Flashcards in CV Physiology Deck (32):
What does CO equal (equation)? What is the Fick principle (equation)? What is MAP? What is MAP (equation)? What happens to CO during exercise? What happens to diastole timing with incr. HR?
CO=rate of O2 consumption/ (arterial O2 content-venous O2 content)
MAP=COxTPR=2/3 diastolic pressure + 1/3 systolic
Early in exercise: HR and SV incr., but SV reaches a limit and only HR can increase
With incr. HR, diastole shortens, eventually leading to decr. CO
What is SV (equation)? What causes it to increase? When is it decreased?
Incr. with incr. contractility, incr. preload, decr. afterload
A failing heart has decr. SV (diastolic or systolic dysfunction)
What things incr. contractility? Decr.
Catecholamines: incr. activity of Ca pump in SR
Incr. IC Calcium
Decr. EC Na (Na/Ca pump)
Digitalis: blocks Na/K pump leading to less EC Na
beta 1 blockade (decr. camp)
HF with systolic dysfunction
Non-dihydropyridine Ca channel blockers
What things incr. myocardial oxygen demand? According to laplaces law, what things incrase wall tension/decrease it?
Incr. heart rate
Incr. diameter (incr. wall tension)
wall tension is incr. by pressure and radius and decr. by wall thickness
How is preload approximated? What does it depend on? What medications decrease it? How is afterload approximated? How does the LV compensate for incr. afterload? Why? What decr. afterload? What decr. afterload and preload?
Venous tone and circ. blood volume
Venodilators decr. preload
approx. by MAP
Incr. in afterload leads to incr. in pressure leads to incr. wall tension. To compensate for this incr. wall tension, the LV incr. wall thickness (hypertension to cardiac hypertrophy)
Vasodilators (hydralazine) decr. afterload
ACEI and ARBs decr. both preload and afterload
What is the ejection fraction (equation)? What does it tell you? What is a normal value? What are the values in diastolic and systolic HF?
Index of ventric. contract=55%=decr. in syst., normal in diastolic
What is the idea behind a starling curve? What increases a starling curve? Decreases?
Force of contraction proportion to end diastolic length of muscle fibers (preload)
Incr. with catecholamines, positive inotropes
Decr. with loss of myocardium, beta blockers, ca channel blockers, dilated cardiomyopathy
How are resistance pressure and flow related? What is Q related to (equation)? What incr./decr. resistance? How is the total resistance of a vessel in series calculated? In parallel? What does viscosity depend on? What else can increase it? Decrease it? What vessels account for most of TPR? What vessels store the most? What does organ removal result in? Which vessels ahve the highest total cross sectional area and lowest flow velocity?
delta P = Q x R
Q=flow velocity (v) x cross sectional area (A)
Capillaries have highest A and lowest v
viscosity and length incr. resistance while incr. radius decreases it.
TR=R1+R2 etc. (series)
1/TR=1/R1 +1/R2 (parallel)
Viscoisty depends on hematocrit
Can be increased in mult. myeloma, etc.
Decr. in anemia.
Explain the cardiac portion of a cardiac and vascular function curve. What increases/decreases it? What are the the increases/decreases like? Dependent/indep. variables? Same questions for a vascular function curve. What does the intersection of curves mean when they're combined? What changes occur in exercise? In HF?
It has an upward slant then plateaus.
Y axis is cardiac output (dependent)
X axis is RA pressure or EDV (independent)
When RA pressure is held constant, an incr. in HR, contractility, or a decr. in afterload will incr. the slope and move the end CO value up. The opposites will decrease it.
It starts plateaued then curves down.
The point where it meets the x axis is the mean systemic pressure.
Y axis is venous return (indep); same x axis (depen)
When blood volume or venous tone increases, the curve shifts to the right, but the slope does not change, which changes the mean systemic pressure.
When SVR decreases, the slope becomes more negative (less flat).
Intersection of curves=operating point of heart (venous return and CO are equal).
In exercise, incr. inotropy and decr. SVR maximize CO (both curves move up so operating point is at a high CO)
In HF, inotropy incr. so fluid is retained which results in incr. preload. The CO point moves down but the venous return curve moves up so the operating point isn't quite so low.
What are the phases of a pressure volume loop? How does incr. preload affect it? Incr. Afterload? Incr. contractility?
Isovolumetric contraction-mitral valve closing to aortic valve opening
Systolic ejection-aortic valve opening and closing
Isovolumetric relaxation-aortic valve closes and mitral valve opens
Rapid filling-soon after MV opens
Reduced filling-just before mitral valve closes.
Incr. preload-incrases stroke volume (EDV), moves right side of curve to right
Incr. afterload-raises the maximum up (incr. aortic pressure), moves ESV to the right (decr. SV)
Incr. contractility-moves ESV to the left (incr. EF and incr. SV)
What signifies S1? Where is it best heard? S2? S3? What is it associated with? When is it normal? S4? What is it associated with? Best heard?
S1-mitral and tricusp closure-At mitral area
S2-aortic and pulmonary valve closure-LUSB
S3-In early diastole, high pressure atrial state (mitral regurg, HF, dilated ventricles, rapid ventricular filling.
Normal in pregnant women and children
S4-In late diastole (atrial kick). Best heard at apex in LLD. High atrial pressure. Ventricular hypertrophy.
Explain the 5 waves of the jugular venous pulse.
a wave-atrial contraction. Absent in a-fib
c wave-RV contraction (tricuspid bulging into atrium)
x descent-atrial relaxation and downward displacement of closed tricup. during ventricular contraction. Absent in tricuspid regurg.
v wave-incr. right atrial pressure due to filling against closed tricusp. valve
y descent-RA emptying into RV.
Waht causes normal splitting? What is it like? What causes wide splitting? What is it like? Fixed splitting? Paradoxical splitting?
Inspiration-drop in intrathoracic pressure leads to incr. venous return leading to delayed closure of pulmonic valve.
It also leads to inccr. pulm. capacity of pulm. circ. which has the same effect.
Therefore, during inspiration, the pulmonic closure is later than the aortic closure leading to a split. During expiration, they occur at the same time.
Seen in conditions that delay RV emptying (pulm. stenosis and RBBB) leading to a delayed sound during insp. and exp. but still more delayed during insp.
Seen in ASD. Left to right shut leads to incr. RA and RV volumes leading to incr. flow through pulmonic vlave so that there is a great and equal delay of the pulmonic closure leading to a split that is the same in both insp. and exp.
Delayed aortic valve closure (aortic stenosis, LBBB). Aortic valve closes much later. Therefore, during insp., when the pulmonic valve is delayed, there is no splitting, but during expiration, there is a split due to the delayed aortic closure.
What murmurs are best heard in the aortic area? Are they systolic, pancystolic, diastolic, or systolic ejection murmurs? LMSB? Pulmonic area? Left infraclavicular region? Tricuspid area? Mitral area?
Systolic: aortic stenosis, flow murmur, aortic valve sclerosis
LEFT MIDDLE STERNAL BORDER
diastolic: aortic regurgitation, pulmonic regurg
systolic: hypertrophic cardiomyop.
Continuous murmur: PDA
Systolic ejection murmur: pulmonic stenosis, flow murmur (physiologic or due to ASD)
Pansystolic: tricuspid regurg, VSD
Diastolic murmur: tricuspid stenosis, ASD
systolic: mitral regurg
diastolic: mitral stenosis
What effect do inspiration, hand grip, valsalva, standing up, and rapid squatting have on heart sounds and why?
Incr. venous return to right atrium
Incr. intensity of right heart sounds
Incr. intensity of MR, AR, VSD murmurs
VALSALVA, STANDING UP
Decr. intensity of most murmurs (including AS)
Incr. intensity of hypertrophic cardiomyopathy murmur
MVP: earlier onset of click/murmur
Incr. venous return and incr. preload
Decr. intensity of hypertrophic cardiomyopathy murmur
incr. intensity of AS
MVP: later onset of click/murmur
Describe the aortic stenosis heart sound? Where is it best heard? Where does it radiate? How does it effect pulses? What symptoms does it lead to? What are some causes? Decribe MR/TR. Where is MR loudest/radiate to? Causes? Where is tricusp/radiate to? Causes? Same questions for MVP. Same questions for VSD? Same questions for AR. Same questions for MS
Crescendo decrescendo systolic ejection murmur.
Loudest at heart base; radiates to carotids
Pulses are weak with a delayed peak
Syncope, Angina, and dyspnea
Age related calcification or early onset calcification due to biscupid aortic valve
Holosystolic, high pitched blowing murmur
Mitral: apex and radiates to axilla. Due to IHD (post MI), MVP, LV dilatation, RF
Tricuspid: loudest at tricuspid area and to RSB, RV dilatation, RF
late systolic crescendo murmur with midsystolic click (due to sudden tensing of chordae tendinae). Bst over apex. Loudest just before S2. usually benign but can lead to infective endocarditis. Myxomatous degeneration (Marfan, Ehler Danlos), RF, chordae rupture
Holosystolic, harsh sounding murmur. Tricuspid area
High pitched blowing early diastolic decrescendo murmur. Long diastolic murmur and signs of hyperdynamic pulse when severe. Aortic root dilatation, biscuspid aortic valve, endocarditis, RF.
Follows opening snap. Delayed rumbling late diastolic murmur (decr. interval between S2 and OS correlates with incr. severity). LA>>>LV during diastole. RF. Can lead to LA dilatation
Continuous machine like murmur. Loudest at S2. Congenital rubella or prematurity. left infraclavicular area.
What are the parts of a myocardial action potential? How do they differe from skeletal muscle?
phase 0=rapid uprstroke and depolarization-voltage gates na channels open
phase 1=initial repolarization-na+ channels inactivate. K channels begin to open
phase 2=plateau-Ca channels open balancing out k efflux. Ca entering leads to contraction
phase 3=rapid repolarization=massive k efflux due to opening of voltage gated slow k channels and closure of ca channels
phase 4=resting potential=high K perm. through k channels
Has no plateau
cardiac nodal cells spontaneously depolarize (funny current channels)
Cardiac myocytes are electrically coupled to each other by gap junctions
What are the phases of the pacemaker action potential? Where do they occur? How do ACh and adenosine affect HR and how? What about catecholamines? What about symp stimulation?
SA AND AV NODES.
phase 0=upstroke-opening of Ca channels. Fast Na channels are permanently inactivated. Slow conduction velocity which prolongs transmission from atria to ventricles
phase 1 and 2=absent
phase 3=inactivation of ca channels and act. of k channels (repolarization)
phase 4=slow spontaneous depolarization as Na conductance incr. (If (funny current)). Leads to automaticity of SA and AV nodes. The slope or phase 4 determines heart rate.
ACH/ADENOSINE: Decr. rate of diastolic depolarization and decr. HR
CATECHOL: Incr. depolarizaiton and HR
SYMPATHETIC: Incr. the chance that If channels are open and thus incr. HR
What is the order of pacemakers and their rate? What is the conduction pathway? What is the pacemaker? Where is the AV node located?
SA>AV>bundle of His/Purkinje/ventricle
Sa node to atria to AV node to common bundle to bundle branches to fascicles to purkinje fibers to ventricles
AV node-posteroinferior part of interatrial septum
What is the p wave on ECG? PR interval (normal)? QRS complex (normal)? QT interval ? T wave? What might t wave inversion mean? J point? ST segment? U wave causes?
P wave-atrial depolarization
PR interval-time from start of atrial depol to ventricular depol (<120msec)
QT interval-ventricular depol, contraction, repol
T wave-ventricul repol. (inversion could mean recent MI)
J point-junction between QRS complex and ST segment
ST segment-isoelectric, venttricles depol.
U wave-hypokalemia, bradycardia
What is torsades de pointes? What can it progress to? What predisposes to it? Causes? Treatment?
polymorphic vent. tachy characterized by shifting sinusoidal waveforms on ECG.
What is congenital long QT syndrome? What does it incr. risk for? What are two genetic sydromes/symptoms? What are five drugs that induce long QT?
Inherited disorder of myocardial repol (ion channel defects)
Incr. risk of torsades de pointes and sudden cardiac death
Drugs, Decr. K+, decr. Mg+
Romano Ward: Only heart
Jervell and lange-neielsen syndrome: long QT and sensorineural deafness
Drug induced (ABCDE)
Anti "C"ychotics (Haldol)
What is brugada syndrome? epidem? ECG pattern? Increased risk of what? How is it treated?
ECG: pseudo RBBB and ST elevations in V1-V3.
Incr. risk of ventr. tachyarrhythmias and SCD
Prevent SCD with inmplantable cardioverter-defibrillator (ICD)
What is wolff-parkinson-white syndrome? pathophys? ECG findings? What might it result in?
Abnormal fast accessory conduction pathway that bypasses AV node leading to early partial ventricular depol leading to delta wave, widened QRS complex and short PR interval.
May result in reentry circuit leading to supraventricular tachycardia
What is the pattern of A-fib? What are its associations? What can it lead to? Treatment?
irregularly irregular. No discrete P waves. Irregularly spaced QRS waves.
Hypertension, CAD, Rheum heart disease, binge drinking, HF, valvular disease, hyperthyroidism
Atrial stasis-->cardioembolic events
rate control (beta blocker, Ca channel blocker, digoxin)
rhythm control (IC or III antiarrhythmics)
cardiversion (pharm or electric)
What is the pattern of atrial flutter? How is it managed? Definitive treatment?
Rapid succession of identical back to back atrial depol waves (Saw tooth appearance)
Management similar to a-fib
Waht is the pattern of v-fib? Prognosis/treatment?
completely erratic rhythm with no identifiable waves
Fatal w/o immediate CPR and defib
What is 1st degree AV block like? symptoms/risks? Treatment? 2nd degree mobitz type 1 (weckebach)? 2nd degree mobitz type II? 3rd degree?
PR interval is prolonged to >200 msec. Benign and asymp. No treatment?
WENCKEBACH/MOBITZ TYPE I
Progessive lengthening of PR interval until a beat is dropped. Usually asymp. Variable RR interval with a pattern (regularly irregular)
MOBITZ TYPE II
Dropped beats that are not preceded by a change in length of PR interval. May progress to 3rd degree block. Pacemaker
Atria and ventricles beat independently of each other. Both present, but no relation. Atrial rate faster.
What releases ANP? Why? Mechanism of action? What are its reults? Same qustions for BNP? What is it used to diagnose? Treat?
high blood volume and incr. atrial pressure
vasodilation and decr. na reabssorption at the Renal collecting tubule
Dilates afferent renal arterioles and constricts efferent arterioles leading to diuresis and aldosterone escape
similar action to ANP but with longer half life
Used to diagnose and treat HF.
What are the two baroreceptors? Location? To where do they transmit and through what nerve? What do they respond to? How would they response to hypotension? Carotid massage? What is the cushing reaction?
Aortic arch via vagus nerve to solitary nucleus of medulla (respond to change in BP)
Carotic Sinus (CNIX) to solitary nucleus of medulla (change in BP)
Hypotension: decr. baroreceptor firing leading to incr. symp. and decr. parasymp. leading to vasoconstriction and incr HR, contract. and BP (severe hemorrhage)
Carotid massage: incr. pressure on carotid sinus leading to decr. symp, incr. parasymp and decrease HR
hypertension, bradycardia, and respiratory depression due to incr. intracranial pressure
What are the peripheral chemoreceptors? What are they stimulated by? What are the central chemoreceptors stimulated by?
carotid and aortic bodies (decr. PO2, incr. PCO2, and decr. pH)
Changes in pH and PCO2 (of brain interstitial fluid which is influenced by arterial CO2) but no PO2.