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| Question | Answer |
|---|---|
| which coronary artery supplies the SA and AV nodes? | RCA |
| which coronary artery supplies the inferior portion of the left ventricle? where does this artery come from? | posterior descending/interventricular artery; 80% of the time from RCA, 20% of time from CFX (off of LCA) |
| where does Coronary artery occlusion most often occur? | anterior interventricular septum/apex; LAD |
| what supplies the anterior interventricular septum/apex? | LAD |
| when do coronary arteries fill? | diastole |
| which is the most posterior part of the heart? what can this cause if enlarged? | left atrium; dysphagia (compression on esophagus), and voice hoarseness from compression on recurrent laryngeal nerve (branch off of vagus) |
| what can cause left atrium hypertrophy? | mitral stenosis |
| when else can you see hoarseness of the voice due to recurrent laryngeal nerve disruption (other than LA hypertrophy)? | aortitis on left recurrent laryngeal nerve |
| how do you measure CO? what is FIck's way of doing it? | HR x SV; rate of O2 consumption/ (arterial O2 -venous O2 content) |
| how do you calculate MAP? what is another way ? | MAP= 1/3 systolic pressure + 2/3 diastolic; MAP = CO x TPR |
| how do you calculate the pulse pressure? what measure estimates for pulse pressure? | systolic pressure-diastolic; SV |
| how can you calculate the SV? another way? | CO/HR; EDV-ESV |
| during exercise, what happens do the CO? why? | increases due to HR increase |
| what happens to the CO if the HR gets too high? what is this called? | not enough time for diastolic filling, so that CO goes down; ventricular tachycardia |
| what is the sodium/calcium exchanger? does it have calcium come in or out? does slowing it down increase or decrease ionotropy? does increased extracellular sodium increase or decrease ionotropy? | a secondary energy dependent (dependent on ATP dep. Na/K exchanger) exchanger that pumps Ca out using the sodium concentration gradient that has sodium wanting to come in; Ca out; decrease; decrease (increases Na conc gradient) |
| what are cardiac glycosides and what do they do to ionotropy and how? | digitalis; they increase ionotropy by blocking the ATP dep. Na/K exchanger so that increased intracellular sodium decreases the concentration gradient for the Na/Ca exchanger |
| what is stroke volume affected by? | Preload, Afterload, Ionotropy (contractiliy) |
| what increases ionotropy generally? name 4 specific examples. | whatever increases intracellular calcium; catecholamines (increaes activity of Ca pump in SR); digitalis (blocks concentration gradient for Na/Ca exchanger); increased intracellular calcium somehow; decrease extracellular sodium (decreases conc gradient o |
| how do catecholamines increase ionotropy? | by increasing Ca pump in SR |
| Name 5 situations that decrease ionotropy? | beta blockade (decrease cAMP); acidosis; hypoxia, hypercapnea; heart failure (systolic dysfunction); Non-dihydropyridine Ca channel blockers |
| in what situations does SV increase? when does it decrease? | exercise, anxiety, pregnancy; failing heart |
| what four components effect myocardial O2 demand? | heart size, heart rate, heart contractility, increased afterload |
| what estimates the preload or EDV? | the right atrial pressure |
| what does the right atrial pressure estimate? | ventricular EDV/preload? |
| what does the mean arterial pressure estimate? | afterload |
| what does the aortic pressure estimate? pulmonic artery pressure? | afterload of the LV, afterload of the RV |
| what type of drugs decrease preload? give an example. | venodilators; Nitroglycerin |
| what type of drugs decrease afterload? give an example. | arterial dilators (hydralazine) |
| how does hydralazine work? | cGMP decreases IP3 levels which decreases Ca pump action at SR |
| T/F nitroglycerin decreases afterload | false- decreases preload |
| in what three situations is preload increased? | exercise, increased blood volume, sympathetic increase |
| what is a measure for the initial length of cardiac muscle fiber? what property is this proportional to? | preload; SV |
| what does EF measure for? | ventricular contractility |
| how do you measure EF? | SV/EDV; (EDV-ESV)/EDV |
| what is the EF normally? | greater than 55% |
| in what pathology is the EF decreased? | heart failure |
| what drives flow? what is flow inversely proportional to? | pressure gradient drives capillary flow (thus arterial pressure-venous pressure or MAP -RAP); resistance (which is proportional to viscosity and inversely proportional to radius to the fourth); SO flow through capillaries is dictated by : 1) pressure diff |
| how do you measure Q? (flow) | (MAP-RAP)/TPR (pressure gradient/resistance) |
| how do you measure RAP? what does it represent? | from the CVP (just from a central venous catheter- measure pressure!) CVP~RAP (PCWP~LAP) |
| what is resistance directly proportion to? inversely proportional to? | viscosity; radius to the fourth power |
| what happens to resistance (and thus flow) when the radius decreases by 2? | resistance increases by 16 and thus flow decreases by 1/16 |
| what does viscosity depend a lot on? what happens to flow if viscosity increases, why? | hematrocrit; flow decreases because resistance increases with increased viscosity and flow is inversely proportional to flow |
| what increases hematocrit? thus what do these properties do to viscosity, and thus resistance and thus flow? | polycythemia, hyperproteinemic states (multiple myeloma), hereditary sphercytosis; viscosity up, resistance up, flow down |
| what are the most common locations of coronary arter occlusion? | LAD>RCA>circumflex |
| what is the cause of MI when there is no arterial damage? | cocaine! |
| when do you start to see microscopic changes | |
| after an MI? gross changes? | 2-4 hours; 1 day |
| what do you grossly one day after an MI? what | |
| is the greatest risk? | pale with tetrazolium stain; dark mottling either wise; arrythmia |
| what do you see microscopically around 12-24 hours after an MI? | contraction band necrosis, early coag. necrosis and early neutrophil emigration |
| what cause contraction band necrosis post MI? | reperfusion injury - calcium influx causes hypercontraction of myofibrils in dead cells |
| what do you see microscopically 2-4 days after an MI? grossly? what is the greatest risk? | neutrophil emigration, hyperemia due to dilated vessels, acute inflammation, coag. necrosis; hyperemia; risk for arrhythmia |
| what do you see microscopically 5-10 days after an MI? grossly? what is the greatest risk? | macrophage infiltrate starts around 3 days; hyperemic border but centrally yellow brown softening- maximal yellow at ten days due to macrophagal destruction of structural comp; risk for free wall rupture, tamponade,papillary muscle rupture, IV septal rupt |
| what do you see microscopically 7 weeks after an MI? grossly? what is the greatest risk? | gray white patchy tissue (noncontractile dysfunctional); contracted scar complete; risk for ventricular aneurysm |
| what is the gold standard of MI diagnosis in first 6 hours? afterwards? up to what? | ECG; cardiac troponin I; 10 days |
| when is CK MB useful in MI diagnosis? why is not as specific as cardiac troponin I? | reinfarction on top of acute MI; also released from skeletal muscle |
| T/F AST can be found in heart and skeletal muscle | true |
| what ECG changes do you see on a subendocardial infarct? transmural? | ST depression on ECG; ST elevation on ECG |
| in which type of MI do you see more necrosis ? | transmural (subendocardial is <50% ischemic necrosis of ventricular wall) |
| what leads show an anterior wall infarct? (LAD) anteroseptal (LAD)? | VI-V4; V1-V2 |
| what leads show anterolateral infarct (LCX)? lateral wall (LCX)? | V4-V6; I, avL |
| what leads show inferior wall infarct (RCA)? | II, III, aVF |
| what is an important cause of death before reaching the hospital in MI? when else is it common? | cardiac arrythmia (V fib); first few days while in hospital |
| what is the mcc of hospital death due to an MI? | cardiogenic shock due to left heart failure |
| what is Dresslers syndrome and what does it result in? | autoimmune phenonomenon few weeks post MI; fibrinous pericarditis |
| what valves are affected most in rheumatic heart disease? | mitral>aortic>tricuspid |
| what is the early mitral lesion in RHD? late? | stenosis; regurg |
| with what disease are Aschoff bodies associated? what are they? what are they surrounded by? | RHD myocarditis; granulomas with giant cells; Anitschkows cells (activated histiocytes) |
| T/F you can detect elevated ASO titers in RHD | true |
| antibodies to what protein cause RHD? what type of hypersensitivity? | M protein; II |
| what happens to the left atria with mitral valve regurg? what does this predispose to? | dilation; embolus |
| what does FEVERSS stand for in RHD? | fever; erythema marginatum; valvular damage; ESR increased; Red hot joints (migratory polyarthritis); subcutaneous nodules; St. Vitus' dance (chorea) |
| what causes the hypotension in cardiac tamponade? what are other signs of cardiac tamponade? | decreased CO from compression of the heart, increased JVD, distant heart sounds, increased HR, pulsus paradoxus |
| what should you be thinking with distant heart sounds and increased heart rate? | cardiac tamponade |
| what is pulsus paradoxus? what else is it called? what can cause it? | exaggerated decrease in pulse (and systolic bp) during |
| inspiration; Kussmauls pulse; cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup | |
| how does tertiary syphilis effect the aorta? | disrupts vaso vasorum of aorta leading to vessel wall weakening and aortic dilation and aneurysm- also dilates aortic valve and regurg |
| what is "tree bark " appearance of aorta and what leads to it? | calcification of aortic root and ascending aortic arch; tertiary syphilis |
| what is a bounding pulse a sign of? | aortic regurg |
| what are the most common heart tumors overall? where do they occur? | mets ; pericardium |
| what are the most common primary heart tumors in adults? where do they occur? | myxomas; atria (left esp) |
| what are the most common primary heart tumors in children? what are they associated with? | rhabdomyomas; tuberous sclerosis |
| what is kussmaul's sign? what is it seen in? | increase in JVP on inspiration; cardiac tumors |
| what causes varicose veins? what do they predispose to? | chronically increased venous pressure (pregnancy, obesity, prolonged standing, OCPs, age) causes valve incompetence; poor wound healing varicose ulcers |
| do varicose veins predispose to thromboembolism? | no the stasis in DVT do |
| where is the mc location of varicose vein? where else? | superficial saphenous veins; esophageal, anorectal, left scrotal sac |
| what causes raynauds disease? | decreased blood flow to skin due to arteriolar vasospasm in response to cold temp or emotional stress |
| what can cause raynauds phen? | SLE, CREST, Buergers |
| what causes a presentation of nodular densities on CXR, RBC casts, saddle nose deformity, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea? | Wegeners |
| what is the pathology see in wegeners? what is a strong marker of disease? how is it treated? | necrotizing granulomas in lung and upper airway, necrotizing glomerulonephritis, focal necrotizing vasculitis; cANCA; cyclophosphamide, corticosteroids |
| what size vessels does wegeners target? | small/medium |
| what vasculitis is similar to wegeners but lacks | |
| granulomas? what is a marker for it? what size vessels does it affect? | microscopic polyangitis; pANCA; small |
| what signs do small vessel inflammation cause? medium? large? | palpable purpura; vessel thromboses, infection, aneurysms; loss of pulse, stroke |
| what vasculitis has p ANCA as a marker? what is the pathology? what is the presentation? | Churg Strauss; granulomatous vasculiits with eosiniphilia; small vessel disease- adult onset asthma, sinusitis, skin lesions, peripheral neuropathy (wrist food drop) |
| what size vessels does sturge weber disease affect? name four manifesations. | capillary sized blood vessels; port wine stain (nevus flammeus) on face, ipsilateral leptomeningeal angiomatosis, seizures, early onset glaucoma |
| what is the most common form of childhood systemic vasculitis? which vessels does it effect? | henoch schonlein purpura; skin (buttocks and legs); joints (arthralgia), GI (intestinal hemorrhage, melena, abd pain), renal- nephropathy |
| which vasculitis is associated with IgA nephropathy? | HSP (bergers when just nephropathy) |
| T/F HSP lesions are of different ages | false- thats polyarteritis nodosa |
| which vasculitis is associated with thromboangitis obliterans? what is it strongly associated with? what are the symptoms | buergers; smoking; intermittent claudication, superficial nodular phlebitis, raynauds phenomenom, resting pain on forefoot |
| what acute vasculitis effects asian children? what is the presentation? treatment? | kawasaki disease; mucocutaneous lymph node syndrome, fever, CORONARY aneuryms; iV ig and aspirin (acute and self limited) |
| what is the pathology seen in polyarteritis nodosa? what viral infection is it associated with? what type hypersenstivity? | segmental transmural vasculitis with fibrinoid necrosis; hep B; type III (immune complex mediated) |
| where is polyarteritis nodosa not seen? where i it seen? | pulmonary; renal and visceral |
| what small/medium vasculitis causes multiple aneurysms, is immune complex mediated, and causes constrictions on arteriogram (bead like formation? where does it usually effect causing what? | PAN; renal and visceral (fever, weight loss, malaise, abdominal pain, melena, headache, myalgia, hypertension, neurologic function, cutaneous eruptions) |
| how do you treat PAN? wegeners? | corticosteroids and cyclophosphamide; ditto |
| which pulseless disease has an increased ESR and affects female less than 40 y/o? what kind of pathology happens and where? | takayasus; granulomatous thickening of aortic arch and/or proximal great vessels causes narrowing |
| what does FAN MY SKIN On Wednesday for takayasus mean? | fever, arthiritis, night sweats, myalgia, skin nodules, Ocular disturbances, weak pulses |
| which arteriritis is also called giant cell arteritis? what arteries does it affect? are the lesions focal or continuous? | branches of carotid artery, temporal, opthalmic (can lead to irreversible blindness); focal |
| what is the most common vasculitis?how does it present? what else is it associated with? | temporal arteritis; jaw claudication, impaired vision, unilateral headache; polymyalgia rheumatica |
| which two vasculitides are associated with an increased ESR? | temporal and takayasus |
| what is a benign capillary hemangioma of infancy? what is its destiny? | strawberry hemangioma; regresses |
| what is a benign capillary hemangioma of the elderly? what is its destiny? | cherry hemangioma; does not regress (increases with age) |
| what is a polypoid capillary hemangioma? what is it associated with? what is its destiny? | pyogenic granuloma; pregnancy and trauma; can ulcerate and bleed |
| what is a glomus tumor? | benign, painful, red blue tumor under fingernails (from modified smooth muscles of glomus body) |
| what is an angiosarcoma? what is it associated it? | highly lethal vascular malignancy of the liver associated with vinyl chloride, arsenic, ThO2 (thorotrast) |
| what is bacillary angiomatosis? what is it often confused with? what is infection is it associated with? | benign capillary skin papules found in AIDS; Kaposis sarcoma; bartanella henselae |
| what is lymphangiosarcoma, what is it associated with? | lymphatic malignancy; persistent lymphedema seen in post radical mastectomy |
| what is kaposis sarcoma? | ... |
| what are nitroglycerin and isosorbide dinitrate used for? | angina, pulmonary edema, aphrodisiac and erection enhancer; vasodilate (veins more than arteries) by releasing NO in smooth muscle causing increase in cGMP |
| how is the high first pass metabolism of isosorbide dinitrate solved? | sublingual nitroglycerin give; mononitrate has less |
| what is the toxicity of nitro products? | reflex tachycardia, hypotension, flushing, headache |
| what causes monday disease? how does it result? | industrial nitro exposure; tolerance is lost over the weekend |
| T/F nitroprusside is used for angina | false- malignant hypertension |
| what are four malignant hypertension treatments? | labetalol, nitroprusside, fenoldopam, diazoxide |
| how is nitroprusside different from the other nitrates? | short acting; direct release of NO; cyanide toxicity (releases CN) |
| what is fenoldopam and what is it used for? | dopamine D1 receptor agonist; relaxes renal vascular smooth muscle- malignant hypertension |
| what is diazoxide and what is it used for? what is its toxicity? | potassium channel opener- hyperpolarizes and relaxes vascular smooth muscle used for malignant hypertension; hyperglycemia (reduces insulin release) |
| what is the goal in antiaginal therapy> | reduce Myocardial O2 consumption: reduce end diastolic volume, blood pressure, heart rate, contractility, and ejection time |
| what two drugs are used in combination for anginal therapy? what can replace them? | nitrates and beta blockers; nifedipine can act as a nitrates, and verapamil can act like beta blockers |
| which beta blockers are contraindicated in anginal therapy and why? | pindolol and acebutolol because they are partial agonists |
| what is the cause of normal S2 splitting? | inspiration causes decreased intrathoracic pressure (increases capacity of pulm circulation) which increases blood flow through the RV (delaying pulmonic valve closure) and aortic valve closes earlier because of decreased return of blood to left heart |
| what can cause wide splitting of S2? | anything that delays pulmonic valve closure: R BBB, pulmonic stenosis |
| what can cause fixed splitting of S2? what else does this defect cause? | ASD; diastolic rumble across tricuspid valve (diastolic murmur) and systolic flow murmur (increased flow across pulmonic valve) |
| what can cause paradoxical splitting? what happens on inspiration? | whatever delays aortic valve closing (L BBB, aortic stenosis); the split in S2 come closer together |
| what can cause Systolic ejection murmur other than aortic stenosis? where is it heard? | hypertrophic cardiomyopathy; left sternal border |
| where is the aortic area and what can be heard there? | Right 2-3 intercostal; systolic ejection murmur- caused by stenosis, increased flow, aortic valve sclerosis |
| where is aortic regurg heard? pulm regurg? | left/right sternal border; left/right sternal border |
| what systolic murmur is heard at right/left sternal border? diastolic? | hypertrophic cardiomyopathy; pulm or aortic regurg |
| where is the pulmonic area and what is heard there? | left 2-3 intercostal; systolic ejection murmurs: pulmonic stenosis, ASD (Flow murmur) |
| can you hear any diastolic murmurs at the aortic or pulmonic areas? | no |
| where is the tricuspid area and what can you hear there? | lower left parasternal border; diastolic murmur: tricuspid stenosis or ASD (flow murmur), systolic murmur: tricuspid regurg or VSD |
| where do you hear a VSD and when? what does it sound like? | left lower parasternal border (tricuspid area); holo systolic; harsh |
| where is the mitral area? and what can be heard there? | apex of the heart; systolic murmur: regurg; diastolic: stenosis |
| what is heard with mitral stenosis and where? | at apex hear diastolic murmur |
| what is heard with mitral prolapse and where? | at apex hear late systolic murmur (mcc of nonfunctional regurg- functional cause in LV dilation) and midsystolic click |
| what can cause pulmonic regurg? | dilation of pulmonic artery (d/t ASD from increased blood flow to right side of heart) |
| when are right heart sounds increased? left heart sounds? | with inspiration; with expiration (d/t increased blood flow through each respectively) |
| other than LV dilation and mitral prolapse, what else can cause mitral regurg? | ischemic heart disease (to papillae for ex) |
| what causes Tricuspid regurg? | RV dilation or endocarditis (both by Rheumatic fever) |
| what heart sounds are increased with increased TPR? what increases TPR? | left heart sounds (Mitral regurg and prolapse); squatting, hand grip |
| where does tricuspid regurg radiate to? mitral regurg? | right sternal border; axilla |
| what part of systole is mitral regurg? prolapse? | holosystolic; late systolic (heard best at S2) |
| what is the most frequent valvular lesion? what causes it? what does it predispose to? | mitral prolapse; myxomatous degeneration, rheumatic fever, chordae rupture; infective endocarditis |
| T/F mitral prolapse is a worrisome finding | false- usually benign |
| which diastolic blowing murmur can present with increased pulse pressure? what are the other symptoms? what can cause it? | aortic regurg; bounding pulses and head bobbing; aortic root dilation, bicuspid valve, rheumatic fever |
| what murmurs do vasodilators decrease the intensity of? | aortic regurg |
| Name the murmur: ejection click, midsystolic click, opening snaP? | aortic stenosis, mitral prolapse, mitral stenosis |
| what causes a machine like murmur? and when is it heard? what causes it? | PDA; all through out (loudest at S2); congenital rubella |
| or prematurity | |
| what can cause LA dilation? how does this present clinically? | mitral stenosis; dysphagia and voice hoarsness |
| what is the mcc of mitral stenosis? | prior rheumatic fever |
| other than aortic regurg, what else can bicuspid aortic valve lead to? why? | aortic stenosis because bicuspid valves are more prone to fibrotic thickening and thus quicker calcifications |
| what does age related calcifications on valves lead to? | aortic stenosis |
| what is pulsus parvus et tardus? in what state does it occur? what can it lead to? | weak pulses in comparison to heard sounds; aortic stenosis; syncope |
| what murmurs are accentuated presystolically and why? | mitral and tricuspid valve stenosis d/t atrial contraction |
| what murmur are eliminated with atrial fibrillation? | atrioventricular because lack of atrial contractility in late diastole |
| when does atrial contraction occur? | late diastole |
| at what point in the action potential does cardiac contraction occur? | at plateau |
| T/F contractility depends on muscle length | false- contractility/ionotropy is the ability to generate force at A GIVEN LENgth; dep on Ca!! |
| what is the PR interval normally? | <200 ms |
| what is the QRS complex length normally? | <120 ms |
| what slows the PR interval? | conduction through the AV node (so slowed Ca current) |
| what increases the QRS complex length? | L or R BBB |
| what interval measures the mechanical contraction? | QT (QRS is just ventricular depol) |
| what does a T wave inversion indicate? | recent MI |
| what can cause a U wave? | hypokalemia, bradycardia |
| what is the order in speed of conduction? how about in terms of pace of pacemakers? | purkinje > atria >ventricles> AV node; SA >AV >bundle of His/purkinje/ventricles |
| where can you find the AV node? | in the medial of the RA wall, next to the tricuspid valve, at the bottom of the interatrial septum |
| how long is the QT interval | around 400 ms |
| what does long QT interval predispose to? | ventricular tachycardia or Torsade pointes which can lead to V fib |
| what are the most likely causes of congenital long QT syndrome? what can they present with? | defect in cardiac sodium or potassium channels; sensorineural deafness |
| what are Jervell and Lange Nielsen syndromes? | congenital long QT syndromes |
| what is wolff parkinson white syndrome caused by? what do you see on ECG? what can it lead to? | accessory conduction pathway (bundle of Kent) bypassing AV node leading to early ventricular depol; delta wave on ECG; reentry current leading to SVT |
| what is the rhythm of atrial fib? what do you see on ECG? what can it predispose to? | irregularly irregular; no discrete P waves; atrial stasis and stroke |
| how do you treat a fib? | beta blocker or calcium channel blocker plus embolus prophylaxis (warfarin) |
| what do see on ECG with atrial flutter? how do you treat? | sawtooth appearance (identical back to back depol waves); attempt to convert back to sinus with IA, IC or III antiarrhythmics |
| what is first degree AV block defined by? how do you treat? | PR interval > 200 ms; asymptomatic, not necessary |
| what is 2nd degree AV block Mobitz type 1? how do you treat? | progressive lengthening of PR interval until beat dropped (P not followed by QRS); asymptomatic usually |
| what is 2nd degree AV block Mobitz type II? what does it predispose to? | dropped beats that are NOT preceded by change in length of PR interval; dangerous can lead to third degree AV nodal block |
| what is 3rd degree AV block? how is it treated? which is faster atrial or ventricular rate? | atria and ventricle beat completely independent of each other- both P and QRS complexes but have no relation to each other; pacemaker; atrial |
| what microbial infection can cause 3rd degree block? | Lyme disease |
| what is V fib? how do you treat? | completely erratic rhythm with no identifiable waves; fatal without CPR and defib |
| what is the atrial response to blood volume? | ANP and ADH (ADH important for hemorrhage) |
| how does ANP work? | generalize vascular relaxation and increases GFR (by afferent dilation and efferent constriction) |
| how does ANP promote diuresis? | by increasing GFR |
| what contributes to the "escape from aldosterone" mechanism? | ANP released from increased blood volume increases GFR (as well as generalized vasculature relaxation via cGMP) |
| how do beta and alpha receptors increase CO and TPR? | increases heart rate and contractility (both increase CO) ;venous constriction and arteriolar constriction (first increases CO and the other increases TPR) |
| how does RAAS increase CO and TPR? | aldo increases CO and angiotensin II increases TPR (vasoconstriction) |
| what stimulated the sympathetic response when there is decreased MAP? the RAAS system? | decreased stretch on carotid sinus causes activation via medullary vasomotor center; JGA senses decreased MAP AND- sympathetic activation from decreased carotid sinus stretch causes renin receptor activation (beta 1) |
| T/F Aortic arch receptors respond to increases and decreases in BP | false only increases |
| how does the aortic arch baroreceptor respond to increases in BP? | via vagus nerve to medulla |
| how does the carotid sinus baroreceptor respond to increases and decreaes in BP? | via glossopharyngeal nerve to solitary nucleus of medulla |
| what does decreased stretch on carotid sinus cause? increased stretch? | decreased afferent firing which leads to increased efferent sympathetic firing; increased afferent firing which leads to decreased efferent sympathetic firing |
| in what situations should you try a carotid massage? why does it help? | arrhthmymials (particulary atria), decreases HR |
| where are peripheral chemoreceptors located? central? | carotic and aortic bodies; brain interstital luid |
| which chemoreceptors respond more to changes in PO2? pCO2? | peripheral; central |
| which organ gets the largest share of CO? which gets the highest blood flow per gram of tissue? ` | liver; kidney |
| where is the largest arteriovenous O2 difference? how do you meet increases in O2 demand here then? | heart- 100% always extracted!; by increasing blood flow |
| what anti arrhythmics can induce torsade de pointe? | quinidine and sotalol (class IA, K+ channel blocker) |
| what is magnesium helpful in treating? | seizures in ecclampsia; effective in torsade de pointes and digoxin toxicity |
| what is used for digoxin toxicity other than Fab - Dig? | Mg, Lidokaine, stabilization of potassium |
| what is autoregulation? | how blood flow to an organ remains constant over a wide range of perfusion pressures |
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juniebug26
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