Blonder Flashcards
1
Q
VSD
A
Most common congenital heart disease at birth, only accounts for 10% of adult congenital due to spontaneous closure.
2
Q
VSD
4 Types
A
InfundibularVSD
Membranous VSD
Inlet Defect VSD
Muscular VSD
3
Q
InfundibularVSD
A
below the aortic and pulmonic valves, leading to progressive aortic regurgitation, the hallmark.
4
Q
Membranous VSD
A
also called conoventricular, deficencyof the membranous septum.
5
Q
Inlet Defect VSD
A
av canal, Down’s
6
Q
Muscular VSD
A
in the trabecular system, 5-20%
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
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
9
Q
VSD-Pathophysiology 1
A
- Small or Restrictive VSD have orifice diameter
- R shunt with no LV volume overload
- No pulmonary Hypertension
10
Q
VSD-Pathophysiology 2
A
•Moderate sized defect, >25%-
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
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
13
Q
VSD-Pathophysiology
Endocardial Scarring
A
bc blood is spurting into other ventricle
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
15
Q
VSD-Clinical
Small defect
A
small L>R shunt, asymptomatic adults
16
Q
VSD-Clinical
Moderate sized defect
A
either asymptomatic or mild CHF in children, usually gets smaller with growth and may have AR
17
Q
VSD-Clinical
Large VSD
A
Usually early presentation with CHF in infancy or Eisenmenger’sin late childhood, early adulthood.
18
Q
VSD
PE
A
large holosystolic, LSB, 2ndor 3rdICS, thrill
19
Q
VSD
EKG
A
66% of small are normal.
20
Q
VSD
Echo
A
test of choice
amount of flow across defect
21
Q
VSD
CT/MRI
A
excellent for complex lesions
22
Q
VSD
Cath
A
less important now with advanced Echo and MR
23
Q
What is a shock?
A
when you feel the heart sound
24
Q
Tetralogy of Fallot
4 Features
A
- RVOT obstruction
- VSD
- Aorta overrides IVS
- Concentric RVH
25
TOF
10% of CHD
one of most common cyanotic congenital heart disease
26
TOF
The need for medical intervention
is dependent on the degree of RVOT obstruction
27
Tetralogy of Fallot
RVOT obstruction
pulmonic stenosis..
28
Tetralogy of Fallot
Aorta overrides IVS
get blood from right and left ventricle going out systmically
29
Tetralogy of Fallot
Concentric RVH
consequence of everything else
30
ASD-Summary
ASD is an open communication between the atria via a defect in the intra-atrial septum
31
ASD-Summary
Septum
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
32
ASD-Summary
PFO
Patent Foramen Ovaleis a foramen covered by the septum primumbut is not sealed shut in 20% of normal subjects
33
ASD
Diagnosis
made primarily by echocardiography
34
ASD-Summary
Transient R>L shunting
occurs in most patients during the onset of ventricular contraction, explaining neurologic events in non cyanotic patients.
35
ASD Right to Left shunt get a?
stroke in right to left shunt bc clot goes to brain
36
ASD right to left shunt extra shunting of blood from right is done by
oxygen
37
ASD right to left shunt size of hole
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)
38
ASD right to left shunt don't want right sided resistance to increase bc
you will eventually need a heart and lung transplant
39
ASD right sided volume overload is well tolerated for?
years
40
ASD
essential htn causes increased resistance
(increased afterload), left ventricle will thicken, then right will thicken then right will dialate
41
ASD is what kind of problem?
volume problem which the heart tolerates better than increased resistance
42
Volume problems effect what first?
right ventricle
43
ASD
modality of choice for diagnosis and characterization of the defect?
Echocardiography
44
Bicuspid Aortic Valve
MVP-MyxomatousMitral Valve
ASD-Atrial Septal Defect
Ventricular Septal Defect
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
45
ASD
Second most common
adult congenital after Bicuspid AV
46
ASD
Usually asymptomatic
until adulthood
47
ASD
Complications include
* Atrial Arrhythmias
* Paradoxical Embolus
* Cerebral Abcess
* Right Heart Failure
* Pulmonary Hypertension>EisenmengerSyndrome
48
ASD
Atrial Arrhythmias
most common is afib, premature atrial beats then go into fib
49
ASD
Paradoxical Embolus
dvt then stroke
50
ASD
Cerebral Abcess
infection embolizes across asd into brain
51
ASD
Right Heart Failure
happens after 25 years of volume overload, rigth ventricle starts to fail
52
ASD
Pulmonary Hypertension>EisenmengerSyndrome
media and intima scrinch down and you increase resistance, pressure goeas up and r vent fails
53
ASD
Types
Secundum ASD
Primum ASD
Sinus Venosus ASD
54
Secundum ASD
* 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
55
Primum ASD
* 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
56
Sinus VenosusASD
•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
57
ASD
Scimitar Syndrome
* 1. Partial anomalous venous return
* 2. Hypoplasia of a lobe of the right lung
* 3. Thoracic aorta>Pulmonary artery collaterals
58
ASD Pathophysiology
The shunt depends on the size of the defect
the compliance of the right and left ventricles, and the phases of contraction (systole/diastole, atrial ventricular, early or late in phase)
59
ASD Pathophysiology
Most shunts start
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
60
ASD Pathophysiology
Shunt flow leads to a “useless circuit”
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
61
ASD Pathophysiology
Shunt flow leads to a “useless circuit” Leads to
Right heart volume overload, well tolerated for years, but can cause Pulmonary Hypertension and Eisenmengers
62
normally right sided is a?
fifth of the left sided
63
cad is a disease of the left ventricle most of the time bc
the left ventricle has to do more work bc the resistance is 5x higher than that of the r ventricle
64
ASD Natural Histroy
•Lesions
65
ASD Clinical Manifestation
Most patients with ASD and significant shunt flow (>2:1)
will become symptomatic and require surgical repair by age 40
32-55
66
ASD Clinical Manifestation
Atrial Arrhythmias
make pts decompensate
20% atrial fibrillation or flutter, increases with advancing age
At risk for embolic events, including stroke, including paradoxical stroke, systemic emboli
67
ASD Clinical Manifestation
Migraine cephalgiamay be associated
study is not panning out, just as many pts that got procedure had migraine resolution as those that had them closed?
maybe some association
68
ASD Clinical Manifestation
Pulmonary Hypertension and Eisenmengersyndrome, requires
>2.5:1 shunt
69
ASD Clinical Manifestation
Cyanosis
Usually associated with concomitant Pulmonic Valve Stenosis or Eisenmengers
70
ASD
Physical findings are related to three things
* Size and location of defect
* Size of the shunt
* Pulmonary Artery Pressure (resistance)
71
ASD PE
Precordium
* RV Heave
| * Palpable PA at upper LSB
72
ASD PE
Heart Sounds:
* Wide fixed split S2
* Increased P2 with Pulmonary Hypertension
* S1 split with increase in Tricuspid component
73
ASD PE
Heart Murmurs:
* SEM Upper LSB from increased flow
| * Early DM, upper LSB from PI secondary to pulmonary hypertension
74
Infective Endocarditis (SBE, ABE)
not subacute anymore
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
75
IE Usually presents
acutely not sub acutely (as before antibiotic age)
76
IE Careful clinical history focused on
indwelling prosthetic devices such as; IV catheters, orthopedic hardware, cardiac devices.
aortic and mitral valve replacements
iv drug abuse
dialysis
hypoalimentation
chemo ports
77
IE IV drug use/abuse
is one of the most important factors
78
IE PE should focus on
new regurgitant murmurs and CHF
79
IE Look for stigmata of endocarditis to include
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.
80
ASD is what heart sound?
second
81
IE Blonder overview
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)
82
IE Murmur overview Blonder
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
83
IE Diagnosis
* 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.
84
IE blonder diagnosis
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
85
IE Duke Criteria
Definite IE
* 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
86
IE Duke
Possible IE
* 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
87
Duke Major Criteria
* 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
88
Viridans Strep
Most common Ie most common oral pathoge
89
HACEK group
require special cutlure so let them know what you are looking for
90
IE
if pt is on antibiotics
you will not get a culture so keep this in mind
91
IE
most common cause
no endocarditis at al
| l, made a mistake, hard to diagnose and hard to treat, culture negative endocarditis is 5-8% of endocarditis
92
Typical micro organism for IE from two separate blood cultures;
* Viridans Stre0
* Strep gallolyticus (bovis)
* HACEK group
* Staph aureus
* Community acquired enterocci or
93
Other things to look for in Duke majore
anemia, valve regurg sick, nausea anorexic
if the pt comes in late they could have glomerulonephritis along with the lesions
94
Positive Echocardiogram in IE
vegetations and clumps of bacteria on valves on maybe on the wall
95
Duke minor
* Predisposition
* Fever (100.4 F, 38 C)
* Vascular findings
* Immunologic findings
* Positive blood cultures not meeting above major criteria
* Serologic evidence of infection
96
Blood cultures for IE
* 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.
97
Try to make diagnosis of IE before?
antibiotics but the pts health is always number 1
98
Echocardiogram
Should be obtained in all patients of IE
a TTE first, TEE if indicated
99
TTE
transthoracic echo, transducer on chest 5 different views
100
TEE
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
101
IE
Questions?
high fevers sick for weeks it will be anemic, treat quick or people will die
102
Atrial Fibrillation (AF) overview
* 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
103
Afib main risk
cardiac emboli, to the brain, 50% of strokes to brain come from this
104
A fib antithrombin drugs overview
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
105
A fib pearls
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
106
Af risk factors
* More common in men
* Increases with age
less than 1% in 20s
15% in 80s
107
AF reduces cardiac output by
decreasing filling from increased rate encroaching on diastolic filling time and loss of atrial contribution to ventricular filling
108
AF etioloy
whatever is most common heart disease in your local
medication can cause
* 1. Hypertensive Heart Disease
* 2. CHD
* 3. RF in underdeveloped countries
* 4. Hyperthyroidism
* 5. Genetic (likely most common)
minor abnormality of dna junction inbetween strands cause afib
109
AF
Changes in the
refractory period of the underlying atrial musculature
110
AF what often precipitates?
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
111
AF may be?
valvularor non-valvular
treatment is warfarin
112
AF
Always address?
underlying cause
ie; postop cardiac surgery, hyperthyroidism, mitral valve disease, pulmonary disease, etc.
113
AF Classification
1. Paroxysmal
2. Persistent
3. Long standing persistent
Permanent AF-
114
AF Classification
1. Paroxysmal
AF that terminates spontaneously or with intervention within 7 days of onset. Episodes may recur with variable frequency
115
AF Classification
2. Persistent-
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
AF Classification
3. Long standing persistent
AF that has lasted for more than 12 months.
117
AF Classification
Permanent AF
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
Low Risk AF
* 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
Recurrent AF
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
Subclinical AF
AF detected in asymptomatic patients without a prior diagnosis. Many of these patients have paroxysmal AF.
121
Afib Evaluation of the Patient
* 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
Anti Coagulation predictor
CHA2DS2-VASc: This is becoming the most useful tool for deciding risk of stroke to determine whether to anti-coagulate
123
CHA2DS2-VASc
* 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
aortic plaque
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
CHA2DS2-VASc score and stroke risk/year
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
AF-Anti Coagulant Meds
| Warfarin
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
AF Anticoagulants NOAC (Novel Oral Anti Coagulants)
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
Afib Evaluation
* 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
Afib Treatment, Tale of 2 Cities
* 1. Rate Control-patient is appropriately anti-coagulated and the rate is controlled by AV blockers.
* 2. 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
no Plavix for
afib
131
valvular afib is directly tied to
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
PVC’s overview
* Premature Ventricular Complexes-PVC
* Premature Ventricular Beats-PVB
* Wide QRS (>=120msec)
* Full compensatory pause
* SN doesn’t “see” the PVC.
133
PVC salvo
2 in a row
134
PVC multiform
more than one qrs morphology
135
PVC bigeminy
every second beat is a pvc
136
PVC vt ventricular tachycardia
3 or more pvcs in a row polymorphic or torsades de pointes
137
pvc polymophic
multiform
138
Mechanisms of PVCs
* Re-entry
* Enhanced normal or abnormal automaticity
* Triggered activity resulting from after depolarizations
139
PVC Associated Conditions
* Hypertension and LVH
* Acute MI
* CHF
* Hypertrophic Cardiomyopathy
* Congenital Heart Disease
* Idiopathic VT
140
PVC Treatment
* 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
PVC Facts
* 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
Presence of PVC’s with ACS (acute coronary syndromes)
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
PVC
Reassurance is the mainstay of treatment with patients who have no
structural or significant electrical abnormalities (WPW, etc).
144
PVC
Occur in patients without
structural heart disease, and with various levels of severity of heart disease.
145
PVC
Frequency and complexity have
no bearing on prognosis, only in ACS and post MI.
146
PVC
The severity of LV function determines
prognosis, not the frequency or complexity of the PVCs
147
PVC
Pharmacologic Treatment
* 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
PVC serious palpitation symptoms
pt feels like they will die, syncope, blackouts, underlying heart disease
149
syncope could be
vtac, intermittent vfib, psvt at rates of 240 thatt reduces co, afib with fast hr of 200
150
flecainide incanide suppressed pvcs,
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
PVC full compensatory pause
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
PVC frequency
30 beats is sustained
less than 30 not sustained
153
PVC Multiform
more than 1 qrs morphology of the pvc
coming from more than 1 area (torsades de pointes)
154
most pvcs are from
reentry
155
most pvcs are from
normal hearts
156
what treatment usually for pvcs?
none
157
Pvc with amiodarone
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
AV Block Major Causes
Physiologic and Pathophysiologic
* 1. Increased vagal tone (cam cause syncope)
* 2. Fibrosis and sclerosis of conduction system (some of these cause scarring that causes this)
* 3. IHD
* 4. Cardiomyopathy and myocarditis
* 5. Congenital heart disease
* 6. Familial AV Block
159
1s degree AV block is a prolongation of
pr interval, prolongation of over .20 seconds, it is rate dependant, prolongation of conduction between the atria and the ventricle.
160
early rapid filling phase then the
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
AV Block-Physiologic/Pathophysiologic
Other causes-hyperkalemia,infiltrativemalignancies,neonatalLupus, severe hypo or hyperthyroidism, trauma,degenerativeneuromuscular disease
162
AV Block Iatrogenic
Drugs
Digitalis, calcium channel blockers, beta blockers, amiodarone, adenosine
163
AV Block Iatrogenic everything besides drugs
* Cardiac Surgery
* Catheter ablation of arrhythmias
* TranscatheterVSD closure
* Alcohol Septal ablation for HOCM
* TAVr(TranscatheterAV replacement)
164
AV Block-Definition
•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
AV Block Fibrosis and sclerosis of the conduction system accounts for
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
AV BLock IHD (Ischemic Heart Disease) accounts for
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
AV Block Familial AV Block
may be transmitted as an autosomal dominant trait
168
AV Block Drugs
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
AV Block A variety of procedures performed on the heart may result in
AV block.Theseinclude valve replacement, catheter ablations, closure of VSD’s, alcohol septal ablations and TAVr.
170
Types of AV Block
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•First Degree AVB
•Second Degree AVB:
•MobitzType I
•MobitzType II
Third Degree AVB (complete heart block)
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First Degree AVB
prolongation of pr interval
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MobitzType I
progressive PR interval prolongation precedes a nonconductedP wave
wenckebach
count pwaves to qrs complexes 8:7 ex
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MobitzType II
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
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Third Degree AVB (complete heart block)
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
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AV block examples
pdf 1.4 and 1.5 from sep 15
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Aortic Stenosis overview blonder
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.
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issue with aortic stenosis is
knowing when to and getting it fixed
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in bicuspid valves there may be a mess up in the
media of ascending aorta 20% of people with bicuspid valves get ascending aortic anuerysms
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always look for this with pt iwth
bicuspid valve
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timing of valve is tough to know
when to change
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the big clumps are calcium and are what cause the ? with aortic stenosis
obstruction
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AS in Adults
* 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).
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2nd most common cause of lv outflow obstruction is
hypertorphic obstructive cardiomyopathy, most common cause of sudden death playing sports
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2nd most common cause of death in athletes
coronary artery anomalies
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Bicuspid AV
* 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
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Senile AS
* 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.
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The obstruction to outflow from the LV causes
LVH first, then LA dilatation, finally LV dilatation CHF and death
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Aortic Stenosis 3 cardinal symptoms are
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
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no lvh
no severe aortic stenosis
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echo measures normal left ventricle is normal up to
0.9 or 1.0 over is lvh is they are up to 2. something is severe
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after lvh left vetnricle dialates in AS
this is late in disease and yo must replace valve
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left atrium dialates early in disease in as
so this will tell you if it is severe also
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dyspnea on exertion or sob
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
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less than 10% of pts have heart disease with chest pain
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
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Is pe diagnostic for AS
yes if done correctly
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Echocardiography is indicated if significant AS
is suspected
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As diagnostic pearls
* 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.
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ejection murmur means
systole, crescendo decrescendo, after you hear a few of them you will know
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innocent murmurs
are ejection murmurs but you can tell if it is not innocent by physical exam
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AS radiates where?
into carotids and on the clavicles so you can hear it easy bc bone transits sound so good
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AS degree of symptoms
* 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
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PE in AS
1
* 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)
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functional class 3 symptoms of AS
sob on more than ordinary activity
look at sob color copb blue bloater pink puffer
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shock
when you can feel a sound
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thrill
if you can feel a murmur
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shudder
when you can feel as in carotid if feels like a cat purring
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PE in As
2
* 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.
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HOCM
hypertrophic obstructive cardiomyopathy
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AS echo
* 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.
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AS pressure diff
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
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Patients with acute mitral regurgitation are often gravely ill
with significant hemodynamic abnormalities that require urgent medical and usually surgical treatment
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Etiology Of Acute Mitral Regurg
Only 2 basic mechanisms
* 1. Ruptured mitral chordae tendinaedue to myxomatousdisease (was called MVP), infective endocarditis, trauma, rheumatic heart disease (either acute or chronic) or spontaneous rupture.
* 2. Papillary muscle rupture due to acute MI or trauma or pap muscle displacement due to ischemia or MI.
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Etiology Prosthetic Valves (can fail acutely and cause)
Acute Mitral Regurg
* Tissue valve leaflet rupture due to degeneration, calcification or endocarditis
* Impaired closure of mechanical valve due to thrombosis, infection, pannus.
* Paravalvular regurgitation
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Acute mitral regurg
Pathophysiology
* 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
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Acute mitral regurg basic path
usually stiff and not compliant so when it happens all thepressure goes back into the lungs and can kill you
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Clinical Manifestations of acute mitral regurg
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.
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PE for acute mitral regurg
* 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.
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acute mitral regurg testing
* 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.
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Acute mitral regurg Medical Stabilization
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.
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Acute MR Endocarditis
This is one of the absolute indications for surgery in SBE, or ABE.
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Ischemic Acute MR
* 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.
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Chronic Mr Management
* 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)
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chronic mr Pathophysiology and Natural History
* 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
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Pathophysiology Phases of chronic MR
* Compensated Phase
| * LVEDD
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ef should be normal or high with severe mitral regurg bc
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
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Pathophysiology of chronic mr
Decompensated Phase
* LVEF7 cm, LVESD>4.5cm.
| * Very important to recommend surgery prior to decompensation as surgical results are very poor in these patients.
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Etiology of Chronic Mr
•5 “parts” of the MV apparatus:
* 1. Leaflets
* 2. Mitral Annulus
* 3. Chordae Tendinae
* 4. LA
* 5. LV (papillary muscle, regional LV dysfunction at the origin of the muscle, etc)
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chordae tendinae in MR
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?
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papillary muscle is pulled down when
ventricle is enlarged for any reason
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MV Leaflets
MR may occur due to
* 1. Myxomatous MV (MV Prolapse)
* 2. Rheumatic changes (underdeveloped countries)
* 3. SBE (acute)
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Myxomatous MV in mr
not a sydrome,
imprortant lies in amount of mitral regurg no the amount that goes back into the atrium
most common
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Mitral annulus MR
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)
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Chordae Tendinae MR
* Rupture-usually acute (severe mitral regurg)
* Fixation from RF (and leaflets)
* Disruption from SBE-usually acute
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Left Atrium MR
* 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
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Left Ventricle MR
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
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Atrial Fibrillation in MR
* 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
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Ischemic Heart Disease and MR
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).
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if papillary muscles don't contract
you get prolapse leading to regurg, with ischemia first thing that goes is mechanics
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symptoms of MR
* Dyspnea on Exertion (DOE)
* Fatigue
* Palpitations-especially with atrial fibrillation
* CHF decompensation, orthopnea, PND, Functional Class III or IV
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orthopnea
sign of heart fialure decompensation
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PND
he likes this for decompensated hf
paroxysmal nocturnal dsypnea
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signs of Mr
* 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.
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holosystolic murmur in mr
most important for dx
high frequency blowing in quality easy to hear
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if you feel heave
ef is 35% or lower
think Mr
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MR treatment
* 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
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treat mr if
regurg volume back to la is 35% or above
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MR drugs overview
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
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MR surgery
* Mitral Valve Repair favored over Replacement
| * Percutaneous Mitral “Clip” (help repair valve percutaneously)
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Mitral Stenosis
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
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MS blonder overview
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
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MS rheumatic fever
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
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MS rheumatic disease etiology
* 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
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RF is a late sequelae of
Group B strep infections, usually the throat, not treated with effective antibiotics. It is an autoimmune disease, requiring weeks to develop.
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Chronic MS etiology
RHD
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chronic ms symptoms
Symptoms are DOE, PND, orthopnea and fatigue
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chronic ms symptoms are due to
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
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as la pressure goes up it reflects into
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
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MS Other symptoms
hemoptysis, atrial fibrillation, thromboembolism, chest pain (from pulmonary hypertension).
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hemoptysis in ms
due to long standing high pressure in the lungs, rare bc normally picked up before this happens
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afib in ms
common, get acutely il, heart fails and yuou lose atrial kick
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chest pain from pulmonary htn in ms
usually young ladies get this really bad
cant get pregnant with ms bc you ahve pulmonary htn
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syddenham chorea
nuerologic manifestation of rhuematic fever
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MS-Atrial Fibrillation
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.
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PE in MS
* 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
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Cardiac auscultation (after inspection and palpation) findings in ms
* 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).
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Opening Snap, follows S2, severe shortens the A2-OS interval
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)
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Mid diastolic murmur (rumble), heard at apex, with pre systolic accentuation (if in NSR). in ms
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
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MS testing
* 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.
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AR overview
* 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.
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AR blonder pearls
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
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AR Etiology
Valvulard isease
* 1. RF (rheumatic fever)
* 2. Senile AV (atherothrombotic)
* 3. IE
* 4. Trauma (usually don't live)
* 5. Myxomatousdegeneration
* 6. Degeneration of a Bioprosthetic AVR (aortic valve replacement)
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Myxomatous degeneration
marfans ehlers danlos ankylosing spondylitis
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AR Etiology
Aortic Root Dilatation
* 1. Marfans, can also involve the leaflets
* 2. Dissecting AA
* 3. Non dissecting AA
* 4. Ankylosing Spondylitis (murry strumpels disease?)
* 5. Becet’s, syphilis(tertiary), Osteogenesis Imperfecta, Psoriatic Arthritis, etc
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AR
PE
* 1. Bounding pulse, large pressure-pulse and pulse-pressure lead to many signs like Demecet’s, Traub’s, Quinkepulse, etc
* 2. Early diastolic decresendo murmur(starts when aortic valve closes, 2nd heart sound), LSB, 4-5thICS, or RSB in AA
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demecets
head bob
276
traubs
pistol shot sound over capillaries
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quince pulse
capular bed
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acute ar vs chronic ar
acute aortic regurg not as comon as chronic but must act fast
longer the more severe, can be trauma or infective endocarditis
