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IPAP > Cardio Block 2 > Flashcards

Cardio Block 2 Flashcards

1
Q

What is the most important and weakest part of the visit when assessing heart valves?

A

PE- weakest

Hx/Diagnostic study- strongest

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2
Q

What are the common causes of aortic valve diseases?

A

Congenital bi/unicuspid- most common congenital heart Dz, seen in PTs <70y/o

Degenerative Ca+- wear/tear from atherosclerosis/CAD, seen in PTs +65/yo

Worldwide- RF, usually mitral valve involvement then aortic valve

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3
Q

How much of an AS occlusion is needed for Sxs?

What is the bodies remodeling response to AS/inc AL and what other issue can be forced to develop?

A

90% for Sxs to appear

Concentric hypertrophy, can lead to MR

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4
Q

What is the sequence of pathophysiologic changes seen in AS?

A

AS, Outflow obstruction, Inc EDP, Concentric* LVH, LVF, CHF, Subendocardial ischemia

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5
Q

Why does exertion syncope occur with AS during exercise?

Why does CHF occur?

A

LV can’t increase CO, dilation causes decreased cerebral perfusion pressure

Inc AL causes contractile dysfunction and inc LV diastolic volume/press, pressure backs into pulmonary vessels, inc alveoli congestion

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6
Q

What are the S/Sxs of AS

How are AS seen on PE?

A

Prolonged ASx period:
Exertion induced dyspnea, angina, dizziness

Harsh Cresc/Decresc at RUSB w/ bell/diaphragm, radiates to carotid
Narrow pulse pressure
Displaces PMI

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7
Q

Define Pulsus Parvus et Tardus

How does AS cause angina?

A

Weak and late/slow rising best appreciated at carotid/PMI and carotid at same time

Imbalance between supply/demand
Inc LVDP reduces coronary perfusion pressure gradient

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8
Q

How does AS present on ECG?

What Sx is seen in PTs w/ severe form?

A

LVH, LAE, possible A-Fib

A-Fib leading to HF/Stroke

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9
Q

Where is A-Fib seen on an EKG?

How does AS appear on CXR?

A

Bi-phasic in V1 or Lead 2

LVH, Calcified leaflets, CHF if advanced

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10
Q

How does Echo appear on Echo?

Bicuspid aortic valves are associated w/ increased risks for ?

A

TTE shows inc wall thickness and determines severity

Aneurysm and Dissections

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11
Q

If AS can’t be seen w/ Echo, what test is ordered?

Who else receives this test?

A

CT or MRI

Candidates for Transcatheter Aortic Valve Replacement (TAVR)

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12
Q

When do AS PTs get an Exercise Test?

How are AS PTs treated?

A

Asx severe AS to confirm absence of Sxs

Limit activity
No optimal pharm Tx
Caution w/ anti-hypertensive meds
NO diuretics

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13
Q

How often do AS PTs receive Echos?

A 
At Dx
Mild= Q3-5yrs
Mod= Q1-2yrs
Sev= Q6-12mon
Any time Sxs change
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14
Q

What is the only true effective Tx for PTs w/ severe AS?

What is the alternate procedure for kids and young adults w/ congenital AS?

A

Valve replacement- preferred method is transcatheter aortic valve replacement

Balloon aortic valvuloplasty

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15
Q

What type of PT gets a mechanical valve and what prophylaxis do they get?

Who gets a bioprosthetic valves?

A

Younger PTs, Coumadin

PTs that won’t live more than 10yrs, no coumadin

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16
Q

What is the prognosis of AS?

What AS PTs do we screen for unnoticed Sxs?

A 
ASx- near normal survival
Angina= <5yrs
Syncope= <3yrs
Dyspnea= <2yrs
A-Fib precipitates overt HF and increases mortality rates

ASx PTs

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17
Q

What is the normal cross sectional area of the aortic valve?

What is the most common etiology of AI in developed countries?

A

3-4cm^2

Congential bicuspid
Dilation of aortic root- Marfans/Ehlers-Danlos

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18
Q

Acute AI is a medical emergency if it appears in ? situations?

A 
Native valve
Endocarditis
Aortic dissection
Traumatic rupture of leaflets
Iatrogenic- failed valvotomy/valve repair
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19
Q

What is the sequence of pathophysiology events that occur in AI?

Acute AR is usually associated with rapid decompensation due to ?

A

AR, Vol overload, LV dilation, Wide Pulse Pressure, Inc wall tension, Pressure overlaod, LVH

Inability to accomodate inc end DBP

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20
Q

How is Chronic AR different than Acute?

How does this compensation cause a widened pulse pressure and what is unique about this change?

A

Dilation w/ less hypertrophy
Drop in aortic diastolic pressure

High LVSV, reduced DBP= Wide pulse pressure, HALLMARK of AR**

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21
Q

How does acute AI present?

How does chronic AI present?

A

Acute Pulmonary Edema

Wide pulse pressure, CHF Sxs, Angina, Atypical chest pain

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22
Q

What are 5 Signs associated w/ AI and what are they all indicative of an increased risk for?

A 
De Musset- head bobbing w/ systole
Corrigans- water hammer
Quincke- nail bed pulsations
Traube- pistol shot heard over radial/femoral
Duroziez- to and fro heard over femoral

Inc stroke volume and widened pulse pressure

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23
Q

What type of murmur is AI?

AI valve etiology is best hear at ? while root etiology is best hear at ?

A

High pitched, blowing diastolic murmur at Erb’s point w/ PT leaning fwd and exhaling

Valve= LSB 2/4ICS
Root= RSB and apex
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24
Q

Define Austin Flint murmur

A

Low rumble during mid systolic sound from normal diastolic flow from LA hitting anterior leaflet of MV, which is partially closed due to inc force of AR

AR + physiological MS w/out opening snap

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25
Q

How does AI look on EKG?

How does it look on CXR?

A

LVH, LAE, LAD
Strain pattern
LBBB
A-Fib

Acute= pulmonary edema/congestion
Chronic= cardiomegaly, dilated ascending aorta
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26
Q

Why do PTs w/ AI get a radionuclide angiography/MRI?

What two tests can be ordered as follow up tests?

A

Initial and Serila assessment of LV volume and function at rest

Root angiography- hymodynamic measurements

Cardiac cath- when non-invasive tests are inconclusive/discrepant results

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27
Q

How are AI PTs managed with pharmaceuticals?

A

Nothing in ASx
ACEI, D-CCB or Hydralazine in severe cases w/ preserved LV function
BBs in PTs w/ Sxs or reduced LV function who are not surgical candidates

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28
Q

When do AI PTs get surgery?

A

Sxs and NYHA >2
EF <50%
ASx severe AI while undergoing CABG or surgery

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29
Q

What are the 3 ways to classify infective endocarditis?

What heart valve d/o is commonly affected by infective endocarditis?

A

Clinical- sub/acute
Host substrate- native, prosthetic, IVDA
Microbe- Staph, Strep

AS

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30
Q

Majority of US infective endocarditis PT are ? old and w/ ? issues

What valves are usually infected?

A

+60
Pre-existing structural heart Dz

AV > TV > PV
Drug abuse= TV

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31
Q

?? is the most common underlying cardiac condition in PTs w/ infective endocarditis

What PT population is at an increased risk of infective endocarditis?

A

MVP

Hypertrophic cardiomyopathy, especially w/ outflow obstructions

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32
Q

What risk factor is among the highest risk factors for subsequent infective endocarditis cases?

Nonbacterial thrombotic endocarditis can occur spontaneously in PTs w/ ? systemic illnesses?

A

Previous endocarditis

Marantic endocarditis of malignancy
Libman-Sacks endocarditis in Lupus Eryth.

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33
Q

What are the most common microbes in endocarditis on native valves?

What microbes are most common in IVDU PTs?

A

Strep, mainly Viridans
Staph A

Staph A
Strep

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34
Q

What are the most common microbes in prosthetic valve endocarditis when PT has had surgery within the past year?

What two microbes are the most common in PTs w/ prosthetic valves and surgery was more than 1yr ago?

A

Staph Epidermis
Staph A

Strep
Staph A

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35
Q

What are the risk factors for endocarditis

A 
Age >60
Male
Structural heart Dz
Prosthetic valves
Congenital heart Dz
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36
Q

Define Pentology of Fallot

A 
VSD
PS
Misplaced aorta
Thickened RV wall
ASD
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37
Q

What are the non-heart Dz risk factors for endocarditis

A 
Indwelling catheter (chronic hemodyalisis)
IV drugs
Hx of endocarditis infection
Poor dental hygiene
HIV
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38
Q

What conditions are needed inside of the body for endocarditis to start an infection process?

What is the most common cause of endocarditis adherence?

A

Endocardial surface injury
Platelet/fibrin thrombus formation
Bacteria enters circulation
Bacteria adherence to injured sites

Turbulent blood flow

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39
Q

Sterile vegetation is able to adhere to surfaces due to ?

What additional issue does this adherence material offer than promotes infections?

A

Fibrin deposits

Covers and protects vegetation from host defenses

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40
Q

Acute endocarditis usually presents with ? 2 Sxs and is due to ? microbe

Subacute endocarditis is usually due to ?

A

Rapid/high fever, New murmur
Staph

Low fever, non constitutional Sxs

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41
Q

50% of endocarditis PTs complain of ? issue

In 5-10% of cases, what is the chief complaint?

A

MSK Sxs- flank arthritis to diffuse myalgias

Low back pain/low grade fever w/ no osteomyeltitis or epidural abscess

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42
Q

What are the primary cardiac Dzs of endocarditis?

What are the secondary phenomena?

A

CHF signs from valve insufficiency

Focal neural from embolic stroke
Back pain w/ vertebral osteomyelitis

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43
Q

What are the common complaints of endocarditis PTs who abuse IV drugs?

How are acute and subacute infectious endocarditis Dxs differentiated?

A

Dyspnea, Cough, Angina
Due to TV involvement and secondary embolus in pulmonary vasculature

Subacute (Strep)= fever, fatigue, anorexia, back pain and weight loss
Less common Sxs= CVA or CHF

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44
Q

What are the 4 symptoms and 4 signs that appear in high frequency (>40%) of endocarditis?

A 
S= Fever, Chills, Weakness, Dyspnea
Sxs= Fever, Murmur, Skin lesion/emboli, Petechia
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45
Q

What are the S/Sxs of moderate frequency (10-40%) of endocarditis?

A

S: Olser nodes(painful)/Janeway lesion (painless), Splinter hemorrhages, Splenomegaly, Stroke, HF, Pneumonia, Meningitis
Sxs= Sweat, Anorexia, Cough, Stroke, Rash, N/V, HA, Myalgias/Arthralgias

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46
Q

What are the low frequency (<10%) S/Sxs of endocarditis?

How is steps are taken and labs ordered to help Dx endocarditis?

A

S: New murmur, Retinal lesion, RF
Sx: Ab pain, Delerium/coma, Hemoptysis, Back pain

Hx, PT, Blood culture, Echo, EKG, CXR

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47
Q

What murmur presents w/ hemoptysis?

What criteria is used to diagnose definite or possible endocarditis?

A

MS

Modified Duke criteria
Definitive= 2 major, 1 major 3 minor, 5 minor
Possible= 1 major 1 minor, 3 minor

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48
Q

What is unique about the presence of Strep Bovis/Strep Gallolyticus

Major criteria for Duke criteria include ?

A

Colorectal cancer

1) Typical microbes= Two +Blood cultures drawn 12hrs apart
2) Skin microbes= 3 or 4 or more blood cultures w/ first and last drawn at least 1hr apart
3) Single +Blood culture for Cox Burnetii (Q Fever) or Phase 1 IgG Ab titer >1:800

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49
Q

What are the 5 minor criteria of Duke Criteria?

A 
IV drug use/Prosthetic heart valve
Fever + 100.4/38*C or higher
Vascular phenomenon
Immunologic phenomenon
Microbe evidence- only one positive
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50
Q

What labs are ordered for PTs w/ suspected endocarditis?

What are the major criteria for Echo?

A

Chem 7, CBC, UA, Blood cultures

Vegetation, New regurgitation, Abscess, TTE- initial TOC (large vegetations, quantifies dysfunction, non-invasive and easy)
TEE- >90% specific and more sensitive (small vegetation, prosthetic valves, prior valve abnormality, bad windows/deformity)

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51
Q

What type of EKG changes can indicate endocarditis?

What is the most common risk factor for enteric gram-negative endocarditis?

A

Conduction d/o, blocks- indicate peri-valvular involvement

Health care contact, not IV drug use

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52
Q

What is the diagnostic procedure of choice for suspected atrial myxomas?

If the search continues to be negative, what two microbes are considered last?

A

2D echo

Marantic/Libman-Sacks (Lupus and Myxoma)

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53
Q

HACEK spp microbes are mostly ?

Coxiella Burnetti

A

Oral flora, often w/ Hx of peridontal Dz

Exposure to raw milk, farms or rural areas

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54
Q

Brucella spp

Bartonella spp

A

Ingestion of contaminated milk/milk products

Henslae- Cat
Quintana- human body lice; homeless, alcohol abuse

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55
Q

Chlamydia psittaci

Nutritionally variant streptococci

A

Bird exposure

Slow/indolent course, MOST common

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56
Q

Legionella spp

Aspergillus and non-candidal fungus

A

Contaminated water, often nosocomial outbreaks, usually prosthetic valves

Prosthetic valves

57
Q

Initial labs for endocarditis include ? and usually reveal ? results

A

CBC w/ Diff, Serum E+, Renal function, UA

Subacute= Fe like anemia, WBC normal
Acute= Inc WBC especially if Staph A is the cause
Proteinuria and hematuria are common

58
Q

What test is King for endocarditis?

What if this initial test is negative?

A

TEE

Repeat Q3-5 days

59
Q

If PT is unstable and must be given ABX prior to culture draw, when is the preferred time to draw blood?

How long does ABX Tx last?

A

Give ABX after all 3 cultures are drawn, minimum of 2

4-6wks

60
Q

What ABX is used for empiric Tx of endocarditis?

What is used for Strep, Staph or PCN allergy?

A

IV vancomycin- covers Staph (methicillin susceptible and resistant), Strep and Enterococci

Strep- IV Penicillin G 12-18M units

Staph (Oxacillin susceptible)- IV Nafcillin + Gentamicin or Cefazolin + Gentamicin

Staph (Oxacillin resistant)- IV vancomycin

PCN allergy- Ceftriaxone + Gentamycin or Vancomycin
(Dont give Gentamycin alone)

61
Q

What are the potential complications of endocarditis Tx?

A 
Emboli
CHF
Abscess- seen w/ TEE
Intracranial hemorrhage
Immune complex glomerulonephritis
62
Q

What endocarditis PTs get surgery?

A 
Refractory pulmonary edema
Severe valve regurgitation
Obstruction w/ cardiogenic shock
HF of any degree
Local infection complications
Relapsing/refractory bacteremia despite ABX therapy
63
Q

What is the Tx step for infective endocarditis that has no available effective anti-microbial therapy

What are the relapse chances?

A

Fungi, Brucella, Pseudomonas aerugiosa (DM), L sided Staph

Usually w/in 2mon
Inc w/ prosthetic valves
Continued IV drug use

64
Q

What are the mortality chances of infective endocarditis?

When is it recommended to give PTs prophylaxis?

A

In hospital- 23% or less
6mon- 27% or less
50% if infected w/ fungus or P. aeruginosa

Prostetic valves/materials
Prior Hx of IE
Unrepaired cyanotic congenital heart Dz

65
Q

What PTs are at highest risk for IE and need prophylaxis?

A

Repaired congenital heart dz w/ residual shunts/regurgitation at/near site of repair

First 6mon after congenital dz repair w/ catheter/occlusion device

Valve regurgitation due to structurally abnormal valve in transplanted heart

66
Q

What PTs are NOT given prophylaxis for IE?

A

Congenital bicuspid valve
Acquired native aortic/mitral valve dz
MVP w/ regurgitation
HCM w/ latent/resting obstruction

67
Q

What is the DOC for IE prophylaxis?

What ABX are used for PTs that are allergic to this prophylaxis?

A

2g Amoxicillin
Post-procedure ABX are not required

Allergic to PCN=
Cephalexin
Clindamycin
Azithromyin/Clarithromycin

68
Q

What are the murmurs associated w/ MS, MR and MVP?

What PT population tends to get it?

A 
MS= opening snap
MR= blowing holosystolic
MVP= mid-systolic click

Young females w/ 2:1 W/M, younger ages in 3rd world countries, 2-3 decades post-infection

69
Q

What is the pathophysiology of MS?

How does PHTN look on EKG?

A

MS, Fixed CO, Inc LA Press, Inc pulm press, Inc hydrostatic press, Plasma in lungs, CHF dyspnea

P wave >2.5mm in Lead 2

70
Q

What are the two types of PHTN that develop due to MS?

How do they form?

A

Passive- inc pressure due to backward flow from LA press (most common)

Reactive- hypertrophy of pulmonary artery

71
Q

What is the end result of MS?

What are the main S/Sxs of MS?

A

R sided HF due to RVH, and TR

Progressive dyspnea w/ exertion
Hemoptysis

72
Q

How does a MS murmur sound?

What PE finding indicates the severity of MS?

A

Low rumbling decrescendo diastolic rumble
heard w/ bell @ LLD

Duration

73
Q

How does MS look on EKG?

How does it look on CXR?

A

LAE (P-mitrale)
RVH
RAD
Possible A-fib

LAE, Pulmonary congestion, Kerley B lines, Prominent pulmonary arteries

74
Q

What Dx test is done for suspected MS and can confirm Dx?

What can be seen on this test?

A

TTE

Thick MV leaflets (fish mouth)
Severity of mean gradient
Potential LA thrombus

75
Q

TEEs should always be performed for ? 2 reasons?

How is MS treated?

A

ID LA thrombus
Eval MV morphology and hemodynamics in PTs w/ sub-optimal TTE

Na restriction/Diuretics
BB
Non-DHP CCB
Digoxin- rate control A-fib
Anti-coagulants- A-fib or thrombus
ACEIs can be used but have delayed benefit
76
Q

Since sudden death from MS is rare, all PTs need to ?

What is the best/definitive Tx for MS?

A

Exercise

Valvotomy/replacement
Percutaneous mitral balloon valvotomy is PREFERRED unless congenital MS

77
Q

What is the f/u schedule for MS PTs after Tx?

What is the normal MV size?

A 
Known MS and changing Sxs
Serial echo for ASx
Routine TTE:
Q3-5yrs MVA >1.5cm (mild)
Q1-2yrs MVA 1-1.5cm (mod)
Annually MVA <1cm (sev)

4-6cm^2

78
Q

MR usually effects ? PTs and involves ? leaflet?

What is the most common cause of degenerative MR in the US?

A

F>M
Posterior leaflet

MVP

79
Q

What are the etiology causes of Primary MR?

What are the secondary causes?

A

Congenital, RH, IE, MVP, Trauma

HOCM, Acute MI, Ischemic Dz, LV dysfunction, RF

80
Q

Define Acute MR

A 
Sudden usually from damage to valve:
Post-MI
Ruptured chordae from IE
Blunt trauma to chest
Deteriorated chordae from CT Dz (Marfans, Ehlers-Danlos)
81
Q

Define Chronic MR

A

Myxomatous degeneration of valve
Rheumatic deformity
Congenital defect
Calcification of annulus

82
Q

Severity of MR is based on what 5 things?

A 
Opening size during regurg
Systolic gradient between LA/LV
Systemic resistance on LV
LA compliance
Duration of regurg
83
Q

What are the 3 direct consequences of MR

One of these consequences is different than MS how?

A

Elevated LA volume/press
Reduction of Fwd CO
Diastolic volume stress on LV

MS= fixed forward CO

84
Q

What is the difference in pathophysiology between Acute and Chronic MR

A

Acute=
Normal LA, High LA pressure, High Pulmonary venous press, Dec CO

Chronic=
Inc LA size, normal LA/pulmonary press, low fwd CO

85
Q

What is the difference in Tx of Acute and Chronic MR?

What are the primary Sxs of each?

A 
Acute= no fluids
Chronic= fluids
Acute= pulmonary edema, needs emergent surgery
Chronic= low CO
86
Q

How does acute MR present on PE?

A 
Apical thrill if severe
Soft S1 w/ wide split S2
Loud P2 (PHTN always)
Enlarged LV 
L displacement of PMI
87
Q

How does chronic MR present on PE?

Why is one of these Sxs unique and differentiating from acute?

A

Loud, high pitched holosystolic at apex and radiates to axilla best heard at axilla in LLD w/ diaphragm
Loud S2
Intensifies w/ hand grips
May radiate to back

Chronic doesn’t have PHTN, quiet P2

88
Q

How does MR look on EKGs?

How does it look on CXR?

A

A-fib, LAE, LVH

Cardiomegaly
LAE, LVH
Annular calcification

89
Q

What’s the difference between acute/chronic MR on CXR?

What Dx test can be done?

A

Acute= pulmonary edema

TTE
Echo
Exercise Doppler Echo- for ASx PTs w/ severe MR

90
Q

How is acute MR Tx?

How is Chronic MR Tx?

A

Acute= dec preload w/ diuretics, vasodilators

Chronic= no benefit from meds
Vasodilators (ACEI) to dec AL
Goal is surgery 
Tx HTN
Anti-arrhythmics
MVP/Afib= anticoagulation
91
Q

If MR is acute and secondary to papillary rupture, what is the Tx of choice?

A

Valve replacement

If HOTN/cardiogenic shock is present, aortic balloon pump can be used to increase organ perfusion and decrease MR

Normotensive PTs- vasodilators decrease AL

92
Q

What is the prognosis for mild/mod/sev MR?

How is MVP defined on Echo?

A 
Mild= stable for yrs
Mod-Sev= surgery within 10yrs or death

Billowing of mitral leaflets 2mm or more above annual plane

93
Q

MR is associated w/ ? CT D/ox?

A

Marfann- ectopia lentis, pectus excavatum, pes planus, wrist/thumb sign

Ehlers-Danlos Syndrome

Osteogenesis imperfecta

94
Q

Define Ebstein’s Abnormality

A

Congenital malformation of TV and RV due to improper development of TV in first 8wks of gestation

95
Q

Define MVP Syndrome

A 
DEFAMED MP
Dyspnea
Exercise intolerance
Fatigue
Anxiety
Mild to Stabbing chest pain
Emoblic phenomena
Dizziness
S/Sxs of MR
Palpitation
96
Q

What type of murmur is MVP?

What causes one of the identifying features?

A

Mid systolic click w/ late systolic click

Snapping of chordae during systole when valve bows into atria

97
Q

What bedside maneuver accentuates MVP?

What diagnostic imaging is used?

A

asd

Echo

98
Q

What test is ordered for PTs w/ suspected MVP or ASx w/ MVP?

How often are they followed up on to track progression?

A

Echo

Only w/ change of Sxs

99
Q

How is MVP managed?

How is MVP syndrome managed?

A

ASA
A-Fib= anti-coag therapy or TIA while on ASA
No prophylaxis

Reassurance/life style changes
Avoid caffeine/ETOH
Avoid stress/fatigue

100
Q

PT w/ late systolic murmur and mids-ystolic click can move the click later into systole by ? maneuver?

TS usually found with other valve lesions, especially ? but rarely ?

A

Squatting

Common- MS from RH
Rarely- congenital, carcinoid syndrome, RA/metastatic tumors

101
Q

S/Sxs of TS?

What type of murmur is it?

A

Abd distension
Hepatomegaly
JVP w/ A-waves

Low pitch tumble hear on LLSB w/ bell w/ possible opening snap

102
Q

What maneuvers make TS louder?

How does it appear on EKG and CXR?

A

Inspire
Leg raise
Squat

RAE w/ absence of RVH
RAE

103
Q

How is TS Dx?

How is it Tx?

A

Echo

Reduce preload w/ diuretics
Surgery for other valve repair
Percutaneous balloon dilation

104
Q

What can cause/lead to TR?

A

RDz on MS to TR from PHTN w/ RV enlargement
IE
Ebstein- most common
Carcinoid syndrome from Lungs or GI- rare

105
Q

How does TR present on PE?

What findings will be found on PE?

A

Palpitations w/ A-Fib
Abd fullness
Prominent V-waves

RV heave
Ascites
Pulsatile liver edge

106
Q

What type of murmur is TR?

What makes it louder or quieter?

A

Blowing holosystolic heart at LLSB w/ diaphragm

Iinc w/ inspiration
Dec w/ valsalva/standing

107
Q

What EKG changes are seen w/ TR?

What will be seen on CXR?

A

RAE, RVH, A-Fib

RAE, RVH

108
Q

How is TR treated?

What usually causes PS?

A

Diuretics for volume/congestion
Severely Sxs= surgery

Congenital- most common
Carcinoid syndrome from Gi tumor metastasizing to liver and releasing serotonin metabolites into blood forming plaques

109
Q

What are the S/Sxs of PS?

What is seen on PE?

A

ASx to exertional dyspnea
Exercise induced fatigue/syncope
Sxs of R HF

RV impulse w/ left parasternal lift
S2 split and S4

110
Q

How does PS sound?

How often are these PTs f/u on?

A

Crescendo-decrescendo systolic murmur heard w/ bell or diaphragm at LUSB and accompanied w/ early ejection click

ECG for baseline and Q5-10yrs
RVH present

111
Q

When/why would cardiac cath be done on PS PT?

A

R sided Swan Ganz cath to w/ Doppler

PTs w/ peak gradient greater than 36mm
Balloon valvotomy candidates

112
Q

How is PS treated?

How does PHTN look on EKG?

A

Severe w/ surgery
Balloon valvotomy via cath is usually effective

Peaked P-wave 4-6mm tall in Lead 2

113
Q

What causes PR?

What PTs usually get this?

A

PHTN

Tetrology of Fallot

114
Q

What heart dz is associated w/ rheumatic d/os?

What are the S/Sxs of PR?

A

PI

Exertional dyspnea, chest pain, syncope
Fatigue
Anorexia/abd pain
Ortner’s Syndrome- cough, hemoptysis, hoarsness (2nd one, MS)

115
Q

What doe PR sound like?

Define the Graham-Steele murmur

A

Early diastolic murmur w/ ejection click

Result of PHTN- high pitched decrescendo diastolic murmur hear at LSB

116
Q

How is PR treated?

What is the difference between ASD murmur and PR murmur?

A

Diuretic, O2, HTN treatments

ASD- Fixed split S2, no inc w/ inspiration
PR- wide split

117
Q

What type of murmur does HOCM create?

Which holosystolic murmur inc w/ inspiration?

A

High pitched cresc/decresc mid-systolic murmur heard on LLSB

TR

118
Q

What is the relation between a VSD size and its sound?

HF is considered the final/most severe form of heart Dz including ? 6

A

Smaller= louder

Coronary artherosclerosis
HTN
MI
Valve Dz
Congenital HDz
Cardiomyopathies
119
Q

What are the 3 things that cause HF?

A

Inc Preload
Inc Afterload
Dec contractility

120
Q

Low CO and inc AL causes decreased ? which causes what chain reaction?

What is the sequence of pahtologial events leading to CHF?

A

RAAS, causes fluid overload

LV dysfuntion 
Dec contractility/CO
Catecholamine produciton- Epi, NorEpi
Inc Afterload/BP
Inc wall tension
121
Q

What are two meds given to reduce catecholamine production during HF?

Which drug is best for HF?

A

BBs, ACEIs- dec PL, AL and contractility

BBs

122
Q

What is the number one Dz that increases Afterload?

HF is a ? problem

A

HTN

Diastolic

123
Q

What are the 5 Tx goals of HF?

What med can be used to decrease Preload?

A

Manage oxygenation/ventilation
Treat unstable arrhythmia
Dec PL/AL
Improve contractility

Nitro, BB, Loops/Thiazide

124
Q

What meds can be used to decrease after load?

What drugs can be used to inc contractility?

A

ACEI, BB, Hydrochlorothiazide, Chlorthaladone

Dobutamine, Digoxin, NorEpi, Epi

125
Q

What 2 meds are used last for HF and affects the pump?

Pulmonary edema occurs as a secondary result to ? HF

A

CCB, Digoxin
Only used if dec PL/AL isn’t successful

Backwards

126
Q

What is the difference between Diastolic Dysfunction and Systolic Dysfunction?

What is the difference between forward and backward HF?

A

Dys- ineffective ventricle filling (hypertrophy)
Sys- ineffective ventricle emptying

Fwd- can’t maintain CO to meet demand
Rvs- can’t accommodate venous return causing congestion

127
Q

What’s the difference between Low and High output failure?

What causes 70% of HFrEF?

A

Low- poor CO
High- inc metabolic demand

CAD

128
Q

Reduced ejection fraction is anything below ?

What is the cellular response to the first sign of ischemia?

A

40%
40-50= gray area

Hibernation

129
Q

What are the 3 things that cause constrictive cardiomyopathy?

What causes transient and permanent Diastolic Dysfunction?

A

Amylodosis, Sarcoidosis, Hemachromatosis

Transient- ischemia
Permanent- Hypertrophy, restrictive cardiomyopathy, MIs

130
Q

Inc LV filling pressure produces ?

What is the cause of R sided HF when not caused by L sided HF?

A

Venous congestion upstream

Issue in the lungs

131
Q

What processes can cause impaired contractility?

What can cause increased after load?

What can cause impaired diastolic filling?

A

CAD (MI, transient ischemia)
Chronic volume overload (MR, AR)
Dilated cardiomyopathy

Severe AS
Uncontrolled/severe HTN

LVH
Restrictive cardiomyopathy
Myocardial fibrosis
Transient ischemia
Tamponade/constriction of pericardium
132
Q

What is the CO equation

A

CO= SV x HR

133
Q

What is the Preload equation

What happens if AL and Contractility are the same?

A

Wall tension at end of diastole
EDV/EDP

Inc Pre-Load, Frank Starling adjusts

134
Q

What is the Afterload equation

How does inc Afterload result in a dec SV?

A

Wall tension during contraction
SBP

LV pressure increases
Inc SBP
Less shortening of myocardial fibers
Dec SV

135
Q

What is Contractility?

What does this measurement reflect?

A

Strength of contraction
Independent of AL or PL

Chemical/Hormone influence of contraction
Consistent AL and PL, but inc of Contractility= efficient emptying of ventricles

136
Q

S/Sxs of HFrEF?

What type of dysfunction is this?

A

Paradoxysmal dyspnea and fatigue

Primary systolic dysfunction

137
Q

Once we have cardiac remodeling, what 3 neuro-hormonal mechanisms are activated?

A

RAAS
Adrenergic
Hypothalamic Neuro Hypophyseal system

138
Q

With over stimulation of RAAS, what type of renal consequence is seen?

A

Renal free water absorption

Dilutional hypnatremia

IPAP (212 decks)

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