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110 Cards in this Set
- Front
- Back
What is contained in the carotid sheath?
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VAN
internal jugular vein (lateral) common carotid artery (medial) vagus nerve (posterior) |
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What are the 2 coronary arteries?
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right coronary artery (RCA) - acute marginal artery (supplies RV) and often posterior descending artery (supplies posterior septum)
left main coronary artery - gives off left anterior descending (supplies apex and AV septum) - also left circumflex artery - supplies posterior left ventricle |
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What are the AV and SA nodes commonly supplied by?
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RCA
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right dominant heart vs. left dominant heart
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80% people are right dominant - the RCA supplies the PDA
20% of people are left dominant - the LCX supplies the PDA |
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What is the most common location for a coronary artery occlusion?
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LAD - which supplies the anterior intraventricular septum - called the widow maker
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When do coronary arteries fill during?
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diastole
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What can enlargement of the most posterior part of the heart cause?
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left atrium is the most posterior part of the heart - if it enlarges it can cause dysphagia (from compression of esophageal nerve), horseless (compression of recurrent laryngeal -
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What happens to CO during exercise?
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initially increases because of increased SV. After prolonged exercise CO increases because of increased HR
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What happens if the HR gets too fast?
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person will have decreased CO - because of decreased filling during diastole (ex. ventricular tachycardia)
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CO =
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SV x HR
SV = EDV - ESV Fick's Principle CO = rate of O2 consumption/(arterial O2 content - venous O2 content) |
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mean arterial pressure =
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2/3 diastolic pressure + 1/3 systolic pressure
MAP = CO x total peripheral resistance (TPR) |
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Pulse pressure =
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systolic pressure - diastolic pressure
pulse pressure is proportional to the stroke volume |
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What affects stroke volume?
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contractility, afterload, preload
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What increases contractility?
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- catecholamines (increased activity of Ca2+ pump in sarcoplasmic reticulum)
- increased intracellular calcium - decreased exracellular sodium (decreased activity of Na+/Ca2+ exchanger) - digitalis (increased intracellular sodium, resulting in increased Ca2+) |
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What decreases contractility?
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- B1 blockade
- heart failure - acidosis - hypoxia/hypercapnea - non-dihydropyridine Ca2+ channel blockers |
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What increases stroke volume?
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pregnancy, anxiety, exercise
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What is the SV in a failing heart?
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decreased
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Myocardial O2 demand is increased by what?
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increase in afterload, increase in contractility, increased heart rate, increased heart size (increased wall tension)
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preload is what?
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end diastolic volume
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afterload is what?
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mean arterial pressure = 2/3 diastolic pressure + 1/3 systolic pressure
mean arterial pressure = CO x TPR (total peripheral resistance) |
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what do venodilators do?
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decrease preload - decrease return to the heart
ex. nitroglycerin |
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What do vasodilators do?
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decrease afterload (arterial)
ex. hydralazine |
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What increases preload?
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exercise (slightly), increased blood volume (overtransfusion), and excitement (sympathetics).
Preload pumps up the heart |
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The force of contraction is related to what?
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the initial length of cardiac muscle fiber (preload)
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What increases and decreases the contractile state of the myocardium?
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increases: sympathetic stimulation, catecholamines, digitalis
decreases: pharmacologic depressants, loss of myocardium (MI) |
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EF = what?
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EF = SV/EDV
EF = (EDV-ESV)/EDV it is a measurement of the ventricular contractility normal EF > 55% |
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Normal EF is what?
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> 55%
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change in pressure = what?
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change in pressure = Q x R
(similar to V = IR) |
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What does resistance =?
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R = 8nl/(pi r^4)
n = viscosity l = length r = radius as the radius decreases the resistance increases a lot! |
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What is an example of resistance in parallel?
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Systemic circulation with the aorta
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What is an example of resistance in series?
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blood flow within individual organs
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What is viscosity most dependent on?
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hematocrit
viscosity increases with: - polycythemia - hyperproteinemic states (multiple myeloma) - herediary spherocytosis |
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What does a pressure gradient do?
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drives flow from high pressure to low pressure
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How does resistance, length, viscosity, and radius all affect each other?
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resistance is proportional to viscosity and length and inversely proportional to the radius
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What accounts for the most resistance in the blood?
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arterioles - regulate capillary flow
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What is the operating point of the heart?
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Where venous return and CO are equal
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What are the 4 phases of the left ventricle?
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MV closes - isovolumetric contraction (period of highest O2 consumption) - AV opens - systolic ejection - AV closes - isovolumetric relaxation - MV opens - rapid filling (period right after mitral valve opens) - reduced filling (period just before mitral valve closure)
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S1
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Mitral and Tricuspid valve closure
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S2
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Aortic and pulmonary valve closure
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S3
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rapid filling - after S2- in early diastole during rapid ventricular filling phase. Associated with increased filling pressures and more common in dilated ventricles (normal in children and pregnant women)
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S4
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usually pathologic
stiff left ventricle - so left atrium must kick to get more blood into the left ventricle - happens late diastole *Associated with ventricular hypertrophy |
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What are the waves in the JVP?
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upstrokes: a,c,v
downstrokes: xy in order: a - atrial contraction increase in pressure *MV closes c- RV contraction (tricuspid valve bulges into the atria causing increased pressure) x - relaxation of the right atria v - filling of the right atria from the veins y - opening of TV - blood flows form RA to RV - decreased pressure in RA |
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What is S2 splitting? What is normal splitting?
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The the aortic valve closes before the pulmonary valve
normal splitting: When you breath in decrease in intrathoracic pressure - more blood returns to the heart so pulmonary valve closes even later (to accommodate for the increase in blood volume) - the aortic valve closes earlier because less blood to the left side of the heart (held up in the lungs) |
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What is wide splitting? What do you see it in?
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pulmonic sound is always very delayed
see in conditions that delay RV emptying (pulmonic stenosis, or right bundle branch block) - have exaggerated splitting regardless of breath |
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Fixed splitting
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seen in ASD
shunt present that causes blood to flow from the left side of the heart through the right - so increased flow through the pulmonary valve regardless of the breath, pulmonary closure is greatly delayed |
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Paradoxical splitting
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seen in conditions that delay LV emptying (aortic stenosis, left bundle branch block). The valve sounds are reversed - P2 closes before A2 - when inspire - loose splitting (P2 takes longer)
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What are the listening posts of the heart?
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'Are People That Mean'
Aortic (right 2nd intercostal space): systolic murmur: aortic stenosis, flow murmur, aortic valve sclerosis Pulmonary (left 2nd intercostal space) systolic murmur: pulmonic stenosis, flow murmur (ASD) Ticuspid (left 4th intercostal space): pansystolic murmur: TR, VSD diastolic murmur: TS, ASD Mitral (left 5th intercostal space): systolic murmur: MR diastolic murmur: MS |
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murmur in ASD
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commonly a pulmonary flow murmur (from increased flow through the pulmonary valve) and a diastolic rumble (increased flow across tricuspid); blood flow across the actual ASD does not cause a murmur because no pressure gradient. Murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilation of pulmonary artery
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holosystolic blowing murmur
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MR or TR
mitral: loudest at the apex and radiates to the axilla. enhanced by maneuvers that increase TPR (squatting, hand grip) or LA return (expiration). MR is often due to ischemic heart disease, mitral valve prolapse or LV dilation. tricuspid: loudest at tricuspid area and radiates to right sternal border. enhanced by maneuvers that increase RA return - inspiration. TR is due to RV diltaion or endocarditis. Both MR and TR can be due to rhematic fever |
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What increases MR?
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things that increase TPR - squatting or hand grip
things that increase flow to LA - expiration |
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What increases TR?
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inspiration (increases RA return)
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Crecendo-decrescendo murmur
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AS - systolic ejection murmur following ejection click (EC: due to abrupt halting of valve leaflets). LV > aortic pressure during systole. Radiates to carotids/apex.
Pulsus parvus and tarvus can lead to syncope. Often due to age-related calcific aortic stenosis or bicuspid aortic valve |
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Where does AS radiate?
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to the carotids
can see pulsus tardus and parvus |
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holosystolic, harsh murmur
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VSD - it is the loudest at the tricuspid area
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Mitral prolapse
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late systolic cresendo murmur with midsystolic click (MC; due to sudden tension of chordae tendineae). Most frequent valvular lesion. Loudest at S2. usually benign. Can predispose to infective endocarditis. Can be caused by myxomatous degeneration, rhematic fever, or chordae rupture. Enhanced by maneuvers that increase TPR (squatting or hand grip)
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Aortic regurgitation
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immediate high-pitched blowing diastolic murmur. Wide pulse pressure when chronic; can present with bounding pulses and head bobbing. Often due to aortic root dilation, bicuspid aortic valve, or rheumatic fever
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Mitral stenosis
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following opening snap (OS; due to tensing of chordae tendineae). delayed rumbling late diastolic murmur. LA>LV pressure during diastole. Often occurs secondary to rhematic fever. Chronic MS can result in LA dilation. Enhanced by maneuvers taht increase LA return (expiration)
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machine like murmur
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PDA. Loudest at S2
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What is cardiac muscle contraction dependent on?
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extracellular Ca2+ - it enters the cells during plateau of action potential and stimulates calcium release from the cardiac muscle sarcoplasmic reticulum (calcium induced calcium release)
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Cardiac muscle vs. skeletal muscle
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cardiac muscle action potential has a plateau, which is due to Ca2+ influx
- cardiac nodal cells spontaneously depolarize, resulting in automaticity due to If channels - cardiac myocytes are electrically coupled to each other by gap junctions |
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Ventricular action potential
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phase 0: rapid upstroke - Na+ rushes into the cell to depolarize it
phase 1: initial repolarization - inactivation of Na+ channels and opening of K+ channels (K+ goes outside of the cell) Phase 2: plateau - Ca+ channels open and Ca2+ goes into the cell - balances K+ going out of cell - Ca2+ triggers calcium release from sarcoplasmic reticulum and myocyte contraction Phase 3: rapid repolarization - massive K+ efflux due to opening of slow K+ channels and closure of Ca2+ channels Phase 4: resting potential = high K+ permeatiblity through K+ channesl |
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when does myocyte contraction occur?
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during plateau phase - when Ca2+ rushes into the cell (causes more Ca2+ release from sarcoplasmic reticulum)
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pacemaker action potential
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occurs in the SA and AV nodes
Phase 0: upstroke - depolarization via opening of Ca2+ channels - Ca2+ goes inside cells (no fast Na+ channels) - results in a slow conduction velocity to prolong transmission from the atria to the ventricles phase 2: absent phase 3: Ka+ channels open - K+ goes outside the cell (repolarization) - Ca2+ channels close phase 4: slow diastolic depolarization - membrane potential spontaneously depolarizes as Na+ conductance increases (If different from the INa in the myocyte). Accounts for autoaticity of SA and AV nodes. |
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What does the slope of phase 4 determine?
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phase 4 is when If (Na+) channels are open - the slope determines the heart rate. Ach decreases the rate of diastolic depolarization and decreases the heart rate. catecholamines increase the depolarization and increase the heart rate. Sympathetic stimulation increases the change that If channels are open
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What is the speed of conduction difference between the AV, SA node, bundle of His?
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purkinje>atria>ventricles>AV node
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What does the P wave represent?
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Atrial depolarization
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What does the PR interval represent?
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delayed conduction through AV node because of Ca2+ channels (should be less than 200 ms)
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What does the QRS complex represent?
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ventricle depolarization - should be less than 120 ms
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What does the QT interval represent?
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mechanical contraction of the ventricles
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What does the T wave represent?
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Ventricular repolarization - can be inverted after a MI
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What represents atrial repolarization?
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nothing - it is masked by ventricular depolarization
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ST segment
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isoelectric, ventricles depolarized
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What does the U wave represent?
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hypokalemia, bradycardia ( it is depressed segment after the T wave)
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What does the delay of firing between the SA and AV node allow for?
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filling of the ventricles
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Torsades de pointes
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ventricular tachycardia is shifting sinusoidal waveforms on ECG. Can progress to V-fib. Anything that prolongs the QT interval can predispose to torsades de pointes
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Congenital long QT syndromes
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usually due to defects in Na+ or K+ channels - can present with severe congenital sensorineural deafness (Jervell and Lange Nielsen syndrome)
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Wolff-Parkinson-White syndrome
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ventricular preexcitation syndrome. Accessory conduction pathway from atria to ventricle (bundle of kent), bypassing AV node. As a result, ventricles begin to partially depolarize earlier, giving rise to delta wave. may result in reentry current leading to supraventricular tachycardia
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delta wave
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increase in voltage right before QRS segment - classic for wolff-parkinson-white syndrome
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irregularly irregular ECG
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Atrial fibrillation - chaotic and erratic baseline with no discrete P waves in between irregularly spaced QRS complexes. Can result in atrial stasis and lead to stroke
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treatment for A-fib?
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B-blocker, Ca2+ channel blocker; prophylaxis against thromboembolism with warfarin (Coumadin)
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Holiday heart syndrome - risk of it?
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A-fib - risk of thromboembolism - from static blood in atria - risk of clots
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sawtooth pattern
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Atrial flutter - rapid succession of identical, back to back atrial depolarization waves. Try to convert back into sinus rhythm. Use class IA, IC, or III antiarrhythmics.
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treatment for Atrial flutter?
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IA, IC, or III antiarrhythmics
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AV block 1st degree
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PR interval is increased (greater than 200 ms). Asymptomatic
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AV block - 2nd degree - Mobitz type I (Wenckebach)
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Progressive lengthening of PR interval until a beat is dropped (a P wave not followed by QRS). Usually asymptomatic
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AV block 2nd degree - Mobitz type II
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Dropped beats that are not preceded by a change in length of PR interval. The abrupt, nonconducted P waves result in a pathologic condition. Often found as a 2:1 block, 2 P waves to 1 QRS complex. May progress to 3rd degree block
*normal PR intervals |
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AV block 3rd degree
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atria and ventricles beat independently of each other, but both P and QRS are present. P waves bear NO relation to QRS complexes. Atrial rate is faster than the ventricular rate
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What can cause a 3rd degree AV block? What is the treatment?
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Lymes disease can cause it
treat with a pacemaker |
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Ventricular fibrillation
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completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation.
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What maintains the mean arterial pressure?
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decrease in MAP causes:
1) medullary vasomotor center senses decreased baroreceptor firing - increases sympathetic activity (B1: increases heart rate and contractility - increased CO, a1: venoconstriction, increased venous return - increased CO, also a1 causes arterial vasoconstriction - increased MAP 2) JGA senses decreased MAP (effective circulating volume) - increased renin release - RAAS system - (AT II - vasoconstriction - increased TPR, aldosterone increased blood volume - increased CO) |
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What is released in a response to increased blood volume and atrial pressure?
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ANP from the atria - causes generalized vascular relaxation. Constricts efferent renal arterioles, dilates afferent arterioles. Involved in escape from aldosterone mechaism
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Where are baroreceptors located? What do they respond to?
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In the carotid sinus (respond to increases and decreases in BP via glossopharyngeal nerve to solitary nucleus of medulla) and aortic arch (respond only to increases in BP - via vagus nerve to medulla)
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What happens to baroreceptors during hypotension?
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decreased BP - decrease stretch on baroreceptors - decreased firing - causes increased sympathetic firing and decreased parasympathetic firing - vasoconstriction, increased in HR, contracitility and blood pressure - important response to hemorrhage
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What happens to baroreceptors during carotid massage?
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increased stretch - increased firing of receptors - decreased HR (trick the medulla to think that there is increased BP)
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What are the 2 types of chemoreceptors?
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1) peripheral - carotid and aortic bodies respond to decreased PO2 (<60 mm Hg), increased PCO2, and decreased pH of the blood
2) central - respond to changes in pH and PCO2 of brain interstitial fluid. Do not directly respond to PO2. Responsible for cushing reaction - increased intracranial pressure constricts arterioles - cerebral ischemia - hypertension (sympathetic response) - reflex bradycardia. *cushing's triad: hypertension, bradycardia, respiratory depression 2) central |
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cushing's reaction
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increased intracranial pressure constricts arterioles - cerebral ischemia - hypertension (sympathetic response) - reflex bradychardia
*cushing's triad: hypertension, bradycardia, respiratory depression |
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What gets the largest share of systemic cardiac output?
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liver
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What gets the highest blood flow per gram of tissue?
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kidney
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Where is O2 extraction 100%?
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in the heart - increased O2 demand is met by increased coronary blood flow, not by increased extraction of O2
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What are the normal pressures in the heart?
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RA <5
RV <25/<5 PA <25/10 PCWP (LA pressure) <12 LV <130/10 Aorta <130/90 |
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What is PCWP?
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pulmonary capillary wedge pressure - an approximation of LA pressure
measured with Swan-Ganz catheter |
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What is autoregulation?
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how blood flow to an organ remains constant over a wide range of perfusion pressures
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What does the heart do to autoregulate?
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local metabolites - O2, adenosine, NO
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What does the brain do to autoregulate?
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local metabolites - CO2 (pH)
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What does the kidneys do to autoregulate?
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myogenic and tubuloglomerular feedback
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What does the lungs do to auto-regulate?
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hypoxia causes vasoconstriction - so blood does not go to areas of the lung that don't have oxygen
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How does skeletal muscle autoregulate?
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local metabolites - lactate, adenosine, K+
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How does skin autoregulate?
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sympathetic stimulation most important mechaism - temperature control
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What is the starling equation?
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Pnet = Kf (Pc-Pi) - (pic - pii)
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What causes edema?
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edema - excess fluid outflow into interstitum commonly caused by:
- increased Pc (heart failure) - decreased plasma proteins (decreased pi c; nephrotic syndrome, liver failure) - increased capillary permeability (increased Kf; toxins, infection, burns) - increased interstitial osmotic pressure (increased pi i; lymphatic blockage) |