Week 4 - Cardiac Physiology Flashcards

Question

Semilunar Valve Open ## Footnote Semilunar Valve Function

Answer 1

-as ventricles contract, intraventricular pressure rises -blood is pushed up against semilunar valves and forces them open

Answer 2

-as ventricles relax, intraventricular pressure falls -blood flows back from arteries filling cusps of semilunar valves and forcing them to close

Answer 3

-stimulated by nerves and self-excitable (automaticity) -contracts as a unit -long (250 ms) absolute refractory period

Answer 4

**initiate action potentials** -unstable resting potentials (pacemaker cells) -Ca2+ influx for rising phase of A.P. (depolarization) coming from ECF + ICF

Answer 5

heart block

Answer 6

arrythmia if not in sync

Answer 7

bottom -> up

Answer 8

top -> bottom

Answer 9

-impulse starts at **SA node + action potential spreads throughout R + L atria** -simultaneously, impulse goes to **excite AV node via internodal pathway** -impulse passes from **atria to ventricles through AV node** (separated by fibrous ring) -**A.P. briefly delayed at AV node** (0.1 sec) to ensure atrial contraction precedes centricular contraction to allow complete ventricular filling -impulse travels rapidly **down interventricular septum by Bundle of HIS** -impulse rapidly disperses **throughout myocardium by Purkinje Fibers** -rest of ventricular cells activated by gap junctions

Answer 10

slow Ca2+ channels (L type) | Na+ channels are inactivated due to depolarization state

Answer 11

ensure atrial contraction precedes ventricular contraction to allow for complete ventricular filling | 0.1 sec delay

Answer 12

**ensures adequate ejection time (ensures ventricular filling)** -plateau due to activation of slow-L type Ca2+ channels

Answer 13

**Phase 0**: fast Na+ channels **Phase 1**: Na+ channels inactivated, Cl- in, K+ out **Phase 2**: slow Ca2+ channels in, K+ out (so repolarization is not as fast) **Phase 3**: Ca2+ channels close, big K+ efflux (out) **Phase 4**: Na+/K+ pump (resting state)

Answer 14

**20% from ECF triggers larger release of Ca2+ from ICF (80%)** -leads to cross bridge cycling / contraction

Answer 15

1. A.P. in cardiac contractile cell 2. travels down T-tubules 3. entry of small amount of Ca2+ from ECF and release of large amount of Ca2+ from ICF 4. increase in cytosolic Ca2+ 5. troponin-tropomyosin complex in thin filaments pulled aside 6. cross-bridge cycling between thick and thin filaments 7. thin filaments slide inward between thick filaments 8. contraction

Answer 16

**ensures alternate periods of contraction and relaxation which are essential for pumping blood** -do not want another A.P. to happen quickly/prevent adequate time to fill/contract -delay filling w/ blood before contraction begins | **summation of A.P. and tetanus is impossible**

Answer 17

**SA node -> AV node** (atria to atria) **AV node -> bundle branches** (atria to ventricular septum) **Bundle Branches to Purkinje Fibers** (ventricular septum to apex + ventricular walls)

Answer 18

SA node generates impulse and atrial excitation begins

Answer 19

impulse delayed at AV node

Answer 20

impulse passes to heart apex and ventricular excitation begins

Answer 21

ventricular excitation complete

Answer 22

when they contract, they "wring" the blood from the apex to the base where the major arteries exit

Answer 23

**stimulates the heart** -epinephrine and norepinephrine

Answer 24

**inhibits the heart's activity** -by Vagus nerve stimulation

Answer 25

**atrial depolarization** -electrical signal first then muscle contracts -SA node (RA) -> AV node (LA)

Answer 26

**AV nodal delay** -ensures ventricular filling

Answer 27

**ventricular depolarization** -atria repolarizing simultaneously -gets electrical signal before contraction

Answer 28

time during which the ventricles are contracting and emptying

Answer 29

ventricular repolarization

Answer 30

time during which ventricles are relaxing and filling

Answer 31

1. SA node (atrial pacemaker cells) 2. AV node 3. Common Bundle (Bundle of HIS) 4. R + L Bundle branches 5. Purkinje Fibers 6. Ventricular muscle

Answer 32

**period of rapid filling** -blood from atria rushes into ventricles | ventricular diastole

Answer 33

**diastasis** -only blood coming back to the heart goes from atria to ventricles -finished one cardiac cycle -AV valves open and filling with blood | ventricular diastole

Answer 34

**atria contract** -dump 20-30% of final ventricular volume into ventricles -not requried for operation -used in cases where heart needs more capacity rquired to pump than at rest (ex. exercise) | atrial systole

Answer 35

**all 4 valves are closed; volume in the ventricles is constant; cannot open because there is not enough pressure** -blood isn't going anywhere -leads to emptying of ventricles during systole -ventricular contraction begins -> increased vent. pressure -> close AV valves **-before ventricular pressure is great enough to push semilunar valves open, both entrance and exit valves are closed/contracting** -eventually pressure will increase enough to open AV valves and fill again -occurs during S1 | no change in volume, no overall change in length

Answer 36

**ventricular pressure is sufficient enough to push semilunar valves open** -blood leaving ventricles, volume decreases -heart muscle contracts and increases pressure -blood ejects from pulmonary artery and aorta -AV valves closed | ventricular ejection

Answer 37

1/3 filling of ventricles (70% emptying)

Answer 38

2/3 filling of ventricles (30% emptying)

Answer 39

**all 4 valves are closed; no volume change** -drop in intraventricular pressure back to low diastolic values -relaxation -> backflow closes semilunar valves -> all 4 valves closed -increased arterial pressure closes semilunar valves

Answer 40

**greater than 100 bpm** -increased ventricular filling = shortened disatole (relaxation) -less O2 to tissues -decreased EDV = decreased SV + C.O.

Answer 41

**less than 60 bpm** -decreased HR = decreased C.O.

Answer 42

regularity or spacing of ECG waves

Answer 43

**variation from normal rhythm and/or excitation of the heart** -A flutter -A fib -V Fib

Answer 44

**usually 200-350 bpm** -no ventricular filling

Answer 45

**random, uncoordinated excitation and contraction** -most common cause of clots -blood pools at bottom of the ventricle + valves so coagulation and clots form / pump out to the rest of the body | treated with heparin or coumadin

Answer 46

**life threatening rhythm starting in ventricles** -triggered by heart attack

Answer 47

**block somewhere in the excitatory and conducting pathway** -absent T wave on EKG | AV node block very common, artificial pacemaker needed

Answer 48

**PVCs (premature ventricular contraction) prior to receiving electrical conduction** -ventricular tachycardia

Answer 49

short circuit develops in atria resulting in rapid heart beat that stops abruptly

Answer 50

damage of the heart muscle

Answer 51

**inadequate delivery of oxygenated blood to heart tissue** -decreased blood flow = cells die -tissue damage = LV hypertrophy pulling chordae tendonae + papillary muscles away -> regurgitation | may result in Mitral Regurgitation

Answer 52

death of heart muscle cells

Answer 53

**blood vessel supplying area of heart becomes blocked (clot or vascular spasm)** -commonly coronary artery blocked -ST elevation on EKG

Answer 54

intensity (loudness), frequency (pitch) & quality

Answer 55

**related to opening** -closure sounds = S1 + S2 -audible with stethoscope

Answer 56

**early and late diastolic filling events of the ventricle** -S3 + S4 -not usually audible with stethoscope

Answer 57

between S1 and S2

Answer 58

between S2 and S1

Answer 59

**closure of the mitral and tricuspid valves** -signifies beginning of systole -frequency = 50-60 Hz -time = 0.15 sec -heard during isovolumetric contraction | "lub"

Answer 60

1. Structural Integrity of the Valve 2. Velocity of Valve Closure 3. Status of Ventricular Contraction 4. Heart Rate 5. Transmission Charcateristics of Thoracic Cavity and Chest Wall

Answer 61

-**inadequate coaptation of mitral valve** (SOFT S1) - ex. severe MR -**loss of leaftlet tissue** (SOFT S1) -thickness/mobility of valve: 1. **mild to mod Mitral Stenosis** (LOUD S1) - increased LA pressure causes leaftlets to be widely separated (pushing blood through semi-hard leaftlets; stiff noncompliant valves and chordae tendonae 2. **Calcified Mitral Valve**(SOFT S1) - long standing MS immobilizes the valve

Answer 62

**determined by position of mitral valve at onset of ventricular systole; position of mitral valve is altered by timing of atrial/ventricular systole (PR interval)** -**long PR (SOFT S1)**: longer diastolic fill time -> LV pressure increases -> mitral valve leaftlets slowly drift together -> lesser distance between leaftlets -**short PR (LOUD S1)** : when atrial/vent. systole coincide; mitral leaftlets are farther apart at onset of vent. systole -> close with high velocity; decreased PR = not enough time to close/ fill w/ blood

Answer 63

-**increased myocardial contractility** increases rate of LV pressure (LOUD S1) - exercise, high output state -**decreased contractility** (SOFT S1) - M.I., myocarditis

Answer 64

-**tachycardia** (LOUD S1) - decreased PR interval; wide opened valves to due short diastole; increased contractility

Answer 65

-obesity, emphysema, pericardial effusion decrease intensity of auscultory events (SOFT S1) -thin chest wall increases intensity (LOUD S1)

Answer 66

1. Mitral Stenosis (MS) 2. Mitral Valve Prolapse (MVP) 3. Exercise 4. Tricuspid Stenosis (TS) 5. Atrial Septal Defect (ASD) 6. Anomalous Pulmonary Venous Cnnected with Increased Tricuspid Flow

Answer 67

1. Mitral regurgitation 2. Calcific Mitral Stenosis (immobile mitral valve) 3. Severe Atrial Regurgitation 4. LBBB (decreased LV contractility)

Answer 68

increased pressure = increased force of contraction

Answer 69

**floppy leaflet gain velocity by snapping** -not anchored as well + turbulent blood flow

Answer 70

increased HR -> decreases PR interval -> decreases EDV

Answer 71

increased pressure = increased force of contraction

Answer 72

**increased LA pressure more than RA** -LA flow to RA -increased blood flow to RA -increased contractility to force shut smaller = louder murmur (less space for blood flow)

Answer 73

PV connected to LV instead of RV

Answer 74

backflow into LA but valve doesn't close all the way

Answer 75

**valve is stuck in closed position but opens slightly** -immobile mitral valve

Answer 76

tricuspid regurg; one leaflet not closing

Answer 77

blocking bundle branch = decreased LV contractility

Answer 78

**closure of the aortic and pulmonic valves** -signifies beginning of diastole/end of systole -frequency = 80-90 Hz -time = 0.12 sec -heard during isovolumetric relaxation | short and sharp sound / "dub"

Answer 79

**AV valve closes before PV valve (not synchronized)** < 30 ms expiration, 40-50 ms inspiration increase in pulmonary blood flow that occurs with inspiration when increased venous return to R side of heart delays closure of pulmonic valve | (normal during inspiration)

Answer 80

changes in intrathoracic pressure during inspiration

Answer 81

usually seen in RBBB

Answer 82

usually seen in pulmonary stenosis

Answer 83

**seen during expiration instead of inspiration; PV closes before AV valve** -**Aortic Stenosis**: push blood, harder to get out, takes longer for aortic pressure to reach LV pressure -**LBBB**: delayed depolarization of LV + delayed closing of aortic valve -**HCM**: increase force; delay in conduction, obstruction issue

Answer 84

**no change in S2 with deeper inspirations** -ASD -R Ventricular Failure -no change bc ASD is more hemodynamically significant than increase in volume of blood from inspiration increased pulmonary blood flow from increased preload from L -> R shunt of blood across ASD delays closure of PV

Answer 85

**Associated w/ LV failure** -only heard with bell of stethoscope -normal in children and young people w/o abnormalities -suspect CHF and fluid overload if pt over 40 -occurs during 2/3 diastole (diastasis) **-rush of blood from atria to ventricles during rapid filling phase -> vibration in blood** -frequency = 20-30 Hz -time = 0.1 sec | rare extra heart sound occurring after S2

Answer 86

**caused by vibration of ventricular wall during atrial contraction** -associated with stiffened ventricle (low ventricular compliance) **-atrial contraction -> rapid flow of blood from atria to noncompliant ventricle -> vibration in blood** -heard in pts with Ventricular Hypertrophy and Myocardial Ischemia, sometimes athletes -frequency = < 20 Hz | comes just before S1

Answer 87

**velcro sound you can hear throughout the cardiac cycle** -recent upper respiratory tract infection -chest pain that is better with leaning forward and worse with lying down | pericarditis

Answer 88

relaxation / ventricular filling | takes more time than systole

Answer 89

contraction / ejection

Answer 90

**less filling time** - greater than 100 bpm -decreased C.O. = less O2 to tissues -O2 demand exceeds supply -decreased diastole = decreased pumping time = decreased O2 supply

Answer 91

**abnormal sounds produced due to abnormal / turbulent blood flow through abnormal heart valves** -ex. stenosis or regurgitation (incompetence) -holosystolic, crescendo-decrescendo, decrescendo

Answer 92

**narrow or stiff valve that does not open completely** -produces a whistling sound

Answer 93

**valve does not close properly and remains open** -produces a swishing or gurgling sound

Answer 94

**Rheumatic Fever** -autoimmune disease triggered by streptococcus bacterial infection

Answer 95

**produced during ventricular systole** -between S1 (closing of mitral valve) and S2 (closing of aortic valve) -ventricles have difficulty pushing blood -ex. aortic stenosis + mitral regurg -**crescendo-decrescendo**: aortic stenosis, pulmonic stenosis -**holosystolic**: mitral regurg, tricuspid regurg | (lub - mumur - dub)

Answer 96

**produced during ventricular diastole** -between S2 and S1 -ex. aortic regurg + mitral stenosis, pulmonic regurg, stenosis of mitral or tricuspid | (lub - dub - mumur - lub)

Answer 97

**continuous sound** mitral regurg, tricuspid regurg or VSD | systolic

Answer 98

**high "lub" sound, soft "dub" sound** aortic stenosis, pulmonic stenosis, "innocent" mumur | systolic; louder then gets softer

Answer 99

Patent Ductus Arteriosus (PDA)

Answer 100

increased loudness | harder to push blood

Answer 101

1. faintest murmur that can be heard (with difficulty) 2. murmur is also a faint murmur but can be identified immediately 3. moderately loud 4. loud with a palpable thrill 5. very loud, but still need stethoscope 6. loudest and can be heard without a stethoscope

Answer 102

aortic murmur | may raidate to R neck

Answer 103

pulmonic murmur | may radiate to back

Answer 104

tricuspid murmur | usually does not radiate

Answer 105

mitral valve murmur | may radiate to axilla

Answer 106

-blood has trouble exiting the ventricle through tight valve (aortic stenosis) -flowing through valve that should be closed tightly but is not (mitral regurgitation) -hole exists where it should not within ventricular septum and blood crosses from high pressure side to low pressure side (VSD)

Answer 107

**usually "diamond shaped;" brief little radiation** -common in children and young adults -always systolic, less than 3/4 intensity -other heart sounds and pulses are normal

Answer 108

-blood is having trouble leaving the atrium to the ventricle because the valve is partially shut; thin walled aorta on top so gravity should allow blood to easily flow to ventricles (mitral stenosis) -ventricular outflow tract can not stay shut, radiates inferiorly, best heard with patient sitting up and leaning forward (aortic regurg)

Answer 109

**maintain forward flow and prevent reversal flow** -valves open and close in response to pressure gradients between cardiac chambers

Answer 110

-**valvular stenosis**: narrowing -**valvular incompetence**: regurgitation

Answer 111

**incompetent MV does not close properly resulting in abnormal leaking of blood from LV to LA (decreased SV)** -**sound**: holosystolic, radiates to axilla, heard in apex -**compensatory mechanisms**: increase SV + EF, LV/LA dilation, LV volume overload -tries hard to pump out leftover blood = hypertrophy

Answer 112

**normal LA, increased LA pressure, acute pulmonary edema (backflow from LV -> LA -> lungs)** -**sound**: decrescendo systolic murmur -**caused by**: **Ineffective Endocarditis** (IV drug use); **Ischemic Heart Disease** (papillary muscle rupture -> ischemia); **Mitral Valve Prolapse** (chordal rupture/mid-systolic click); **chest trauma**

Answer 113

**dilated / compliant LA; increased pressure LA, fatigue, A-fib** -LA dilated -> electrical conduction doesnt reach all tissues since MV is stretched -**causes**: myxomatous degeneration, M.I., dilated LV -**auscultory findings**: soft S1, increased P2 -**hyperdynamic LV** = brisk carotid upstrokes, increased LV apical impulse, LV lift, RV tap

Answer 114

**mitral valve is tight so blood cannot completely get out of the atrium during diastole** -increased HR = decreased diastole as pressure increases -**sound**: mid systolic rumbling after opening snap; best heard at apical region and does not radiate -**auscultory findings**: crescendo-decrescendo, S1 variable intensity, increased P2 -**echocardiogram findings**: thickened/deformed MV leaftlets; doppler gradient -restriction of blood flow from LA to LV during diastole -MV gradient increases LA pressure

Answer 115

-Rheumatic Fever (99%) -Congenital -Prosthetic wave stenosis -Mitral annular calcification -Left atrial myxoma -Damage from Endocarditis

Answer 116

**blood pools in LA -> increased pressure LA (blood cannot flow to LV) -> backup to lungs -> increased lung pressure -> pulmonary HTN -> RV fail** -Pulmonary HTN -RV pressure overload

Answer 117

-**A-fib**: embolus fomration from valves not moving/stagnant -**Systemic thromboembolisation**

Answer 118

-fatigue, low output state (decreased C.O.) -peripheral edema + hepatosplenomegaly -hoarsness (recurrent laryngeal nerve palsy)

Answer 119

**displacement of abnormally thickened mitral valve leaftlet displaced into atrium while in systole** -mid-systolic click w/ late systolic murmur -can develop into mitral regurg if severe

Answer 120

**aortic valve narrows and creates turbulent blood flow across the narrowed aortic valve, resulting in the heart working harder by creating pressure to move blood** **across the stenotic valve** -increased pressure and force from LV (LV pressure overload) **causes**: congenital bicuspid valve, wear + tear from age, Rheumatic Fever -**sound**: crescendo-decrescendo in systole radiates to carotids -**gradient progression**: increase 6-10 mmHg a year -**risk factors**: age over 70, C.A.D., hyperlipidemia, chronic renal failure -**symptom triad**: angina pectoris (5 years), syncope ( 2-3 years), CHF (1-2 years, end stage) -leads to sudden death

Answer 121

**valve cannot fully close leading to backflow of blood to LV** -hear turbulence in diastole after aortic valve should have fully closed (after S2) -LV volume overload -**increased HR **= decreased diastolic fill time -**increased pressure aorta** = leaky valve + backflow -**compensatory mechanisms**: LV dilation + LVH, increased LV compliance, peripheral vasodilation -**severity dependent on**: size of regurgitant orifice, diastolic pressure gradient between aprtic valve + LV, HR or duration of diastole

Answer 122

-congenital bicuspid valve -ineffective endocarditis -acute aortic dissection (Marfan's Syndrome or EDS) -Rheumatic Fever -prolpase and congenital VSD -HTN -syphillis -connective tissue disorders

Answer 123

**sudden AoV incompetence** -rare unless dissection event -noncompliant LV -acute pulmonary edema

Answer 124

**long term, asymptomatic** -progressive LV dilation -orthopnea, PND (paroxysmal nocturnal dyspnea) -frequent PVCs -widened pulse pressure greater than 70mmHg -low diastolic pressure less than 60mmHg -hyperdynamic LV (increase systolic BP to push blood out)

Answer 125

**rhythmic bobbing/nodding of head in synchrony with heart beat** -syphillic aortis -rheumatic fever -aneurysm

Answer 126

carotid pulse that is forceful and suddenly collapses (rapid upstroke)

Answer 127

pulsations in capillary bed of nail

Answer 128

**audible diastolic murmur heard over femoral artery when compressed by bell of stethoscope** -**auscultation** - diminished A2, decrescendo diastolic blowing murmur @ LSB, Austin Flint murmur (diastolic flow rumble @ apex)

Answer 129

-**LV volume**: normal -**Wall thickness**: conc. LVH -**LV compliance**: stiff compliance -**LV diastolic pressure**: increased -**LV systolic pressure**: increased -**LVEF**: normal

Answer 130

-**LV Volume**: dilated -**Wall thickness**: normal. toslightly increased -**LV compliance**: increased compliance -**LV diastolic pressure**: normal to slightly increased -**LV systolic pressure**: normal to slightly increased -**LVEF**: increased

Answer 131

**O2 rich blood from aorta mixes with O2 poor blood from pulmonary artery, putting strain on heart** -connection of aorta + pulmonary artery -increased BP in lung arteries -LA -> RA -> Rv (increased pressure RV) -sounds like continuous machinery murmur in both systole and diastole