Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
BR-Cardiovascular
5/16/06
| Question | Answer |
|---|---|
| Antihypertensives | Captopril, Clonidine, Enalapril, Furosemide, Hydralazine, Hydrochlorothiazide, Losartan, Metoprolol, Nifedipine, Nitroglycerin, Prazosin, Propranolol, Verapamil |
| Antianginal | Diltiazem, Nefedipine, Nitroglycerin, Propranolol |
| Class IA Antiarrhythmics (Na and K blocker; Inc QRS and QT); dec myocardial excitability, conduction velocity, contractility and automaticity; prolong refractory period and block vagal stimulation of AV node | Amiodarone, Procainamide, Quinidine, Disopyramide |
| Class 1B Antiarrhythmics (Activates K channels; Dec QT only); suppress SA and AV nodal conduction to improve resting potential duration | Lidocaine, Phenytoin, Mexiletine, Tocainide |
| Class IC Antiarrhythmics (Strong Na blocker; Inc QRS only) | Encainide, Propafenone, Flecainide |
| Class II Antiarrhythmics (B-blockers; Inc PR interval; neg chronotrope, dec sinus rhythm) | Esmolol, Atenolol, Propranol, Sotalol, Metoprolol |
| Class III Antiarrhythmics (K channel blockers; Inc QT only) | Amiodarone, Ibutilide, Sotalol |
| Class IV Antiarrhythmics (Ca channel blockers; Inc PR interval; Dec sinus and AV rhythm) | Verapamil, Diltiazam |
| Class I Side Effects | Torsade's (Inc QT; IA only); Dec Force (neg inotropic); Proarrhythmic; Do NOT give to CHF patients |
| Class II/IV Side Effects | Dec force (neg inotropic); Dec Rate (neg chronotropic) |
| Class III Antiarrhythmics Side Effects | Torsade's (Inc QT); Dec Rate (neg chronotropic); Proarrhythmic; Do NOT give if pt is Bradycardic |
| Antihhyperlipidemic | Cholestyramine, Clofibrate, Gemfibrozil, Lovastatin, Nicotinic Acid |
| Antimicrobials | Aminoglycoside, Ampicilin, Chloramphenicol, Methicilin, Penicilin, Tetracycline, Vancomycin |
| Cyclosporin in cardiac pt | used to prevent acute rejection of heart and renal transplants by inhibiting T-helper cell activation (via inhibition of IL-2) |
| Immunosuppressives | Glucocorticoids, Cyclosporine |
| Inotropic drugs (increase cardiac output) | Digoxin, Digitalis, Dobutamine, Dopamine |
| Myocardial Infarction drugs | Aspirin, Ticlopidine |
| Where do B-blockers work in CV system? | they inhibit renin release |
| Where do ACE inhibitors work? | they inhibit renin's ability to convert angiotensin I to angiotensin II |
| What do ARBs do? | they prevent antiotensin II from increasing preload, afterload and remodeling of the heart |
| What do diuretics and vasodilators do in the CV system? | inhibit increased preload and afterload of heart by lowering blood volume and pressure |
| Antihypertensive drug categories | Diuretics (Hydrochlorothiazide, Loops), Sympathohplegics (Clonidine, Methyldopa, Hexamethonium, Reserpine, Guanethidine, Prozasin, b-blockers), Vasodilators (Hydralazine, minoxidin, nifedipine, verapamil, nitroprusside), ACE-i (captopril), ARBs (losartan) |
| Antihypertensive diuretics | Hydrochlorothiazide; (adverse effects: hypoK, hyperLipidemia, hyperUricemia, lassitude, hyperCa, hyperGlycemia) |
| Antihypertensive diuretics | loop diuretics; (adverse effects: K+ wasting, metabolic alkalosis, hypotension, OTOTOXICITY) |
| Antihypertensive sympathoplegic | Clonidine; (adverse effects: dry mouth, sedation, severe rebound HTN) |
| Antihypertensive sympathoplegic | Methyldopa; (adverse effects: sedation, positive Coomb's test) |
| Antihypertensive sympathoplegic | Hexamethonium; (adverse effects; severe orthostatic hypotension, blurred vision, constipation, sexual dysfxn) |
| Antihypertensive sympathoplegic | Reserpine; (adverse effects: sedation, depression, nasal stuffiness, diarrhea) |
| Antihypertensive sympathoplegic | Guanethidine; (adverse effects: orthostatic and exercise hypotension, sexual dysfxn, diarrhea) |
| Antihypertensive sympathoplegic | Prozasin; (adverse effects: 1st dose orthostatic hypotension, dizziness, HA) |
| Antihypertensive sympathoplegic | b-blockers; (adverse effects: impotence, asthma, CV effects (bradycardia, CHF, AV block), CNS effects (sedation, sleep alterations)) |
| Antihypertensive Vasodilator | Hydralazine; (adverse effects: nausea, HA, lupus-like syndrome, reflex tachycardia, angina, salt retention); *use with b-blockers to prevent reflex tachy and a diuretic to block salt retention* |
| Antihypertensive Vasodilator | Minoxidil; (adverse effects: hypertrichosis (hair growth), pericardial effusion, reflex tachycardia, angina, salt retention); *use with b-blockers to prevent reflex tachy and a diuretic to block salt retention* |
| Antihypertensive Vasodilator | Nifedipine, Verapamil; (adverse effects: dizziness, flushing, constipation (verapamil), nausea) |
| Antihypertensive Vasodilator | Nitroprusside; (adverse effects: cyanide toxicity d/t CN release) |
| Antihypertensive ACE inhibitor | "Captopril"; (adverse effects: HyperKalemia; Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy probs (fetal renal damage), Rash, Inc renin, Lower angiotensin II) |
| Antihypertensive ARB | Losartan; (adverse effects: fetal renal toxicity, hyperKalemia) |
| Acetazolamide site of action | prox tubule; carbonic anhydrase-i; self-limited NaHCO3 diuresis/depletion of HCO3- stores; Uses: Glaucoma, urinary alkalization, metabolic alkalosis, altitude sickness; (Toxcitiy: hyperChloremic metabolic ACIDosis, neuropathy, NH3 toxicity, sulfa allergy |
| Mannitol (Osmotic) Diuretic site of action | proximal tubule and descending loop of Henle and collecting duct |
| Furosemide (Loop) diuretic site of action | thick ascending loop; inhibit cotransport of Na/K/2Cl; no urine [ ]; LOSE Ca; Uses: Edema (CHF, cirrhosis, neprhotic syndrome, pulm edema), HTN, hyperCa; (Toxicity = "OH DANG;" ototoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis, gout) |
| Thiazide (hydrochlorothiazide) diuretic site of action | distal tubule; inhibits NaCl reabsorption; DEC Ca excretion (opp loops); Uses: HTN, CHF, hypercalciuria, nephrogenic diabetes insipidus; (Toxicity: hypoKalemic met alkalosis; hyponatremia; HyperGLUC = hyperGlycemia, -Lipidemia, -Uricemia, -Calcemia; sulfa |
| Potassium sparing diuretic site of action | The K STAys (spironolactone, triamterene, amiloride, eperlone); junction of distal tubule and collecting tubule; Uses: hyperaldosteronism, K+ depletion, CHF; (Toxicity: hyperKalemia, endocrine effects (spironolactone = gynecomastia/antiandrogen effects) |
| ADH antagonist diuretic site of action | collecting duct |
| Spironolactone | competitive aldosterone receptor antagonist |
| Diuretics that increase Urine NaCL | all types: carbonic anhydrase inhibitors, loop diuretics, thiazides, K-sparing |
| Diuretics that increase Urine K+ | all types except K-sparing |
| Diuretics that decrease blood pH, causing metabolic acidosis | carbonic anhydrase inhibitors, K-sparing |
| Diuretics that increase blood pH, causing metabolic alkalosis | loop diuretics, thiazides |
| Diuretics that increase Urinary Ca | loop diuretics |
| Diuretics that decrease Urinary Ca | thiazides |
| Hydralazine | antihypertensive; inc cGMP to relax smooth m (vasodilates arterioles > vv); reduces afterload; Uses: severe HTN, CHF; (Toxicity: compensatory tachy, fluid retention, lupus-like syndrome) |
| Nifedipine, verapamil, diltiazam | CCBs; block voltage-dep channels on cardiac/smooth muscle to reduce contractility; Uses: HTN, angina, arrhythmias; (Toxicity: cardiac depression, peripheral edema, flushing, dizziness, constipation) |
| Verapamil | CCB that has greatest effect on decreasing cardiac muscle contracility |
| Nifedipine | CCB that has greatest effect on decreasing smooth muscle contracility; does NOT cause arrhythmias |
| Captopril, Enalapril, Lisinopril | ACE-i; dec AT-II (No bradykinin inactivation = vasodilation); inc renin d/t loss of feedback inhib; Uses: HTN, CHF, diabetic renal dz; (Toxicity: "CAPTOPRIL" = cough, angioedema, proteinuria, taste change, hypOtension, Pregnancy (fetal renal damage), rash |
| Losartan | ARB; does not cause cough; use when pt cannot stand ACE-i |
| Nitroglycerin, Isosorbide dinitrate | vasodilators (vv >> aa; inc NO and cGMP for smooth m relaxation; Uses: angina, pulmonary edema; (Toxicity: tachycardia, hypotension, HA, "monday dz") |
| Goal of antianginal therapy | reduce myocardial O2 consumption by decreasing 1 or more of the following: end diastolic vol, BP, HR, contractility, ejection time; the use of nitrates + b-blockers has greatest effect overall on dec BP, HR and O2 consumption |
| Nifedipine, Verapamil | CCBs; N is similar to nitrates (dec end diastolic vol, BP, ejection time, but reflexes inc contractility and HR) and V is similar to b-blockers in effect (inc end diastolic vol and ejection time, dec BP, contractility, HR) |
| Digitalis, Digoxin (cardiac glycosides) | inhibits Na/K ATPase = inc in intracellular Na and Ca = Positive inotropy; Inc PR, Dec QT, Scooping of ST segment, T-wave inversion; Uses: CHF (inc contractility) and Atrial Fib (dec AV node conduction); (Toxicity: N/V/D, blurry yellow vision, arrhythmias |
| CCBs | inhibit voltage-gated Ca channels |
| B-agonists | activate voltage-gated Ca channels |
| Digoxin | 75% bioavailability; urinary excretion; (Toxicity: renal failure (dec excretion), hypokalemia, quinidine (dec clearance); ANTIDOTE = slowly normalize K+, Lidocaine, Cardiac pacer, Anti-dig Fab fragments |
| LDL Lowering drugs | HMG-CoA reductase inhibitors ("statins") >> Niacin = Bile Resins (Cholestyramine, Colestipol), Cholesterol absorption blocker (Ezetimibe) > Fibrates (Gemfibrozil, Clofibrate, etc) |
| TG lowering drugs | Fibrates >>> Niacin = HMG-CoA Reductase Inhibitors |
| HDL Raising Drugs | Niacin > HMG-CoA Reductase Inhib = Fibrates |
| Side effects of Niacin | red, flushed face (can be dec w/aspirin or long-term use); try to get pt to tolerate b/c it can raise HDL and lower LDL |
| Lipid lowering drugs that cause Elevated LFTs | HMG-CoA red inhib, Fibrates, rarely cholesterol absorption blocker (ezetimibe) |
| HMG-CoA Reductase Inhibitors MOA | prevent conversion of HMG-CoA to cholesterol in hepatocytes |
| Niacine MOA | Inhibits cholesterol conversion to VLDL in hepatocytes; less circulates in blood |
| Resins MOA | prevents reabsorptionof bile acids from GI into hepatocytes; pts hate tase and have GI discomfort |
| Gemfibrozil MOA | activates Lipoprotein lipase to convert VLDL into IDL; can cause myositis |
| Heart development | mesoderm; paired endocardial tubes; lateral and cephalic folding; primitive heart dilates in 5 areas (truncus arteriosus, bulbus cordis, primitive ventricle, primitive atrium, sinus venosus) |
| Truncus arteriosus | ascending aorta, pulmonary trunk/artery; divided by aorticopulonary septum |
| Bulbus cordis | smooth parts of R ventricle (conus arteriosus) and L ventricles |
| Primitive ventricle | R and L ventricles (trabeculated) |
| Primitive atrium | R and L atria (trabeculated) |
| Sinus venosus | R horn = smooth part of R atrium; L horn = coronary sinus; oblique vein |
| R common and anterior cardinal veins | superior vena cava |
| Septum primum, septum secundum, AV cushion form the: | atrial septum |
| Foramen ovale | communication btw R and L atria formed by walls of septum primum and septum secundum; Persistance/patency = mc atrial septal defect |
| Aberrant development of aorticopulmonary septum causes: | Tetralogy of Fallot |
| Aorticupulmonary septum, R and L bulbar ridges, atrioventricular cushion form the: | Interventricular septum |
| Aortic arch 3 | forms bilateral common carotid arteries |
| Aortic arch 4 | forms aorta on left and proximal subclavian artery on right |
| Aortic arch 6 | forms ductus arteriosus and part of pulmonary trunk |
| Paired dorsal aortae that run on ventral surface of embryo form: | descending aorta when they coalesce |
| Vitelline veins | ductus venosus, hepatic sinusoids, IVF, portal vein, superior and inferior mesenteric vv |
| Umbilical veins | no adult vascular structures; L vein connects to ductus venosus & carries O2-blood (80% sat) from placenta to fetus; L vein = ligamentum teres hepatis |
| Anterior Cardinal veins | forms internal jugular vein and superior vena cava |
| Posterior Cardinal veins | form IVC, common iliac vv, azygos v, and renal vv |
| The umbilical ciruculation | the only other place besides lungs where artery carries deO2 blood; the paired arteries carry deO2 to placenta and single vein brings O2-blood to fetus |
| 1st aortic arch | part of maxillary artery |
| 2nd aortic arch | stapedial and hyoid arteries |
| Umbilical arteries | MEDIAL umbilical ligaments |
| Ductus arteriosus | ligamentum arteriosum |
| Ductus venosus | ligamentum venosum |
| Foramen ovale | fossa ovalis |
| Allantois | urachus; MEDIAN umbilical ligament (urachal cyst or sinus permits urine to drain from bladder) |
| Notochord | nucleus pulposus |
| Fetal blood flow: oxygenated blood | the majority reaches heart via IVC and is diverted thru foramen ovale and pumped out aorta towards head |
| Fetal blood flow: deoxygenated blood | arrives in the SVC and is expelled thru pulmonary artery and ductus arteriosus to lower body of fetus |
| Fetal circulation: changes at birth | deep breath = dec pumonary resistance and inc L atrial pressure (versus R atrial pressure); foramen ovale closes; Inc in O2 inhibits prostaglandins, causing closure of ductus arteriosus w/in first days of life |
| Indomethacin Therapy | closes patent ductus arteriosus |
| Alprostadil (PGE1) Prostaglandin Therapy | keeps an patent ductus arteriosus open (in case of a heart defect) |
| Down syndrome heart defects | endocardial cushion defects can manifest as atrial septal or ventricular septal defects |
| Atrial septal defect | 90% are d/t septum secundum; L to R shunt; asymptomatic until 30s; murmur, R ventricular hypertrophy; female |
| Coarctation of aorta | infantile (proximal to PDA) versus Adult (constriction at closed ductus arteriosus, distal to origin of L subclavian v); weak pulses in lower limbs; males and females with Turner's syndrome |
| Paradoxical emboli | originate in venous circulation, pass thru patent foramen ovale or ASD to produce symptoms on arterial side |
| Patent ductus arteriosus | may be d/t premature birth w/hypoxemia or structural defects; continuous MACHINERY murmur; 2nd mc CHD |
| Tetralogy of Fallot | overriding aorta, VSD, pulmonary stenosis, hypertrophy of R ventricle; possible cyanosis, R to L shunt, boot-shaped heart; pt "squats" to relieve symptoms; can survive to adulthood |
| Transposition of great arteries | separate pulmonary and systemic circuits = incompatible with life unless a shunt exists; cyanosis at birth; a/w diabetic mothers |
| Ventricular septal defect | mc CHD; membranous (90%) or muscular; L to R shunt; LOUD HOLOSYSTOLIC murmur means small defect (can close spontaneously); large = heart failure at birth |
| Dextrocardia | heart is on R side of thorax; isolated cases a/w other organ anomalies |
| Situs Inversus | transposition of al organs; a/w "Kartagener's Syndrome" w/immotile cilia d/t dynein arm defect (lung dz and sterility); heart is usu normal |
| Eisenmenger's syndrome | the change from a L to R shunt to a R to L shunt secondary to increasing pulmonary HTN; usu d/t chronic adaptive response to pre-existing L to R shunt such as VSD |
| Right coronary artery | supplies SA and AV nodes and inferior portion of left ventricle via posterior descending artery (right dominant heart) |
| Coronary artery occlusion | most commonly occurs in left anterior descending artery, which supplies anterior IV septum |
| Coronary artery dilation | occurs during diastole |
| Left atrium of heart | the most posterior portion of the heart; enlargement can cause dysphagia |
| Depolarization of nodal tissues versus muscular cardiac tissue | Ca2+ versus Na+; Ca channels are slower allowing for prolongation of AV transmission btw atria and ventricles |
| Drugs that treat arrhythmias can also cause them | digoxin, class Ia (quinidine, disopyramide), Class Ic (propafenone, flecainide, ecainide) and Class II (propranolol) |
| Sympathetic CHOLINERGICS | mediate vasodilation in skin vessels; activated in response to inc body temp or alcohol (vessels dilate, AV anastomoses close and heat is lost to atmosphere); the opposite occurs w/dec core body temp |
| Increased intracellular Ca (drug-mediated or d/t sympathetic b-receptor stimulation) | allows for increased INOTROPIC effects of heart; greater contractility |
| Greater preload (inc filling of ventricles) | stretches myocytes and induces stronger contraction |
| Afterload (aortic pressure) | influenced by total peripheral resistance of body; heart must work harder if afterload is high otherwise cardiac output falls |
| Renin-Angiotensin-Aldosterone System | responds to changes in arterial pressure by altering salt and water retention by kidneys; low bp inc renin release (converts angiotensinogen to AT1 in liver, AT1 --> AT2 in lungs via ACE; AT2 constricts arterioles and inc release of aldosterone (Na/Water) |
| Atrial natriuretic peptide | responds to bp changes; Inc BP = Inc stretch in Atrial Myocytes which releases ANP; ANP inhibits contraction of smooth muscle, inc Na and water excretion and inhibits renin release |
| Antidiuretic hormone/ADH/AVP | responds to rapid blood loss; released from pituitary to work on kidney to dec urine output and retain water; also constricts arterioles to inc peripheral vascular resistance |
| Baroreceptor reflex | affects total vascular resistance; carotid bodies (sense arterial pressure) send afferent signals via CNIX to induce efferent signals via CNX to influence HR; inc BP = inc vagal output and dec HR; Dec in BP = Dec in vagal output and inc HR |
| Layers of a muscular coronary artery | adventitia, vasa vasorum, external elastic lamina, media, internal elastic lamina, endothelium |
| Anastamoses between R and L coronary arteries | Septal branch and Apex |
| P wave | atrial depolarization |
| PR interval | 0.12 - 0.2 seconds; measures time btw atrial and ventricular polarization |
| QRS interval | usu <0.1 second; reflects duration of ventricular depolarization |
| T wave | ventricular depolarization |
| Torsades des Pointes | ventricular tachycardia d/t anti-arrhythmic drugs, especially quinidine; long QT interval and "short-long-short" sequence prior to inception of tachycardia; ECG shows series of upward pointing QRS complexes followed by series of downward pointing complexe |
| Atrial Flutter | regular, saw-tooth pattern of back-to-back atrial depolarizations (P wave); usu near 300/min; QRS complexes are present |
| Atrial Fibrillation | chaotic, erratic baseline w/o discrete P waves in between irregularly spaced QRS complexes (AV node is bombarded by impulses; wide QRS complexes = abberent "Ashman" beats |
| Ventricular Fibrillation | completely irratic rhythm without any identifiable waves; fatal w/o immediate defibrillation; atria may be dissociated |
| Wolff-Parkinson-White Syndrome | accessory AV conductions (bundle of Kent) bypassing AV node; aterograde or retrograde - ventricles partially depolarize early producing blurred QRS slope (delta-waves); reentry currents lead to supraventricular tachycardia |
| Myocardial infarctions can cause | both second degree and third degree heart blocks |
| First degree heart block | long PR interval (>0.2 sec); AV nodal anomaly; b-blockers, digitalis, CCBs |
| Second degree heart block: Mobitz type 1, Wenckebach | Progressively increasing PR interval until QRS wave is lost; defective AV node; common; no Tx required |
| Second Degree Heart Block: Mobits type 2 | defectiv His-Purkinje system; constant PR interval with random dropped QRS complexes; Tx = pacemaker |
| Third Degree Heart Block | Atria and ventricles contract independently; Rate of ventricular contraction is determined by His-Purkinje system; may need pacemaker |
| Ventricular action potentials | depolarized by Na, K+ efflux plateaus with Ca influx; Ca triggers SR to release more Ca and contract myocytes; Massive K efflux repolarizes as Ca channels close (Phases 0 thru 4) |
| Pacemaker (SA and AV nodes) Action Potentials | depolarization initiated by Ca (not Na), which is slower than myocytes to prolong transmission btw atria & ventricles; No plateau; slow diastolic depolarization; ACh decreases HR, Catecholamines (NE, E) inc HR (aka rate of diastolic depol of SA node) |
| Fick Equation | calculates either CO or oxygen consumption: CO = (O2 consumption)/([O2] in pulmonary v - pulmonary a) |
| Cardiac output | Stroke volume x HR; inc during exercise initially d/t inc in SV and d/t inc in HR after prolonged exercise; if HR is too high, diastolic filling is incomplete and CO decreases (ex: v-tach) |
| Mean arterial pressure | cardiac output x total peripheral resistance OR 1/3 systolic + 2/3 diastolic |
| Pulse pressure | systolic - diastolic; (approximates the stroke volume) |
| Stroke volume | Cardiac output / Heart rate OR End diastolic volume - End systolic volume |
| Ejection fraction | (Stroke Volume / End diastolic volume) x 100%; Normal >55% |
| Relationship between arteriolar diameter and systemic resistance | if radius is increased by 2, the resistance drops by 16 fold (R = 1/r^4) |
| What happens to blood flow resistence when vessels run parallel to each other? What affects viscosity? | It lowers total resistance (ex: capillary beds); inversely proportional to the radius^4; directly proportional to viscosity (ex: polycythemia, hyperproteinemia (multiple myeloma), hereditary spherocytosis) |
| Stroke volume is affected by (SV CAP) | contractility, afterload, and preload; it increases with elevated preload and contractility and decreases with decreased afterload |
| Contractility and SV increase with | Catecholamines (inc Ca pump in SR); Inc intracellular Ca; Dec extracellular Na; Digitalis (in intracellular Na and Ca); anxiety, exercise, pregnancy |
| Contractility and SV decrease with | b1 blockade; Heart failure; Acidosis; Hypoxemia/hypercapnea |
| Myocardial O2 demand increases with | inc Afterload, inc Contractility, inc HR, in Heart size (inc wall tension) |
| Preload | represents ventricular end diastolic volume; it increases w/exercise, overtransfusion, and excitement; It can be decreased by venous dilators (ex: Nitroglycerin); force of contraction is proportional to initial length of cardiac muscle fiber |
| Afterload | represents diastolic arterial pressure (proportional to peripheral resistance); It can be decreased by vasodilators (ex: hydralazine) |
| Isovolemic contraction | period btw mitral valve closure and aortic valve opening; period w/highest O2 consumption |
| Systolic ejection | period btw aortic valve opening and closing |
| Isovolemic relaxation | period btw aortic valve closing and mitral valve opening |
| Rapid filling | period just after mitral valve opening |
| Slow filling | period just before mitral valve closure |
| S1 sound | mitral and tricuspid valve closure |
| S2 sound | aortic and pulmonary valve closure |
| S3 sound | at end of rapid ventricular filling; a/w dilated CHF |
| S4 sound | "atrial kick;" high atrial pressure/stiff ventricle; a/w hypertrophic ventricle |
| S2 splitting | aortic valve closes before pulmonic; the difference is increased during inspiration |
| Normal S2 splitting | aortic closes before pulmonic valve |
| Paradoxical splitting | a/w aortic stenosis; pulmonic valve closes before aortic valve |
| Jugular venous distention | a/w right heart failure |
| Cardiac myocyte physiology in contrast to skeletal muscle | contraction relies on calcium-induced calcium release; cardiac myocyte APs have a plateau d/t Ca influx; cardiac nodal cells spontaneously depolarize, resulting in automaticity; cardiac myocytes are electrically coupled together via gap junctions |
| Smooth muscle contraction | AP depolarizes membrane, voltage-gated Ca channels open, inc intracellular Ca binds to Calmodulin; Calmodulin activates myosin light chain kinase; phosphorylation = relaxation, myosin light chain phosphatase permits x-bridging & contraction |
| Conduction to contraction | depolarization - T tubule opens Ca channel and SR Ca release - binds troponin C & conformational change moves tropomyosin out of myosin binding groove on actin - myosin hydrolyzes ATP for power stroke with contracts "HIZ" bands (lenght stays constant) |
| Aortic arch baroreceptor | transmits via vagus nerve to medulla; responds ONLY to increased BP |
| Carotid sinus baroreceptor | transmits via glossopharyngeal nerve to medulla |
| Hypotension | low arterial pressure, low stretch, low afferent baroreceptor firing = INC efferent SYMP firing and dec parasymp stimulation = VASOCONSTRICTION, INC HR, contractility, INC BP; (important response to severe hemorrhage) |
| Carotid massage | by increasing pressure on the carotid artery, the vessels stretches and DECREASES HR |
| Peripheral chemoreceptors | carotid and aortic bodies respond to low PO2 (<60mmHg), high PCO2 and low pH |
| Central chemoreceptors | respond to pH and pCO2 changes in CSF which are influenced by arterial CO2. NO direct response to O2 levels; Responsible for Cushing's rxn to ICP (hypertension (symp response), bradycardia (parasymp response)) |
| Circulation through liver | gets largest share of systemic cardiac output |
| Circulation through Kidney | gets highest blood flow per gram of tissue |
| Circulation through the heart | large arteriovenous O2 difference; Inc O2 demand is met by Inc coronary blood flow NOT by inc extraction of O2 |
| Pulmonary capillary wedge pressure (PCWP) | is a good approximation of LEFT ATRIAL pressure; measured with Swan-Ganz catheter; usu <12mmHg |
| Right atrial pressure | <5mmHg |
| Right ventricle pressure | <25/<5mmHg |
| Pulmonary artery pressure | <25/10mmHg |
| Left atrial pressure | PCWP; <12mmHg |
| Left ventricular pressure | <130/10mmHg |
| Aortic pressure | <130/90mmHg |
| Autoregulation of blood flow | alterations meet demands of tissue |
| Factors determining autoregulation of Heart blood flow | local metabolites: O2, adenosine, NO |
| Factors determining autoregulation of Brain blood flow | Local metabolites: CO2 (pH) |
| Factors determining autoregulation of Kidney blood flow | Myogenic and tubuloglomerular feedback |
| Normal blood composition | 8% of total body weight; 45% = hematocrit (formed elements: RBC, WBC, platelets); 55% = plasma (water, ptns, salts, fats, vitamins) |
| Serum | Plasma minus the clotting factors (ex: fibrinogen) |
| Starling forces | determine fluid movement by osmosis thru capillary membranes; Net filtration = the difference btw capillary fluid pressure and osmotic pressure |
| Pc = capillary pressure AND (pi)i = interstitial fluid colloid osmotic pressure | moves fluid out of capillary |
| Pi = interstitial fluid pressure AND (pi)c = plasma colloid osmotic pressure | tends to move fluid into capillary |
| Edema | excess fluid outflow into interstitium d/t: Inc capillary pressure (ex: HF); Dec plasma ptns (ex: nephrogenic dz or liver failure); Inc capillary permeability (ex: toxins, burns, infxn); Inc interstitial colloid osmotic pressure (ex: lymphatic blockage) |
| Atherosclerosis | the deposition of lipids into the INTIMA of elastic and lg/med muscular arteries leading to FIBROSIS and CALCIFICATION |
| Risk factors for Atherosclerosis | hyperlipidemia, DM, smoking, HTN, obesity, (family Hx, age, male, OCPs, elevated homocystein level) |
| Pathogenesis of Atheroma formation in Atherosclerosis | monocytes adhere to vessel wall, enter tissue, become MQs; transform into FOAM CELLS w/ingestion of oxidized LDL; accumulation in INTIMA w/release of factors to aggregate platelets, FGF (smooth muscle); plaque calcifies around central core of cholesterol |
| Complications of Atheroma in Atherosclerosis | plaque rupture, FATTY STREAKS, ischemic heart dz or MI; stroke; renal artery ischemia; death |
| Vitamin E | inhibits oxidation of LDL and its absorption by MQs |
| Superoxide, NO, Hydrogen peroxide | promote oxidation of LDL and blood vessel injury |
| HDL | works to remove cholesterol from tissues and plaques; exerts protective effect; levels are increased by EXERCISE |
| Familial Dyslipidemias | type IIb (combined hyperlipidemia) and IV (hypertriglyceridemia) are most common |
| Familial hypercholesterolemia (type IIa) | high LDL, elevated cholesterol, DEC LDL RECEPTORS; Xanthomas; (Tx = cholestyramine, lovastatin & niacin for homos) |
| Combined Hyperlipidemia (type IIb) | elevated LDL, VLDL, TG and Cholesterol; d/t hepatic overproduction of VLDL (Tx = cholestyramine, lovastatin & niacin for homos) |
| Hypertriglyceridemia (type IV) | elevated VLDL, TGs (cholesterol may be normal); d/t hepatic overproduction/dec clearance of VLDL; a/w diabetes, obesity, pregnancy, alcoholics; (Tx = wt loss, low fat diet, niacin, clofibrate or lovastatin) |
| Progression of atherosclerosis; and locations | fatty streaks --> proliferative plaque --> complex atheromas; abdominal aorta > coronary artery > popliteal artery > carotid artery |
| Symptoms and Complications of atherosclerosis | Angina, claudication, may be asymptomatic AND aneurysms, ischemia, infarcts, peripheral vascular dz, thrombus, emboli |
| Monckeberg Arteriosclerosis | calcification of arteries, especially radial or ulnar; usu benign |
| Arteriolosclerosis | HYALINE THICKENING of small arteries in ESSENTIAL HTN; hyperplastic "ONION SKINNING" in MALIGNANT HTN |
| Hypertension | age, obesity, diabetes, smoking, genetics, black, 90% essential d/t inc CO and TPR; 2* cases d/t renal dz; Malignant = severe/rapid progression |
| Characteristics of essential hypertension | BP >140/90 on 3 separate occasions; Hypertrophy of LV; Onion-skinning of vessel walls; Retinal hemorrhage; Predisposition to ischemic heart disease |
| Hypertrophy of left ventricle | a/w hypertension, left-sided valvular disease (ex: aortic stenosis or mitral regurgitation) |
| Secondary hypertension | a/w Renal Diseases (MCC; Parenchyma, Renal a. stenosis (atherosclerosis in black males, fibromuscular dysplasia in white females), activated RAAS) AND Endocrine dzs (1* Aldosteronism, Pheochromocytoma, Hyperthyroidism) |
| Fibromuscular dysplasia of renal artery | "beads on a string" sign on radiograph; common in white females; cause of secondary HTN |
| Malignant Hypertension | rapid course; results in end organ damage (CV - vascular damage, aortic dissection; Pulmonary - edema; Renal - "flea-bitten kidneys," azotemia; Ocular - fundal hemorrhage, papilledema; CNS - encephalopathy, seizure, coma); Death d/t CVA; Young Black Males |
| Arteriovenous fistula aneurysm | d/t trauma; causes high output cardiac failure |
| Atherosclerotic aneurysm | d/t atherosclerotic or coronary artery dz; usu in DESCENDING AORTA btw renal aa and iliac bifurcation |
| Berry aneurysm | congenital weakness at cerebral bifurcations esp Circle of Willis; usu hemorrhage into SUBARACHNOID SPACE; a/w polycystic kidney dz (AD dz on Chrom 16) |
| Dissecting aneurysm | a/w HTN, Marfan's, cystic medial necrosis; Tearing pain (separation of tunica media from aortic wall) |
| Syphilitic aneurysm | tertiary syphilis obiliteration of vaso vasorum w/necrosis of media; ASCENDING AORTA w/ aortic valve insufficiency; |
| Mycotic (infectious) aneurysm | inflammation usu d/t salmonella; ABDOMINAL AORTA |
| Syphilis | STD caused by Treponema pallidum (spirochete); painless hard chancre; if untreated, it causes rashes, lymphadenopathy, condyloma lata, Argyll Robertson pupils (accommodation, but no constriction) and aneuyrisms |
| Ischemic heart disease | inadequate supply of O2 relative to demand of heart, resulting in damage to cardiac tissue; most often caused by atherosclerosis; Exercise tolerance testing is good way to diagnose subacute coronary occlusion |
| 4 types of ischemic heart disease | Angina Pectoris, Myocardial Infarction, Chronic Ischemic Heart Disease, Sudden Cardiac Death |
| Angina pectoris | paroxysmal attacks of retrosternal pain that may radiate to face/arms; a/w diaphoresis & nausea; CAD narrowing >75%; Three types: Stable, Prinzmetal's (Variant) and Unstable |
| Stable Angina | mc; induced by exercise, relieved by rest, d/t stenosis of coronary arteries |
| Prinzmetal's (variant) angina | episodic pain at rest; attacks are unrelated to activity, BP, or HR, but are d/t coronary vessel VASOSPAM; significant artery stenosis is present |
| Cocaine use | can cause coronary vasospasm and myocardial ischemia; it stimulates release of endogenous catecholamines (dopamine, NE, E) |
| Amphetamine use | prevents the reuptake of endogenous catecholamines |
| Unstable angina | occurs at rest or with increasing frequency, severity or duration; d/t RUPTURED atherosclerotic PLAQUE w/subsequent thrombosis and embolization; Activated platelets help thrombosis and vasospasm; Microinfarcts may occur |
| Myocardial infarction | tissue death d/t lack of perfusion; mc d/t atherosclerosis, plaque rupture, thrombosis; Endocardium is most vulnerable; can be: Non-transmural and Transmural; cardiac enzymes are released by damaged myocytes |
| Non-transmural (non-Q-wave) Infarct | diffuse coronary atherosclerosis w/dec coronary flow; Rupture/thrombosis is followed by clot lysis and loss of perfusion to inner 1/3 of muscular wall; ST segment DEPRESSION on ECG |
| Transmural Infarct | Atherosclerotic plaques rupture; Platelet-mediated thrombosis OCCLUDES vessel and blood flow is lost to entire muscular wall; ST segment ELEVATION on ECG |
| Left anterior descending coronary artery | mc artery involved in acute MI; infarcts affect LV near apex or anterior part of intraventricular septum |
| ST elevation is pathognomonic for: | Transmural (Q-wave) infarcts |
| ST depression | is not pathognomonic for non-transmural infarcts, it can also be produced by digitalis drugs |
| Red versus Pale Infarcts | Red (hemorrhagic) = occur in loose tissues w/collaterals (ex: lungs, intestines, or following reperfusion); Pale Infarcts = solid tissues w/single blood supply (ex: brain, heart, kidney, spleen) |
| Evolution of MI | Coronary artery occlusion: LAD > RCA > Circumflex; Day 1 (coagulative necrosis, dark, PMN recruitment); Days 2-4 (inflammation, hyperemia, PMN emigration, necrosis, yellow & soft); Days 5-10 (granulation tissue, MQ, PMNs); 7wks (Gray/white scar tissue) |
| Acute MI Symptoms and Diagnosis | Severe retrosternal pain, L arm/jaw pain, SOB, fatigue, adrenergic sx; ECG w/in 6hrs; later - troponin-I, CK-MB, LDH1, AST, ECG changes |
| Cardiac troponin I for diagnosis of MI | rises after 4hrs; stays elevated for 7-10days; Most SPECIFIC marker |
| CK-MB for diagnosis of MI | Test of choice w/in 1st 24hrs |
| LDH1 for diagnosis of MI | former test of choice; stays elevated for 2-7 days post-MI |
| AST for diagnosis of MI | nonspecific; can be found in liver, cardiac and skeletal muscle cells |
| ECG changes a/w MI | ST elevation (transmural), ST depression (subendocardial infarct), Q waves (transmural infarct) |
| MI Complications | Arrhythmia (early); LV failure/pulmonary edema; Cardiogenic shock (high mortality); Rupture of ventricular free wall, septum, papillary m (day 4-10) w/cardiac tamponade; Thromboembolism (mural); Fibrinous pericarditis (day 3-5); Dressler's syndrome (wks) |
| Dressler's Syndrome | autoimmune phenomenon a/w MI, resulting from fibrinous pericarditis (friction rub) several wks post-MI |
| Greatest danger of sudden cardiac death d/t arrhythmias | w/in 1-3hrs post-MI |
| Greatest danger of left ventricular free wall rupture | w/in 4-8 days post-MI (heart has yellow infarct w/red border and angiogenic/fibroblastic proliferation) |
| Chronic Ischemic Heart Disease | d/t Congestive heart failure; hypertrophy of heart and cardiac decompensation occur d/t infarction; usu in ELDERLY |
| Sudden Cardiac Death | unexpected death from cardiac failure w/in 2hrs of MI; a/w marked atherosclerosis and d/t arrhythmias |
| What is the most common cause of post-MI arrhythmias? | re-entry circuits, refractory tissue (unidirectional block), slow conduction velocity and an initiating event (premature beat) |
| Congestive heart failure | a clinical dz where heart can't pump enough blood to meet metabolic needs of body; hormonal changes (RAA and sympathetic activation), peripheral vasoconstriction and myocardial dysfunction all play a role |
| Cor pulmonale | right heart failure secondary to lung disorders which leads to pulmonary arterial hypertension |
| Left-sided CHF | Pulmonary edema/Paroxysmal Nocturnal dyspnea (pulm venous pressure; hemosiderin MQs), Orthopnea (can't be supine), S3 sound; d/t ischemia (CAD), HTN, valvular dz, myocarditis, cardiomyopathy, congenital heart dz, pericardial dz |
| Right-sided CHF | Nutmeg liver (central venous pressure; hepatomegaly/ascites), Peripheral Edema (pitting in ankles), Distention of neck vv; d/t Cor pulmonale |
| Myocarditis | inflammation of cardiac muscle; MCC is Coxsackie B virus (toxoplasmosis, S. aureus, C. diptheriae, Chaga's dz, Lyme dz, hypersensitivity rxns); Muffled S1, Audible S3, Mitral Regurgitation, Cardiomegaly |
| Trypanosoma cruzi | causes Chagas dz; transmitted by Reduvid bug; can cause myocarditis |
| Borrelia burgorferi | a spirochete that causes Lyme dz; Stage 1 = erythema chronicum migrans; Stage 2 = cardiac (myocarditis) and neurogenic probs; Stage 3 = arthritis |
| Causes of irreversible, dose-dependent cardiotoxicity | Doxorubicin, daunorubicin, anthracylines (used to tx breast cancer, lung cancer and ALL) |
| Endocarditis | inflammation of heart lining/CT; d/t Rheumatic heart dz (or rheumatic fever) OR Infectious causes (bacteria, damage, vegetative growth) |
| Characteristics of Endocarditis | Janeway lesions (peripheral nodular hemorrhages); Osler's Nodes (tender on fingers/toe pads); Splinter hemorrhages (finger nails), roth spots (retina), splenomegaly, petechiae; Commonly Mitral or Aortic valve (tricuspid = IVDA) |
| Acute Endocarditis | d/t Staph aureus; rapid onset; fever, anemia, embolic events, murmur |
| Subacute Endocarditis | d/t Strep viridans; poor dentition or oral surgery in pt w/preexisting heart dz; Onset over 6mo; Tx = IV Abx |
| Nonbacterial (marantic) endocarditis | a/w metastatic cancer; sterile fibrin deposits on heart valves; can cause cerebral infarct |
| Libman-Sacks endocarditis | a/w SLE; auto-antibody damage/vegetations to both sides of valve; no embolisms |
| Culture negative endocarditis | a/w HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) |
| Prosthetic valves predispose pts to | endocarditis caused by Staph epidermitis |
| Tumors of heart | Metastatic (2*) are most common; Primary tumors are very rare; Atrial myxomas are the most common 1* tumor in adults; Rhabdomyomas are mc primary tumor in children (a/w tuberus sclerosis) |
| Antiphospholipid syndrome | common in SLE; d/t Abs to phopsholipids that produces a hypercoagulable state leading to thrombotic disorders and multiple spontaneous abortions |
| Rheumatic Fever and Heart Disease | a/w pharyngitis w/GAS (b-hemolytic; S pyogenes); w/o Tx (PCN), Abs form via antigenic mimicry & fibrous bridges in hi pressure valves (MITRAL > aortic >>tricuspid); Aschoff bodies (granuloma in giant cell), polyarteritis, Erythema marginatum, hi ESO titer |
| Rheumatic Fever: FEVERSS | kids 5-15yo; fever, erythema marginatum, valvular damage, elevated ESR, Red-hot joints (polyarteritis), Subcutaneous nodules, St. Vitus' dance (chorea); myocarditis can cause heart failure and death |
| Bacterial Endocarditis: From Jane | Fever, Roth's spots, Oslers nodes, Murmur, Janeway lesions, Anemia, Nail-bed hemorrhage, Emboli |
| Cardiac Tamponade | compression of heart by fluid (ex: blood) in pericardium, leads to dec cardiac output; pressure in all 4 chambers equilibrates; Pulsus paradoxus; ECG - electrical alternans (beat-to-beat alterations in height of QRS) |
| Dilated cardiomyopathy | mc type; dilated "balloon" ventricles; idiopathic, a/w coxsackie B, alcoholics, Chagas, lithium, doxorubicin; Decreased Ejection Fraction and PVCs (systolic dysfxn) |
| Hypertrophic cardiomyopathy (aka: idiopathic hypertrophic subaortic stenosis) | AD seen in Young Athletes; asymmetric, involves IV septum; Mitral Regurgitation; S4, cardiomegaly, dyspnea, syncope, murmur; Relieved by Squatting and worsened w/activity |
| Restrictive cardiomyopathy | Stiffenen heart muscle (a/w sarcoidosis, amyloidosis); Peripheral Edema, ascites, JVD; (differentiate from constrictive) |
| Idioapthic dilated cardiomyopathy (mc cause), Tx = | Digitalis, ACE inhibitors, Heart Transplant, Chronic Anticoagulation |
| Senile Amyloidosis is derived from | tranthyretin |
| Primary amyloidosis is d/t | amyloid light chain (AL) ptn from immunoglobulin light chains; seen in plasma cell disorders |
| Mitral Stenosis | usu d/t Rheumatic Heart Disease; Opening Snap |
| Mitral Regurgitation | 50% d/t Rheumatic Heart Disease; S3; Holosystolic Murmur loudest at apex |
| Aortic Stenosis | Calcification/thick valve; Crescendo-Decrescendo Systolic Ejection Murmur (do NOT give b-blockers) |
| Aortic Regurgitation | S3, High pitched Blowing Decrescendo Diastolic Murmur; wide pulse pressure |
| Mitral Valve Prolapse | mc valvular lesion; Late Systolic Murmur w/midsystolic click; found in young women or Marfan's pts; d/t tissue laxity; Murmur is exagerated by Valsalva and reduced by sqatting; Require endocardial prophylaxis prior to dental procedures |
| Ventricular Septal Defect | holosystolic murmur |
| Patent ductus arteriosus | Continuous machine-like murmur; Loudest at S2 |
| Systolic Ejection Murmurs | Aortic or Pulmonic valve stenosis, Hypertrophic Cardiomyopathy |
| Holosystolic Murmur | Mitral or Tricuspid Regurgitation, Ventricular Septal Defect |
| Late Systolic Murmur | Mitral Valve Prolapse |
| Early Diastolic Murmur | Aortic or Pulmonoic Valve Regurgitation |
| Mid-to-late Diastolic Murmur | Mitral Stenosis |
| Continous Diastolic Murmur | Patent Ductus Arteriosus |
| Churg-Strauss Peripheral vascular dz | Granulomatous inflammation; a/w ASTHMA, EOSINOPHILIA |
| Henoch-Schonlein Purpura vascular dz | IgA immune complex mediated; Atopic (allergic) pt; URTI in KIDS; renal deposits, PALPABLE PURPURA |
| Kaposi's Sarcoma vascular dz | AIDS; malignant vascular tumor in HOMOSEXUALS; a/w HHV-8 |
| Kawasaki's Disease vascular dz | Acute necrotizing; YOUNG KIDS |
| Rendu-Osler-Weber Syndrome vascular dz | AD hemorrhagic telangiectasia; MORMONS |
| Polyarteritis nodosa vascular dz | p-ANCA necrotizing degeneration of media; a/w HEPATITIS B infxn |
| Takayasu's Arteritis | "pulseless dz;" damage of AORTIC ARCH; loss of carotid, radial and ulnar pulses; Young ASIAN FEMALES |
| Temporal Arteritis | nodular inflammation of branches of carotid; HA, VISUAL deficits; elevated ESR, ELDERLY; mc vasculitis in US |
| Thromboangiitis Obliterans (Buerger's dz) vascular dz | full thickness vessel inflammation, extends to nerves w/ occlusive lesions in extremities; Raynaud's Phenomenon; young JEWISH MALE SMOKER; may lead to gangrene |
| Von Hippel-Lindau vascular Dz | AD (chrom 3); Hemangioblastomas of cerebellum; inc risk of RENAL CELL CARCINOMA |
| Wegener's Granulomatosis vascular dz | c-ANCA: necrotizing Granulomatous lesions in KIDNEY and LUNG; ulcers in NASAL SEPTUM |
| Serum sickness | generalized deposition of immune complexes (TYPE III HYPERSENSITIVITY); more rare now d/t less frequent use of animal serum |
| Details about Cardiac Tamponade | fluid in pericardial sac (mc d/t neoplasms, pericarditis, uremia); Ventricular filling is limited & CO is low; Tx = Pericardiocentesis |
| Pericarditis | d/t idiopathic or Coxsackie A or B; JVD, inc Jugular venous pressure w/inspiration (Kussmaul's Sign); Pericardial Friction Rub, Distant heart sounds; ST ELEVATION; can lead to constrictive pericarditis |
| Differences btw ST elevation in MI and Pericarditis | in MI, the ST elevation is followed by a depression of the ST segment and QRS changes |
| Shock | a metabolic state where O2 delivery doesn't match O2 demand; tachycardia, hypotension, oliguria, mental changes, weak pulses, cool extremities |
| Autoregulation of heart is altered to meet demands of tissues via | Nitric oxide and Adenosine |
| Cardiogenic shock | d/t pump failure; arrhythmias, HF, intracardiac obstruction or MI |
| Hypovolemic shock | d/t volume loss; blood, E-lyte, fluid or plasma loss; burns, severe vomiting or diarrhea |
| Obstructive shock | extracardiac obstruction of blood flow; d/t aortic dissection, cardiac tamponade, pulmonary embolism |
| Septic shock | d/t inc venous capacitance; from G(-) endotoxemia, direct toxic injury or DIC; a/w Vasodilation, Hypotension, and WARM EXTREMITIES |
| Neurogenic shock | d/t massive peripheral vasodilation; from severe cerebral, brain stem or spinal cord injury |
| Clinical Manifestations of Shock | acute tubular necrosis, necrosis of brain, fatty change in liver/heart, patchy hemorrhages in colon, pulmonary edema |
| CV Manifestations of DM | large vessel ATHEROSCLEROSIS, MIs, CAD, Restrictive cardiomyopathy; Transposition of great arteries in fetus |
| Hyperthyroidism effects on CV System | Palpitations, Systolic HTN, Fatigue, Sinus Tachycardia |
| Hypothyroidism effects on CV System | Decreased CO, HR, BP, pulse pressure; Cardiomegaly, Bradycardia |
| Kwashiorkor effects on CV System | Thin, pale, flabby heart; Low Cardiac Output and low Systolic Pressure |
| Malignant Carcinoid effects on CV System | Right-sided heart lesions; Coronary artery spasm (angina) |
| Obesity effects on CV System | Inc total blood volume; Inc Cardiac Output; HTN; CAD, Cardiac Hypertrophy |
| Pheochromocytoma effects on CV System | HTN, myocardial necrosis, LV hypertrophy |
| Rheumatoid Athritis effects on CV Stystem | Pericarditis, Coronary Arteritis |
| SLE effects on CV Systems | Pericarditis, Libman-Sacks endocarditis, Anti-phospholipid syndrome |
| Thiamine Deficiency effects on CV System | High output cardiac failure; Tachycardia, S3, Systolic Murmur |
| leukocytoclastic angiitis | hypersensitivity vasculitis w/fragmented neutrophils; PCN may be an antigenic trigger |
| acebutolol and pindolol | not recommended in angina patients b/c they can exacerbate sx; these have intrinsic sympathomimetic properties |
| beta-blockers in general | are the only drugs that are proven to prolong a pt's life w/ coronary dz and are a first line agent in chronic angina (except acebutolol and pindolol) |
| Treatment of atrial fibrillation and flutter | digoxin |
| Treatment of supraventricular tachycardias | adenosine, amiodarone, disopyramide, quinidine |
| thiazide diuretics decrease the excretion of Ca | indapamide, hydrochlorothiazide, metolazone (can treat edema and hypertension) |
| congenital arteriovenous fistulas in limbs | pathognomonic = increased O2 content; warmth, swelling |
| Symptoms of complete heart block | HR around 40bpm b/c ventricles are controlling rhythm; pulse pressure is high (normal is 30-50); elevated stroke volume causes a larger rise and fall in pressure btw systole and diastole |
| Marfan's syndrome | fibrillin mutation |
| Amlopidine | CCB; used to treat mild/moderate HTN and angina |
| Terazosin | alpha-1 adrenergic receptor blocking agent; used to treat HTN and BPH |
| Enalapril | ACE-i; used to treat HTN and CHF |
| Propranolol | non-selective b-1 (neg inotropic/neg chronotropic) and b-2 (bronchoconstriction) receptor blocker; used to treat HTN |
| Cardiac defect most commonly a/w Down Syndrome | endocardial cushion defect (MR, duodenal atresia "double bubble," simian crease) |
| 22q11 cardiac defects | truncus arteriosus, tetralogy of fallot |
| congenital rubella cardiac defects | Septal defects, PDA |
| Infantile coarctation of the aorta | aortic stenosis proximal to insertion of ductus arteriosus (preductal); check for weak or absent femoral pulses |
| Adult type coarctation of the aorta | stenosis DISTAL to ductus arteriosus (postductal); a/w notching of ribs, HTN in upper extremities and weak pulses in lower extremities; |
| Right to left shunts (early cyanosis) = "Blue Baby" syndrome | 3 Ts = Tetralogy, Transposition, Truncus; children may squat to increase venous return |
| Left to right shunts (late cyanosis) = "Blue Kids" | VSD (mc congenital cardiac anomaly) > ASD (loud S1, fixed split S2) > PDA (close w/indomethacin); Inc pulmonary resistance d/t arteriolar thickening, progressive pulmonary HTN can reverse shunt (Eisenmenger's) |
| Common congenital malformations | heart defects, hypospadias, cleft lip (w/ or w/o palate), congenital hip dislocation, spina bifida, anencephaly, pyloric stenosis w/projectile vomiting |
| Carotid Sheath Structures | VAN = Internal jugular VEIN (lateral), Common carotid ARTERY (medial), VAGUS nerve (posterior) |
| Recurrent laryngeal nerve supplies all intrinsic muscles of larynx except: | cricothyroid; it is a branch of CNX |
| The left recurrent laryngeal nerve wraps around the: | arch of the aorta and ligamentum arteriosum; damage results in hoarseness (complication of thyroid surgery) |
| The right recurrent laryngeal nerve wraps around the: | right subclavian artery; damage results in hoarseness (complication of thyroid surgery) |
Created by:
bscaryp