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Pathophysiology - MD > Week 4 - Cardiac Physiology > Flashcards

Week 4 - Cardiac Physiology Flashcards

1
Q

Heart Location

A

-superior surface of the diaphragm
-left of the midline
-anterior to the vertebral column
-posterior to the sternum

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2
Q

Pericardium

A

double walled sac composed of:
-superfician fibrous pericardium
-deep, 2 layer serous pericardium separated by fluid filled pericardial cavity

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3
Q

Parietal Layer of Pericardium

A

lines the internal surface of the fibrous pericardium

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4
Q

Visceral Layer of the Pericardium

A

aka epicardium
-lines the surface of the heart

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5
Q

Function of the Pericardium

A

-protects and anchors the heart
-prevents overfilling of the heart with blood
-allows for the heart to work in a relatively friction free environment

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6
Q

Epicardium

Heart Wall

A

visceral layer of the serous pericardium

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7
Q

Myocaridum

Heart Wall

A

cardiac muscle layer forming the bulk of the heart

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8
Q

Fibrous Skeleton

Heart Wall

A

criss corssing interlacing layer of connective tissue

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9
Q

Endocardium

Heart Wall

A

endothelial layer of the inner myocardial surface

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10
Q

Secretory Lining

Pericardial Sac

A

secretes pericardial fluid
-provides lubrication to prevent friction between pericardial layers

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11
Q

Pericarditis

A

inflammation of the pericardial sac
-can cause compression of the heart

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12
Q

Complications of Pericarditis

A

Cardiac Tamponade
-extra fluid can cause compression around the heart
-Cardiac Tamponade is an emergency in which the heart cannot fill with blood due to compression
-C.O. is reduced
-can also result from pleural effusion (chemo or lung cancer)

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13
Q

Vessels Returning Blood to the Heart

A

SVC, IVC, R + L Pulmonary veins

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14
Q

Vessels Conveying Blood Away from the Heart

A

-pulmonary trunk (splits onto R & L PA)
-ascending aorta (brachiocephalic, left common carotid, subclavian arteries)

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15
Q

Why is the L Ventricle most inferior?

A

most important part of the heart is protected

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16
Q

Pulmonary Artery

A

only artery w/ deoxygenated blood

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17
Q

Pulmonary Vein

A

only veing with oxygenated blood

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18
Q

Vessels that Supply/Drain the Heart

(Anterior View)

A

arteries:
-R & L coronary arteries (AV groove)
-marginal
-circumflex
-anterior interventricular arteries

veins:
-small cardiac
-anterior cardiac
-great cardiac

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19
Q

Vessels that Supply/Drain the Heart

(Posterior View)

A

arteries:
-R coronary artery (AV groove)
-posterior interventricular artery

veins:
-great cardiac vein
-posterior veing to LV
-coronary sinus
-middle cardiac vein

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20
Q

Atrioventricular Valves

(AV Valves)

A

prevent backflow into atria when ventricles contract
-tricuspid valve (RA + RV)
-mitral valve (LA + LV)

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21
Q

Chordae Tendonae

A

anchor AV valves to papillary muscles and prevent valves from being inverted
-large M.I. -> ruptured chordae tendonae -> prolapse, murmur

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22
Q

Semilunar Valves

A

prevent backflow of blood into ventricles
-aortic semilunar (LV + aorta)
-pulmonary semilunar (RV + pulmonary trunk)

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23
Q

AV Valve Open

AV Valve Function

A

-blood returning to heart fills atria, putting pressure on AV valves
-AV valves forced open
-ventricles fill and AV valves hang limp into ventricles
-atria contract and force additional blood into ventricles

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24
Q

AV Valve Closed

AV Valve Function

A

-vnetricles contract forcing blood against AV valve cusps
-AV valves close
-papillary muscles contract and chordae tendonae tighten, preventing valve flaps from everting into atria

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25
Q

Semilunar Valve Open

Semilunar Valve Function

A

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

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26
Q

Semilunar Valve Closed

Semilunar Valve Function

A

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

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27
Q

Heart Muscle

Cardiac Muscle Contraction

A

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

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28
Q

Autorhythmic Cells

Cardiac Muscle Contraction

A

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

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29
Q

What prevents the SA node from firing?

A

heart block

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30
Q

What happens if the heart does not contract as one unit?

A

arrythmia if not in sync

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31
Q

Contraction goes from…

A

bottom -> up

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32
Q

Electrical Activity goes from…

A

top -> bottom

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33
Q

Electrical Acitivty of the Heart

A

-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

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34
Q

The rising phase of action potential is due to…

A

slow Ca2+ channels (L type)

Na+ channels are inactivated due to depolarization state

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35
Q

Purpose of AV Nodal Delay

A

ensure atrial contraction precedes ventricular contraction to allow for complete ventricular filling

0.1 sec delay

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36
Q

Purpose of Prolonged Positive Phase (Plateau) + Prolonged Contraction

A.P. of Cardiac Contractile Cells

A

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

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37
Q

Steps of Ventricular Muscle Action

(Contraction)

A

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)

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38
Q

Ca2+ Entry

Electrical Activity of the Heart

A

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

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39
Q

Excitation-Contraction Coupling

Cardiac Contractile Cells

A
  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
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40
Q

Purpose of Longer Refractory Period

A

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

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41
Q

Sequence of Excitation

A

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)

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42
Q

Start of the P Wave

Heart Excitation Related to EKGs

A

SA node generates impulse and atrial excitation begins

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43
Q

Entire P Wave

Heart Excitation Related to EKGs

A

impulse delayed at AV node

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44
Q

P Wave -> Q Wave

Heart Excitation Related to EKGs

A

impulse passes to heart apex and ventricular excitation begins

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45
Q

Q Wave -> RS Wave

Heart Excitation Related to EKGs

A

ventricular excitation complete

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46
Q

Why are bundles of cardiac muscle spirally wrapped around the ventricle?

A

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

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47
Q

Sympathetic Nervous System

A

stimulates the heart
-epinephrine and norepinephrine

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48
Q

Parasympathetic Nervous System

A

inhibits the heart’s activity
-by Vagus nerve stimulation

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49
Q

EKG: P Wave

A

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

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50
Q

EKG: PR Segment

A

AV nodal delay
-ensures ventricular filling

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51
Q

EKG: QRS Complex

A

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

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52
Q

EKG: ST Segment

A

time during which the ventricles are contracting and emptying

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53
Q

EKG: T Wave

A

ventricular repolarization

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54
Q

EKG: TP Interval

A

time during which ventricles are relaxing and filling

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55
Q

Sequence of A.P. Conduction

A
  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
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56
Q

1st 1/3 Filling of Ventricles

Cardiac Cycle

A

period of rapid filling
-blood from atria rushes into ventricles

ventricular diastole

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57
Q

2/3 FIlling of Ventricles

Cardiac Cycle

A

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

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58
Q

3/3 Filling of Ventricles

Cardiac Cycle

A

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

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59
Q

Period of Isovolumetric Contraction

Cardiac Cycle

A

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

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60
Q

Period of Ejection

Cardiac Cycle

A

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

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61
Q

Period of Rapid Ejection

Cardiac Cycle

A

1/3 filling of ventricles (70% emptying)

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62
Q

Period of Slow Ejection

Cardiac Cycle

A

2/3 filling of ventricles (30% emptying)

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63
Q

Period of Isovolumetric Relaxation

Cardiac Cycle

A

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

64
Q

Tachycardia

A

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

65
Q

Bradycardia

A

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

66
Q

Heart Rhythm

A

regularity or spacing of ECG waves

67
Q

Arrythmia

A

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

68
Q

Atrial Flutter

Arrythmias

A

usually 200-350 bpm
-no ventricular filling

69
Q

Atrial Fibrillation

A Fib

Arrythmias

A

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

70
Q

Ventricular Fibrillation

V Fib

Arrythmias

A

life threatening rhythm starting in ventricles
-triggered by heart attack

71
Q

Heart Block

A

block somewhere in the excitatory and conducting pathway
-absent T wave on EKG

AV node block very common, artificial pacemaker needed

72
Q

Ectopic Focus

A

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

73
Q

PVST (Paroxysmal Supraventricular Tachycardia)

A

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

74
Q

Cardiac Myopathy

A

damage of the heart muscle

75
Q

Myocardial Ischemia

Cardiac Myopathy

A

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

76
Q

Necrosis

Cardiac Myopathy

A

death of heart muscle cells

77
Q

Acute Myocardial Infarction

(heart attack)

Cardiac Myopathy

A

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

78
Q

Heart Sounds Characteristics

A

intensity (loudness), frequency (pitch) & quality

79
Q

High Frequency Sounds

A

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

80
Q

Low Frequency Sounds

A

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

81
Q

When can ventricular systole be heard?

(Contraction)

A

between S1 and S2

82
Q

When can ventricular diastole be heard?

(Relaxation)

A

between S2 and S1

83
Q

S1 Sounds

A

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

“lub”

84
Q

Factors Affecting S1 Sounds

(Mitral + Tricuspid)

A
  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
85
Q

Structural Integrity of the Valve

Factors Affecting S1

A

-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

86
Q

Veolicty of Valve Closure

Factors Affecting S1

A

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

87
Q

Status of Ventricular Contraction

Factors Affecting S1

A

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

88
Q

Heart Rate

Factors Affecting S1

A

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

89
Q

Transmission Charcateristics of Thoracic Cavity and Chest Wall

Factors Affecting S1

A

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

90
Q

Conditions Causing Loud S1

A
  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
91
Q

Conditions Causing Soft S1

A
  1. Mitral regurgitation
  2. Calcific Mitral Stenosis (immobile mitral valve)
  3. Severe Atrial Regurgitation
  4. LBBB (decreased LV contractility)
92
Q

Mitral Stenosis

(mild to moderate)

Conditions Causing Loud S1

A

increased pressure = increased force of contraction

93
Q

Mitral Valve Prolapse

(MVP)

Conditions Causing Loud S1

A

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

94
Q

Exercise

Conditions Causing Loud S1

A

increased HR -> decreases PR interval -> decreases EDV

95
Q

Tricuspid Stenosis

Conditions Causing Loud S1

A

increased pressure = increased force of contraction

96
Q

Atrial Septal Defect

(ASD)

Conditions Causing Loud S1

A

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)

97
Q

Anomalous Pulmonary Venous Connection with Increased Tricuspid Flow

Conditions Causing Loud S1

A

PV connected to LV instead of RV

98
Q

Mitral Regurgitation

(MR)

Conditions Casuing SOFT S1

A

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

99
Q

Calcific Mitral Stenosis

Conditions Casuing SOFT S1

A

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

100
Q

Severe Atrial Regurgitation

Conditions Casuing SOFT S1

A

tricuspid regurg; one leaflet not closing

101
Q

LBBB

(Left Bundle Branch Block)

Conditions Casuing SOFT S1

A

blocking bundle branch = decreased LV contractility

102
Q

S2 Sounds

A

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”

103
Q

Normal Split S2 Sound

A

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)

104
Q

Physiologic Cause of Split S2 Sound

A

changes in intrathoracic pressure during inspiration

105
Q

Wide Split S2 Sound

A

usually seen in RBBB

106
Q

Wide Fixed Split S2 Sound

A

usually seen in pulmonary stenosis

107
Q

Paradoxical Split S2 Sound

A

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

108
Q

Fixed Split S2 Sound

A

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

109
Q

S3 Sounds

A

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

110
Q

S4 Heart Sounds

A

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

111
Q

Pericardial Rub

A

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

112
Q

Diastole

A

relaxation / ventricular filling

takes more time than systole

113
Q

Systole

A

contraction / ejection

114
Q

Increased HR = shorter diastole…

A

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

115
Q

Heart Murmurs

A

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

116
Q

Stenosis

A

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

117
Q

Incompetence/Regurgitation

A

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

118
Q

Most Common Cause of Stenosis + Incompetence

A

Rheumatic Fever
-autoimmune disease triggered by streptococcus bacterial infection

119
Q

Systolic Murmurs

A

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)

120
Q

Diastolic Mumurs

A

produced during ventricular diastole
-between S2 and S1
-ex. aortic regurg + mitral stenosis, pulmonic regurg, stenosis of mitral or tricuspid

(lub - dub - mumur - lub)

121
Q

Holosystolic

A

continuous sound
mitral regurg, tricuspid regurg or VSD

systolic

122
Q

Crescendo-Decrescendo

A

high “lub” sound, soft “dub” sound
aortic stenosis, pulmonic stenosis, “innocent” mumur

systolic; louder then gets softer

123
Q

Both Systolic and Diastolic Murmur

A

Patent Ductus Arteriosus (PDA)

124
Q

Increased pressure across valve leads to…

A

increased loudness

harder to push blood

125
Q

Grading Murmurs

A
  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
126
Q

What murmur do you hear at RUSB?

A

aortic murmur

may raidate to R neck

127
Q

What murmur do you hear at LUSB?

A

pulmonic murmur

may radiate to back

128
Q

What murmur do you hear at LLSB?

A

tricuspid murmur

usually does not radiate

129
Q

What murmur do you hear at apex?

A

mitral valve murmur

may radiate to axilla

130
Q

Causes of Systolic Murmurs

A

-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)

131
Q

Innocent Murmurs

Systolic Murmur

A

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

132
Q

Causes of Diastolic Murmurs

A

-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)

133
Q

Normal Valve Function

A

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

134
Q

Two Types of Valve Disease

A

-valvular stenosis: narrowing
-valvular incompetence: regurgitation

135
Q

Mitral Regurgitation

A

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

136
Q

Acute Mitral Regurgitation

A

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

137
Q

Chronic Mitral Regurgitation

A

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

138
Q

Mitral Stenosis

A

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

139
Q

Causes of Mitral Stenosis

A

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

140
Q

Complications fo Mitral Stenosis

A

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

141
Q

Symptoms Unrelated to Severity of Mitral Stenosis

A

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

142
Q

Symptoms Related to Severity of Mitral Stenosis

Due to Pulmonary HTN ot RV Failure

A

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

143
Q

Mitral Valve Prolapse

(MVP)

A

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

144
Q

Aortic Stenosis

A

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

145
Q

Aortic Regurgitation

A

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

146
Q

Causes of Aortic Regurgitation

A

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

147
Q

Acute Aortic Regurgitation

A

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

148
Q

Chronic Aortic Regurgitation

A

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)

149
Q

DeMusset’s Sign

Signs of Hyperdynamic LV

A

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

150
Q

Corrigan’s Pulse

Signs of Hyperdynamic LV

A

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

151
Q

Quincke’s Pulsations

Signs of Hyperdynamic LV

A

pulsations in capillary bed of nail

152
Q

Durozier’s Murmur

Signs of Hyperdynamic LV

A

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)

153
Q

LV Pressure Overload

(Aortic Stenosis)

A

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

154
Q

LV Volume Overload

(Mitral + Aortic Regurgitation)

A

-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

155
Q

Patent Ductus Arteriosus

(PDA)

A

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

Pathophysiology - MD (7 decks)

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