasodilation Positive inotropes, vasodilators. BP / O2 consumption unchanged |
|
|
Betablockers and CHF
|
can be used to treat left ventricular dysfunction in stable patients. In conjunction with ACE inhibitors or diuretics.
many use labetalol, pindolol, carvedilol, celiprolol, nebivolol because vasodilating beta-blockers good for CHF |
|
|
Capopril
|
-pril = ace inhibitor
only ace inhibitor with a sulfur group in it, can cause allergic reactions |
|
|
Cardiogenic syncope
|
syncope due to decreased perfusion
Stoke-Adam Syndrome Cam be due to tachycardia or bradycardia. Cardiac output = Stroke volume x heart rate. Tachycardia decreases stroke volume and bradycardia decreases heart rate. Less than 30 BPM or greater than 180 BPM. Any arrhythmia will change CO, normal rhythm = optimal |
|
|
Brady arrhythmias Causes
|
SA node dysfunction: hard to distinguish from physiologic sinus bradycardia, increases in frequency after 50
Transient AV block: common in young due to increased vagal tone, persistent failure rare in adults |
|
|
Bradyarrhythmic syncope symptoms
|
Fatigue, chronotropic incompetence, exercise intolerance, abrupt syncope (no prodrome), may be difficult to see on ECG
|
|
|
SA node location / blood supply
|
Located at right atrial-superior vena caval junction
Arteries: RCA 60% flow (SA node artery), Left circumflex 40% flow |
|
|
SA node bradyarrhythmia extrinsic factors
|
reversible underlying cause
autonomic (vasovagal, carotid hypersensitivity), drugs, hypothyroidism, hypoxia, sleep apnea, hypothermia, high intracranial pressure |
|
|
SA node bradyarrhythmia intrinsic factors
|
degenerative (fibrous replacement), MI (often inferior wall MI), inflammatory damage, amyloidosis, iatrogenic (radiation, breast cancer), trauma
|
|
|
Sick sinus syndrome
|
seen more often in elderly, causes arrhythmias
increased fibrous tissue in SA node One type is tachy-brady which alternates between the two arrhythmias |
|
|
SA & AV node dysfunction clinical
|
Can be asymptomatic, may give pre-syncope lightheadedness, syncope, palpitations
|
|
|
AV node dysfunction
|
Can see ventricular dysfunction. If AV node becomes pacemaker, slower rhythm, P-R interval abnormal.
|
|
|
AV node innervation
|
Blood from AV nodal artery & first septal perforator of the left anterior descending artery.
Gets postganglionic sympathetic inervation, and parasympathetic innervation. His bundle / distally are unaffected by ANS. |
|
AV block ECG classification
|
1st degree = P-R > .2s (one big box)
2nd degree = P-R > .2s and not every P results in QRS Morbitz type 1: P-R progressively prolonged until QRS drop Morbitz type 2: multiple P for every QRS 3rd degree = no association of P with QRS |
|
|
AV block etiology
|
Lev's disease: degenerative sclerosis, common, 40+, faster with DM, HTN, atherosclerosis
Autononomic causes: carotid hypersensitivity, vasovagal dysfunction Metabolic: hyperkalemia, hypomagnesemia, hypothyroidism, adrenal insufficiency Drugs, infectious processes, AV valve endocarditis, congenital, iiatrogenic, inflammatory, infiltrative (amyloidosis, sarcoidosis, hemochromatosis), neoplastic, MI (LAD) |
|
|
Bradyarrhythmia testing
|
ECG
Holter (ECG for 20-30 days) ETT Exercise tolerance test, show ischemia or chronotropic incompetence Electro physiologic study = catheter with multiple stimulation / reception sites. Can measure conduction time from different points. (pictured) |
|
|
Clinical presentation of tachyarrhythmic syncope
|
Dizziness, lightheadedness, palpitations (more easily felt), sense of impending doom. Paroxysmal
|
|
|
Tachyarrhythmic syncope types
|
Supraventricular: syncope depends on ventricular conduction rate, often doesn't cause syncope unless with a structural heart disease
Ventricular: syncope dependent on rate (>180), can degenerate into V fibrillation, dangerous |
|
|
Types of SVT (Supraventricular tachycardia)
|
Paroxysmal atrial tachycardia (150-250)
Flutter due to intra-atrial reentry (250-350) Fibrillation due to atrial multifocal rhythm (350-450) AV nodal reentry (created in AV node) Atrioventricular reentry (WPW) |
|
|
Supraventricular tachycardia causes syncope more often if paired with:
|
Heart disease compromising cardiac output, mitral stenosis, cerebrovascular disease, vascular tone / blood volume disorders, pregnancy
|
|
|
atrial flutter = sawtooth
atrial fibrillation P waves too fast to see |
|
Reentry mechanism
|
Anytime there is mismatch in conduction reentry is possible, just need to create a circuit long enough that repolarization is possible before a full loop.
To fix this give adenosine, stops everything. |
|
|
Wide vs narrow tachycardia
|
Narrow = supraventricular
Wide = ventricular, no P waves because AV node isn't creating stimulation, may see retrograde because AV stimulates atria. |
|
|
WPW Atrioventricular reentry (AVRT)
Wolff-parkinson-white |
Direct conduction from atria to ventricle via accessory fibre. Clinical = tachycardia / syncope
ECG: Short P-R, wide QRS (wider than 2 boxes), delta wave (before the R) |
|
|
Ventricular tachycardia with syncope
|
Common cause of syncope, especially if associated with structural disease. Can degenerate in ventricular fibrillation.
Wide QRS |
|
|
Ventricular tachycardia structural causes
|
Ischemic cardiomyopathies = most frequent. MI, ischemia. ECG: Q-waves, LBBB, ST abnormalities
Aortic Valvular Stenosis: LVH Hypertrophic obstructive cardiomyopathy: LVH, left axis deviation Congenital heart disease: RVH, Right axis deviation (from pulmonary hypertension) |
|
|
Ventricular tachycardia repolarization causes
|
Long QT syndrome, caused by medications (antiarrhythmics, tricyclics, erythromycin)
Genetic (familial long QT syndrome) Has a longer relative refractory period, which could allow for a ventricular stimulated Q during the T and push the ventricle into tachycardia (wide) Torsade de pointes |
|
|
Treatment of Bradycardia
|
Determine if primary or secondary
If secondary, correct underlying cause. If primary, pacemaker may be needed, and is the general treatment for chronic bradycardia |
|
|
Acute pharmacological treatment of bradycardia
|
Isoproterenol, sympathomimetic (b1/b2 agonist) must be given IV
atropine: anticholinergic (m2) also can't be used chronically |
|
|
Treatment of Tachycardia
|
Drugs for supraventricular, but not first line for ventricular
Correct underlying cause may need ICD (implantable cardioverter defibrillator) |
|
|
Pacemaker depolarization
|
Depolarizes from right ventricle base, then up septum
Has a wide QRS, pacer spike = tell tale sign Antitachycardia pacemaker capable of either capturing rhythm by speeding up then slowing back down. Or can cardiovert with a shock to normal rhythm. Needs to be large for battery |
|
|
Non-arrhythmic syncope of cardiogenic origin (structure affecting volume)
|
Atrial myxoma (reduced preload) from tumor
mitral stenosis (reduced preload) restrictive cardiomyopathy (reduced filling) pericardial constriction (reduced filling) pericardial tamponade (reduced filling) myocardial disease (reduced afterload) from MI aortic outflow obstruction (reduced SV) aortic stenosis (reduced SV) hypertrophic cardiomyopathy (reduced SV, reduced filling) |
|
|
other non-arrhythmic syncope due to reduced preload
|
pulmonary embolism
pulmonary hypertension orthostatic hypotension (most common) blood loss, dehydration exacerbate. Or abnormal vasoconstriction reflex, or with antihypertensives, vasodilators, antidepressants |
|
|
Reflex syncopes
|
neurocardiogenic (abnormal reflex / vagal response)
situational syncope (fear) carotid hypersensitivity All have increased vagal tone causing bradycardia, and withdrawal of sympathetic tone causing vasodilation |
|
|
Neurocardiogenic (vasovagal) syncope
|
cardioinhibitory = increased parasympathetic activity causing bradycardia
vasodepressor = sympathetic withdrawal causing vasodilation / drop in BP usually some combination of the two common, account for 1/2 of all syncope episodes, have presyncope, recur, and have triggers Sphincter control maintained, motionless |
|
|
Situational syncope
|
cardioinhibitory and vasodepressor
often fright induced often have urinary / GI symptoms along with it (micturition, defecation) |
|
|
Neurogenic syncope clues
|
consider if autonomic dysfunctions present (bladder control, constipation, sweat problems, erectile dysfunction) or with peripheral neuropathies (diabetic, alcoholic, amyloid, nutrition), or other neuropathic degenerative diseases
|
|
|
Cerebrovascular disease symptoms with syncope
|
have other symptoms of focal ischemia (side weakness, diplopia, ataxia, sensory disturbances, dysarthria)
|
|
|
Syncope from seizure
|
have a prodrome, tonic clonic (tonic = seize up quickly, clonic = alternate between seizing and relaxing), postictal state (confusion for 5-30 minutes post seizure)
|
|
|
Antiarrhythmatic class 1a
|
sodium channel blocker, lengthens repolarization
proarrhythmic, not used for chronic treatments. Sometimes used for acute situations of supraventricular tachycardia quinidine, procainamide |
|
|
Antiarrhythmic class 1b
|
sodium channel blocker, shortens repolarization
IV for ventricular tachycardia. lidocaine. hepatic metabolism |
|
|
Antiarrhythmic class 1c
|
Slow conduction
Flecainide, propafenone can be used acute or chronically for supraventricular tachycardia proarrhythmic with ischemia |
|
|
Antiarrhythmic 2
|
beta blockers, -olol
slow heart, negative inotropic, can be used for SVT and VT. Good to treat ischemic heart, cannot use with COPD |
|
|
Antiarrhythmic class 3
|
Potassium channel blockers, prolong action potential
amiodarone (also class 1, 2, 4 effects), good for most arrhythmias except torsades (prolongs P-R) |
|
|
Amiodarone
|
class 3, although also 1, 2, 4 effects, prolongs AP
treats most arrythmias, except torsades SE many: pulmonary fibrosis!, cataracts, thyroid disease, hepatopathy, dermatosis (blue). most non-reversible. |
|
|
Antiarrhythmic class 4
|
Ccb, treats SVT angina and hypertension
Decreases cardiac output, do not use in CHF |
|
|
Normal arrhythmias
|
sinus arrhythmia = normal variation in heart rate
sinus tachycardia = reactive to stressors, drugs, anemia, ETOH, shock. max 160-180. Treat cause Sinus bradycardia: normal in athletes, only treat if symptoms |
|
|
Supraventricular tachycardia
|
HR:140-240, caused by reentry mechanism
Either AVNRT or AVRT (WPW usually) Abrupt onset, rapid but regular, rare syncope NARROW QRS, no or reversed P waves |
|
|
SVT treatment
|
Vagal maneuvers (rub eyelids / massage carotids if clear ultrasound)
AV node blockers (adenosine) careful with COPD bronchospasms Cardioversion (shock) unless digoxin toxic, leading to arrhythmia RFA (radio frequency ablation) catheter burns off problem area |
|
|
AV nodal reentrant tachycardia
|
narrow complex
|
|
|
Wolf parkinson white (SVT)
|
aberrant conduction fibers create reentry circuit
Short PR, wide QRS, delta wave 30% develop atrial fibrillation / atrial flutter, may degenerate to VT |
|
|
WPW fibers
|
Kent fibers = between atria and ventricle
Mahaim fibers = near AV node |
|
|
Orthodromic vs Antidromic WPW
Concealed |
Orthodromic = antegrade down AV node, retrograde up accessory pathway (narrower QRS)
Antidromic = antegrade down accessory pathway, retrograde up AV node Concealed = retrograde, may be invisible on ECG unless tachycardic |
|
|
WPW treatment
|
radio frequency angioplasty = best
do not use AV node suppressants with wide complex SVT (antidromic), decreases accessory refractory and increases AV refractory, hastening tachycardia. Narrow SVT treat with AV nodal blockade. if hemodynamic unstable, cardiovert. |
|
|
Atrial fibrillation
|
Regularly irregular QRS, noise instead of P waves, not all ventricular beats produce peripheral pulse (may not have preload)
common in elderly, with structural defect, thyroid problems, COPD, holiday ETOH heart, post heart surgery Not usually life threatening, can cause tachycardia mediated cardiomyopathy, hypotension if mitral stenosis or if pregnant !Big worry = embolic events! Transient ischemic attack, cerebrovascular accident |
|
|
Tachycardia mediated cardiomyopathy
|
heart rate goes fast for a long time, weakening myocytes and attenuating myocyte function
|
|
|
Holiday Heart
|
Atrial fibrillation in healthy person 1-4 days after alcohol consumption
treat rate control, CCb or Bb |
|
|
Atrial Fibrillation emboli
|
TEE, trans-esophageal echocardiogram important
need to look for clots before returning to sinus rhythm. Via cardioversion may need anticoagulant, if pharmacological cardioversion then time consuming and want anticoagulants for all that time |
|
|
Atrial fibrillation anticoagulation
|
Heparin first (no factor 10), followed by long term warfarin (slow, vit K dependent factors)
CHAD score determines risk of emboli, need for anticoagulants CHF=1, HTN=1, Age>75=2, DM=1, Stroke/TIA=2 1-2 = intermediate, 3-4 =high risk anticoagulants Everyone gets aspirin |
|
|
Atrial fibrillation , slow vs fast ventricular response
|
slow = get bradycardia, may need pacemaker
fast = can cause tachycardia mediated cardiomyopathies, can cause VT |
|
|
Atrial flutter (persistent atrial contractions)
|
COPD or structural heart disease, atria 250-350 sawtooth formation, 1:1 or more
can also cause emboli, need anticoagulant often treat with radio frequency ablation Need to differentiate from MAT |
|
|
Multifocal atrial tachycardia
|
3 different P waves creating arrhythmia
need to treat underlying condition, often hypoxemia |
|
|
Benign Premature ventricular contraction (PVC)
|
skipped beats. always resolve with exercise. no association with structural heart disease (if you have this probably not PVCs)
Treat with: K+, MG++, or Thyroid issue, no class 1 or 3 due to QT prolongation and proarrhythmatic |
|
|
ICD
|
implantable cardioverter defibrillator
|
|
|
Ventricular tachycardia
|
Sustained, or nonsustained (3 or more beats, less than 30 seconds). NSVT.
with structural heart disease, poor prognosis ICD with low ejection fraction. Acute can treat with amiodarone or lidocaine (3) or lidocaine (1b) |
|
|
Ventricular tachycardia associations
|
sudden death, early morning (autonomic)
structural heart diseases: CAD, hypertrophic cardiomyopathy, CHF, aortic stenosis, congenital heart diseases, prolonged QT, Brugada arrhythmia electrolyte abnormalities |
|
|
Brugada Arrhytmia
|
Right ventricle, spontaneous, can lead to VT
Repolarization problem appears as landslide on ECG |
|
|
Ventricular tachycardia treatment
|
common post reperfusion, not poor prognosis
Treat acute with lidocaine / amiodarone if stable, if unstable = cardiovert Chronic = ICD |
|
|
Long QT
|
Congenital abnormalities (Jervel-Nielsen, Romano-Ward)
Acquired (drugs, electrolyte, metabolic) Causes torsades de pointes (especially with Class 1 and 3) |
|
|
Coronary artery disease CAD
|
or obstructive coronary artery disease, results in angina (clinical term for cardiac chest pain)
Usually described as a pressure, sometimes pain radiates down left arm. |
|
|
Stable angina
|
Due to partial CAD obstruction, stable (predictable, pattern), exertional, no intensity variation, relieved with rest / NTG
No acute cardiac compromise, no ECG ischemia. May happen post PTCA and CABG. |
|
|
PTCA
CABG |
percutaneous transluminal coronary angioplasty
coronary artery bypass graft |
|
|
Unstable angina
|
new onset, increase in recurrence pattern, increase in intensity, not relieved with rest or NTG
cardiac compromise, emergency, associated with new partial CAD obstruction. Not associated with permanent myocardial damage, but could progress |
|
|
Prinzmetal angina
|
Vasospastic CAD, transient paroxysmal vasoconstriction, not usually associated with athersclerotic CAD
Paradoxical upright T waves, or T wave increase (decreased regularly, increased during vasospasm) More common in women < 50 |
|
|
Prinzmetal treatment
|
Give NTG acutely, CCb chronically
No beta blockers, leave alpha unopposed, may be agonised by spilling over catecholamines causing further constriction |
|
|
Non-cardiac chest pain causes
|
life threatening: tension pneumothorax, pulmonary embolism, oesophageal rupture, aortic dissection
other: rib fracture, bone metastasis, cholecystitis (gallbladder), pancreatitis, sickle cell crisis, pleurisy, rib fracture, costochondritis (rib or connective tissue), esophagus spasm, pericarditis, gastroesophageal reflux, pneumonia, pleural effusion, herpes zoster |
|
|
Acute coronary syndrome ACS
|
Caused by Unstable angina, subendocardial infarction (NSTEMI, non-ST elevation MI), or STEMI (ST elevation MI)
|
|
|
CAD development
|
|
|
|
STEMI vs UA / NSTEMI
|
Note that UA doesn't necessarily lead to myocardial damage but NSTEMI does
Plaque rupture exposes lipid and causes clotting / thrombus formation |
|
NSTEMI (non-ST elevation MI)
|
Subendocardial damage (the last tissue supplied by vasculature). Acute angina.
No ST elevation, have T inversions or ST depression Partially obstructive thrombus can shed and completely occlude smaller vessels supplying subendocardium. Thrombus = platelet rich |
|
|
Platelets in atherothrombosis
|
1: adhesion, platelets stick to damaged epithelium with exposed lipids / ECM.
2: activation, give off chemicals, begin fibrin formation 3: aggregation = fibrin form between platelets forming clot Aggregation occurs due to 2b3a receptors connecting platelets via fibrinogen Platelet rich for NSTEMI, fibrin rich for STEMI (more spread out, more completely occlusive) |
|
|
MI markers
|
Troponin = earliest release, very good marker
CK-MB = cardiospecific MI marker, slightly slower than troponin but lasts longer 3 days Myoglobin = accurate for muscle damage but not specific for cardiac LDH = ischemia marker, not fast changing so not good immediately |
|
|
NSTEMI ECG
|
ST segment depression isn't good for localizing blocked vasculature (in contrast with STEMI)
|
|
|
STEMI
|
same pathology as NSTEMI, but complete obstruction of larger artery. Result = transmural damage, rather than subendocardial. High risk than NSTEMI
ECG = elevated ST, possible LBBB (if LAD MI), ECG also localizes MI Clot = fibrin rich |
|
|
coagulation cascade
|
Intrinsic pathway = surface contact with ECM, activating factors leading to factor 10 activation
Extrinsic pathway = tissue factor (7) released from within endothelium with damage, also activates factor 10. Prothrombin > thrombin, fibrin > fibrinogen. Fibrin bound thrombin = building block for clots. |
|
Left coronary artery
|
Gives up Left anterior descending artery and Circumflex artery
LAD gives of diagonals Circumflex gives off obtuse marginals Ramus intermedius = variant, sometimes between LAD and Circumflex |
|
Right coronary artery
|
Posterior descending artery
posterior left ventricular branches Usually dominant (supplies posterior descending artery) |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Atrioventricular / interventricular planes of view
|
|
|
|
LAD stenosis
|
|
|
Time lapse of myocardial damage in MI
|
|
|
|
Transmural anterior wall MI, AWMI
Showing on V1-6 as ST elevation (gravestone hump) |
|
|
inferior wall MI, IWMI
Showing especially on aVF (best for inferior) also lead 2 May want to get a V4R lead here to check health of right ventricle |
|
|
Pathological Q waves indicative of old MI, see in AVF 2 and 3 most likely inferior wall MI
|
|
|
See AVF involvement check RV4 incase IWMI with Right ventricular involvement, pictured here on RV4
|
|
|
IWMI nitroglycerin
|
Cannot give nitroglycerin incase of right ventricular involvement. Decreases preload already from deficient RV. Nitroglycerin will decrease venous return and decrease preload as well.
|
|
|
NSTEMI streatment
|
Prevent full occlusion (MI)
2b-3a inhibitor (thrombus formation), aspirin, heparin |
|
|
STEMI treatment
|
fibrinolytic therapy, or percutaneous coronary intervention (PCI) (balloon with catheter, stent)
|
|
|
Long term management of ACS
|
Clopidogrel (antiplatelet), ASA, Bb, ACE-I, statin
|
|
|
Hypertension
|
risk for end organ damage, Heart (CAD, CHF), brain (stroke), kidney (renal disease). M&M increase with age and systolic BP. complications = more often in morning
Stage 1 = 140-159/90-99 Stage 2 = >160/>100 High prevalence, 60% treated, 35% controlled |
|
|
L-arginine
|
can help lower BP through production of NO
|
|
|
Primary (essential) hypertension
|
Idiopathic, can be sympathetic hyperactivity (white coat), can be resistant hypertension (3 classes of medications but still not controlled)
BP > 140/90. !Ages 25-50 (biggest differentiator)! 95% of hypertension. Exacerbated by obesity, tobacco, ETOH, NSAIDs, estrogen, erythropoietin, sodium diet |
|
|
Secondary hypertension
|
renovascular disease (most common cause), adrenal disease (endocrine), pheochromocytoma (sympathetic tumors creating catecholamines)
Can be the cause of resistant hypertension Bruits = secondary hypertension, renal artery stenosis! Can also find abnormal pulse, thyromegaly, or flushing with pheochromocytoma !Age <20 or >50! greatest differentiating factor Pregnancy BP >140/90 @20 weeks = preeclampsia, followed by eclampsia (seizures) |
|
|
Secondary hypertension labs
|
Bun (blood urea nitrogen), creatinine (GFR), Urinary analysis, CBC, glucose, lipids, CRP (inflammation), serum potassium (hypokalemia drives hypertension), thyroid profile (hyperthyroidism drives hypertension)
renal parenchymal disease (increased BUN), hyper aldosteronism (aldosterone elevated), pheochromocytoma, renal ultrasound (renal disease, stenosis), contrast from imaging studies can predispose for renal disease |
|
|
Hypertensive crisis
|
Emergency, diastolic > 130
can have hypertensive encephalopathy, nephropathy, CHF, MI, aortic dissection, preeclampsia Malignant hypertension = end organ damage with !papilledema! (hypertensive retinopathy) |
|
|
Hypertensive urgency
|
can be asymptomatic, BP > 220/125 but stable
|
|
|
Hypertension lifestyle adjustments
|
Sodium reduction, avoid NSAIDs, limit ETOH, smoking cessation, exercise / weight
treat comorbidities (DM, CVA, CAD, CKD (chronic kidney disease), PAD (peripheral arterial disease)) |
|
|
Hypertension medical therapy
|
Diuretics, ACE-I / Betablockers, CCb (-dipines)
if resistant consider aldactone (competitive inhibitor of aldosterone, also diuretic) diabetics = ACE-I CKD = ACE-I or ARB african americans = diuretics & CCb |
|
|
Heart failure
|
impaired pumping resulting in vasoconstriction & fluid retention.
CAD and hypertension = most commonly associated. Even among men and women, EF is roughly 50% (norm 55-70%) Can be R or L, systolic or diastolic, chronic or stable |
|
|
Edema with cardiac failure
|
Decreased CO results in decreased renal flow, increased RAAS system and increased sodium retention, edema.
Increased venous pressure (pooling) increased capillary filtration, edema. (pedal edema) |
|
|
Left heart failure
|
blood backs into pulmonary circulation, !pulmonary edema! Dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, fatigue, lower extremity edema, arrhythmias, S3, JVD, wheezing, tachypnea
Causes: CAD, hypertension, cardiomyopathies, valvular disease |
|
|
Right heart failure
|
blood backs into systemic circulation, !tissue edema!, anasarca (generalized), ascites (abdominal), pleural effusion, pericardial effusion
most common cause !left sided heart failure!, hypertension, COPD, pulmonary embolism, RV MI, right ventricular cardiomyopathies !classic triad: JVD, hypotension (reduced preload), clear lungs! |
|
|
Diastolic dysfunction
|
heart unable to relax, expand, or fill sufficiently, inadequate preload. Ejection fraction may actually increase but there won't be enough actual volume of blood
LVH, myocardial fibrosis, restrictive cardiomyopathy, hypertrophic cardiomyopathy, pericarditis, amyloid deposition |
|
|
systolic dysfuntion
|
Heart unable to pump out enough blood
|
|
|
Pathophysiology of hypertrophy
|
Pressure overload= LVH with increased wall thickness due to hypertension or aortic stenosis
Volume overload = dilation due to increased blood volume, also increased wall thickness. Due to mitral / aortic regurgitation |
|
|
Acute heart failure
|
common etiology: Acute MI, dysrhythmia, hypertensive crysis
|
|
|
Chronic heart failures
|
Stable angina (CAD), old MI, cardiomyopathies, valvular disease, chronic arrhythmias,
|
|
|
Good indicators for acute HF
|
JVP > 11cm
S3 |
|
|
HF Classification
|
A = high risk
B = HF but asymptomatic C = symptomatic HF D = end stage HF (despite medical therapy), cannot safely discharge |
|
|
Diagnostic studies
|
Echocardiogram can differentiate between systolic / diastolic
cardiac catheterization = pulmonary capillary wedge pressure |
|
|
Stage A treatments
|
treat comorbidities. ACE-I in some patients (DM)
|
|
|
Stage B treatments
|
ACE-I or ARB, Bb in some
|
|
|
Stage C treatment
|
ACE-I, Bb, treat symptoms as they arise
Sodium restriction, diuretics |
|
|
Stage D treatment
|
Inotropes, transplantation, hospice
|
|
|
ACE-I and ARBs
|
-pril
-sartan |
|
|
DASH diet
|
whole grains, fish, poultry nuts, less red meat, sweets, sugars. Rich in K+, Mg+, Ca+, protein, fiber
protective against CAD, CVA, HF |
|
|
Cardiomyopathies
|
primary disorder, not result of dysfunction of another cardiac structure
|
|
|
Dilated cardiomyopathy
|
Dilated, ventricular enlargement / systolic dysfunction
More in blacks, more in men. Sometimes misdiagnosed as upper respiratory infection |
|
Hypertrophic cardiomyopathy
|
Hypertrophic, myocardial hypertrophy without hypertension / aortic stenosis, diastolic dysfunction
genetic component, 50% are autosomal dominant Syncope, heart failure, palpitations. Present at young age. ECG: LVH, apical hypertrophy causes precordial T wave inversion Slow deterioration, death from VT. Can progress into dilated cardiomyopathy from muscle fibrosis |
|
|
systolic anterior motion of mitral valve
|
Seen with hypertrophic cardiomyopathy, mitral valve pushes against septum obstructing blood flow reducing preload.
Systolic murmur created, improves with leg raising (increased blood to heart, opening up the cavity and preventing the obstruction) Worse murmur with valsalva, increased pressure on heart less volume and increased obstruction |
|
|
Precordial T wave inversion
|
sign of apical hypertrophy (hypertrophic cardiomyopathy)
|
|
|
HCM vs LVH in elderly
|
Associated hypertension, ventricular morphology distorted outflow tract,
Sigmoid septum (pictured), with systolic anterior motion of mitral valve (grandma SAM) |
|
|
Aortic stenosis vs hypertrophic cardiomyopathy
|
Aortic insufficiency murmur common with aortic stenosis.
Pulse pressure increased after premature ventricular contraction (rather than decreased) !Valsalva maneuver makes aortic stenosis murmur lessen, increases with HCM! Normal pulse with aortic stenosis, bisferens with HCM |
|
|
Restrictive cardiomyopathy
|
Restrictive, hardened abnormal filling / diastolic function
similar in presentation to constrictive pericarditis ECG shows a square root sign |
|
|
ECG square root sign
|
shows present of constrictive cardiomyopathy or restrictive pericarditis
|
|
|
Restrictive cardiomyopathy vs Pericarditis Constriction
|
pericardial calcification, thick pericardium. Imaging = best differentiator.
Square root shows up on both |
|
|
p-VAD
|
peripheral ventricular assisting device
Treat those not responding to cardioversion catheters outlet in ventricles Used to be a bridge to transplant, now often a destination |
|
|
Indications for Transplant
|
Mechanical assitance, Class 3 /4 or stage D, severe hypertrophic / restrictive cardiomyopathy, resistant arrhythmias, complex congenital heart disease
|
|
|
Contraindications for transplant
|
Neoplasm, connective tissue disease (harms transplant), primary pulmonary hypertension, Age > 70, severe peripheral vascular disease (difficult to operate), DM with organ damage, severe lung disease (unless heart / lung transplant), HIV / Hep B & C, no support, extreme weights
|
|
|
Transplant status listings
|
1A = cardiac assistance, in ICU
1B = chronic inotropes 2 = improved patients not in immediate need, or with new contraindications |
|
|
Transplant cut
|
cut at atria, actually maintain two sinus rhythms
|
|
|
Transplant rejection
|
Prophylaxis before operation: cyclosporine, corticosteroids, azathioprine
biopsy tested every few weeks, followed by every few months, biyearly the longer after the transplant Use CK-MB test to confirm rejection, and echocardiography for LV function. Symptoms usually similar CHF |
|
|
Transplant Vasculopathy
|
Atherosclerosis caused by accelerated inflammation, almost always happens and is main cause of mortality after first year (before first year is rejection or infection)
|
|
|
Opportunistic infections
|
CMV often transmitted donor to recipient, fever malaise anorexia.
If donor + recipient - then prophylactic ganciclovir or foscarnet, long term use acyclovir. If recipient + less is needed. Bone marrow toxicity from azathioprine sometimes confused with CMV |
|
|
Patent foramen ovalus
|
|
|
|
Atrial septal defect (ASD)
|
more common in females. Small = asymptomatic. !FIXED SPLIT S2! Pulmonic systolic ejection murmur
Primum = lower, RBBB, AV block secundum = mid (most common), incomplete RBBB, notched cortege IW QRS sinus venosus = upper (to SVC) repair if shunt is bigger, asymptomatic without paradoxical emboli. Pulmonary trunk may be enlarged surgery if >1.5% blood mix |
|
|
Eisenmenger syndrome
|
reversal of a Left to right shunt over time due to hypertrophy of the right heart, leads to hypoxia and cyanosis
|
|
|
transesophageal echocardiogram (TEE)
|
needed to look for atrial fib / flutter thrombi
also great for diagnosing congenital heart defects |
|
|
Ventricular septal defect (VSD)
|
higher flow than ASD, more likely to cause tissue damage, associated with endocarditis, holosystolic murmur, systolic thrill. Seen with downs, fetal alcohol syndrome
ECG: normal or RBBB, RVH, LVH. RIsk of arrhythmia Most common and congenital, more likely to self resolve if muscular. Surgery if > 2% blood mix, and if no pulmonary hypertension |
|
|
Patent Ductus Arteriosus
|
Usually closes with decreased prostaglandins, treated with Indomethacin
Loud S2, wide pulse pressure, continuous !MACHINERY MURMUR / THRILLS!!normal hands but pedal toe cyanosis! |
|
|
Univentricle
|
cyanotic on birth, not much to do
|
|
|
Tetralogy of fallot
|
pulmonic stenosis, right ventricular hypertrophy, overriding aorta, VSD
boot shaped heart (due to RVH) Blalock - Taussig repair = shunt from aorta to pulmonary artery for more pulmonary supply |
|
|
Transposition of great arteries
|
right side supplies to aorta instead of pulmonary trunk
Left side supplies to pulmonary instead of aorta Major surgery to correct, only possible if congenital shunt (PDA) is present |
|
|
Turner syndrome (XO)
|
Coarctation of aorta, bicuspid aortic valve (50%), differential pulse (pre vs post coarctation vasculature), hypertension
|
|
|
3 sign for coarctation
|
sigmoid type curve on radiograph above heart
|
|
|
Down Syndrome
|
ASD, VSD, valve defects
|
|
|
Jervell Lange Nielsen syndrome
Romano Ward syndrome |
Long QT syndromes from K/Na pump abnormalities
JLN = AR, congenital deafness RW = AD Treat: Bb, permanent pacemaker, sympathectomy, ICD |
|
|
Mitral regurgitation
|
congenital: trileaflet valve
acquired: degenerative, ischemic, infectious, rheumatic, MVP (pictured), papillary ischemia from IWMI |
|
|
Mitral stenosis
|
!Rheumatic heart disease!
can hear opening snap. Murmur from pulmonary hypertension during diastole (Graham Steel) syncope, due to decreased preload |
|
|
Aortic stenosis
|
usually degenerative (fibrocalcific)
congenital bicuspid valve = faster degeneration echocardiogram valve = too thick |
|
|
Aortic regurgitation
|
congenital with bicuspid valve leads to AS
Secondary to CHF, aortic dissection, aortic aneurysm (makes it difficult to close) Wide pulse pressure from diminished diastolic pressure |
|
Notched P wave limb leads
|
Mitral regurgitation indication, biphasic in precordial
|
|
|
Mitral regurgitation treatment
|
Annular ring, can cause AV block due to inflammation
Can also use valvuloplasty with a balloon pushing the valve open again |
|
Trans catheter aortic valve replacement (TAVR)
|
for people that can't handle surgery
|
|
|
Murmur sounds
|
MR = systolic holosystolic
MS = stenosis mid diastolic (atria contract) AR = low diastolic murmur AS = crescendo-decrescendo PR = graham steell murmur, from pulmonary hypertension such as MS VSD = harsh holocystolic ASD = fixed split S2, systolic ejection murmur PDA = continuous machinery murmur |
|
Epstein's Anomaly
|
Downward placed tricuspid valve
arrhythmias, WPW |
|
|
Pulmonic stenosis
|
congenital, females
P2 = diminished / delayed |
|
|
Metallic Valve problems
|
Annular dehiscence: valve comes off of sutures
Mechanical dysfunction Pannus formation: connective tissue overgrows valve |
|
|
Rheumatic heart disease
|
Group A step infection (beta-hemolytic), usually mitral valve involved, sometimes aortic
Jones criteria: major: carditis, erythema marginatum, sydenham chorea, polyarthritis minor: fever, polyarthralgias, prolonged PR, positive throat, ASO titer (antibodies) 2 major, or 1 major 2 minor Treat with penicillin, prophylaxis once a month for five years |
|
|
Endocarditis
|
Can effect any valve, degenerative, embolisms, can cause abscesses (septal if aortic). Clots over the body = usually what identifies clinically
AV node problems if mitral valve Diagnosed on clinical symptoms, and TEE (gold standard), Cultures not always positive |
|
|
Ascending Aortic Anuerysm
|
Due to connective tissue problems
Pain, SOB (compress pulm trunk), heart failure if regurgitant Wide pulse pressure, Aortic insufficiency Reduce hypertension, surgery if > 6cm |
|
|
Abdominal aortic aneurysm
|
Due to atherosclerosis
Surgery if at 4cm, stent otherwise. May cause renal artery stenosis / hypertension, claudication, pulsatile infraumbilical mass |
|
Aortic Dissection
|
subintimal tear (separates media from intima), false lumen usually larger due to trapping blood
A = ascending, B = only descending Risk: hypertension, pregnancy, coarctation, bicuspid aortic valve, Marfan's Tearing pain along back, asymmetric pulse (depending which way it goes) Complications: extension, tamponade, AI, MI (IWMI) from right coronary artery, rupture |
|
|
Marfans
|
connective tissue disorder
Pectus excavatum, dilation of aorta, arachnodactyly, ocular lense subluxation |
|
|
Aortic dissection prognosis
|
Type A = more dangerous, especially with AI
Type B = nitroprusside, manage complications, stent Chronic if after two weeks, medical therapy |
|
|
Peripheral arterial disease (PAD)
|
disorder from atherosclerosis limiting blood flow to limbs. better with rest. check posterior tibial pulse, everyone should have this, shows presence of PAD
differentiate from lumbar canal stenosis (no association with rest, gets worse if standing still) differentiate from degenerative joint disease (in hip / knee) via tests high mortality, can also lead to stable claudication. Occasionally amputation |
|
|
Claudication
|
pain in limbs from ischemia, associated with limb loss (gangrene)
Symptom of PAD common in population over 70, if less than 40 aorto-iliac, if greater than 40 femoropopliteal. More frequent in diabetics |
|
|
Pseudoclaudication
|
spinal cause, tingling / weakness, clumsiness. Variable onset depending on position. Occurs while standing and not walking (compression of spine). Must sit or change position to relieve
|
|
Diagnosis of PAD
|
!office ABI (ankle-brachial index) (ankle systolic / brachial systolic) Very sensitive! >.9 normal. <.9 = PVD. >1.4 = calcified (noncompressible, diabetics)
ultrasound, MR angiography, pulse volume recordings May help to detect borderline with walking |
|
|
Cilostazol
|
PDE-I, prevents platelet aggregation and vasodilates
treat PAD |
|
|
Treatment
|
Cilostazol, revascularization (if limiting), angioplasty + stent
|
|
|
Venous diseases
|
Deep venous thrombosis, in upper or lower extremities, can travel and cause pulmonary embolism
Vessel damage, venous stasis, hypercoagulable states all lead to DVT. Often unrecognized due to difficult diagnosis (low sensitivity & specificity) Treat with anticoagulation (heparin), catheter thrombolysis, vena-cava filters |
|
|
Hoffman's Sign
|
pain upon flexion / extension of knee, muscle may compress thrombi
|
|
|
DVT diagnosis
|
usually done with ultrasound, if mass is incompressible is likely a thrombus
|
