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;
272 Cards in this Set
- Front
- Back
|
What class are Ca+ channel blockers?
|
Class IV
|
|
|
What are the Class IV antiarrhytmics?
|
Verapamil & Diltiazem
|
|
|
Where do the Ca+ channel blocker primarily work?
|
Primarily affect AV nodal cells by decreasing Ca conduction through myocyte membranes.
|
|
|
What are the main electric changes the Ca+ blockers cause?
|
1. Decrease conduction velocity; 2. Increase ERP; increase PR interval
|
|
|
What are Ca channel blockers mainly used for, an example being?
|
Used for prevention of nodal arrhythmias, ie SVT
|
|
|
What are the symptoms of toxicity of Ca channel blockers?
|
Constipation, flushing, edema, CV Effects: CHF, AV block, sinus depression
|
|
|
Which Ca channel blocker cause torsades de pointes?
|
bepridil
|
|
|
What is adenosines mechanism of action?
|
Increases efflux of K+ causing hyperpolarization of cells
|
|
|
What is adenosine a drug of choice for?
|
Dx/abolishing AV nodal arrhythmias
|
|
|
How long does adenosine last in its cardiovascular actions?
|
Very short acting ~ 15 sec
|
|
|
How K+ work as an antiarrhythmic?
|
Depresses ectopic pacemakers in hypokalemia
|
|
|
When is K+ used in cardiovascular events
|
hypoK+ from digoxin toxicity
|
|
|
When Mg2+ effective as an antiarrhythmic?
|
In torsades de pointes and digoxin toxity
|
|
|
Example: What cellular enzymes are involved in apoptosis?
|
Caspases
|
|
|
Definition of Cardiac Tamponade?
|
compression of heart by fluid in pericardium, leading to decreased CO, equilibrium of diastolic pressures in all 4 chambers
|
|
|
Findings of Cardiac Tamponade?
|
hypotension, increased venous pressure, distant heart sounds, increased HR, pulsus paradoxus, ECG shows electrical alternans
|
|
|
What is Pulsus Paradoxus?
|
(Kussmaul's pulse) decrease in amplitude of pulse during inspiration, seen in severe tamponade, asthma, obstructive sleep apnea, pericarditis, and croup
|
|
|
Cause of serous Pericarditis?
|
SLE, rheumatoid arthritis, viral infection, uremia
|
|
|
Cause of fibrinous pericarditis?
|
uremia, MI, rheumatic fevere
|
|
|
Cause of hemorrhagic pericarditis?
|
TB, malignancy (I.e. melanoma)
|
|
|
Findings of Pericarditis?
|
pericardial pain, friction rub, pulsus paradoxus, distant heart sounds, ECG changes with diffuse S-T elevation, can resolve without scarring or lead to chronic adhesive or chronic constrictive pericarditis
|
|
|
Syphilitic heart disease?
|
tertiary syphilis disrupts the vasa vasorum of the aorta with consequent dilation of the aorta and valve ring, may see calcification of aortic root and ascending arch, leads to tree bark appearance of aorta
|
|
|
Outcome of syphilitc heart disease?
|
can result in aneurysm of the ascending aorta and aortic valve incompetence
|
|
|
Most common primary cardiac tumor?
|
Myxomas are the most common cardiac primary tumor in adults, 90% in atria, usually a ball-valve obstruction in left atria, rhabdomyomas are the most frequent primary cardiac tumor in children (associated with tuberous sclerosis)
|
|
|
Most common overall cardiac tumor?
|
via metastasis from lymphomas and melanomas
|
|
|
Findings of cardiac tumors?
|
Kussmaul's sign: increase in JVP on inspiration
|
|
|
What is telangiectasia?
|
arteriovenous malformation in small vessels, looks like dilated capillaries
|
|
|
What is the hereditary form of telangiectasia?
|
Osler-Weber-Rendu syndrome: autosomal dominant, see nosebleeds and skin discolorations
|
|
|
What is Raynaud's disease?
|
decrease in blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress, most often in fingers and toes
|
|
|
What is Raynaud's phenomenom?
|
when Raynaud's dz is secondary to a mixed connective tissue dz, SLE, or CREST
|
|
|
What is the triad of symptoms for Wegener's Granulomatosis?
|
focal necrotizing vascultitis, necrotizing granulomas in the lung and upper airway, necrotizing glomerulonephritis
|
|
|
Other Symptoms of Wegener's?
|
perforation of nasal septum, chronic sinusiis, otitis media, mastoiditis, cough, dyspnea, hemoptysis, hematuria
|
|
|
Findings of Wegener's Granulomatosis?
|
c-ANCA is a STRONG marker for dz, CXR may reveal large nodular densities, hematuria, and RBC casts
|
|
|
Treatment for Wegener's?
|
Cyclophosphamide and corticosteroids
|
|
|
Other ANCA-associated vasculitides?
|
microscopic polyangitis, primary pauci-immune cresecentic glomerulonephritis, churg-strauss syndrome
|
|
|
What is Sturge-Weber Dz?
|
congenital vascular disorder that affects capillary-sized blood vessels, see port wine stain on face and leptomeningeal angiomatosis
|
|
|
What is Henoch-Schonlein Pupura?
|
most common form of childhood systemic vasculitis
|
|
|
Symptoms of Henoch-Schonlein Purpura?
|
skin rash (palpable purpura), arthralgia, intestinal hemorrhage, ab pain, and melena
|
|
|
What is the common triad of areas affected by Henoch-Schonlein Purpura?
|
skin, joints, and GI
|
|
|
Buerger's dz is also known as?
|
thromboangiitis obliterans
|
|
|
Pathogensis of Buerger's?
|
idiopathic, segmental, thrombosing vasculitis of small and medium peripheral arteries and veins
|
|
|
What type of person is Buerger's commonly seen in?
|
heavy smokers
|
|
|
Symptoms of Buerger's Dz?
|
intermittant claudication, superficial nodular phlebitis, cold sensitivity, severe pain in affected part
|
|
|
Complication of Buerger's Dz?
|
gangrene
|
|
|
Treatment of Buerger's Dz?
|
Smoking cessation
|
|
|
What is Kawasaki Dz?
|
acute, self-limiting dz of infants/kids that causes necrotizing vasculitis of small/medium vessels
|
|
|
Symptoms of Kawasaki Dz?
|
fever, congested conjunctiva, changes in lips/oral mucosa (strawberry tongue), lymphadenitis
|
|
|
Complication of Kawasaki?
|
coronary aneursyms
|
|
|
What is Polyarteritis Nodosa?
|
necrotizing immune complex inflammation of medium-sized muscular arteries
|
|
|
Symptoms of Polyarteritis Nodosa?
|
fever, weight loss, malaise, ab pain, melena, headache, myalgia, HTN, neurologic dysfunction, cutaneous eruptions
|
|
|
Findings of Polyarteritis Nodosa?
|
Hep B seropositivity in 30% of patients, multiple aneurysms and constrictions on arteriogram
|
|
|
Is Polyarteritis Nodosa associated with an ANCA?
|
NO
|
|
|
Treatment of Polyarteritis Nodosa?
|
Corticosteroids, cyclophosphamide
|
|
|
What is Takayasu's arteritis?
|
pulseless dz see granulomatous thickening of aortic arch and/or proximal great vessels
|
|
|
Lab findings with Takayasu's arteritis?
|
increased erythrocyte sedimentation rate (ESR)
|
|
|
Who is commonly affected by Takayasu's arteritis?
|
Asian females under the age of 40
|
|
|
Symptoms of Takayasu's arteritis?
|
fever, arteritis, night sweats, mylagia, skin nodules, ocular disturbances, weak pulses in upper extremities
|
|
|
Adverse effects of Hydrochlorothiazide?
|
hypokalemia, mild hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia
|
|
|
Adverse effects of Loop Diuretics?
|
potassium wasting, metabolic alkalosis, hypotension, ototoxicity
|
|
|
Adverse effects of Clonidine?
|
dry mouth, sedation, severe rebound HTN
|
|
|
Adverse effects of Methyldopa?
|
sedation, postitive Coomb's test
|
|
|
Adverse effects of Hexamethonium?
|
severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction
|
|
|
Adverse effects of Reserpine?
|
sedation, depression, nasal stuffiness, diarrhea
|
|
|
Adverse effects of Guanethidine?
|
orthostatic and exercise hypotension, dizziness, headache
|
|
|
Adverse effects of Prazosin?
|
1st dose orthostatic hypotension, dizziness, headache
|
|
|
Adverse effects of Beta-blockers?
|
impotence, asthma, CV effects (bradycardia, CHF, AV block), CNS effects (sedation, sleep alteration)
|
|
|
Adverse effects of Hydralazine?
|
nausea, headache, lupus-like syndrome, reflex tachycardia, angina, salt retention
|
|
|
Adverse effects of Minoxidil?
|
hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retention
|
|
|
Adverse effects of Nifedipine and Verapamil?
|
dizziness, flushing, constipation (verapamil), AV block (verapamil), nausea
|
|
|
Adverse effect of Nitroprusside?
|
cyanide toxicity (releases CN)
|
|
|
Adverse effect of Diazoxide?
|
hypoglycemia (reduces insulin release, hypotension)
|
|
|
Adverse effects of Captopril, Enalapril, and Fosinopril?
|
hyperkalemia, cough, angioedema, taste changes, hypotension, pregnancy problems (fetal renal damage), rash, increased renin
|
|
|
Adverse effects of Losartan?
|
fetal renal toxicity, hyperkalemia
|
|
|
Mechanism of Hydralazine?
|
increases cGMP, causes smooth muscle relaxation, also vasodilates arterioles more than veins, afterload reduction
|
|
|
Indications for Hydralazine?
|
severe HTN, CHF, first-line therapy for HTN in pregnant women with methyldopa
|
|
|
Mechanism of Minoxidil?
|
K+ channel opener- hyperpolarizes and relaxes vascular smooth muscle
|
|
|
Indications for Minoxidil?
|
severe HTN
|
|
|
What components are in the carotid sheath?
|
internal jugular vein, common carotid artery, vagus nerve
|
|
|
In most cases what supplies the SA and AV nodes?
|
RCA
|
|
|
Where does coronary artery occlusion most commonly occur?
|
LAD
|
|
|
When do coronary arteries fill?
|
diastole
|
|
|
What does enlagement of the left atrium cause?
|
dysphagia or hoarseness
|
|
|
What murmurs do you hear in the aortic area?
|
systolic murmur (aortic stenosis, flow murmur, aortic calve sclerosis)
|
|
|
What murmurs do you hear in the pulmonic area?
|
systolic ejection murmur (pulmonic stenosis, flow murmur, Atrial septal defect)
|
|
|
What murmurs do you hear in the tricuspid area?
|
pansystolic murmur (tricuspid regurg, vent septal defect) and diastolic murmurs (tricuspid stenosis, atrial septal defect)
|
|
|
What murmurs do you hear in the mitral area?
|
systolic murmurs (mitral regurg) and diastolic murmurs (mitral stenosis)
|
|
|
How are cardia output, stroke volume and heart rate related?
|
CO = SV x HR
|
|
|
What happens to caridac output if the heart rate is too high?
|
diastolic filling is incomplete and CO decreases
|
|
|
What is the pulse pressure?
|
systolic pressure - diastolic pressure
|
|
|
What is the mean arterial pressure?
|
2/3 diastolic pressure + 1/3 systolic pressure
|
|
|
What does a P wave represent?
|
Atrial Depolarization
|
|
|
How long does the PR interval normally last?
|
<200 msec
|
|
|
What wave represents atrial repolarization?
|
none. It is hidden by the QRS complex
|
|
|
The QRS complex represents what?
|
ventricular depolarization
|
|
|
What measures contraction of the ventricles?
|
The QT interval
|
|
|
When will you see a U wave? (2 situations)
|
Hypokalemia, Bradycardia
|
|
|
What does the T wave represent?
|
Ventricular repolarization
|
|
|
What is the atrioventricular delay?
|
100msec delay of signal firing in AV node. Allows for ventricular filling
|
|
|
What is Torsades de pointes?
|
Ventricular tachycardia with shifting sinusoidal waves on ECG
|
|
|
What can Torsades de pointes progress to?
|
V-fib
|
|
|
What predisposes to Torsades de pointes?
|
anything that prolongs the QT interval (Class III antiarrythmic drugs, Class Ia antiarrhythmics (quinidine))
|
|
|
In what disease do you see a delta wave?
|
Wolff-Parkinson-White Syndrome
|
|
|
Describe the pathogenesis of Wolff-Parkinson-White Syndrome
|
A conduction pathway from the Atria to Ventricle that bypasses the AV node. Ventricles depolarize earlier than usual causing a Delta wave
|
|
|
What may Wolff-parkinson white syndrome cause
|
supraventricular tachycardia
|
|
|
What part of the kidney tubule secretes renin?
|
Juxtaglomerular Apparatus
|
|
|
What is the primary effect of Angiotensin II?
|
Vasoconstriction causing increased TPR
|
|
|
What is ANP?
|
Atrial Naturetic Peptide. diuretic released from atria.
|
|
|
What are the effects of ANP?
|
vascular relaxation. Constricts renal efferent arteriole and dilates afferent arterioles.
|
|
|
Cardiac mm contraction is based on?
|
extracellular calcium (calcium-induced calcium release)
|
|
|
What cause the plateau in cardiac mm AP?
|
Calcium influx
|
|
|
What is responsible for spontaneous depolarization (automaticity) in cardiac nodal cells?
|
Funny channels
|
|
|
Cardiac myocyctes are electrically coupled together by?
|
Gap junctions
|
|
|
Rapid upstroke - voltage gated Na channels open
|
Phase 0 (Ventricular AP)
|
|
|
initial repolarization - inactivation of VG Na channels - Voltage gated k channels begin to open
|
Phase 1 (Ventricular AP)
|
|
|
Plateau - Ca influx through voltage gated ca channels balances k efflux. Ca induced Ca release from sarcoplasmic reticulum
|
Phase 2 (Ventricular AP)
|
|
|
Rapid repolarization - massive k efflux due to opening of voltage gated slow K channels and closure of VG Ca channels.
|
Phase 3 (Ventricular AP)
|
|
|
Resting potential - high K permeability
|
Phase 4 (Ventricular AP)
|
|
|
Upstroke - opening of voltage gated Ca channels
|
Phase 0 (Pacemaker AP)
|
|
|
Type of cardiac cells with absent plateau during AP.
|
Nodal cells.
|
|
|
Inactivation of Ca channels and increased activation of K channels
|
Phase 3 (Pacemaker AP)
|
|
|
Slow diastolic depolarization - due to increased Na conductance via funny channels
|
Phase 4 (Pacemaker AP)
|
|
|
What part of the AP determines the HR?
|
Slope of phase 4 in the SA node
|
|
|
What effect does Ach have on nodal cell AP?
|
Decreases the rate of diastolic depolarization
|
|
|
What effect sympathetic stimulation have on the funny Channels?
|
Increases the chance they are open
|
|
|
How does atrial fibrillation appear on EKG?
|
Erratic baseline with no discrete P waves in between irregularly spaced QRS complexes.
|
|
|
Atrial fibrillation can lead to what? Treatment?
|
Atrial stasis and stroke; Warfarin
|
|
|
How does atrial flutter appear on EKG?
|
Rapid succession of identical, back-to-back atrial depolarization waves. Have sawtooth appearance.
|
|
|
Treatment of atrial flutter?
|
Class 1A, 1C, or III antiarrhythmics
|
|
|
How does 1st degree AV block appear on EKG?
|
PR interval prolonged. Asymptomatic
|
|
|
How does 2nd degree AV block (Mobitz type I) appear ?
|
Progressive lengthening of PR interval until a beat is dropped. Usually Asymptomatic
|
|
|
How does 2nd degree AV block (Mobitz type II) appear ? Usually there are 2 P waves to 1 QRS response (when the beat is dropped)
|
Dropped beats that are not preceded by a change in the length of PR interval
|
|
|
How does 3rd degree AV block appear ?
|
Atria and Ventricles beat independently of eachother. P waves bear no relation to QRS complexes
|
|
|
Treatment? What disease causes 3rd degree block?
|
Pacemaker. Lyme disease
|
|
|
How doesventricular fibrillation appear on EKG?
|
Completely erratic rhythm with no identifiable faves. Fatal without CPR and defibrillation.
|
|
|
Mechanism of action of Nifedipine/Verapamil/Diltiazem?
|
block voltage-dependent L-type calcium channels of cardiac and smooth muscle→decreased contractility
|
|
|
Order of selectivity of CCBs for vascular smooth muscle
|
nifedipine>diltiazem>verapamil
|
|
|
Order of selectivity of CCBs for heart
|
verapamil>diltiazem>nifedipine
|
|
|
Clinical use and toxicity of CCBs
|
Uses: HTN, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's; Toxicity: Cardiac depression, peripheral edema, flushing, dizziness, constipation
|
|
|
Drugs that preferentially dilates veins by release of NO→increased cGMP and smooth muscle relaxation
|
Nitroglycerin, isosorbide dinitrate
|
|
|
Clinical use of nitroglycerin and isosorbide dinitrate
|
angina, pulmonary HTN, aphrodisiac and erection enhancer
|
|
|
Drug who's toxicity includes tachycardia, hypotension, flushing, headache, Monday disease with industrial exposure
|
Nitroglycerin, isosorbide dinitrate; Monday disease-develop tolerance for vasodilating effects during work week with loss of tolerance over weekend leading to tachycardia, dizziness, headache on reexposure.
|
|
|
Treatment options for malignant hypertension
|
1) Nitroprusside: short acting, ↑ cGMP via direct release of NO; 2) Fenoldopam: Dopamine D1 agonist-relaxes vascular smooth muscle; 3) Diazoxide: K+ channel blocker-hyperpolarizes and relaxes vascular smooth muscle
|
|
|
Determinants of myocardial O2 consumption (MVO2)
|
end diastolic volume, blood pressure, heart rate, contractility, ejection time (attempt to reduce MVO2 in antianginal therapy)
|
|
|
Effect of nitrates in antianginal therapy
|
↓end diastolic volume, ↓blood pressure, ↑ heart rate (reflex response), ↑ contractility (reflex response), ↓ejection time = ↓MVO2 (Nifedipine has similar actions)
|
|
|
Effect of β blockers in antianginal therapy
|
↑end diastolic volume, ↓blood pressure, ↓ heart rate, ↓ contractility, ↑ejection time = ↓MVO2 (Verapamil has similar actions)
|
|
|
Effect of Nitrates + β blockers in antianginal therapy
|
No effect or ↓end diastolic volume, ↓ blood pressure, ↓ heart rate, little/no effect on contractility, little/no effect on ejection time = ↓↓ MVO2
|
|
|
These drugs are contraindicated in angina
|
Labetalol, pindolol, acebutolol-partial agonists
|
|
|
Lipid-lowering drug class with strongest effect on LDL
|
HMG-CoA reductase inhibitors (lovastatin, pravastatin, simvastatin, atorvastatin); also ↑ HDL and ↓TGs
|
|
|
Myositis is a side effect of these lipid-lowering agents
|
HMG-CoA reductase inhibitors and Fibrates
|
|
|
Mechanism of action Niacin
|
inhibits lipolysis in adipose, reduces VLDL secretion into circulation; (strongest elevator of HDL, ↓LDL and TGs, causes flushing which can be ↓ with aspirin or long-term use
|
|
|
Lipid-lowering agents with adverse effects of ↑ TGs, ↓ absorption of fat soluble vitamins, poor taste and GI discomfort
|
Bile acid resins (cholestyramine, colestipol); ↓ LDL, slightly ↑ HDL by preventing intestinal reabsoption of bile acids which forces liver to use cholesterol to make more
|
|
|
Lipid-lowering drug that inhibits cholesterol reabsorption at small intestine brush border
|
Ezetimibe; no effect on HDL or TG, rare ↑ LFTs
|
|
|
Most effective agents for decreasing TG's
|
Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate): upregulate LPL causing TG clearance; modest ↓ in LDL and ↑ HDLside effects include myositis and elevated LFTs
|
|
|
Pharmacokinetics of Digoxin
|
75% bioavailable, 20-40% protein bound, Half-life = 40 hrs, urinary excretion
|
|
|
Cardiac drug that inhibits Na+/K+ ATPase
|
Digoxin (cardiac glycosides)-results in indirect inhibition of Na+/Ca2+ exchanger→↑ Ca2+ concentration→positive inotropy
|
|
|
Clinical use of cardiac glycosides (Digoxin)
|
CHF (↑ contractility), atrial-fib (↓ AV node conduction, depression of SA node)
|
|
|
Toxicity of Digoxin
|
ECG changes: ↑ PR, ↓ QT, scooping of ST segment, T-wave inversion; also ↑ parasympathetic activity (nausea, vomiting, diarrhea, blurry yellow vision (thing Van Gogh!), arrhythmia
|
|
|
These factor increase risk of digoxin toxicity
|
renal failure (decreased excretion), hypokalemia (potentiates drug's effect), quinidine (decreases clearance and displaces from tissue-binding sites)
|
|
|
Antidote for cardiac glycoside toxicity (digoxin)
|
slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+
|
|
|
Mechanism of action of Na+ channel blockers
|
Local anesthics. Slow or block conduction (especially in depolarized cells). ↓slope of phase 4 depolarization, ↑ threshold for firing in abnormal pacemaker cells. State dependent (selective for frequently depolarizing tissue)
|
|
|
Which class of antiarrhythmics do Quinidine, Amiodarone, Procainanide and Disopyramide belong to?
|
Class IA: ↑ AP duration, ↑ ERP, ↑ QT interval; used for atrial and ventricular arrhthmias, especially reentrant and ectopic supraventricular and v-tach.
|
|
|
Toxicity of Quinidine
|
Chinchonism-haeadache, tinnitus; thrombocytopenia; torsades de pointes (prolonged QT interval)
|
|
|
Antiarrhythmic that can cause SLE-like syndrome
|
Procainamide
|
|
|
Class IB antiarrhythmics
|
Lidocaine, Mexiletine, Tocainide, (Phenytion): ↓ AP duration
|
|
|
Uses for Lidocaine, Mexiletine, Tocainide
|
acute ventricular arrhythmias (especially post-MI) and digitalis-induced arrhythmias; affect ischemic or deoplarized Purkinje and ventricular tissue
|
|
|
Toxicity of Class IB antiarrhythmics
|
local anesthetic, CNS stimulation/depression, cardiovascular depression
|
|
|
Class IC antiarrhythmics
|
Flecainide, encainide, propafenone
|
|
|
Clinical uses for flecainide, encainide, propafenone
|
V-tachs that progress to VF and intractable SVT. Usually only last resort in refractory tachyarrhythmias. No effect on AP duration, increase Phase 3 K+ conductance.
|
|
|
Class of antiarrhythmics that can be proarrhythmic, especially post-MI (contraindicated)
|
Class IC; significantly prolong refractory period in AV node
|
|
|
Electrolyte abnormality that ↑ toxicity of all Class I antiarrhythmics
|
Hyperkalemia
|
|
|
Class II antiarrhythmics
|
β-blockers: propanolol, esmolol (short acting), metoprolol, atenolol, timolol
|
|
|
Mechanism of Class II antiarrhythmic
|
↓CAMP, ↓ Ca2+ currents. Supress abnormal pacemakers by ↓ phase 4 slope. AV node particularly sensitive-↑ PR interval
|
|
|
This class of antiarrhythmics is used for V-tach, SVT, slowing ventricular rate during a-fib and a-flutter
|
β-blockers (Class II)
|
|
|
Toxicity of β-blockers
|
Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask signs of hypoglycemia. Metoprolol can cause dyslipidemia.
|
|
|
Drug class of sotolol, ibutilide, bretylium, amiodarone
|
K+ channel blockers-Class III antiarrhythmics
|
|
|
Mechanism of action of K+ blockers
|
↑ AP duration, ↑ ERP. Used when other antiarrhythmics fail. ↑ QT interval
|
|
|
Effects of Sotolol toxicity
|
torsades de pointes, excessive β block
|
|
|
Class III antiarrhythmic that can cause new arrhythmias and hypotension
|
Bretylium
|
|
|
Amiodarone toxicity
|
pulmonary fibrosis, corneal deposits, hepatotoxicity, skin deposits (photodermatitis), neurological effects, constipation, CV effects (bradycardia, heart block, CHF), hypothyroidism/hyperthyroidism (always check LFTs, PFT, TFTs!)
|
|
|
Class III antiarrhythmic that is safe to use in Wolff-Parkinson-White syndrome
|
Amiodarone
|
|
|
Where does the Aortic Arch transmit to? And what does it respond to?
|
Increase in BP, Vagus to Medulla
|
|
|
What does the Carotid sinus transmit to and what does it respond to?
|
Decease in BP, Glossopharyngeal Nerve to Medulla
|
|
|
What do the carotid and aortic bodies respond to?
|
Decrease in PO2, or Increase in PCO2, decrease in blood pH
|
|
|
What is a cushing reaction?
|
Increase in intracranial pressure due to cereberal ischemia
|
|
|
What is the Cushing triad?
|
Hypertension, bradycardia, respiratory repression
|
|
|
What organ receives the highest share of CO?
|
Liver
|
|
|
Which organ receives the highest blood flow through gram of tissue
|
The kidney
|
|
|
What are the normal pressures in each area of the heart?
|
RA-5, RV-25/5, PA-25/10, LA-12, LV 130/10, Aorta-130/80
|
|
|
Factors that determine autoregulation for the heart?
|
Adenosine, O2, NO
|
|
|
Factors that determine autoregulation for the brain?
|
CO2, pH
|
|
|
Factor that determine autoregulation in the lungs?
|
Hypoxia-vascoconstriction
|
|
|
Factors that determine autoregulation in the kidneys?
|
Myogenic and tubuloglomerular feedback.
|
|
|
Which starling forces pull fluid out of a capillary?
|
Capillary (+) and Interstitial Fluid Pressure (-)
|
|
|
Which starling forces keep fluid in a capillary?
|
Plasma colloid osmotic pressure (+), and interstitial fluid pressure (+)
|
|
|
What syndromes decrease plasma protein levels?
|
Nephrotic Syndrome, liver failure
|
|
|
Which congenital heart defects result in early cynaosis?
|
Terribe Ts (5): tetralogy, transposition, truncus, tricuspid atresia, and TAPVR, due to right to left shunt
|
|
|
Which congenital heart defects result in late cyanosis?
|
VSD>ASD>PDA due to reversal of left to right shunt.
|
|
|
What is Eisenmengers syndrome?
|
Untreated VSD, ASD< or PDA leads to Pulm HTN causes shunt reversal to R to L shunt causing late cyanosis
|
|
|
4 Features of Tetralology of Fallot
|
Pulmonary Stenosis, RVH, Overriding Aorta, VSD
|
|
|
What Congenital Heart defect is caused by the failure of the aorticopulmonary septum to spiral?
|
Transposition of the great vessels
|
|
|
What is the difference between infantile and adult coarctation of the aorta?
|
Infantile is preductal, adult is postductal also asc with rib notching, unequal pulses in the extremities and Turners Syndrome
|
|
|
What drug keeps the ductus arteriosis patent?
|
Prostanglandin E1 and low 02 concentration
|
|
|
What drug should you use to close a patent ductus arteriosis?
|
High 02 and Indomethacin
|
|
|
Congenital Defects Associated with Downs Syndrome?
|
ASD, VSD, AV septel defect
|
|
|
Congenital Defects Associated with Rubella?
|
Septal defects, PDA, pulmonary artery stenosis
|
|
|
Congenital heart defects associated with 22q11 syndrome?
|
Truncus Arteriosis, Tetrology of Fallot
|
|
|
What are risk factors for hypertension?
|
Increase age, obesity, diabetes, smoking, genetics, black>white>asian
|
|
|
What are cutaneous findings of Hyperlipedemia?
|
Atheromas, Xanthomas, and corneal arcus
|
|
|
What is Mockenberg Arteriosclerosis?
|
Calcification in the media of the arteries, especially radial or ulnar. Benign.
|
|
|
What are the features of arteriolosclerosis?
|
Hyaline thickening of small arteries in hypertension with hyperplastic onion skinning in malignant hypertension
|
|
|
What are the features of athleroscleoris?
|
Fibrous plaques and atheromas form in intima of arteries
|
|
|
What are risk factors for athlerosclerosis?
|
Smoking, diabetes, hypertension, hyperlipedemia, family history
|
|
|
How does ischemic heart disease manifest?
|
Angina, Myocardial Infarction, Sudden Cardiac Death, Chronic Ischemic Heart Disease
|
|
|
Where does a red infarct occur?
|
Liver, lungs, intestines, follows a repurfusion injury
|
|
|
Where does a pale infarct occur?
|
Occurs in tissue with single blood supply like heart, kidney, and spleen.
|
|
|
How do catecholamines and Digitalis increase heart contractility?
|
Catecholamines: increase intracellular Ca (increase activity of Ca pump in sarcoplamic reticulum)Digitalis: blocks Na/K ATPase pump --> increase in intracellular Na --> increasing intracellular Ca
|
|
|
How does nitroglycerin affect ventricular EDV?
|
Venodilator: decreases preload
|
|
|
How does hydralazine affect MABP?
|
Vasodilator: decreases afterload(less force to pump against)
|
|
|
How does an increase in stroke volume affect:PreloadAfterloadContractility
|
Preload increasesAfterload decreasesContractility increases
|
|
|
What is the basic Frank-Starling principle?
|
Force of contraction is proportional to the inital length of cardiac muscle fiber (preload)ie: more it fills, harder it pumps
|
|
|
Calculate Ejection Fraction
|
EF = SV/EDV = (EDV-ESV)/EDV(this is an index of contractility)
|
|
|
How is vascular resistance r/t viscosity and vessel lumen?
|
Resistance ~ viscosity ~ 1/radius^4(Arterioles account for most of PVR)
|
|
|
What are the phases of the cardiac cycle?
|
1. Isovolumic contraction (highest O2 consumption)2. Systolic ejection3. Isovolumic relaxation4. Rapid filling, reduced filling
|
|
|
What is S3? When is it heard?
|
Early diastole, during the rapid filling phase.Blood rushing into a volume overloaded chamber (turbulant)(common in dilated ventricles, normal in children)
|
|
|
What is S4?When is it heard?
|
Late diastole; atrial kickBlood entering a noncompliant vessel (ie: a thick left ventricle
|
|
|
Jugular Venous Pulse (JVP) waves
|
a wave: atrial contractionc wave: RV contraction (causes tricuspid valve to bulge into RA)v wave: increased atrial pressure due to filling against closed tricuspid valve
|
|
|
When will you normally hear S2 split?Inspiration or Expiration
|
InspirationIncreased negative pressure and lung expansion causes an increase in preload. An increased blood volume in RV caused the pulmonic valve to stay open longer.
|
|
|
Wide splitting of S2Disease?
|
Associated with pulmonic stenosis
|
|
|
Fixed splitting of S2Disease?
|
Associated with ASD (atrial septal defect)
|
|
|
Paradoxical Splitting of S2Disease?
|
Associated with aortic stenosis
|
|
|
Heart: Holosystolic Blowing murmurDisease?
|
Mitral/tricuspid Regurgitation
|
|
|
How can one distinguish which side a murmur is on?(ie- if it is a right or left sided murmur?)
|
Right: will increase in intensity with INSPIRATIONLeft: will increase with intensity with EXPIRATION
|
|
|
Crescendo-decrescendo systolic ejection murmurDisease?
|
Aortic Stenosis(also has pulses parvus et tardus)
|
|
|
olosystoic, HARSH-sounding murmur (loudest at tricuspid area)Disease?
|
VSD
|
|
|
Mid-systolic CLICK
|
followed by a murmurDisease?
|
|
|
Blowing diastolic murmurpresenting with a wide pulse pressureDisease?
|
Aortic regurg
|
|
|
SNAP and RUMBLING late diastolic murmurDisease?
|
Mitral Valve Stenosis
|
|
|
Continous machine-like murmurDisease?
|
PDA
|
|
|
What are the different possible embolus types?
|
Fat, Air, Thrombus, Bacteria, Amniotic fluid, Tumor
an embolus moves like a FAT BAT |
|
|
What are fat emboli associated with?
|
Long bone fractures and Liposuction
|
|
|
What is an important possible complication of amniotic fluid emboli?
|
DIC, especially postpartum
|
|
|
A patient presents with chest pain, tachypnea, and dyspnia, what is a likely cause?
|
Pulmonary embolus
|
|
|
Approximately 95% of pulmonary emboli arise from what?
|
Deep leg veins
|
|
|
What predisposes a patient to developing Deep venous thrombosis?
|
Virchow's Triad
1. Stasis 2. Hypercoagulability 3. Endothelial damage DVTs can lead to pulmonary embolism |
|
|
What clinical findings are associated with bacterial endocarditis?
|
Bacteria FROM JANE
Fever Roth's spots Osler's nodes Murmur Janeway lesions Anemia Nail-bed hemorrhage Emboli |
|
|
What are Roth's spots?
|
round white spots on the retina surrounded by hemorrhage
|
|
|
What are Osler's nodes?
|
tender raised lesions on finger or toe pads
|
|
|
What are Janeway lesions?
|
small erythematous lesions on palm or sole
|
|
|
What valve is most frequently involved in bacterial endocarditis?
|
Mitral Valve
EXCEPTION: in IV drug users the Tricuspid valve is most commonly involved. -don't tri drugs |
|
|
What are the organisms that cause Acute and Subacute Bacterial endocarditis? What are the valves and vegetations like in each case?
|
Acute: S. Aureus (high virulence)
large vegetations on previously normal valves Subacute: Viridans streptococcus (low virulence) Smaller vegetations on congenitally abnormal or damaged valves. Sequela of dental procedures. More insidious onset. |
|
|
What are the possible complications of bacterial endocarditis?
|
Chordae rupture
Glomerulonephritis Suppurative pericarditis Emboli |
|
|
What are some causes of NON-bacterial endocarditis?
|
endocarditis secondary to malignancy or hypercoagulable state (marantic/thrombotic endocarditis)
|
|
|
What is the causative agent of Rheumatic Fever? What possible serous complication can it lead to?
|
Group A beta-hemolytic streptococci
May lead to rheumatic heart disease |
|
|
What are the clinical findings associated with Rheumatic heart disease?
|
FEVERSS
Fever Erythema marginatum (presence of pink rings on the trunk and inner surfaces of the arms and legs which come and go) Valvular damage ESR-increased Red-hot joints (migratory polyarthritis) Subcutaneous nodules St. Vitus' dance (Chorea) |
|
|
What heart valves are involved in Rheumatic heart disease?
|
Mitral>Aortic>>tricuspid
Therefore, the high pressure valves are affected most |
|
|
What histological findings are associated with rheumatic heart disease?
|
Aschoff Bodies (granuloma with giant cells), Anitschkow's cells (activated histocytes)
|
|
|
Would you see elevated ASO titers in Rheumatic heart disease?
|
Yes
|
|
|
What mediates the damage that occurs in rheumatic heart disease?
|
The damage is immune mediated (type II hypersensitivity), and is not a direct effect of the bacteria
|
|
|
Where are the most likely sites for a coronary a. occlusion?
|
LAD > RCA > circumflex
|
|
|
What are the symptoms of MI?
|
diaphoresis, nausea, vomiting, severe retrosternal pain, pain in L arm and/or jaw, SOB, fatigue, adrenergic sx
|
|
|
What micro pathology changes occur on the 1st day of MI?
|
first 2-4 hrs: no visible change by light microscopy; coagulative necrosis: contraction bands visible after 4hrs, release of contents of necrotic cells into blood and beginning of neutrophil emigration
|
|
|
What gross pathology changes occur on the 1st day of MI?
|
occluded artery causes infarct; dark mottling; pale with tetrazolium stain
|
|
|
What pathology changes occur on days 2-4 of MI?
|
tissue surrounding infarct shows acute inflammation; dilated vessels (hyperemia); neutrophil emigration; muscle shows extensive coagulation; note: RISK for ARRYTHMIA on days 2-4 post MI
|
|
|
What pathology changes occur 5-10 days after MI?
|
Gross: hyperemic border, central yellow-brown softening (max yellow and soft by 10 days); Micro: outer zone shows ingrowth of granulation tissue, macrophage and neutrophils present; note: RISK for FREE WALL RUPTURE 5-10 days post MI
|
|
|
What pathology changes can be seen 7 wks after MI?
|
Gross: recanalized artery, gray-white scar; Micro: contracted scar is complete; note: RISK for VENTRICULAR ANEURYSM
|
|
|
How do you diagnose MI?
|
first 6 hrs: ECG = gold standard! ECG changes include: ST elevation (=transmural infarct), ST depression (=subendocardial infarct), or pathological Q waves; cardiac troponin I rises after 4 hrs and is elevated 7-10 days (=more specific than other protein markers)
|
|
|
What are some MI complications?
|
1. cardiac arrhythmia = important cause of death before getting to hospital, common in first few days; 2. LV failure and pulmonary edema; 3. cardiogenic shock: large infarct = high risk mortality; 4. rupture: ventricular free wall rupture → cardiac tamponade, papillary rupture muscle → severe mitral regurg., interventricular septal rupture → VSD; 5. aneurysm formation: decr. CO, risk of arrhythmia, embolus from mural thrombus; 6. fibrinous pericarditis: friction rub 3-5 days post-MI; 7. Dressler's syndrome = autoimmune phenomenon causing fibrinous pericarditis several wks post-MI
|
|
|
What is dilated (congestive) cardiomyopathy?
|
most common cardiomyopathy (90% of cardiomyopathies), causes systolic dysfunction; d/t: chronic Alcohol abuse, Beriberi, Coxsackie B virus myocarditis, chronic Cocaine use, Chagas' dz, Doxorubicin toxicity, and peripartum cardiomyopathy; Note: heart dilates and looks like balloon on CXR
|
|
|
What is hypertrophic cardiomyopathy?
|
hypertrophy causing diastolic dysfunction, often asymmetric involving interventricular septum; normal heart size; 50% of cases are auto-dominant; cause of sudden death in young athletes; Note: findings include: loud S4, apical impulses, systolic murmur; trx: beta-blocker or verapamil
|
|
|
What is restrictive/obliterative cardiomyopathy?
|
cardiomyopathy that causes diastolic dysfunction; d/t sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis, Löffler's syndrome, and hemochromatosis
|
|
|
What are the signs of CHF?
|
dyspnea on exertion, cardiac dilation, pulmonary edema, paroxysmal nocturnal dyspnea, orthopnea, hepatomegaly (nutmeg liver), ankle and sacral edema, jugular venous distention
|
|
|
What are the most common causes of R heart failure?
|
R heart failure most often d/y L heart failure. Isolated R heart failure usually d/t cor pulmonale.
|
