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CV Exam III > Blonder > Flashcards

Blonder Flashcards

1
Q

VSD

A

Most common congenital heart disease at birth, only accounts for 10% of adult congenital due to spontaneous closure.

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2
Q

VSD

4 Types

A

InfundibularVSD

Membranous VSD

Inlet Defect VSD

Muscular VSD

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3
Q

InfundibularVSD

A

below the aortic and pulmonic valves, leading to progressive aortic regurgitation, the hallmark.

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4
Q

Membranous VSD

A

also called conoventricular, deficencyof the membranous septum.

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5
Q

Inlet Defect VSD

A

av canal, Down’s

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6
Q

Muscular VSD

A

in the trabecular system, 5-20%

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7
Q

VSD rarely missed bc

A

they have long loud holosystolic murmur at left sternal border similar to mitral and tricuspid regurg, they are difficult to tell apart

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8
Q

VSD-Pathophysiology

Direction and severity

A

determined by functional size and the ratio of pulmonary to systemic vascular resistance

usually blood flows left to right to start out bc easier to get blood out of right than left

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9
Q

VSD-Pathophysiology 1

A
  • Small or Restrictive VSD have orifice diameter
  • R shunt with no LV volume overload
  • No pulmonary Hypertension
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10
Q

VSD-Pathophysiology 2

A

•Moderate sized defect, >25%-

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11
Q

VSD-Pathophysiology 3

A
  • Large VSD, >=75% of annulus
  • Moderate to large L>R shunts with LV volume overload, if uncorrected leads to
  • PHTN develops with pulmonary arterial obstructive disease
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12
Q

VSD-Pathophysiology 4

A
  • Progressive pulmonary hypertension leads to RV pressures approaching systemic
  • Leads to reversal of shunt with R>L flow
  • Hypoxemia and cyanosis develop
  • This is Eisenmengersyndrome, and when coupled with VSD is called EisenmengerComplex
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13
Q

VSD-Pathophysiology

Endocardial Scarring

A

bc blood is spurting into other ventricle

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14
Q

VSD-Pathophysiology

left ventricle pushes blood up towards pulmonary artery

A

when it pushes it across, this happens during systole so the blood flows right into the pulmonary artery and it floods the artery quick and they get sob etc
can get endocarditis, pretty common

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15
Q

VSD-Clinical

Small defect

A

small L>R shunt, asymptomatic adults

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16
Q

VSD-Clinical

Moderate sized defect

A

either asymptomatic or mild CHF in children, usually gets smaller with growth and may have AR

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17
Q

VSD-Clinical

Large VSD

A

Usually early presentation with CHF in infancy or Eisenmenger’sin late childhood, early adulthood.

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18
Q

VSD

PE

A

large holosystolic, LSB, 2ndor 3rdICS, thrill

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19
Q

VSD

EKG

A

66% of small are normal.

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20
Q

VSD

Echo

A

test of choice

amount of flow across defect

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21
Q

VSD

CT/MRI

A

excellent for complex lesions

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22
Q

VSD

Cath

A

less important now with advanced Echo and MR

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23
Q

What is a shock?

A

when you feel the heart sound

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24
Q

Tetralogy of Fallot

4 Features

A
    1. RVOT obstruction
    1. VSD
    1. Aorta overrides IVS
    1. Concentric RVH
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25
Q

TOF

10% of CHD

A

one of most common cyanotic congenital heart disease

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26
Q

TOF

The need for medical intervention

A

is dependent on the degree of RVOT obstruction

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27
Q

Tetralogy of Fallot

RVOT obstruction

A

pulmonic stenosis..

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28
Q

Tetralogy of Fallot

Aorta overrides IVS

A

get blood from right and left ventricle going out systmically

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29
Q

Tetralogy of Fallot

Concentric RVH

A

consequence of everything else

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30
Q

ASD-Summary

A

ASD is an open communication between the atria via a defect in the intra-atrial septum

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31
Q

ASD-Summary

Septum

A

when 2 pieces come apart it is patent foramen ovale (pfo), pfo is not a disease, 20-25% of adults have a flap that opens, bubble study you inject saline into vein, you can see it go into the the atria and back and forth if there is a shunt, more difficult to see left to right shunt,

always a little bit of both in asd

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32
Q

ASD-Summary

PFO

A

Patent Foramen Ovaleis a foramen covered by the septum primumbut is not sealed shut in 20% of normal subjects

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33
Q

ASD

Diagnosis

A

made primarily by echocardiography

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34
Q

ASD-Summary

Transient R>L shunting

A

occurs in most patients during the onset of ventricular contraction, explaining neurologic events in non cyanotic patients.

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35
Q

ASD Right to Left shunt get a?

A

stroke in right to left shunt bc clot goes to brain

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36
Q

ASD right to left shunt extra shunting of blood from right is done by

A

oxygen

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37
Q

ASD right to left shunt size of hole

A

cause more blood being shunted, or resistance (if high systemic ressitance the left ventricle will put out more pressure, if you have a higher pulmonary resistance the rigth ventricle will actually be putting out more flow than the left ventricle so you will get even more shunting causing hypoxia, so you get eisenmengers (clubbed sob)

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38
Q

ASD right to left shunt don’t want right sided resistance to increase bc

A

you will eventually need a heart and lung transplant

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39
Q

ASD right sided volume overload is well tolerated for?

A

years

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40
Q

ASD

essential htn causes increased resistance

A

(increased afterload), left ventricle will thicken, then right will thicken then right will dialate

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41
Q

ASD is what kind of problem?

A

volume problem which the heart tolerates better than increased resistance

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42
Q

Volume problems effect what first?

A

right ventricle

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43
Q

ASD

modality of choice for diagnosis and characterization of the defect?

A

Echocardiography

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44
Q

Bicuspid Aortic Valve

MVP-MyxomatousMitral Valve

ASD-Atrial Septal Defect

Ventricular Septal Defect

A

Not sure why but these were altogether right after ASD, volume overload and echo. they were also before this slide

Other common defects
•Tetrologyof Fallot
•Ebstein’s
•Eisenmenger
•PDA

I think they might be volume overload problems

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45
Q

ASD

Second most common

A

adult congenital after Bicuspid AV

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46
Q

ASD

Usually asymptomatic

A

until adulthood

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47
Q

ASD

Complications include

A
  • Atrial Arrhythmias
  • Paradoxical Embolus
  • Cerebral Abcess
  • Right Heart Failure
  • Pulmonary Hypertension>EisenmengerSyndrome
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48
Q

ASD

Atrial Arrhythmias

A

most common is afib, premature atrial beats then go into fib

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49
Q

ASD

Paradoxical Embolus

A

dvt then stroke

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50
Q

ASD

Cerebral Abcess

A

infection embolizes across asd into brain

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51
Q

ASD

Right Heart Failure

A

happens after 25 years of volume overload, rigth ventricle starts to fail

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52
Q

ASD

Pulmonary Hypertension>EisenmengerSyndrome

A

media and intima scrinch down and you increase resistance, pressure goeas up and r vent fails

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53
Q

ASD

Types

A

Secundum ASD

Primum ASD

Sinus Venosus ASD

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54
Q

Secundum ASD

A
  • 70% of ASD
  • More common in females
  • Due to defects in the foramen ovalis
  • Usually not associated with other cardiac defects

in the middle of septum

usually you get urology problems too but not this one

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55
Q

Primum ASD

A
  • Large
  • 15%-20% of ASD
  • Almost always associated with defects in the AV valves or Ventricular septum
  • AV Canal, or EndocardialCushion Defect is the complete form

patient is more sick

in the bottom of the septum

tricuspid and mitral valve can get clefts leading to insufficiency

can get catheter into left atrium and left ventricle or right side respectively called canals..

look at patients palms to see if they are anemic

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56
Q

Sinus VenosusASD

A

•5%-10% of ASD

•Often associated (>90%) with anomalous pulmonary vein insertion
1 or more that feed right atrium instead of left atrium, essentially same as septal defect bc you get oxygenated blood in right atrium

  • Two types:
    • Superior Sinus Venosus-SVC Defect
    • Inferior Sinus VenosusDefect-IVC Defect

at the top of the septum in right atrium by sa node

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57
Q

ASD

Scimitar Syndrome

A
    1. Partial anomalous venous return
    1. Hypoplasia of a lobe of the right lung
    1. Thoracic aorta>Pulmonary artery collaterals
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58
Q

ASD Pathophysiology

The shunt depends on the size of the defect

A

the compliance of the right and left ventricles, and the phases of contraction (systole/diastole, atrial ventricular, early or late in phase)

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59
Q

ASD Pathophysiology

Most shunts start

A

L>R, but all large shunts have some R>L

most shunts start left to right bc resistance to ejection of the left ventr is greater than the resistance of the right, as pulmonary vascular resistance goes up the shunting starts to change to right to left you get clubbing and cyanosis

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60
Q

ASD Pathophysiology

Shunt flow leads to a “useless circuit”

A

Shunt flow leads to a “useless circuit”

of blood through the defect, into the RA,RV,PA,LA back to RA. The flow may be trivial or as much as 8:1, but more likely 2:1-5:1.

measure amount of blood going through heart to the amount going to the systemic circuit

5: 1 means five times more blood going across asd than out of the left ventricle
2: 1 is the cutoff where they need intervention

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61
Q

ASD Pathophysiology

Shunt flow leads to a “useless circuit” Leads to

A

Right heart volume overload, well tolerated for years, but can cause Pulmonary Hypertension and Eisenmengers

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62
Q

normally right sided is a?

A

fifth of the left sided

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63
Q

cad is a disease of the left ventricle most of the time bc

A

the left ventricle has to do more work bc the resistance is 5x higher than that of the r ventricle

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64
Q

ASD Natural Histroy

A

•Lesions

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65
Q

ASD Clinical Manifestation

Most patients with ASD and significant shunt flow (>2:1)

A

will become symptomatic and require surgical repair by age 40

32-55

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66
Q

ASD Clinical Manifestation

Atrial Arrhythmias

A

make pts decompensate

20% atrial fibrillation or flutter, increases with advancing age

At risk for embolic events, including stroke, including paradoxical stroke, systemic emboli

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67
Q

ASD Clinical Manifestation

Migraine cephalgiamay be associated

A

study is not panning out, just as many pts that got procedure had migraine resolution as those that had them closed?

maybe some association

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68
Q

ASD Clinical Manifestation

Pulmonary Hypertension and Eisenmengersyndrome, requires

A

> 2.5:1 shunt

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69
Q

ASD Clinical Manifestation

Cyanosis

A

Usually associated with concomitant Pulmonic Valve Stenosis or Eisenmengers

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70
Q

ASD

Physical findings are related to three things

A
  • Size and location of defect
  • Size of the shunt
  • Pulmonary Artery Pressure (resistance)
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71
Q

ASD PE

Precordium

A
  • RV Heave

* Palpable PA at upper LSB

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72
Q

ASD PE

Heart Sounds:

A
  • Wide fixed split S2
  • Increased P2 with Pulmonary Hypertension
  • S1 split with increase in Tricuspid component
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73
Q

ASD PE

Heart Murmurs:

A
  • SEM Upper LSB from increased flow

* Early DM, upper LSB from PI secondary to pulmonary hypertension

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74
Q

Infective Endocarditis (SBE, ABE)

not subacute anymore

A

bc it is often acute

janeway lesions, roth spots, osler nodes want to heal before they start, they are autoimmune antibodies reacting with other parts of the bod

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75
Q

IE Usually presents

A

acutely not sub acutely (as before antibiotic age)

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76
Q

IE Careful clinical history focused on

A

indwelling prosthetic devices such as; IV catheters, orthopedic hardware, cardiac devices.

aortic and mitral valve replacements

iv drug abuse

dialysis

hypoalimentation

chemo ports

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77
Q

IE IV drug use/abuse

A

is one of the most important factors

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78
Q

IE PE should focus on

A

new regurgitant murmurs and CHF

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79
Q

IE Look for stigmata of endocarditis to include

A

petichiae hemorrhage, Roth spots, Janeway lesions, Osler nodes. Remember most of these are signs of sub acute, not acute disease and they will be absent.

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80
Q

ASD is what heart sound?

A

second

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81
Q

IE Blonder overview

A

bacteria eat up structures (staph and psuedomonas cause this

right sided mostly tricuspid

left sided is both valves over there

right sided endocarditis is iv drug abusers pacemakers laying across tricupid valve (usually no problem bc the pressure is usually not that great)

damage then thrombus is a great place for the bacteria to seed

s. aureaus is most common cause of acute bacterial endocarditis, esp drugs and iv catheters (coagulase neg staph and other skin ones)

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82
Q

IE Murmur overview Blonder

A

listen for aortic and mitral regurg tricuspid and maybe pulmonic

easier to hear in left side murmurs bc the resistance so the pressure gradient is higher. drop in pressure produces acoustic energy from left ventircle to left atrium

to tell diff of tricuspid and mitral, if you take a breath in the tricuspid gets louder, neck veins are big with tricuspid regurg

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83
Q

IE Diagnosis

A
  • Modified Duke criteria are used.
  • The diagnosis is usually straight forward if the pathogen is obtained on blood culture, it is likely to cause endocarditis and there is evidence of endocardial involvement.
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84
Q

IE blonder diagnosis

A

have to have bacteria that causes endocarditis, subsrate for endocarditis to grow, suually produces valvular insufficiency

prosthetic valves can get bacteria on them so it can be stenotic

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85
Q

IE Duke Criteria

Definite IE

A
  • Pathologic criteria
  • micro organism recovered from tissue (embolus, abscess, culture)
  • Histologic proof of organism
  • Clinical criteria
  • 2 major or
  • 1 major and 3 minor
  • 5 minor
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86
Q

IE Duke

Possible IE

A
  • 1 major and 1 minor
  • or 3 minor
  • Rejected IE
  • firm alternative diagnosis or
  • resolution of manifestations with 4 days of antibiotics or
  • No pathologic evidence of IE at surgery or autopsy after only 4 days of Rx
  • Does not meet criteria above
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87
Q

Duke Major Criteria

A
  • Positive blood culture
  • Typical micro organism for IE from two separate blood cultures;
  • Persistently positive blood cultures;
  • blood cultures drawn more then 12 hours apart, or
  • ¾ positive cultures
  • Single positive culture for Coxiella burnetii or antiphase I IgG antibody titer >1:800
  • Evidence of endocardial involvement
  • Very important
  • Positive echocardiogram
  • New valvular regurgitation
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88
Q

Viridans Strep

A

Most common Ie most common oral pathoge

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89
Q

HACEK group

A

require special cutlure so let them know what you are looking for

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90
Q

IE

if pt is on antibiotics

A

you will not get a culture so keep this in mind

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91
Q

IE

most common cause

A

no endocarditis at al

l, made a mistake, hard to diagnose and hard to treat, culture negative endocarditis is 5-8% of endocarditis

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92
Q

Typical micro organism for IE from two separate blood cultures;

A
  • Viridans Stre0
  • Strep gallolyticus (bovis)
  • HACEK group
  • Staph aureus
  • Community acquired enterocci or
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93
Q

Other things to look for in Duke majore

A

anemia, valve regurg sick, nausea anorexic

if the pt comes in late they could have glomerulonephritis along with the lesions

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94
Q

Positive Echocardiogram in IE

A

vegetations and clumps of bacteria on valves on maybe on the wall

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95
Q

Duke minor

A
  • Predisposition
  • Fever (100.4 F, 38 C)
  • Vascular findings
  • Immunologic findings
  • Positive blood cultures not meeting above major criteria
  • Serologic evidence of infection
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96
Q

Blood cultures for IE

A
  • Obtain blood cultures prior to iniation of antibiotics, if feasible (“do no harm”)
  • At least 3 sets of cultures
  • Separate sites, not catheter (could have bacteria)
  • Typical organisms are Staph Aureus, viridanstrep, strep bovis, enterococci and HACEK group.
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97
Q

Try to make diagnosis of IE before?

A

antibiotics but the pts health is always number 1

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98
Q

Echocardiogram

Should be obtained in all patients of IE

A

a TTE first, TEE if indicated

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99
Q

TTE

A

transthoracic echo, transducer on chest 5 different views

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100
Q

TEE

A

transesophageal echo

pt swallows echo probe, and look at heart from esophagus gives you great view of left atrium mitral valve left ventricle and not a great view of the right side

only use if didnt get it on tte so dont do it if youre looking at the right side

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101
Q

IE

Questions?

A

high fevers sick for weeks it will be anemic, treat quick or people will die

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102
Q

Atrial Fibrillation (AF) overview

A
  • The most common cardiac arrhythmia
  • The RR interval follows no repetitive pattern
  • No distinct “P” waves, undulation of the baseline, atrial rate 300-600 beats/minute
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103
Q

Afib main risk

A

cardiac emboli, to the brain, 50% of strokes to brain come from this

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104
Q

A fib antithrombin drugs overview

A

dabigatran pradaxone only direct thrombin inhibitor others are factor Xa inihibitors, upset stomach reflux

xarelto rivaraxaban bc its once a day

eliquis epixiban twice a day

endoxaban once a day

these drugs are expensive

warfarin is what you take when you cant afford these ones

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105
Q

A fib pearls

A

and undulation of baseline, bc atria is trying to depolarize, it looks like a bag of worms when you go to surgery

when heart rate goes up it encroaches on diastole and the heart fails, lost atria to fill you raise heart rate so there is less time to fill passively and you get heart failure

diagnose immediately based on pulse, atrial rate is between 3 amd 6oo beat per minute

irregular distances between complexes

no obvious p waves seen

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106
Q

Af risk factors

A
  • More common in men
  • Increases with age

less than 1% in 20s

15% in 80s

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107
Q

AF reduces cardiac output by

A

decreasing filling from increased rate encroaching on diastolic filling time and loss of atrial contribution to ventricular filling

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108
Q

AF etioloy

A

whatever is most common heart disease in your local

medication can cause

    1. Hypertensive Heart Disease
    1. CHD
    1. RF in underdeveloped countries
    1. Hyperthyroidism
    1. Genetic (likely most common)

minor abnormality of dna junction inbetween strands cause afib

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109
Q

AF

Changes in the

A

refractory period of the underlying atrial musculature

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110
Q

AF what often precipitates?

A

PAC (APBs) often precipitate atrial fib of all kinds

pts who develop it have it precipitated by premature atrial beats, if you can suppress them you might be able to suppress afib for a time

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111
Q

AF may be?

A

valvularor non-valvular

treatment is warfarin

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112
Q

AF

Always address?

A

underlying cause

ie; postop cardiac surgery, hyperthyroidism, mitral valve disease, pulmonary disease, etc.

113
Q

AF Classification

A
  1. Paroxysmal
  2. Persistent
  3. Long standing persistent

Permanent AF-

114
Q

AF Classification

  1. Paroxysmal
A

AF that terminates spontaneously or with intervention within 7 days of onset. Episodes may recur with variable frequency

115
Q

AF Classification

  1. Persistent-
A

AF that fails to self-terminate within 7 days. Episodes often require pharmacologic or electrical cardioversion to restore NSR (Normal Sinus Rhythm). AF generally progresses.

116
Q

AF Classification

  1. Long standing persistent
A

AF that has lasted for more than 12 months.

117
Q

AF Classification

Permanent AF

A

patients with persistent AF where a joint decision has been made by the patient and clinician to no longer pursue a rhythm control strategy

going to treat with a method of anticoag and rate control

118
Q

Low Risk AF

A
  • Used to be called “Lone” AF.
  • 15-30% of AF
  • Younger male patients
  • Frequently familial, low risk of thrombo-embolus (CHA2DS2-VASc score of 0). (this one more complete than just chads)
119
Q

Recurrent AF

A

90% of AF patients have asymptomatic recurrent episodes lasting up to 48 hours

afib pulse is completely random and the volume varies from beat to beat so after a long pause it is more full and higher.

pulse is totally erratic

120
Q

Subclinical AF

A

AF detected in asymptomatic patients without a prior diagnosis. Many of these patients have paroxysmal AF.

121
Q

Afib Evaluation of the Patient

A
    1. H&P
  • History of palps, syncope, dyspnea, fatigue. Precipitating causes include exercise, emotion, alcohol-Holiday Heart.
  • PE-mitral valve disease, especially MS, CHF findings, etc.

binge drinking

from aldehydes of alcohol

may hear mitral regurg and could be reason they have afib or mighthear mitral stenosis that always leads to afib

122
Q

Anti Coagulation predictor

A

CHA2DS2-VASc: This is becoming the most useful tool for deciding risk of stroke to determine whether to anti-coagulate

123
Q

CHA2DS2-VASc

A
  • C=Congestive Heart Failure
  • H=Hypertension
  • A2=Age>=75 (2 points) (65-74 1 point)
  • D=Diabetes Mellitus
  • S2=Stroke, TIA or Thromboembolus(2 points)
  • V=Vascular Disease (prior MI, PAD, aortic plaque)
  • A=Age (65-74) 1 point
  • Sc= Sex category, Female (1 point) (lady with htn you are a candidate for a nowak?)
124
Q

aortic plaque

A

usually accounts for 30% of stroke, usually source of cryptogenic (dont know where it came from), embolic and debris below carotids and vertebrals, treat with statins

eating fish reduces risk

125
Q

CHA2DS2-VASc score and stroke risk/year

A

0 0.2%
1 0.6%
2 2.2% (higher than risk of nowak

when nowaks were developed warfarin is horrible

with warfarin inr needs to be between 2 to 3)

3     3.2%
4     4.8%
5     7.2%
6     9.7%
7     11.2%
8     10.8%
9     12.2%
126
Q

AF-Anti Coagulant Meds

Warfarin

A

Warfarin

1954 FDA approval

“WARF”=Wisconsin Alumni Research Foundation

Derived from “sweet clover animal feed” spoiled with a fungus, discovered at the University of Wisconsin.

cows were aborting baby cows bc of this

First oral anti coagulant

Measured by INR (International Normalized Ratio)

Therapeutic range 2.0-3.0 for atrial fibrillation stroke prevention

127
Q

AF Anticoagulants NOAC (Novel Oral Anti Coagulants)

A

used for nonvalvular afib

  • NOAC (Novel Oral Anti Coagulants) are replacing warfarin in many patients
  • No blood testing necessary
  • These drugs interfere very little with other drugs and virtually no foods
  • As of this date there are 3 available
  • One Direct Thrombin Inhibitor, Pradaxa, dabigitran
  • 2 Factor Xainhibitors
  • Xarelto(rivaroxaban)
  • Eliquis(apixaban)
128
Q

Afib Evaluation

A
  • EKG-rhythm, rate, other abnormal findings, LVH, ST changes, QRS width, QT interval, PR interval.
  • Echocardiogram-chamber sizes and function, valvularfunction, pulmonary artery pressures (Pulmonary Hypertension).

history is most important then echocardiogram

129
Q

Afib Treatment, Tale of 2 Cities

A
    1. Rate Control-patient is appropriately anti-coagulated and the rate is controlled by AV blockers.
    1. Rhythm Control-effort is made to anti-coagulate and restore NSR by meds or electrical cardioversion. A TEE may be used to rule out LA thrombus prior to cardioversion. (athletes control this one)

no real advantage in mortality for either of these, so you can anticoag and control the hr

aspirin for afib is useless

130
Q

no Plavix for

A

afib

131
Q

valvular afib is directly tied to

A

heart valve disease usually mitral valve, mit regurg is more common, put mitral stenosis on warfarin

you can give beta blockerto keep hr low when the pt goes into afib

132
Q

PVC’s overview

A
  • Premature Ventricular Complexes-PVC
  • Premature Ventricular Beats-PVB
  • Wide QRS (>=120msec)
  • Full compensatory pause
  • SN doesn’t “see” the PVC.
133
Q

PVC salvo

A

2 in a row

134
Q

PVC multiform

A

more than one qrs morphology

135
Q

PVC bigeminy

A

every second beat is a pvc

136
Q

PVC vt ventricular tachycardia

A

3 or more pvcs in a row polymorphic or torsades de pointes

137
Q

pvc polymophic

A

multiform

138
Q

Mechanisms of PVCs

A
  • Re-entry
  • Enhanced normal or abnormal automaticity
  • Triggered activity resulting from after depolarizations
139
Q

PVC Associated Conditions

A
  • Hypertension and LVH
  • Acute MI
  • CHF
  • Hypertrophic Cardiomyopathy
  • Congenital Heart Disease
  • Idiopathic VT
140
Q

PVC Treatment

A
  • Avoid stimulants if desired.
  • Since the PVC’s are not a disease, avoiding stimulants is entirely up to the patient
  • Stimulants include caffeine, nicotine, alcohol (a little complicated), pseudoephedrine, elicit drugs (cocaine, methamphetamine, etc).
141
Q

PVC Facts

A
  • One of the most common presenting complaints to a Cardiologist’s office.
  • Presents with palpitations
  • Syncope is an alarm that this IS SERIOUS
  • Almost always of NO significance
  • Often over emphasized by patient and occasionally by the PCP
142
Q

Presence of PVC’s with ACS (acute coronary syndromes)

A

is a bad prognostic sign, but the rules for PVCs in healthy individuals are totally distinct from these patients, and are almost always benign.

143
Q

PVC

Reassurance is the mainstay of treatment with patients who have no

A

structural or significant electrical abnormalities (WPW, etc).

144
Q

PVC

Occur in patients without

A

structural heart disease, and with various levels of severity of heart disease.

145
Q

PVC

Frequency and complexity have

A

no bearing on prognosis, only in ACS and post MI.

146
Q

PVC

The severity of LV function determines

A

prognosis, not the frequency or complexity of the PVCs

147
Q

PVC

Pharmacologic Treatment

A
  • Usually not required
  • Most benign Rx is Beta Blocker
  • Lowest effective dose
  • More classical anti-dysrhythmias are relatively contra indicated
  • Refer to EP Cardiologist for Complex drugs and/or ablation.
148
Q

PVC serious palpitation symptoms

A

pt feels like they will die, syncope, blackouts, underlying heart disease

149
Q

syncope could be

A

vtac, intermittent vfib, psvt at rates of 240 thatt reduces co, afib with fast hr of 200

150
Q

flecainide incanide suppressed pvcs,

A

cast trial showed that these half died that got the drug, if heart was normal arrhythias was low, but if you had cad it caused arhythmias

151
Q

PVC full compensatory pause

A

sinus node doesnt know the pvc occured so when pvc gets to atrium it depolarizes it and they colide, so sinus beat doesnt do anything,

152
Q

PVC frequency

A

30 beats is sustained

less than 30 not sustained

153
Q

PVC Multiform

A

more than 1 qrs morphology of the pvc

coming from more than 1 area (torsades de pointes)

154
Q

most pvcs are from

A

reentry

155
Q

most pvcs are from

A

normal hearts

156
Q

what treatment usually for pvcs?

A

none

157
Q

Pvc with amiodarone

A

treat acls with amiodorane if mi and flurrys of pvcs

amio short term use is fine

long term side effects are life shortening di short of breath, pulmonary fibrosis

158
Q

AV Block Major Causes

Physiologic and Pathophysiologic

A
    1. Increased vagal tone (cam cause syncope)
    1. Fibrosis and sclerosis of conduction system (some of these cause scarring that causes this)
    1. IHD
    1. Cardiomyopathy and myocarditis
    1. Congenital heart disease
    1. Familial AV Block
159
Q

1s degree AV block is a prolongation of

A

pr interval, prolongation of over .20 seconds, it is rate dependant, prolongation of conduction between the atria and the ventricle.

160
Q

early rapid filling phase then the

A

atria contracts to fill ventricle, if the contraction isnt synchronous it doesnt help to fill the ventricle, in normal heart atria contributes 5% or less to CO but in heart failure it goes up to 35% of co

161
Q

AV Block-Physiologic/Pathophysiologic

A

Other causes-hyperkalemia,infiltrativemalignancies,neonatalLupus, severe hypo or hyperthyroidism, trauma,degenerativeneuromuscular disease

162
Q

AV Block Iatrogenic

Drugs

A

Digitalis, calcium channel blockers, beta blockers, amiodarone, adenosine

163
Q

AV Block Iatrogenic everything besides drugs

A
  • Cardiac Surgery
  • Catheter ablation of arrhythmias
  • TranscatheterVSD closure
  • Alcohol Septal ablation for HOCM
  • TAVr(TranscatheterAV replacement)
164
Q

AV Block-Definition

A

•AV Block is defined as a delay or interruption in the transmission of an impulse from the atria to the ventricles due to an anatomic or functional impairment in the conduction system.

165
Q

AV Block Fibrosis and sclerosis of the conduction system accounts for

A

about 50% of cases of AV block and may be induced by several different conditions that often cannot be distinguished clinically. These are frequently progressive to complete heart block.

166
Q

AV BLock IHD (Ischemic Heart Disease) accounts for

A

40% of cases. Conduction distrubancesrange from first degree AVB to complete with either chronic IHD or an Acute MI.

can go from 1st degree to complete block

167
Q

AV Block Familial AV Block

A

may be transmitted as an autosomal dominant trait

168
Q

AV Block Drugs

A

including digitalis, calcium channel antagonists (verapamil and diltiazem), amiodarone, adenosine, and beta blockers can impair AV conduction, occasionally resulting in AV block.

Most are atleastpartially reversible following drug withdrawel.

169
Q

AV Block A variety of procedures performed on the heart may result in

A

AV block.Theseinclude valve replacement, catheter ablations, closure of VSD’s, alcohol septal ablations and TAVr.

170
Q

Types of AV Block

A 
•First Degree AVB
•Second Degree AVB:
     •MobitzType I
     •MobitzType II
Third Degree AVB (complete heart block)
171
Q

First Degree AVB

A

prolongation of pr interval

172
Q

MobitzType I

A

progressive PR interval prolongation precedes a nonconductedP wave

wenckebach

count pwaves to qrs complexes 8:7 ex

173
Q

MobitzType II

A

PR interval remains unchanged prior to a P wave that suddenly fails to conduct to the ventricles

conduction disease is more prominent and the qrs will be more widened, shows you it is not serious if it is narrow and the pt probably will get better

if it is wide they will not get better without a pacemaker

174
Q

Third Degree AVB (complete heart block)

A

No atrial impulses reach the ventricle in 3rdDegree AVB. The block can exist in the AV node or in the infranodal specialized conduction system.

atria are doing their thing and ventricles are doing their thing slower, hr is slower

av dissociation is where atria and ventricles are doing their own thing but ventricles are going fast, vtac, hr is high

175
Q

AV block examples

A

pdf 1.4 and 1.5 from sep 15

176
Q

Aortic Stenosis overview blonder

A

valve disease in adult dongenital or acquired, bicuspid you are born with and the bpdy lays down scar tissue as you get older and it can get stenotic and regurgitant, happens when 25-30 so present between 35-50, valve cusps and base of aorta peaks in 80s and 90s, begins earlier but seen then.

177
Q

issue with aortic stenosis is

A

knowing when to and getting it fixed

178
Q

in bicuspid valves there may be a mess up in the

A

media of ascending aorta 20% of people with bicuspid valves get ascending aortic anuerysms

179
Q

always look for this with pt iwth

A

bicuspid valve

180
Q

timing of valve is tough to know

A

when to change

181
Q

the big clumps are calcium and are what cause the ? with aortic stenosis

A

obstruction

182
Q

AS in Adults

A
  • The most common cause of LV outflow obstruction.

* Etiology has changed over the past 40 years with Bicuspid AV and Senile AS taking over from RF (RHD).

183
Q

2nd most common cause of lv outflow obstruction is

A

hypertorphic obstructive cardiomyopathy, most common cause of sudden death playing sports

184
Q

2nd most common cause of death in athletes

A

coronary artery anomalies

185
Q

Bicuspid AV

A
  • The most common congenital abnormality of the heart
  • Occurs in 1-2% of the population
  • Men out number women 4:1
  • Two cusps instead of three, unequal size, presents in adulthood, younger (35-55 years old) then Senile
186
Q

Senile AS

A
  • Many names, AS of aged, etc.
  • Seems to be associated with atherothrombotic degeneration of the AV (trileaflet) (atherosclerotic is another name)
  • Much older patients, likely in their 80s and 90s.
187
Q

The obstruction to outflow from the LV causes

A

LVH first, then LA dilatation, finally LV dilatation CHF and death

188
Q

Aortic Stenosis 3 cardinal symptoms are

A

DOE, syncope (near syncope, exertional lightheadedness, etc) and angina of effort. Any one of these symptoms are indications for valve replacement as life expectancy is reduced to

189
Q

no lvh

A

no severe aortic stenosis

190
Q

echo measures normal left ventricle is normal up to

A

0.9 or 1.0 over is lvh is they are up to 2. something is severe

191
Q

after lvh left vetnricle dialates in AS

A

this is late in disease and yo must replace valve

192
Q

left atrium dialates early in disease in as

A

so this will tell you if it is severe also

193
Q

dyspnea on exertion or sob

A

is from heart failure, diastolic heart failure, replaced by heart failure with preserved ejection fraction, he thinks it has to do with apex twist no diastolic heart failure

194
Q

less than 10% of pts have heart disease with chest pain

A

usually chest wall or osteopathic from the back easy to determine bc tender during palpation so use omt even this cardiologist uses it, but know bc you cant treat cardiac by cracking back

195
Q

Is pe diagnostic for AS

A

yes if done correctly

196
Q

Echocardiography is indicated if significant AS

A

is suspected

197
Q

As diagnostic pearls

A
  • Look for other causes of symptoms, especially in the aged.

* Coupling the symptoms with echo findings helps lead to proper care. It is usually difficult.

198
Q

ejection murmur means

A

systole, crescendo decrescendo, after you hear a few of them you will know

199
Q

innocent murmurs

A

are ejection murmurs but you can tell if it is not innocent by physical exam

200
Q

AS radiates where?

A

into carotids and on the clavicles so you can hear it easy bc bone transits sound so good

201
Q

AS degree of symptoms

A
  • The degree of symptoms varies widely from patient to patient.
  • There is a long asymptomatic period in each patient.

young can develop it very severe and die before they get symptoms

old people get sob from a ton of things

202
Q

PE in AS

1

A
  • Inspection may find JVD with right heart failure (late finding)
  • There is LVH (non displaced large apex impulse, LV dilatation is late) (it wont be in 5th ic in mid clavivluar it will be to the left and down or maybe in the axilla)
  • A precordial thrill, 3rdinterspace, LSB may be felt.
  • S1 normal, SEM at base, radiates into neck and onto the clavicles (much easier to hear)
203
Q

functional class 3 symptoms of AS

A

sob on more than ordinary activity

look at sob color copb blue bloater pink puffer

204
Q

shock

A

when you can feel a sound

205
Q

thrill

A

if you can feel a murmur

206
Q

shudder

A

when you can feel as in carotid if feels like a cat purring

207
Q

PE in As

2

A
  • Murmur that stops at base of heart and doesn’t radiate into neck is usually not AS, it may be HOCM
  • AS almost always radiates onto the clavicle, it is my “ace in the hole”
  • Severe AS radiates a “shudder” into the carotid, like a cat purring in the neck. You can diagnose AS by careful palpation of the carotids, before you listen to the heart.
208
Q

HOCM

A

hypertrophic obstructive cardiomyopathy

209
Q

AS echo

A
  • AVA= aortic valve area
  • Pressure gradients, mean and max, flow velocity above (distal) to AV and calculated outflow tract dimensions are all utilized to stratify the severity of AS.
  • You must correlate the signs symptoms and echo findings in each patient.
210
Q

AS pressure diff

A

pressure below and above with these you candetermine valve area

.6 is critical

.75 moderate
1 is normal

4cm per second and above is severe

pressure gradeint diff of 40 mm is severe

211
Q

Patients with acute mitral regurgitation are often gravely ill

A

with significant hemodynamic abnormalities that require urgent medical and usually surgical treatment

212
Q

Etiology Of Acute Mitral Regurg

Only 2 basic mechanisms

A
    1. Ruptured mitral chordae tendinaedue to myxomatousdisease (was called MVP), infective endocarditis, trauma, rheumatic heart disease (either acute or chronic) or spontaneous rupture.
    1. Papillary muscle rupture due to acute MI or trauma or pap muscle displacement due to ischemia or MI.
213
Q

Etiology Prosthetic Valves (can fail acutely and cause)

Acute Mitral Regurg

A
  • Tissue valve leaflet rupture due to degeneration, calcification or endocarditis
  • Impaired closure of mechanical valve due to thrombosis, infection, pannus.
  • Paravalvular regurgitation
214
Q

Acute mitral regurg

Pathophysiology

A
  • LA compliance (remember physics) is usually normal, causing an immediate and severe reflection of high pressure from the LA to the pulmonary circulation, causing pulmonary edema. In chronic MR the LA dilates and becomes very compliant, there is no time for LA dilatation in acute MR
  • Also, because the LV is not dilated, much of the cardiac output is diverted into the LA, causing a decrease in effective CO. This causes cardiogenic shock
215
Q

Acute mitral regurg basic path

A

usually stiff and not compliant so when it happens all thepressure goes back into the lungs and can kill you

216
Q

Clinical Manifestations of acute mitral regurg

A

Patients present as the moniker “Acute Severe MR” would suggest with pulmonary edema and cardiogenic shock, they are dying. Only rapid correctly directed care will save their life.

217
Q

PE for acute mitral regurg

A
  • Signs of both APE and Cardiogenic Shock prevail, fast threadypulse, hypotension with hypoperfusion(cold), wet lungs (crackles), extreme air hunger and orthopnea (can’t lay down).
  • There is usually a murmur of MR, but many patients will have a soft or inaudible murmur due to increase in LA pressure diminishing the noise.
218
Q

acute mitral regurg testing

A
  • The diagnosis is made with echocardiography, along with the EKG, CXR and cardiac catheterization
  • Many of these patients will need to be intubated and placed on an ET tube to obtain these tests as their clinical state is as above.
219
Q

Acute mitral regurg Medical Stabilization

A

Most texts mention vasodilators first, but in my experience you need an IABP first, after endotracheal intubation and sedation, often in the Cardiac Cath lab, followed by coronary arteriography. It only takes 2-3 minutes to place an IABP, once the lab and equipment are ready. Also an LVAD will work nicely (but nowhere as available as IABP.

220
Q

Acute MR Endocarditis

A

This is one of the absolute indications for surgery in SBE, or ABE.

221
Q

Ischemic Acute MR

A
  • PCI works well, but may require IABP support.
  • If papillary muscle rupture occurs, only surgery will save your patient’s life. IABP, LVAD may be life saving prior to going to the OR.
222
Q

Chronic Mr Management

A
  • Pathophysiology and Natural History
  • Severity of Valve Lesion
  • Presence of Atrial Fibrillation
  • Effectiveness of Vasodilator Therapy
  • Endocardial Prophylaxis
  • Indications for MV Replacement or Repair (always repair when can and replace when needed)
223
Q

chronic mr Pathophysiology and Natural History

A
  • Most elusive is the transition from compensated to decompensated state (dont want this, act fast)
  • This transition is dependent on the mechanisms of compensation and the severity of the valvular regurgitant volume
  • LV chamber size and function are very important determinants of outcome, both with and without surgery
224
Q

Pathophysiology Phases of chronic MR

A
  • Compensated Phase

* LVEDD

225
Q

ef should be normal or high with severe mitral regurg bc

A

bc it is a volume problem, so it increases preload and it increase the velocity and force of fiber contraction thus increasing the ejection fraction

if ejection fraction is even a little low with mr it requires immediate action

this asd and aortic regurg all have increased ef

226
Q

Pathophysiology of chronic mr

Decompensated Phase

A
  • LVEF7 cm, LVESD>4.5cm.

* Very important to recommend surgery prior to decompensation as surgical results are very poor in these patients.

227
Q

Etiology of Chronic Mr

•5 “parts” of the MV apparatus:

A
    1. Leaflets
    1. Mitral Annulus
    1. Chordae Tendinae
    1. LA
    1. LV (papillary muscle, regional LV dysfunction at the origin of the muscle, etc)
228
Q

chordae tendinae in MR

A

120 in left ventricle lose 3 get some mr lose 15 get severe mr

cordae dont cross to other papillaries

anterior leaflet sticks like a tongue

posterior leaflet is like the rim?

229
Q

papillary muscle is pulled down when

A

ventricle is enlarged for any reason

230
Q

MV Leaflets

MR may occur due to

A
    1. Myxomatous MV (MV Prolapse)
    1. Rheumatic changes (underdeveloped countries)
    1. SBE (acute)
231
Q

Myxomatous MV in mr

A

not a sydrome,

imprortant lies in amount of mitral regurg no the amount that goes back into the atrium

most common

232
Q

Mitral annulus MR

A

MR may occur due to calcification “fixing” the apparatus open, usually not severe, very difficult or impossible to surgically repair (I’ve never seen an attempt to repair surgically)

233
Q

Chordae Tendinae MR

A
  • Rupture-usually acute (severe mitral regurg)
  • Fixation from RF (and leaflets)
  • Disruption from SBE-usually acute
234
Q

Left Atrium MR

A
  • MR begets MR
  • Progressive LA dilatation leads to valve being “pulled apart” as there is continuity of the LA with the leaflets

cant tell transition from la to valve leaflet bc it is continuous so when it enlarges it pulls apart and makes it worse

235
Q

Left Ventricle MR

A

Dilatation of the LV leads to some level of MR in most cases

bc of pulling papillary muscles, cordae tendinae and dilation of the annulus

9/10, dont replace mitral valve bc youll still have the problem

236
Q

Atrial Fibrillation in MR

A
  • May decompensate patient rapidly
  • Due to decreased filling of LV from increased HR (encroaching on diastole when the LV fills, early and mid diastole, passive filling phase) and loss of atrial contribution to LV filling in late diastole
237
Q

Ischemic Heart Disease and MR

A

The papillary muscles contract late in the cardiac cycle, “end circulation” of the muscles can lead to MR by loss of “holding down” the leaflets due to ischemia of the papillary muscles. Chronic MR may develop, and it usually is reversible with revascularization techniques (PCI or CABG).

238
Q

if papillary muscles don’t contract

A

you get prolapse leading to regurg, with ischemia first thing that goes is mechanics

239
Q

symptoms of MR

A
  • Dyspnea on Exertion (DOE)
  • Fatigue
  • Palpitations-especially with atrial fibrillation
  • CHF decompensation, orthopnea, PND, Functional Class III or IV
240
Q

orthopnea

A

sign of heart fialure decompensation

241
Q

PND

A

he likes this for decompensated hf

paroxysmal nocturnal dsypnea

242
Q

signs of Mr

A
  • Precordial Exam
  • LV heave
  • Holosystolic Murmur, or Pan Systolic Murmur (PSM, HSM), at the apex, radiates in direction of MR jet, anterior or posterior (opposite leaflet).
  • Decreased S1, wide split S2 from early A2, occasional S3
  • Rapid rising and falling bounding pulse-volume problem like AR

first heart sound is soft

second widely spilt if severe

  • Echocardiography
  • Chamber size (LA, LV) and function (EF increased at first)
  • Doppler measurements of Flow, regurgitant volume (fraction), direction and volume of jet in LA, etc.
243
Q

holosystolic murmur in mr

A

most important for dx

high frequency blowing in quality easy to hear

244
Q

if you feel heave

A

ef is 35% or lower

think Mr

245
Q

MR treatment

A
  • SVR (systemic vascular resistance determined by arteriolar resistance) (lower peripheral resistace) is the resistance to LV ejection (with a normal AV and LVOT)
  • There is a competition between the periphery and the LA for blood flow in systole. LA resistance is determined by LA size and compliance.
  • Vasodilators such as ACE or ARB, hydralazine, nitrates (venulardilator) may be usefull
  • If LV systolic dysfunction is present, general CHF meds do apply
246
Q

treat mr if

A

regurg volume back to la is 35% or above

247
Q

MR drugs overview

A

in blacks hydralazine and nitrates are more effective in heart failure in general

nitrates mostly venous unless given iv it is 50/50

nitrates is good drug in high dose for hf

248
Q

MR surgery

A
  • Mitral Valve Repair favored over Replacement

* Percutaneous Mitral “Clip” (help repair valve percutaneously)

249
Q

Mitral Stenosis

A

Clinically significant MS is only due to Inactive Rheumatic Heart Disease in the adult. Rarely mitral annular calcifications leads to MS, not usually of great significance

250
Q

MS blonder overview

A

narrowing of the mitral valve

only clinically significsnt in adult is inactive rhuematic disease

some from mitral annulus calacification, this is what makes up the mitral ring and supports the leaflets made up of muscle and fiber tissue it help keep the valve smaller and together, calcium is from aging so it cant contract usually not a big deal it can just not likely

251
Q

MS rheumatic fever

A

a disease of childhood and young adults. The first onset is almost always in childhood. 50% of patients with RF have no history of same. RF is a disease of populations deprived of antibiotics (3rdworld, abused populations, etc).

can get reoccurunce but not usually bc of antibiotic prop hylaxis

252
Q

MS rheumatic disease etiology

A
  • Rheumatic Heart Disease affects 1 in 3 patients with RF.
  • The mitral valve is involved almost 100% in Rheumatic Heart Disease.

•40% of patients with RHD have isolated MV involvement, 40% more have aortic involvement. (with mitral,)
20% have mitral aortic and tricuspid

253
Q

RF is a late sequelae of

A

Group B strep infections, usually the throat, not treated with effective antibiotics. It is an autoimmune disease, requiring weeks to develop.

254
Q

Chronic MS etiology

A

RHD

255
Q

chronic ms symptoms

A

Symptoms are DOE, PND, orthopnea and fatigue

256
Q

chronic ms symptoms are due to

A

the obstruction of flow from the LA to the LV through the MV. This increases the pressure in the LA, pulmonary vasculature back into the RV and RA. It is the resistance to blood flow that increases the pressure.; The heart always tries to maintain the flow (CO), and thus the pressure rises secondarily. The LV is relatively protected from the problem with normal or low LV pressures

257
Q

as la pressure goes up it reflects into

A

pulmonary capillaries, la starts to dialate and it starts to absorb the volume and decreases pressure, if la is small it is acute, actue ms will kill you with pulmonary edema, mechanical valves with a leaflet get stuck they might make it and go right to surgery

258
Q

MS Other symptoms

A

hemoptysis, atrial fibrillation, thromboembolism, chest pain (from pulmonary hypertension).

259
Q

hemoptysis in ms

A

due to long standing high pressure in the lungs, rare bc normally picked up before this happens

260
Q

afib in ms

A

common, get acutely il, heart fails and yuou lose atrial kick

261
Q

chest pain from pulmonary htn in ms

A

usually young ladies get this really bad

cant get pregnant with ms bc you ahve pulmonary htn

262
Q

syddenham chorea

A

nuerologic manifestation of rhuematic fever

263
Q

MS-Atrial Fibrillation

A

A very common Sequaleaof MS, a fib reduces CO by two mechanisms. The loss of atrial contribution to LV filling and the increase in HR both of which reduce LV filling (passive early and active late). This will frequently precipitate APE.

264
Q

PE in MS

A
  • Mitral facies-pink purple cheeks (maxillary) from decrease in CO and vasoconstriction
  • Pulmonary Hypertension leads to Right Heart Failure with RV enlargement, loud P2, etc
  • Cardiac auscultation (after inspection and palpation) findings: another slide
265
Q

Cardiac auscultation (after inspection and palpation) findings in ms

A
  • Increased S1
  • Single S2
  • Opening Snap, follows S2, severe shortens the A2-OS interval
  • Mid diastolic murmur (rumble), heard at apex, with pre systolic accentuation (if in NSR).
266
Q

Opening Snap, follows S2, severe shortens the A2-OS interval

A

froms tiff mitral valve openeing fully

if valve is severely narrowed the sound is close to second heart sound bc it isnt opening very far

A2-os interval (if this interval is long is it less severe)

267
Q

Mid diastolic murmur (rumble), heard at apex, with pre systolic accentuation (if in NSR). in ms

A

low frequency

usually grade 1 hear with lateral laying

at end of diastole when atrium contracts in normal sinus rhythym there is a presystolic accentuation, the murmur gets louder towards first heart sound bc atrium is contracting and dumping more blood across the mitral valve, hard to get the timing right

listen alot with mitral stenosis so you can hear them

268
Q

MS testing

A
  • EKG-P mitrale(left atrial enlargement), a fib, RVH
  • CXR-LAE, RVH, pulmonary congestion, enlarged PA (hypertension)
  • Echocardiography is now the gold standard. PA pressures, mitral gradients (mean and peak), CO, SV and MVA are all standard.
269
Q

AR overview

A
  • AR is a volume problem like MR. These are well tolerated and the vast majority of patients with AR remain compensated for life. Only when the LV dilates and the EF starts to decrease is your patient in trouble.
  • When this happens intense med Rx may be used but it should just be a bridge to AVR.
270
Q

AR blonder pearls

A

this is a volume problem they are easier than pressure problems

mild or mdoerate volume problems may not even need intervention

maybe echos every 3-5 years

have to find the few that are severe and it could cause problems

can come from leaflets of aortic valve orbase of arotic root, it pulls it apart and expands like an aneurysm which is worse than the valve problem

look for the aortic root with the aortic stenosis also and bicuspid aortic valve

271
Q

AR Etiology

Valvulard isease

A
    1. RF (rheumatic fever)
    1. Senile AV (atherothrombotic)
    1. IE
    1. Trauma (usually don’t live)
    1. Myxomatousdegeneration
    1. Degeneration of a Bioprosthetic AVR (aortic valve replacement)
272
Q

Myxomatous degeneration

A

marfans ehlers danlos ankylosing spondylitis

273
Q

AR Etiology

Aortic Root Dilatation

A
    1. Marfans, can also involve the leaflets
    1. Dissecting AA
    1. Non dissecting AA
    1. Ankylosing Spondylitis (murry strumpels disease?)
    1. Becet’s, syphilis(tertiary), Osteogenesis Imperfecta, Psoriatic Arthritis, etc
274
Q

AR

PE

A
    1. Bounding pulse, large pressure-pulse and pulse-pressure lead to many signs like Demecet’s, Traub’s, Quinkepulse, etc
    1. Early diastolic decresendo murmur(starts when aortic valve closes, 2nd heart sound), LSB, 4-5thICS, or RSB in AA
275
Q

demecets

A

head bob

276
Q

traubs

A

pistol shot sound over capillaries

277
Q

quince pulse

A

capular bed

278
Q

acute ar vs chronic ar

A

acute aortic regurg not as comon as chronic but must act fast

longer the more severe, can be trauma or infective endocarditis

CV Exam III (17 decks)

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