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IPAP > Cardio Block 1 > Flashcards

Cardio Block 1 Flashcards

1
Q

Location, Quality, Duration, Worse/Better, S/Sxs of Angina

A

L: retrosternal; radiates to neck, jaw, arm, shoulder, “elephant on chest”, Levine Sign
Q: pressure/burn/squeeze/heavy
D: 2-10min
A/R: exercise, cold, stress / rest, nitro
S/Sxs: S3 or papillary muscle dysfunction murmur during pain episode, sweating (SNS), Nausea (PNS), Tachy

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2
Q

Location, Quality, Duration, Worse/Better, S/Sxs of Rest or Unstable angina

A 
L: same as angina
Q: same as angina but more severe
D: <20min
A/R: same as angina, dec tolerance for exertion/at rest
S/Sx: transient heart failure can occur
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3
Q

Location, Quality, Duration, Worse/Better, S/Sxs of MI

A

L: substernal, radiates similar to angina
Q: heavy, pressure, burning, burning, constriction
D: >30min, but variable
A/R: unrelieved by nitro/rest
S/Sx: N/V, SoB, sweating, weak

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4
Q

Location, Quality, Duration, Worse/Better, S/Sxs of Pericarditis

A

L: over sternum/apex, radiates to neck or L shoulder
Q: sharp, stabbing, knife-like
D: hrs to days w/ waxing/waning
A/R: deep breath, rotating chest, supine / sitting, leaning
S/Sxs: friction rub (best heard LLD)

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5
Q

Location, Quality, Duration, Worse/Better, S/Sxs of Aortic Dissection

A 
L: anterior chest, radiates to back
Q: excruciating, tearing, knife-like
D: sudden and unrelenting
A/R: HTN, Marfan Syndrome
S/Sxs:aortic murmur, HTN, BP asymmetry, large/displaced PMI
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6
Q

Location, Quality, Duration, Worse/Better, S/Sxs of PE

A 
L: substernal or over site of PE
Q: pleuritic or angina-like
D: sudden onset, lasts minutes-hrs
A/R: breathing worsens it
S/Sxs: tachy, dyspnea, Signs of RVFailure
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7
Q

Location, Quality, Duration, Worse/Better, S/Sxs of PHTN

A 
L: substernal
Q: pressure, oppressive
D: similar to angina
A/R: worse w/ effort
S/Sxs: pain w/ dyspnea, signs of PHTN
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8
Q

What are the key terms associated with the quality of pain for non-cardiac causes of chest pain?

A 
Pneumo w/ pleurisy- pleuritic, local
Spot Pneumo- sharp, very local
MSK d/o- ache
Herpes- burning, itch
Esophageal reflux- burning, visceral discomfort
Ulcer- visceral burning, ache
Gallbladder- visceral
Anxiety- variable and transient
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9
Q

What can be heard/best assessed in the aortic area?

What can be heard/best assessed in the pulmonic area?

A

Ascending aorta
Aortic valve
Ejection clicks
Aortic aneurysms

Pulmonic valve, artery, regurgitation
Lungs

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10
Q

What can be heard/best assessed at Erb’s Point?

A

Aortic/pulmonic origins
HOCM
Aortic insufficiency (blowing)

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11
Q

What does it mean if cardiac pulsations are visible laterally to the LMCL?

What does a sustained apex impulse mean?

A

Cardiac enlargement

LVH

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12
Q

How does aortic dissection effect the PMI?

What else can cause these changes to PMI?

A

Enlarged and displaced

Volume overload, cardiac dilation, hyper-dynamic apical pulse
Pressure overload- hypertrophy, sustained apical pulses

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13
Q

Blocked arteries have what characteristics?

Blocked veins have what characteristics?

A

Diminished/absent pulse, swelling, pain, cold to touch

Swelling, pain

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14
Q

What forms the anterior border of the heart on a lateral view?

What forms the posterior border?

A

Inferior- RV, Superior- pulmonary trunk

LV and part of IVC

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15
Q

Characteristics of the S1

A

Heard at Apex
Forced closure of M/T valves from ventricles in sequence w/ carotid pulse Onset of systole
Mitral= S1 but Tricuspid happens at the same time

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16
Q

Characteristics of the S2

A

Closure of A/P valves from aortic/pulmonary artery pressure
Onset of diastole
A- R2IC, more intense
P- L2ICS

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17
Q

Characteristics of S3 heart sounds

A

Most of the time= pathologic
occurs after S2 during ventricle filling as a dull/low pitched sound indicating a volume overload
Indicative of ventricular failure
Systolic HF

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18
Q

What can cause a volume overload and lead to an S3?

Pathological S3 is AKA ? and usually associated w/ ?

A

CHF, M/T insufficiency

Ventricular gallop- blood entering ventricle during rapid filling phase of diastole creating an early diastole sound and seen w/ swollen lower extremities

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19
Q

Characteristics of S4 heart sounds

A

Low pitch from HTN of any type late in diastole when atria contract before S1, atrial filling against stiff/non-compliant ventricle

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20
Q

What type of PT positioning is needed to listen for an S4?

What is a pathologic S4 AKA ? and is from ?

A

Apex with PT in left lateral decubitus

Atrial gallop from pressure overload from HTN of any type

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21
Q

Define Physiological S2 Splitting

A

Aortic valve closes before pulmonic valve and can be exaggerated by inspiration causing more blood return to RV and prolonging the emptying of the chamber and delay in pulmonic valve closure
Pulmonic region between 2-3LICS

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22
Q

When viewing heart valves from a superior view, what is the sequence of valves from anterior to posterior?

Congenital bicuspid valves are especially linked with what syndrome?

A

Pulmonic Aortic (Ant), Tricuspid Mitral (Post)

Marfan Syndrome

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23
Q

Where is the Mitral Valve located and how many leaflets does it have?

A

Between LA and LV

2: anteromedial, posterolateral

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24
Q

Where is the Tricuspid Valve located and how many leaflets does it have?

A

RA and RV

Anterior, Medial and Posterolateral

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25
Q

What does the RCA supply blood to?

A 
PRAIS P; II, III, aVF
Posterior 1/3 of septum
R atrium/ventricle
AV node
Inf/Post LV
SA  
Posterior descending artery- supplies part of septum and accounts for 85% of PTs having right dominant circulation
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26
Q

What does the Left Main Coronary artery turn into and supply blood to?

A

LAD- ABA; V1-V4
anterior 2/3 of septum, bundle branches, anterior LV (bulk of ventricle)

LCX- SLAP P; V5-V6 
1st diagonal=I, aVL= high lateral
SA node
Lateral LV
Atrium, L
Posterior LV
PDA 8-10% of PTs= Left Dom Circulation
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27
Q

Right dominant circulation means supply from ?

Left dominant circulation means supply from ?

Codominant circulation receives blood from ?

A

RCA

LCX (LMCA)

RCA and Circumflex

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28
Q

What is K role in cardiac action?

What is Ca role in cardiac action?

A

Repolarization of AP

Released from sarcoplasma reticulum from ryanodine receptor/Ca release channel to activates muscle contraction by binding to Troponin C to allow actin-myosin cross bridge to occur to shorten sarcomere.

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29
Q

What is the sequence of structures signals pass through in the hearts conduction system?

A 
SA Node
Inter-atrial/nodal pathways
AV node
AV junction/Bundle of His
Intraventricular septum- bundle branches
Left Anterior/Posterior fascicles
Purkinje fibers
Myocardial cells in ventricles
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30
Q

Define Cardiac Output

A

Measurement of the heart’s primary function of delivering oxygenated blood to tissues
CO= SV x HR

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31
Q

Define Preload

What are the 4 components?

A

Load from IVC/SVC that stretches the heart muscle prior to contraction, the ventricle wall tension at end of diastole

Total blood volume, Distribution of blood volume, Atrial contraction, Compliance

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32
Q

What is used is Preload measured?

How is it measured?

A

Ventricular End Diastolic Volume/Pressure

DIRECTLY measured by L Heart Catheterization
ESTIMATED during R Heart Catheterization from Pulmonary Wedge Pressure

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33
Q

Define Afterload

It is determined by what two factors?

A

Force that LV must pump against

Aortic pressure (mean BP)
Volume of ventricular cavity/thickness of wall
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34
Q

How do the adrenergic NS and catecholamines inc/dec myocardial contractility?

What positive inotropic drugs increase myocardial contractility?

A

Inc Ca by stimulating B1 receptor

Digoxin, Isoproterenol, Dopamine, Dobutamine, Caffeine

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35
Q

What substances decrease myocardial contractility?

A

Negative ionotropic drugs
Anti-arrhythmics- Quinidine, Procainamide, Disopyramide
CCB/BBs

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36
Q

What physiological changes/effects can initially cause tachycardia but at toxic levels/times cause bradycardia?

A 
Hypoxia
Hypercapnea
Ischemia/Infarct
Acidosis
ETOH
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37
Q

What are the H’s of ACLS?

A

Hypovolemia- tachy, narrow QRS; Saline
Hypoxia- brady, cyanosis
H+ excess- low amplitude QRS; Sodium BiCarb
Hypoglycemia- Dextrose
Hypo/perkalemia- po=flat T and origin of U, Mg infusion; per= peaked T, wide QRS; CaCl, NaBiCarb
Hypothermia

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38
Q

What are the T’s of ACLS?

A

Tension Pneumo- brady, narrow QRS
Tamponade- tachy, narrow QRS
Toxins- prolonged QRS
Thrombus- pulmonary= tachy, narrow QRS; acute MI= abnormal ECG

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39
Q

What are the causes of PEA narrow complexes?

What will be seen on EKG?

What type of issues cause it?
What imaging can be done and r/o a DDx?

A

Tamponades, Tension Pneumo, Mechanical hyperinflation, PE

Narrrow QRS, mechanical/RV issue
Acute MI, myocardial rupture
Bedside US: LV hyperdynamic, pseudo-PEA

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40
Q

What are the causes of PEA wide complexes?

What will be seen on EKG?

What kind of issue causes it?

A

Severe hyperkalemia, Na channel blocker toxicity
Wide QRS, metabolic/LV problem
Acute MI pump failure
LV hypo/akinetic, true PEA

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41
Q

Where are baroreceptors located?

What drug influences both inotropic and chronotropic results?

A

Carotid sinus, Aortic bodies, Base of heart

Epi- inc HR, inc contractility

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42
Q

Define Ejection Fraction

A

End diastolic volume ejected from ventricles during systolic contractions used to assess primary cardiac function
Normal= 55-75%
EF= SV/end diastolic volume

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43
Q

How is ejection fraction measured?

A 
Echo- done most of the time
Nuclear Ventriculography (MUGA)
MRI
Gold Standard- cardiac catheterization (R sided is best, exact done w/ L sided)
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44
Q

Cardiac hypertrophy causes what heart sounds that can be heard on physical exam?

What are the disadvantages of this hypertrophy?

A

S3 and S4

Increased stiffness and heart O2 demand

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45
Q

What effects can cause hypertrophy?

What effects can cause dilation?

A

Chronic contraction against high after load

Prolonged increase of EDV/EDP from high preloads

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46
Q

What type of heart performance change occurs with cardiac dilation?

What are the disadvantages of this dilation?

A

Initially, increased Frank Starling that tops out and results in decreased CO

Increased wall stress- LaPlace
Increased myocardial O2 demand

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47
Q

PTs presenting with chest pain need x-rays done within ? time frame?

What types of issues can be seen/identified?

A

30min

Chamber enlargement, Cardiomegaly, Enlarged pericardial sac, Ventricular aneurysms

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48
Q

How long does it take for ventricular aneurysms to appear post-MI?

What are the three types of holosystolic murmurs?

A

7 days

MR*, TR, VSD
Systolic murmurs from papillary muscle rupture

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49
Q

What four issues can be identified in the great vessels on a chest x-ray?

A

Calcification- severity (measured w/ continuous wave Doppler)
Aortic aneurysms
Pulmonary artery dilation
Pulmonary venous congestion

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50
Q

What are the primary indications for ordering a CT for cardiac issues?

A

Gold standard- chronic constrictive pericarditis
Assess great vessels- aortic dissection of STABLE PT
Pericardial abnormalities

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51
Q

CT images of the heart can be used to evaluate what four structures?

A

Great vessels
Pericardium
Myocardium
Coronary arteries

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52
Q

What are Electron Beam CT scanner used for?

A

AKA “ultra fast”
TOC to evaluate pericardial disease and cardiac tumors
Coronary artery calcification- Ca within a vessel

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53
Q

Define Agatstan score

A

Data from EBCT that correlates to atherosclerotic plaque burden, shows CA calcification
Considered cardiac risk predictor independent of other risk factors

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54
Q

MRI of the heart are AKA and best used for ?

What type of material is used the dye?

A

CMR, differentiating tissues even w/out contrast

Gadolinium- find infarcted/viable myocardium

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55
Q

What is a CMRA?

What are they utilized for?

A

Coronary angiography- non=invasive, contrast free image

High sensitivity/accuracy for CAD in LMCA, proximal points of coronary vessels and congenital coronary abnormalities

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56
Q

What are the five modes of an Echo

What are the two types of Echos?

A

1D (M-mode), 2D, 3D, 4D (animations), Doppler- blood flow, function

Trans-Thoracic
Trans-Esophageal- Gold Standard

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57
Q

What are the indications for ordering an echo?

A

Valve lesions- quantifies regurgitation and stenosis
Ventricular assessment- thickness, mass, estimate EJF
CAD- post-MI motion abnormalities, quality of RV function
Cardiomyopathy
Pericardial disease

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58
Q

What type of test would be ordered to assess a suspected stenotic heart valve?

What do all post-MI PTs receive prior to discharge home?

A

Doppler Echo

Echo

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59
Q

What are the 3 types of cardiomyopathy?

What test is always ordered for any type?

A

Dilated, HCM, Restricted

Echo

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60
Q

What is the pay off and down side of using a TTE?

A

Visualize anterior heart- RV
Can’t see posterior heart
Bad window from “fluffy”

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61
Q

What info does TTE provide?

A 
B PLEAV
Blood flow direction (regurg)
Paradoxical septum motion
LA size
Estimated EF
Assess LV/RV dilation
Valve structure assessment
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62
Q

If exact, definitive LV EF is needed, what test?

What if an estimate is needed?

A

L sided cath

TTE

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63
Q

What is the primary advantage of doing TEEs?

A

Increased sensitivity/specificity anatomic abnormality detection
Highly specific for aortic dissection, endocarditis, prosthetic/mechanical valve dysfunction
LA thrombus prior to cardioversion

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64
Q

What additional test can be performed with either TEE or TTE?

TEEs are performed if ? is suspected in the PT?

A

Venous saline agitation- Bubble Study: identifies intracardiac shunt (ASD/VSD)

Thrombus

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65
Q

What is the only study that can be used to visualize/assess the appendage on the LA?

Why is this capability unique/important?

A

TEE

Majority of cardiac thrombus originate from here

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66
Q

TEEs allow for user to focus on one structure at a time in a specific pattern in what sequence?

A 
Mitral valve and L chambers
Aortic valve
L atrial appendage***
R side structures
Interatrial septum
Base
Transgastric area
Aorta- asc and desc
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67
Q

Other than CTs, what is the only other test that allows for visualization and assessment of the aorta, both ascending and descending?

If a PTs BP is below ?/? do NOT put them in scanners, instead order ? study

A

TEE- used for unstable PTs w/ sedation

90/60, TEE

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68
Q

Normal HR for EKG
Normal P wave duration
Normal PR Interval

A

50-100
<0.12 msec
90-200 msec

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69
Q

Normal QRS duration
Normal QTCs
Normal QRS axis

A

75-110 msec
M: 390-450; F: 390-460 msec
-30 - +90*

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70
Q

What are the HR for newborns, 2, 4 and 6yrs old?

A

New: 110-150

2: 85-125
4: 75-115
6: 60-100

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71
Q

What is the criteria for the LAFB and LPFB?

A

LAFB- <0.12 sec, -45 - -90*, delayed precordium transition qR aVL, normal QRS

LPFB- <0.12sec, +90 - +180*, delayed precordium transition rS I, aVL, aR in III and aVF, normal QRS

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72
Q

EKGs must be done within ? minutes of PTs presenting?

What is the dose of MgSulfate used in V-Fib or pulseless V-Tach?

A

10m, same as triage time frame

1-2f IV for polymorphic VT

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73
Q

What is the TOC for assessing the LV function?

What is the TOC for assessing myocardial perfusion?

A

MUGA (AKA Radionuclide Ventriculography)- determines L/R ventricular ejection fraction through T-99m labeling to show blood passing through heart/vessels, ischemia/infarction, and assesses myocardial metabolism

PET scan

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74
Q

Most CA cells work in ? environments

EF from MUGA are usually similar to EJ estimates from ? test?

A

Anaerobic

Echos

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75
Q

What are the advantages of MUGA tests?

What are the disadvantages of MUGA tests?

A

30 FAV
Accuracy, RV /LV info simultaneously, No habitus limitations, 30m or less

RAV
Radiation
No info on valves
Less accurate for PTs w/ arrhythmias

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76
Q

What tags are used in cardiac PET scans?

A

Assessment of perfusion and viability with N-13, Fl-18 or Ru-82 to show areas of impaired flow or injury

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77
Q

When are Holter Monitors used on PTs?

When is an Event/Loop monitor used on PTs?

A

Continuous ECG for 24-48hrs for suspected frequent arrhythmias/syncope or dizzy
Usually the FIRST non-invasive cardiac rhythm assessment ordered

3 days to 3wks for infrequent arrhythmia Sxs or PTs w/ non-Dx Holter evaluation

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78
Q

When is an Implantable Loop recorder used?

A

PTs w/ infrequent but concerning Sxs that suggest pathological arrhythmia/unexplained syncope

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79
Q

What test is ordered for all post-MI PTs prior to starting rehab?

Other reasons for ordering a stress test can include ? four things?

A

Cardiac stress test

Prognosis, Function, Therapy effectiveness, Evaluate exercise induced arrhythmia

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80
Q

What are the absolute contraindications for ordering stress tests?

A 
SPAM HEADS
STEMI <2 days
Physically disables
Acute pericarditis (less than 2wks)
Myocarditis
Sx HOCM
Endocarditis
High ACS risk
HF- decompensated
Severe aortic stenosis
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81
Q

If PT has high risk of ACS, no stress tests can be done. What test needs to be ordered?

What Dx can PT have and STILL do a stress test?

A

Coronary angiogram

Chronic pericarditis (more than 2wks)

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82
Q

Define Baye’s Theorem

A

Probability of a PT having a Dz after a Dx test is completed (Post-Test probability) related to disease probability before the test (Pre-Test Probability) and probability the test provides a true result

Post Test Prob= Pre-Test x Likelihood ratio

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83
Q

When do PTs have a high probability of having CAD

A

> 85%
Angina in older PTs- >40 M; >60 F
Angina in PTs w/ combination of risk factors- DM, Smoking, Hyperlipidemia

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84
Q

When do PT have an intermediate risk of CAD?

A

15-85%
Younger PTs, <40 M; <60 F
Angina or non-angina in older PTs >40 M; >60 F
PTs with multiple risk factors

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85
Q

When do PTs have a low probability of CAD?

A

<15%

Possible angina in PTs w/out combo of risk factors

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86
Q

What baseline EKG abnormalities which preclude EKG based testing?

A 
WALL
WPW
Any ST depression 1mm or more
LVH/Digoxin therapy w/ any ST depression 
LBBB, paced rhythm or non spcifiv IVCD
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87
Q

What is the most common treadmill protocol?

A

Bruce protocol- requires PT to reach 85% of max HR w/ 60-65% sensitive/80-85% specific for CAD
Max= 240 - Age

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88
Q

Cardiac stress tests are performed and continued until one of what four events occur?

A 
PAST
PT is fatigued
Angina
Signs of myocardial ischemia in ECG
Target HR reached
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89
Q

Treadmill stress tests are done to provide info on what 5 things?

A 
Local TREP
Localize areas of ischemia for Tx via Echo, EKG or PET
Therapy decision making
Risk of CV event
Exercise capability
Prognosis
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90
Q

What are the markedly positive test findings of a treadmill stress test?

A 
V SIPS
Ventricular arrhythmia develops
SBP decreases during exercise
Ischemia on EKG within 3min of starting/lasting 5min after stopping
PT can't exercise for 2min
ST depression >2mm
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91
Q

How do pressures change as blood progresses through the heart?

A 
*Low Press
RA: 2-8
RV: 15-30/2-8
PA: 15-30/4-12
PCW: 2-10
*Start of high press
LA: 2-10
LV: 100-140/3-12
Aorta: 100-140/60-90
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92
Q

When measuring wedge pressure via R-sided cath, what is it AKA?

A

Swan Gams R sided cath

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93
Q

What are the therapeutic and diagnostic indications for a L-sided cath?

A

Access through F, B, A and is most common type
Balloon- CAD, C Shock, V stenosis
Intracardiac shunt closure

Cant Left w/ Painful Heart
Coronary anatomy in PUNCS
LV function
Prox aorta dz
Hemodynamics pericardial con/restriction
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94
Q

Where is access for a R-sided cath obtained?

A

Subclavian, Internal Jugular, Brachial or Femoral vein w/ balloon tipped catheter (Swan Ganz) w/out need of fluoroscope

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95
Q

What measurement is indicative of the pressure in the Left Atrium?

When are they done?

A

Pulmonary Capillary Wedge Pressure provides estimation

Admitted ICU, not done on Out-PT basis

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96
Q

What does an elevated wedge pressure mean?

What does a reduced pressure mean?

A

Volume overload- wet (S3 sound, 3rd spacing)

Volume depletion- dry (give fluids)

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97
Q

What are the indications for a R-sided cath?

A

AH AS ES ED PM
Assess filling pressures and CO in PTs w/ HF
Volume/vascular resistance in PTs w/ sepsis
Evaluate intracardiac shunts
Evaluate pericardial disease
Peri-operative monitoring PTs w/ high risk of HF during procedures

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98
Q

What are the relative contraindications for doing caths?

A 
DIPS BARS
Digitalis toxicity
Infection
Psych illness
Stroke in past month
Bleeding
Anemia
Renal impairment
Systemic HTN
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99
Q

What are the primary diagnostic indications for electrophysiologic studies?

What are the primary therapeutic indications?

A

Recurrent/difficult arrhythmia including SVT, V-Tach, sudden death

Assess pharmacologic/implanted device efficacy
Ablation of recurrent arrhythmias unresponsive to medical therapy

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100
Q

What tests can be done for PTs 4 days post-MI to test function?

What are the four steps of the clinical approach to a cardiac PT?

A

Echo, MUGA, Stress test

Anatomic/Physiologic
Etiology
Function

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101
Q

What are the cardinal Sxs of heart dz?

A

D FACES

Palpitations, Dyspnea** Fatigue, Angina, Claudication, Edema, Syncope

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102
Q 
Sxs of MI
Sxs of Angina
Sxs of Pericarditis
Sxs of Aortic Dissection
Sxs of Valve Dz
Sxs of CHF
Sxs of Tamponade
A

Pressure radiating into L arm
Pain resolving w/ rest: pressure, squeeze, tight, heavy
Feels better when leaning fwd
Sharp or ripping/tearing
Associated w/ Sxs: Aortic stenosis= syncope
Swollen extremities
Dyspnea, inability to move fatigue

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103
Q

Atypical MIs can happen in female, elder, or diabetic PTs and can have pain located where or accompanied ?

Any PT with ? pain needs to be worked up as an MI until proven otherwise

A

Neck, Back, Jaw, Head, Belching

Jaw

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104
Q

What two CV causes of chest pain present with dyspnea?

What three non-CV causes of chest pain present w/ dyspena?

A

Angina: 2-10min of pain
MI: +30min of pain

PE, Pneumonia w/ pleurisy, Spot Pneumo

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105
Q

What would be seen on an EKG if PT had PHTN?

What type of EKG axis deviation is seen w/ PEs?

A

Lead 2, Large P-wave +2.5mm w/ dyspnea

Q1S3T3, RAD/ERAD

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106
Q

Pink frothy sputum is usually associated w/?

A

PE or MS

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107
Q

What cardiac issues can cause palpitations?

What are the non-cardiac causes of palpitations?

A

V CAPS
Valve Dz, Cardiomopathy, A-Fib/Flutter, , Prematures, SVT

Anxiety, Stimulants, ETOH
Hyperthyroid- Low TSH, High T3/4, isolated systolic HTN

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108
Q

What are the 3 types of edema?

What is the sequence of edema accumulation?

A

Peripheral
Abdominal (ascites)
Dependent- pitting (3rd spacing)

Lower extremities, neck, ascites

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109
Q

What are the 8 (5 modifiable, 3 non-modifiable) traditional atherosclerotic risk factors?

What is the limit for defining HTN?
What are the ages for m/w when risks increase?

A

Smoking, HTN, Dyslipidemia, DM, Obese/Dec PT
Adv Age, Male, FamHx (consider high risk if adopted)

> 140/90 on three different visits
M:>45; W: >55

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110
Q

Diabetics have a ___ increase for CVDz

What risk factors contribute to metabolic syndrome and which one is omitted?

A

3-5x higher

HTN, Hypertriglyceridemia, Low HDL, Insulin resistance, Visceral obesity (NO LDL)

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111
Q

What type of FamHx is of concern for cardiac PT risk factors?

A

M: 1* relative w/ CAD Dx before 55
W: 1* relative w/ CAD Dx before 65

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112
Q

What are the Non-Traditional risk factors for cardiac PTs?

A 
Homocysteine
Lipoprotein
Small LDL size
Pro-inflammatory markers
Subclinical atherosclerosis
Coronary calcification- seen on EBCT
End stage renal Dz
Chronic inflammatory dz (Chrons, Lupus)
HIV/AIDS
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113
Q

Where does homocysteine come from?

What does it require?

A

Methionine metabolism

B12 and Folate

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114
Q

PTs w/ congenital deficiencies related to homocysteine metabolism will be at early risk of ?

What happens when the AA rises to dangerous levels and what is done about it?

A

Premature atherosclerosis

CV events, PO folate is given but no evidence showing decreased events

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115
Q

What is the circulating lipoprotein that is similar to LDL

Lipoprotein A levels are highly dependent on ? factor

A

Lipoprotein A- B100

Inheritance, >20mg/dl= inc risk of CVDz

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116
Q

LDL numbers are correlated with the levels of ?

What is the acute phase reactant?

A

Insulin resistance

CRP- reflects instability rather than burden and not independently reliable unless PT has INTERMEDIATE risk

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117
Q

What imaging modality is used as a screening tool for CAD in ASx PTs

What is a bad score from this test?

A

CT scan

EBCT score +100= atherosclerotic

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118
Q

Normal chest is ____ than it is _____

Abnormalities of the chest shape can lead to secondary cardiac conditions including ?

A

Wider than deep

PHTN

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119
Q

Define Pectus Excavatum

Define Pectus Carinatum

A

AKA Funnel Chest; lower sternum is depressed causing heart/great vessel compression

Sternum displaced anterior which increases A/P diameter and compresses costal cartilages (COPD/Barrel, Obese, Age)

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120
Q

Define Thoracic Kyphoscoliosis

What leads are Septal, Anterior, Lateral

A

Abnormal spinal curvature and vertebrae rotation deforms the chest, possible abnormal lung sounds

1, 2- Septal
3, 4- Ant
5, 6- Lat

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121
Q

What causes Regularly Irregular HRs

What causes irregular irregular HR?

A

Cadence ie- ventricular trigeminy

A-fib/flutter

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122
Q

What is cyanosis usually associated with?

What is abnormal/different about PTs presentation that are in septic shock?

A

Increased levels of reduced/unsaturated Hgb

HOTN but warm

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123
Q

What are the 3 things that primarily cause peripheral cyanosis?

What causes central cyanosis?

A

Cold/vasoconstriction response, HF, Shock- circulatory failure, PT will be cold w/ HOTN

Complex etiologies causing impaired oxygenation (cardiac/pulmonary R to L shunting

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124
Q

Define Eisenmenger Syndrome

Define Erythrocytosis and when is it seen

A

Condition that causes increased pressure from R side to L side of heart through ASD/VSD

Too many RBCs, seen in PTs w/ chronic etiologies that are compensating to their cyonotic state (CA, Heart Dz/F)

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125
Q

What does Pallor of the sclera indicate

What three areas can be checked?

A

Anemia- inadequate Hgb

Check conjunctiva, lips and mucous membranes

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126
Q

What are causes of bilateral edema?

Severe systemic edema due to cardiac causes may manifest as ? or ?

A 
CV Dz (most commonly HF, especially R sided)
Kidney Dz associated w/ proteinuria, hypoalbuminemia

Sacral edema or Hepatomegaly

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127
Q

What conditions can cause an enlarged PMI?

A

HTN, HCM, LVH, Atrial Myxoma (benign tumor in L atrium that enlarges and act like mitral stenosis, causes shifting of heart, most common benign tumor)

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128
Q

JVP is usually associated with ?

Why is measuring JVP in PTs w/ visible JVD not routinely done?

A

Volume overload like in CHF (+S3)

Little/no benefit since JVD= abnormal increase of CVP

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129
Q

What is the difference between the arterial and venous pulses in the neck?

Where does the JVP fill from?

A 
Arterial= single upstroke
Venous= two peaks and two troughs per cycle

Above from SVC

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130
Q

How does inspiration or posture alter the JVP?

A

Resp- volume of atria increases, dec w/ inspiration

Post- dec as PT sits up and if they’re healthy

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131
Q

Interpretation of the JVP waveform determines ? 3 things

What are the 5 elements of the wave form?

A

Structure, function, electrical abnormalities of heart, primarily on R side

A wave
X descent 
C wave
V wave
Y descent
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132
Q

Characteristics of JVP “a wave”

A

Atrial contraction
Precedes S1 in diastole
Inc A= any condition causing increased resistance to R atrial emptying
No a waves in A-Fib (no S4)

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133
Q

Characteristics of JVP “x descent”

A

Atrial relaxation
Prominent X waves in- constrictive pericarditis, pericardial tamponade
Eliminated by tricuspid regurgitation (pan/holosystolic systolic, blowing murmur)

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134
Q

What is the most common PE finding in PTs w/ constrictive pericarditis?

What other condition also has this finding?

A

Pericardial knock

Cardiac tamponade

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135
Q

Most common PE Dx finding for pericarditis?

Most common PE Dx finding for tamponades and constrictive pericarditis?

A

Friction rub (pericarditis, tamponade, myocarditis)

Pericardial knock

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136
Q

Characteristics of JVP “c wave”

A

Bulging tricuspid valve/ventricular contraction during systolic contraction, mostly not present in every PT

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137
Q

Characteristics of JVP “v wave”

A

Increased atrial pressure during venous return after systole

Especially prominent in PTs w/ tricuspid regurg

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138
Q

Characteristics of “y descent”

A

Reduced pressure w/ tricuspid valve opening and atrial emptying during diastole
Impacted by factors impairing atrial emptying (like a waves)

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139
Q

What will Pericardial Effusion, Constrictive Pericarditis and/or Pericardial Tamponade change to JVP?

A

Parodoxical JVP

Kussmaul sign: JVP rises w/ inspiration

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140
Q

Define Cannon A Waves

What can cause these?

A

Aria contracting against a closed tricuspid valve

A-flutter, Premature atrial rhythm/tachy, 3* block, Ventricular ectopics/tachycardia, Junctional rhythm

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141
Q

Define Large A Waves

What causes them?

A

Increased atrial contraction pressure

Tricuspid stenosis, R HF, PHTN

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142
Q

Someone with a prominent JVP “c wave” has what issue?

What does a Precipitous X Descent mean?

A

Tricuspid Regurgitation

Pericardial constriction or Cardiac tamponade

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143
Q

What causes large V Waves?

A

C-V waves: tricuspid regurg (raised JVP, large V wave, rapid Y descent) or ASD

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144
Q

What causes a Slow, Rapid or Sharp Y descent?

A

Slow- tricuspid stenosis
Rapid- tricuspid regurgitation
Sharp- constrictive pericarditis

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145
Q

Total JVP measurement can also be AKA ?

Normal JVP ____ w/ inspiration

A

H2O JVP

Falls

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146
Q

Kussmaul sign is seen w/ ? JVP finding?

Kussmaul findings suggest ? issues

A

JVP rising w/ inspiration

Impaired filling of RV due to fluid in pericardial space or,
Poorly compliant myocardium/pericardium

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147
Q

What are the DDx for Kussmaul JVP findings

Define the Hepato-Jugular Reflux and who is it seen in

A

Constrictive Pericarditis, Restrictive Cardiomyopathy

PE technique to visualize JVP by pressing on RUQ in PTs w/ RHF or passive hepatic congestion

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148
Q

Define Pulse Pressure

What can cause this to increase or decrease?

A

Difference between Systolic and Diastolic arterial pressures

Inc- aortic regurgitation, conditions that increase SV/contraction
Dec- hypovolemia, severe LVF, mitral stenosis

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149
Q

A full pulse exam includes assessing pulses where?

Palpating pulses has what two purposes

A

Carotid, radial, brachial, femoral, popliteal, posterior tibial and dorsalis pedis

Patency and contraction of LV

150
Q

Which pulse location is the most accurate reflection of the aortic pulse?

All pulses are assessed for what 5 things?

A

Carotid

Rate, Rhythm, Strength, Contour, Symmetry

151
Q

A normal pulse is characterized by what 3 things?

Define the Dicrotic Notch

A

Rapid rise in early systole, Short Plateau, Gradual descent

Interrupts descending limb and represents aortic closure

152
Q

Define Hypokinetic pulse

Define Hyperkinetic pulse

A

Hypo- decreased LV pressure, SV, outflow obstruction

Hyper- increased LV pressure, SV w/ decreased peripheral resistance (hyperthryroid, Epi)

153
Q

Define Bisferiens Pulse

Define Pulsus Alternans

A

Bis- pulse w/ two palpable beats during systole (HOCM, AS/insufficiency, ejection of inc SV like exercise, fever, PDA)

PA- variation in pulse amplitude from changing systolic pressure, confirmed w/ BP (Systolic HF, LV failure-S3)

154
Q

Define Pulsus Parvus et Tardus

Define Pulsus Paradoxus

A

PPT- slow rate of pressure increase, small pulse pressure, late associated w/ severe aortic stenosis (2RICS, old PTs, young congenital)

PP- exaggerated decrease 10mm or more of SBP during inspiration (tamponade, constrictive pericarditis, HOTN shock, obstructive pulmonary dz- asthma/COPD, large PEs)

155
Q

What are the three things that cause restrictive cardiomyopathy?

Stethoscope diaphragm and bell are used for what sounds?

A

Amyloidosis, Sarcoidosis, Hemochromatosis

D- high S1/2, AR, MR, pericardial friction rubs, through precordium
B- more sensitive, low S3/4, MS

156
Q

Define Thrills

Define Heave/Lift

A

Palpable low frequency murmurs most commonly associated w/ grades 4-6

Movement of precordium that’s associated w/ large ventricle or HF

157
Q

What can cause widened splitting of S2

What causes fixed spitting of S2?

A

Delayed P/Early A closures through expiration from RBBB or Pulmonic Stenosis

Constant splitting through exp/inspiration from ASD

158
Q

Define Paradoxical splitting

What part of the cardiac cycle would the tightening of the tendon chordae happen?

A

Reversed splitting- P closes before A from LBBB, AS (dec A), chronic HTN (inc A)

S3

159
Q

What can cause an increased intensity of S3?

Most common etiologies of S4 sounds are from ?

A

Increased venous return to heart- leg raise
Increased arterial press/CO- hand grip, brief exercise

LVH from any cause (HTN)

160
Q

Characteristics of opening snaps

A

Early diastolic high pitched heard between apex and L sternal border most commonly due to MS causing doming of leaflets during diastole
Not changed by respiration
Disappears w/ worsening MS
Reduced interval between A2 and Snap= worsening MS

161
Q

Define the Austin Flint murmur

A

Severe AS
Mitral valve leaflet displacement and turbulent mixing of antegrade mitral and retrograde aortic flow
Mid-diastolic, low pitched rumbling murmur best heard at Apex
“Not a true MS”

162
Q

Characteristics of Ejection Clicks

A

Early Systolic high pitched sound usually from valve dz (AS, PS, Pulmonic Stenosis)
Mid systolic- sudden opening/regurg of M/T valves during systole (MV prolapse)

163
Q

Nearly all diastolic murmurs are ?

Systolic murmurs are either ? or ?

A

Pathologic- MS/TS

Pathologic or benign- AS/PS

164
Q

What info is used to describe murmurs?

Two continuous murmurs

A

TIPS
Time/Duration, Location, Intensity, Pitch/Quality, Shape/Configuration

Venous hum, PDA

165
Q

MR will radiate and be heard ?

AS will radiate and be heard ?

A

Axilla

Neck

166
Q

What are the Grade 1-6 criteria for grading murmurs

A

1- barely audible
2- faint-med intensity
3- easily heard, no thrill
4- easily heard, possible thrill (vibration in stethoscope)
5- easily heard but requires stethoscope to touch chest, possible thrill
6- no stethoscope needed

Grade 3-4= worrisome

167
Q

High frequency pitch/quality implies ?

A

High- increased velocity

Low- reduced velocity

168
Q

Harsh pitch= ?

Blowing pitch= ?

Rumbling pitch= ?

A

Associated w/ severity

Regurgitation murmur

Diastolic in nature- Austin Flint, AR, MR

169
Q

Define Crescendo

Defie Decrescendo

Define Crescendo/Decrescendo

A

Builds intensity

Reducing intensity- early diastolic of AR

Diamond shaped murmur of AS

170
Q

Any factor that increases blood volume/preload will increase murmur intensity w/ ? exception?

How is preload inc/dec

A

MV Prolapse and Hypertrophic Cardiomyopathy- more affected by pressure gradient across valve

Inc w/ venous return, dec w/ less venous return

171
Q

What causes after load to inc/dec?

After load generally augments ? murmurs and reduces ? murmurs

A

Inc- inc systemic vascular resistance (BP at aorta)
Dec by reduced systemic resistance (BP at aorta)

Augments regurg
Reduces stenotic

172
Q

How does inspiration change the action of the heart?

A

Increases preload, augments R sided murmurs and S2 splitting, Decreases venous return to L side of heart/murmurs

173
Q

How does standing change load on the heart?

A

Reduces preload
Augments intensity of MVP (mid systolic click) and HOCM from widened pulse gradient at R atrium
Minimal effect on other systolic murmur

174
Q

How does squatting change load on the heart?

A

Increases preload and afterload
Reduces MVP/HCM intensity
Limited effect on other murmurs- regurg/stenotic

175
Q

How does leg elevations alter blood to the heart?

How can you inc/dec HOCM/MVP?

A

Increases preload, reduces MVP and HOCM

Inc- stand, valsalva
Dec- squat, leg elevate

176
Q

How does valsalva alter blood flow to the heart?

A

Inc then dec afterload and preload

Augments MVP and HOCM intensity from widened pressure gradients to R Atrium

177
Q

How does hand grips alter blood flow to the heart?

A

Increases afterload
Augments MR, MVP, AR, and VSD
Reduces AS, HCM

178
Q

How does amyl nitrate alter blood flow to the heart?

How does phenylephrine alter blood flow?

A

Reduces preload and afterload from vasodilation
Inc HOCM and AS
Reduces MR, AR

Inc afterload
Inc MR, AR
Red HOCM, AS

179
Q

How does amyl nitrate alter blood flow to the heart?

How does phenylephrine alter blood flow?

A

Reduces preload and afterload from vasodilation
Inc HOCM and AS
Reduces MR, AR

Inc afterload
Inc MR, AR
Red HOCM, AS
Stops prolonged erection

180
Q 
Why and when are the following drugs taken through the day?
Lisinopril
Simvastatin
Metformin
Gabapentin
Aspirin
A 
L- BP in morning
S- Cholesterol at bed
M- DM at morning and evening dinner
G- nerve pain, breakfast, lunch and bed
Aspirin- heart health at breakfast
181
Q

What are the two major lipids of plasma

How are they transported?

A

Cholesterol and Triglycerides

Lipoproteins

182
Q

What is the most common clinical manifestation of lipid d/o?

Severe hypertriglyceridemia is primarily associated w/ increased risk of ? but not linked to ?

A

Atherosclerotic cardiovascular dz from inc levels of B-100s

Pancreatitis, but CVDz risk
CV score +5%= statin, don’t worry about TGL

183
Q

Cholesterol is precursor for ?

What are TGLY made of?

A

Fat soluble vitamins
Steroid hormones- cortisol, estradiol, progestins, testosterone

3 FA on glycerol molecule

184
Q

What is the importance of Apolipoproteins

A

Amphipathic molecules on lipoproteins that act as keys to receptors

185
Q

What drugs work in the liver?

How do statins exert their needed effect?

A

Niacin, Statin, Fibrates

Inhibit the rate limiting step in cholesterol synthesis: HMGCoA Reductase which binds ACoA to free cholesterol to make cholesterol esters

186
Q

Where are chylomicrons retrieved from?

What anti-oxidant is found in the blood stream?

A

Lymph system
Apo-B and Apo-C transfer from HDL to chylomicrons

Apo-E

187
Q

Liver uses ? and ? to make VLDL

What medication can be injected to lower cholesterol?

A

Cholesterol and TGLY

PCSK-9i

188
Q

What type/class of drug is used for management of TGLY levels?

What does Niacin do?

A

Fibrates

Cholesterol and TGLY management

189
Q

Macrophages eat bad cholesterol until they die and turn into ?

What are the 3 layers of vessels?

A

Foam cells= atherosclerosis

Intima, Media, Adventicia

190
Q

What is it called when a vessel needs its own blood supply?

A

Vasovasorum- located in adventitia

191
Q

Sequence of events to make atherosclerosis

A

Tear in endothelial layer
LDL/cholesterol enters tear
Monocyte turns in macrophage and eats LDL/cholesterol
Inflammation occurs
Death to foam cells leading to necrosis between intima and media layer
Necrotic area turns into fibrous cap
Cap ruptures and becomes thrombus until dislodged and made into an embolis

192
Q

Difference between exo/indogenous pathways of lipoprotein transport system

A

Slide 16 Lect 5

193
Q

What’s the difference between Primary and Secondary dyslipidiemia

Start checking cholesterol levels in kids at ? age?

A

Primary- genetics
Secondary- weight, DM, renal/thyroid disease

9-11y/o
FamHx- 5y/o
BPs @ 5-6y/o

194
Q

What would a PTs BUN levels be if they have liver dz?

AKAs for HDL, LDL and Chylomicrons

A

0

HDL- Apo-A1
LDL- Apo-B100
Chylomicrons- Apo B-48

195
Q

How often are PTs cholesterol levels screened?

When/how often are PS ASCVD scores calculated?

A

Once every 5yrs starting @ 20y/o, done w/ fasting lipids, LDL levels are NOT included

40-75yrs old Q4-6yrs w/out ASCVD or DM w/ LDL 70-189

196
Q

What lab finding is our marker for identifying PTs what are not responding/handling Statin therapy?

A

ALT elevations

197
Q

What are the 3 areas on the body where excess cholesterol can build up and be externally visible?

What are the two high intensity statins?

A

Xanthelasma, Tendon Xanthomata, Arcus senilus

Atorvastatin- 40-80mg
Rosuvastatin- 20mg

198
Q

What are themoderate intensity statins?

A 
Ator- 10mg
Rosu- 10mg
Simva- 20-40mg
Prava- 40-80mg
Lova- 40mg
Fluva- XL 80mg/ 40mg BID
Pita- 2-4mg
199
Q

What are the two low intensity statins?

Why is statin therapy discontinued?

A

Prava- 10-20mg
Lova- 20mg

Severe muscle Sxs/Fatigue
Work up for possible Rhabdo- order CK, creatinine and UA for myoglobinuria

200
Q

What pre-existing conditions can signal PT will be increased risk for muscle symptoms while using statins?

How long can PTs have muscle Sxs before secondary causes need to be searched for?

A

Hypothyroid, Dec renal/hepatic function, Polymyalgia reheumatica, Steroid myopathy, Vit D deficient, Primary muscle dz

2mon

201
Q

What are the 4 statin benefit groups?

A

Pts w/ clinical ASCVD
LDL 190 or higher
40-75y/o diabetics w/ LDL 70-189
40-75y/o w/ LDL 70-189 AND ASCVD of 7.5% or higher

202
Q

Clinical ASCVD includes ? conditions

A 
TIA
Revascularization
Acute coronary syndromes- MI Hx, angina
Peripheral artery dz
Stroke
203
Q

What type of effects do HMG-CoA reductase inhibitors (AKA Statins) exert?

What type of effects do Bile Acid Sequestrants exert?

A

Dec LDL and TGLY, Inc HDL
Adverse- transaminitis, myopathy

Dec LDL, Inc HDL and TGLY
Adverse- constipation, bloating

204
Q

What type of effects do Cholesterol Absorption Inhibitors exert?

What type of effects does Niacin exert?

A

Dec LDL and TGLY, Inc HDL
Adverse- rare allergic Rxn

Dec LDL and TGLY, Inc HDL
Adverse- flushing (reduced w/ Aspirin, don’t use Naperson)

205
Q

What types of effects do Fibric Acid Derivatives exert?

Don’t treat Triglyceride levels unless they’re above what amount?

A

Dec LDL, Inc HDL and TGLY
Adverse- Nausea, Gallstone

500 or higher (Tx w/ Fibrates, Nicotinic acid, Omega 3 Acids)

206
Q

What are the risk factors for PTs to develop metabolic syndrome?

A 
Abd obesity- +40"/35"
High TGLY- 150 or higher
HDL- less than 40m/50w
BP- 130/85 or higher
Fasting glucose- 110 or higher
(not LDL)
207
Q

What adjunct is given to PTs when treating metabolic syndrome and they have intermediate/high CV risk?

90% of metabolic syndrome treatment errors are primary care issues that include what issues?

A

ASA and lipid management

Wrong drug/dose
PT needs combo Tx
Non-compliant PT

208
Q

What two PCSK9 monoclonal antibodies have shown to further reduce ASCVD risks when added to statin therapies in high risk PTs?

What bile sequestrant and fibrate combo have shown progress in reducing CV events in male populations?

A

Alirocumab and Evolucamab and Ezetimibe

Cholestyramine and Gemfibrozil

209
Q

Which fibrate is contraindicated to use w/ statins?

A

Gemfibrozil- 30x increased risk of myopathy

210
Q

EKG ST elevation means?

ST depression/inversion means?

A

Transmural Ischemia and/or injury

Subendocardial Ischemia w/ abnormal repolarizatiton or death

211
Q

Stable angina= ? compensation

Acute coronary sydrome= ? compensation

A

70% or less occlusion

71% or above
90%= pain at rest

212
Q

While walking, coronary blood flow represents ?% of total CO

A

5%

213
Q

Define Ischemic Heart Dz

Define Angina Pectoris

A

Imbalance between myocardial blood supply and demand leads to hypoxia and increased waste metabolites

Uncomfortable chest sensation from ischemia, most common clinical presentation and most commonly from atherosclerosis

214
Q

Define Stable Angina

Define Variant Angina

A

Transient midline/left anterior angina precipitated w/ activity/emotions causing temporary ST depression and relieved w/ rest

Angina at rest from coronary spasm causing transient ST elevation between midnight and 4am, not ruled out with troponins, r/o by PCI

215
Q

Define Silent Ischemia

Define Unstable Angina

A

ASx ischemia detected by EKG and labs

Increased angina from less exertion or at rest; all PTs are admitted
Change of baseline, first time/new onset, any pain at rest
Time is not issue but typically beyond 20min

216
Q

What is the Fatty Streak

A

Endothelial dysfunction between 17-25y/o
Allows LDL entry and modification and monocyte aggregation
Monocytes-> macrophages and foam cell formation

217
Q

What is needed for oxidation to transform LDL to fatty streaks?

What 3 factors affect coronary vascular resistance?

A

Inflammation

Accumulation of metabolites
Endothelial derived substances (NO- dilation; Endothelin 1- constrictor)
Neural innervation- A adrenergic and B2 adrenergic

218
Q

What drug has positive inotropic effect and utilized as last resort when heart is failing?

One medication that can be given that decreases morbidity and mortality

A

Digoxin

Aspirin

219
Q

What are the 3 major clinical consequences of HDz

A

Myocardial injury- stunned or hibernating
Acute Sxs- un/stable, variant, cardiac syndrome X
Necrosis leading to MI- irreversible, Sx or silent

220
Q

What is cardiac syndrome X

Define Stunned myocardium

A

Young/healthy PT that have heart attack without atherosclerosis and is usually genetically linked

Short term near/total reduction of coronary flow re-established by PCI and followed w/ subsequent, limited LV dysfunction

221
Q

Define Hibernating Myocardium

A

Persistently impaired myocardial and LV function at rest from chronically reduced coronary blood flow but is reversible
This is a chronic stable angina PT*
Conduct PET or Dobutamine Echo to determine perfusion and possible angiography if cells are viable

222
Q

What are the anginal equivalent Sxs?

The mortality rate of stable angina is best predicted by?

A

Dyspnea, Sweating, Fatiuge, Dizzy/Light headed, Gastric urtications

Degree of LV function assessed by Echo (CO, EF), exercise capacity and severity of Sxs

223
Q

What are the 3 anginal equivalents of stable/classic angina?

A

Dyspnea, LV dysfunction (light headed, dizzy), Fatigue

224
Q

Prinzmetal angina spasm is thought to be a combo of what two factors?

What meds can be given?

A

Sympathetic activity and Endothelial dysfunction
Stress test will produce normal test results

CCBs preferred, DO NOT use BB
Nitro can be given acutely

225
Q

Of the 3 major clinical presentations of heart disease, where do the atypicals fall in?

What 3 questions are asked during a diagnostic evaluation of stable angina?

A

Myocardial necrosis leading to MI

Is chest pain substernal, retrosternal, or epigastric?
Sxs brought on predictably by stress or exertion?
PTs Sxs relieved by nitro or within 5min of rest?
3 yes= typical angina
2 yes= atypical angina
Less than 2 yes= non-anginal

226
Q

What are the 5 questions/point scale used for determining risk factor points of CAD?

A 
55 or older male/65 or older female
CAD or CV Dz
Pain not reproducible by palpitation
Pain worse w/ exercise
PT assumes pain is cardiogenic
227
Q

What are the 4 cardinal features of angina

How is it typically described by PTs?

A

Character of discomfort, Site and distribution, Provocation, Duration

Pressure w/ feeling of strangling/anxiety
Atypical PTs describe as vague and atypical

228
Q

What does a peaked P-wave in Lead II mean?

What labs/rads are ordered and in what time frame?

A

PHTN

EKG- 10m, if not diagnostic, repeat 5-10m intervals
CXR- 30m
Fibrinolytics- 30m
PCI- 90m, 120min if transfer is needed
Labs- CBC, Chem-7, Troponin, UA, glucose, lipids
Treadmill test- low/mod risk
Nuclear test- if EKG abnormalities OR,
Exercise echo
Rx Stress Test if PT can't exercise
Coronary angiography if PT is high risk
229
Q

What is the difference between Coronary Angiography and Revascularization

A

CA- dye injection

ReVasc- stent placement

230
Q

What are the 3 criteria are are the end points for stress tests?

A

Sxs limit continuation
Ischemia 0.10mV or more or horizontal ST depression/elevation
BP decrease by 10mmHg or more during exercise

231
Q

What are the 3 criteria for a positive stress test?

A 
Pos= 0.10mV or more horizontal ST depression
Neg= no exercise abnormalities at 85% max HR
Non-Dx= <85% max HR w/ no EKG evidence of ischemia
232
Q

What are the 3 goals of therapy in chronic ischemic heart Dz?

How is stable angina managed?

A

Dec anginal attacks
Prevent acute coronary syndromes-MI
Prolong survival

Type of episode- acute or chronic
First line- nitrates, sublingual
Rest/stop doing activity

233
Q

All PTs with stable ischemic heart disease can get which immunization?

What is the pharmacological treatment for them?

A

Influenza- possible reduced inflammation processes

AKA Vasculo Protective Regiment
Anti-platelet therapy (ASA, Clopidogrel)
Lipid lowering- statin/CSPK9
BBs- meto/?
ACEIs- if high risk PT- lisinopril
Rarely CCBs- last resort
234
Q

What are the uses and perks of using BBs

A

Primary preventinon/first line therapy of anti-angina therapy
Only drug proven to prevent re-infarct and increase survival chances post-MI
HR goal 55-60
Beta 1- pos ion/chornotropic
Beta 2- vaso/broncho dilators

235
Q

What 4 BBs can be selected for use and the perks of use

A

Non-Sel: Propanolol
B1 Sel: Meto/Atenolol
Intrinsic sympathomimetic activity
Alpha/Non-Sel: Carvedilol, Labetolol

236
Q

PTs with ischemia +65y/o get ? BB

PTs under 65 get ? one?

A

Carvedilol

Metoprolol

237
Q

Which BB can be used in pregnancy?

What are the contraindications for using BBs?

A

Labetolol

Brady, below 50bpm
PRI > 0.24, 2* or 3* block
Decomp HF
Hx of asthma
Caution w/ diabetics
238
Q

Don’t use ? class drug in PTs on cocaine?

What CCBs are used?

A

BBs- causes coronary spasms

Diltiazem, Verapamil, Amlodipine preferred
Non-DHPs: Dec ion/chronotropy and after load; C/I in brady or systolic HF
DHPs: dilators that decrease afterload, A/F/N-dipine

239
Q

What is the first line medication for treating PTs/ with ischemic heart dz but have bradycardia or AV blocks

What is a new medication that can be used in place of BB or w/ BB therapy?

A

DHPs- Amlo/Felo/Nifedipine

Ranolazine- late Na channel blocker

240
Q

What are the adverse effects of Organic Nitrates?

What are the adverse effects of BBs

A

HA, HOTN, Reflex Tachy

Brady cardia, dec LV contraction, Bronchoconstriction, masks hypoglycemia, fatigue

241
Q

What are the adverse effects of CCBs

What are the adverse effects of Ranolazine

A

HA, flushing, dec LV contractility on V/D
Bradycardia on V/D
Edema on N/D
Constipation, especially on V

Dizzy, HA, constipation, nausea

242
Q

Post MI, what two meds can be used in combo for anti-platelet therapy?

PTs w/ HTN, previous MI or exertional angina should be placed on ?

A

Aspirin and Clopridgel

BB

243
Q

When art PTs placed on ACEI therapy

A

No benefit to angina, helps reduce remodeling of heart

Benefit for HTN, DM, CKD< LVEF <40% require ACEI

244
Q

Usually monitoring is done on PTs who remain Sx on medical therapy, however revascularization is considered and pursued if ?

A

Angina Sxs don’t respond adequately to drug therapy
Unacceptable s/e on meds
PT is high risk coronary dz and revascularization is known to improve survival

245
Q

What is the CABG to PCI ratio

What determines if a PT gets a PCI or CABG?

A

1 CABG : 3 PCIs

One or two vessel involvement, +70%= PCI
3 vessels or LMain disease w/ intermediate/complex anatomy or impaired left ventricular systolic function= CABG
DM with 2 vessels
Significant LV failure

246
Q

Revascularization by any technique does not reduce MI/death risk from CAD in PTs w/ ? and ?

What was the COURAGE trial and what did it show?

A

Chronic stable angina and preserved left ventricle function, medical management is key

Clinical Outcomes Utilizing Revascularization and AGgressive drug Evaluation- showed PCI was no better than max medical therapy at reducing mortality and cardiac events in PTs w/ stable CAD but may be more effective at long term Sx relief

247
Q

PCI is AKA ?

What drugs are given during this procedure?

What two are given prior to procedure?

A

Percutaneous Transluminal Coronary Angiography- places drug eluding stents in PTs w/ 1 or 2 vessel disease and is Procedure of CHOICE

Abciximab, Eptifibatide, Tirofiban

ASA, Clopidogrel

248
Q

When is a CABG procedure preferred?

When do you do PCIs?

A

Large amount of myocardium is at risk (3 vessels or LM)

STEMI, NSTEMIs not responding to max medical therapy

249
Q

What does CABG stand for?

What are the two types done?

A

Corornary Artery Bypass Grafts

Native veins- section of saphenous “superfluous” vein and sutured from base of aorta to RCA segment down stream of stenosis, high re-occlusion rate

Arterial graft- most common, uses internal mammary “superfluous” branch of subclavian and anastomosed distally to LM/LCX, more resistant/long lasting

250
Q

For revascularization, ALL STEMIs get _____

In order to revascularize a PT, one of what two criteria must be present?

A

Angiography- PCI

Severe/refractory angina
Severe ischemia on stress testing

251
Q

What two meds are always given to PTs prior to PCIs?

A

ASA and Clopidogrel

252
Q

What are the 3 benefits of PCI

What are the 3 benefits of CABG

A

Less invasive, Shorter In-PT and easier recovery, Superior to Rx therapy to relive angina

More effective for long term, Most complete revascularization, Greater survival in PTs w/ greater than 50% LM stenosis or w/ impaired LV function

253
Q

Prinzmetal angina is also associated with what other two issues?

All PTs with DM and CAD are placed on ? med?

A

Raynauds and Migraine HAs

ACEI

254
Q

LDL lowering therapy in PTs w/ Dx or suspected CAD are placed on what 3 meds

What drug is used during the MI algorithm but has not mortality/morbidity benefit?

A

High potency statin, Ezetimibe, PCSK9 inhibitors

Nitro

255
Q

What meds are used when BBs are contraindicated for the prevention of MI and reduce Sxs?

What factor Xa inhibitor can be combo’d with ASA or Clopidogrel?

A

CCBs, Long acting Nitrates

Rivaroxaban, not good for non-compliant PTs

256
Q

When is fibric acid derivatives considered for use?

What are the four functional changes that occur to the heart as scarring?

A

High risk PTs w/ elevated triglycerides and LDL is at target on statin therapy, don’t combine

Stunning, Hibernation, Reconditioning, Remodeling

257
Q

What is the one med we use to stop ventricular remodeling?

What two chemicals are naturally secreted by vessels in response to damage to inhibit platelet aggregation and activation?

A

BBs, ACEIs

Prostacyclin- aggregation and activation
NO- activation and dilation
In presence of injury, become constrictive

258
Q

What are 3 drugs that can decrease anti-thrombotic effects?

Partial occlusion of a vessel leads to ? or ?
Full occlusion leads to ? or ?

A

TPA, NO, Prostacyclin

UA or NSTEMI
STEMI

259
Q

When considering the rupture of a plaque, how do you know if it’s superficial or deep?

There is never a serum biomarker with what heart issue?

A

Superficial/minor- self limiting
Deep w/ obstruction- ACS syndrome

UA, no troponin
Always have one w/ NSTEMI

260
Q

You can’t Dx PT with STEMI if they have a normal ?

How are NSTEMIs initially treated?

A

EKG, must have ST elevation

Medical management for 24-72hrs

261
Q

What are some causes coronary thrombus N/STEMI appearing issues but are non atherosclerotic issues?

What is the one exception?

A

Anemia, HOTN, Stenosis, Aortic Dissection, Procedure complication, Embolic phenomenon, Blunt trauma

Coronary artery spasm- variant or Printzmetal

262
Q

What are some non-atherosclerotic conditions that can be used as DDx for N/STEMI issues?

Acute Coronary Syndrome encompasses ? 3 issues?

A

Lupus, Takayasus, Kawasakis, Giant Cell Arteritis, Polycythemia, Sickle Cell, Cocaine

UA, NSTEMI, STEMI

263
Q

What will a transmural entire thickness MI, what will MI show?

How to distinguish between UA or NSTEMI?

A

STEMI, transmural= entire thickness of wall

Lab test for troponin

264
Q

What are the early changes during trasnmural infarctions

A

2m: ATP decrease
10m: Irreversible injury- VT/VF
24min: Wavy myofibrils
12hr: Hemorrhage, edema
24hrs: Coagulation necrosis- eosinophils
2-4d: Total coagulation necrosis- monocytes
Stopped w/ BB/ACEIs

265
Q

What are the late changes during a transmural infarct?

A

5-7d: yellow softening by macrophages
7+d: granulation/ventricular remodel
7wks: fibrosis and scarring complete, PT can start PT

266
Q

What functional changes can occur during transmural events?

A

Impaired contractility/compliance- hyokinetic, akinetic, dyskinetic seen on echo
Myocardial stunning- limited LV dysfucntion
Ischemic precondition- MI w/ recent angina experience less morbidity/mortality
Ventricular remodel- thinning/dilation of wall

267
Q

What is the most common Sx of cardiac ischemia +85y/o?

What two meds used in combo improve LV function and long term survival?

A

Dyspnea

BB and ACEI, PTs need to be on these upon d/c

268
Q

Every PT with suspected MI is treated the same in what steps?

A

O2, Monitor, IV, Hx, PE, EKG, CXR, Labs- Chem 7 (CK, E+), CBC (anemia), lipids, UA, troponin, CKMB, myoglobin

269
Q

How to diagnose ACS from UA/NSTEMI

What med is not used in PTs w/ UA?

A

Sxs, EKG abnormalities, serum markers of myocardial necrosis

CCBs

270
Q

All inferior wall acute MIs need ? prior to Nitro administration?

What vessel supplies lateral, inferior, septal, anterior areas on EKG

A

Right sided EKG V4R

2, 3, AvF- inf, RCA
1, AvL- LCX or 1st diagonal branch
V1, V2- first 1/3= PDA, bottom 2/3=LAD

271
Q

Pos AVR and V1 mean one of what 2 things?

What vessels supply SA, AV, Bundle, RBB, LBB

A

LM occlusion, PE

SA- RCA in 70%
AV- RCA in 85%
Bundle of His- LAD
RBB- Prox= LAD, Distal= RCA
LBB- Ant= LAD, Post= LAD and PDA
272
Q

How long does it take to rule out a MI w/ no troponin results on labs?

What are the two Troponin Cardiac markers?

A

12hrs= 100% r/o, this is why troponins are never ordered on outpatient basis

I and T, I is most sensitive
Inc of either is Dx for MI

273
Q

What is the use of CKMG for MIs?

What is the first marker to rise and fall within 24hrs?

A

Proves MI re-infarction, rise 5x above baseline is Dx

Myoglobin, CKMB and troponin are second

274
Q

What are the timelines for cardiac biomarkers to rise, peak and return to baseline?

A

Troponin: R 3-4hrs, P 18-36hrs, B 7-10 days

CK: R 3-8hrs, P 24hrs, B 2-3 days

275
Q

How often are repeat EKGs ordered post-MI while inpatient?

On an echo, heart wall motion that is waving =?
If it’s no moving then it’s ?

A

Every day

Dyskinetic
Akinetic

276
Q

How do you rule in/out MIs in pregnant PTs?

What if PE is suspected?

A

CT angiogram

Creatinine >1.5- order VQ scan to r/o PE but don’t order CT angiogram, will kill kidneys

277
Q

What are the 4 classes of drugs used in ischemic heart disease?

What is the trifecta sequence of EKG changes during STEMIs?

A

Anti-platelet, BB, CCB, ACEI

Hyper acute T wave, Depression, Elevation, Q waves

278
Q

What two fibrinolytics are used for MI PTs?

For testing purposes, give MI PTs O2 if puls-ox is below ?

A

TPA (Tenecte,Alte/Reteplase) or Streptokinase

90%

279
Q

What are the 3 steps of UA and NSTEMI treatment plans?

A

Anti-ischemis: BB, nitrates, +/- CCB or ACEI
Anti-thrombotic: anti platelet- ASA/Clopanti,coagulant- LMWH, unfractionated heparin
Adjuncts: statin, ACEIs for ALL Pts

280
Q

Why do we give all PTs w/ MIs BB?

What CCBs do we give for anti-ischemic therapy?

A

Lower mortality rate and sets HR goal of 60bpm, don’t use if less than 50bpm

Non-DHPs: Diltiazem, Verapamil; caution w/ edema and constipation
Don’t use for LV dysfunction

281
Q

Don’t use nitrates as anti-ischemic therapy if it’s ? type of failure

What P2Y12 inhibitors are used for UA/NSTEMI antithrombotic therapy?

What GP2b/3a inhibitors are used?

A

RV failure

Clopidogrel (cheaper, higher bleed risk), Prasugrel, Ticagrelor (lowest chance of causing bleeding, expensive, reversible), Cangrelor

Abciximab, Eptifibatide, Tirofiban
E/T= small molecule agents, don’t induce immune response

282
Q

What anti-coagulants are used in UA/NSTEMI therapy?

A

LMWH- most commonly used, no lab testing, Enoxaparin
UFH- slow onset, monitor PTT, preferred for PCI since it’s reversible
Bivalirudin- used if heparin induced thrombocytopenia occurs

283
Q

What is the MOA and benefit of Bivalirudin use

When/why is Fondaparinux used?

A

Direct thrombin inhibitor
Less associated bleeding

Conservative management of UA/NSTEMI to decrease bleeding
Similar to LMWH, indirect 10a inhibitor but no Thrombin inhibit

284
Q

UA/NSTEMI treatment is conservatively managed w/ meds unless ?

Early invasive management (within 24-48hrs) of UA/NSTEMI is based on ?

A

Ischemic episodes return
Stress test indicates residual inducible ischemia

TIMI risk

285
Q

What are the parts of the Thrombolysis in Myocardial Infarction risk score

A

+65y/o
3 or more risk factors: Age, Sex, FamHx, Smoking, HTN, Hypercholesterol, DM, Obese
Coronary stenosis of 50% or more by angiography
ST deviation on presenting EKG
2 anginal episodes in 24hrs
ASA use in prior 7 days
Elevated troponin or CKMB

0-1: ASA and d/c
3 or more- bad

286
Q

How is STEMI clinically defined on EKG?

When does a MI PT NOT receive nitro?

A

ST elevation in 2 contiguous/precordial leads (2,3,AvF; 1, AvL; V5,V6; V3,V4; V1,V2)
New LBBB
Consistent presentation of ACS

Hemodynamic instable, HF, decreased neurologic function

287
Q

All STEMI PTs get an PO BB within ?? hrs of onset of AMI?

What statin is started ASAP?

A

Within 24hrs unless c/i

Atorvastatin

288
Q

STEMI PTs get Fibrinolytics within ? time frame and under ? condition

What are the absolute contraindications for using Fibrinolytics in MI?

A

90-120min and Sxs are <12hrs old

Prior intracranial hemorrhage
Structural cerebral vascular lesion
Intracranial neoplasm
Ischemic stroke in past 3mon
Active internal bleeding (doesn't include menses)
Suspected dissection/pericarditis
289
Q

? drugs is a venodilator?

What aer the long term management and secondary prevention steps of STEMI

A

Nitro

ACEI w/in 24hrs- includes ASx and EF >40%, all CHF, reduced EF <40%, Anterior wall MI or ARB if can’t tolerate ARB (-sartan)

290
Q

What drugs are not given for long term management/secondary prevention of STEMI?

What type of STEMI PTs get an Aldosterone antagonist?

A

CCBs

HF, Spirinolactone

291
Q

What medicatoin must be stopped in all STEMI PTs

What do all STEMI PTs get prior to d/c

A

NSAID- avoid in HF and reduced LVEF except for ASA

Echo

292
Q

When do STEMI PTs get anti-coag w/ Warfarin?

A

Large anterior MI
LV aneurysm on TEE or Echo(7days post-MI)
LV thrombus

293
Q

What is the dispostion for PTs with likelihood/risks for ACS?

A

Low L/Low R= out PT eval
Intermediate L/Low R= out PT eval
Intermediate/Intermediate= in PT w/ telemetry
Intermediate/high L/High R= Cardiac care unit

294
Q

What are the 5 scenarios that require admission for PTs w/ ACS?

A 
Continuous chest pain
Positive serum makers
Significant/new ST abnormalities
Wellens T-waves- new/deep inversions  
Hemodynamically unstable
High risk stress test results- +/-
295
Q

How is Wellens treated/managed?

A

Deep inverted/biphasic T waves due to LAD occlusion, seen in V2/V3, get to PCI due to poor medical management outcomes

PT may be pain free at time of EKG w/ normal/barely elevated enzymes but are at extremely high risk for massive anterior MI in following days

296
Q

If no cardiologist is present, who manages Wellen Syndrome PTs?

What about STEMI, NSTEMI or angina?

A

Internal Med

STEMI- cardiology or Internal Med
NSTEMI- Internal med, may end at cardiology
Angina- internal med

297
Q

What dosage of aspirin is given to PTs upon arrival?

What anti-depressant can be used for depressed PTs post-MI?

A

81-325mg, 325 preferred and chewed
81mg at discharge

Sertraline or any SSRI

298
Q

PTs presenting with one of these 5 NSTEMI characteristics are sent to cath lab immediatley?

A

Hemodynamic instable/cardiogenic shock(BP 90/60, cold and clammy, AMS, chest pain, “sick” looking”
Severe LV dysfunction/HF
Recurrent/persistent rest angina despite medical therapy
New/worsening MR or new VSD
Sustained ventricular arrhythmias

299
Q

Fibrinolytics AKA thrombolytics have no clear survival benefit for ? cardiac PTs?

When is the use of firbrinolytic preferred?

A

UA or NSTEMI, never ever give
Small area of ischemia will be made worse by swelling

Contraindicated for PCI, no PCI available within next 90min

300
Q

No PT ever goes to CABG without going through ? first

How long after MI does LV aneurysm take to development?

A

PCI

7 days

301
Q

What two meds are used for treating MI induces pericarditis/Dressler’s?

What anti-coag can cause cardiac tamponade if given to these PTs but prevents transmural thrombus

A

ASA, Colchicine (viral= high dose NSAIDs)

Warfarin

302
Q

MI Sinus Brady causes ?

MI Sinus Tachy causes?

A

RCA/Inf Wall- Inc vagal tone, dec SA node perfusion

Ant wall- Pain, Anxiety, volume depletion (dopamine)

303
Q

MI APBs, A-Fib causes ?

MI VPBs, VT and VF causes?

A

HF, Atrial ischemia

HF, Ventricle ischemia

304
Q

MI AB Blocks 1, 2, 3 cause?

A

IMI= inc vagal tone, dec AV perfusion

AMI= destruction of conduction tissue

305
Q

Define Cardiogenic Shock

How is it treated?

A

Dec CO and HOTN w/ poor peripheral perfusion due to >40% LV death

Ionotropic drugs (Dobutamine) but cycle continues until LVAD implant or transplant

306
Q

What test is done prior to all post-MI PT discharge and is is used to gather the most useful prognostic indicator?

PEs are _% sensitive and _% specific for detecting valve Dz

A

Echo to get LVEF

70% and 98%

307
Q

What are the Systolic murmurs by position?

When do the get Echos?

A 
AS- RUSB
PS/PDA- LUSB
HCM- Erb's
TR, VSD- LLSB
MR, MVP- Apex

Grade 3 or higher

308
Q

What are the Diastolic murmurs by postition?

What do all diastolic murmurs gert?

A

PI, Split S2- LUSB
AI- Erb’s
TS- LLSB
MS- Apex

Echos

309
Q

What are the 3 continuous murmurs?

What is the sequence of interventions for brady/BLS?

A

PDA- LUSB
Arteriovenous malformation
Venous hum

Atropine, Transcutaneous Pacing, Dopamine, Epi

310
Q

What vision change can occur w/ Digitalis toxicity?

Pancarditis is AKA ?

A

Yellow vision

Myocarditis

311
Q

What are the 2 types of WPW?

How is it treated?

A

Orthodromic- narrow QRS, symptomatic, Delta waves
Antodromic- wide QRS

Tx w/ Procainimide or conversion
Definitive Tx- ablation

312
Q

What type of BBB is equivalent to STEMI?

VSD is most commonly associated w/ ? and ASDs are most commonly associated w/ ?

A

LBBB

VSD- LBBB
ASD- RBBB, PEs most commonly associated here

313
Q

Sequence of treatment of PSVT

3 PVCs in a row is called ?

A

Stable- vagal, adenosine 6mg/flush, 12mg/flush,

V-tach

314
Q

What are the causes behind Sinus Brady?

A 
BB, CCBs, Digoxin
Inc vagal tone
Hypo thyroid, temp, sugar
SSS
Obstructive apnea
315
Q

If blood glucose is less than 60, what is the Tx?

How many Joules are used for defib on Vfib?

A

Glucose

200J biphasic

316
Q

PT on hydrochlorothizide and develops U-waves, what is the cause?

How is V-tach treated?

A

Hypokalemia

Stable= amiodarone, lidocaine, procainamide
Unstable= cardioversion
Pulseless- defib

317
Q

What meds can cause Torsades?

How is it treated?

A

Antipsychotics, Methadone (SSRIs preferred for depressed MI PTs)

Unstable- defib
Stable- IV MgSulfate and d/c offender

318
Q

What is the most common cause of R sided HF?

A

L sided HF

319
Q

What are the grading scales for systolic murmurs?

A 
1- barely audible
2- faint but immediately audible
3- easily heard
4- easily heard and w/ palpable thrill
5- loud, hear w/ light tough of stethoscope
6- audible w/out stethoscope
320
Q

What are the grading scales for diastolic murmurs?

A

1- barely
2- faint but audible
3- easily heard
4- very loud

321
Q

Murmurs of what characteristics are classified as benign murmurs?

A 
Early/mid systolic- MVP
Soft, grade 1 or 2
Vary w/ respiration
Normal exam/work up
No FamHx
322
Q

What are pathologic murmurs and what do all get for imaging?

A 
All diastolic- MS TS, AR, PR
All pansystolic- MR TR VSD
Late systolic- AS/PS
Loud 
Continuous- venous hum, PDA, AV malformation

ALL GET ECHOS

323
Q

Systolic ejection murmurs

Pansystolic murmurs

A

AS- 2RICS and neck
PS- 2-3LICS

MR- apex to axilla
TR- LLSB to RLSB

324
Q

Late systolic murmurs

Early diastolic murmurs

A

MVP- apex to axilla

AR- L sternum
PR- upper R of sternum

325
Q

Mid to Late diastolic murmurs

Define Acute Rheumatic Fever

A

MS- apex

2-3 wk delayed sequel of pharyngeal infection w/ Group A Strep w/ scarlet fever but not from GAS skin infections

326
Q

What physical response occurs during ARF?

A

Aschoff nodule- source problem of all issues
High fever
Valvulitis, usually mitral
Non-itching pruritis- erythema modulotum
Joint pain starting one at a time
PAINLESS subcutaneous nodules (endocarditis= painful)
Rapid involuntary muscle movement of face

327
Q

What would bee seen on physical exam in PTs presenting weeks after infection but now with ARF?

A

Throat exudates and high fever

No runny nose, cough= GAS don’t cause these

328
Q

What are the major Jones Criteria

A

Joints- migratory polyarthritis in large joints of UE w/ Rubor, Palor, Calor and Tumor
O- myocarditis w/ pericardial effusion
Nodules, subcutaneous
Erythema marginatum
Sydenhams chorea- AKA St Vitus Dance, stops during sleep, rare in adults, rarer in males

329
Q

What imagine modality is used to view Jones Criteria

Firm/painless nodules nearly always occur due to ?

A

Echo, no scanners

Carditis

330
Q

ARF erythema marginatum presents with what characteristics?

A

Non pruritic, non-painful serpentinous eruption on trunk, proximal trunk and center returns to normal before margins

331
Q

What are the minor Jones criteria

A

Arthralgia w/out arthritis
Fever 101-104
Elevated ESR and CRP
Prolonged PR interval**

332
Q

What are the diagnostic tests for RF show on labs/rads

A

Strep culture or Rapid Strep
Strep Ab Titer- ASO or AntiDNase B w/ elevated CRP and ESR

CXR w/ cardiomegaly and/or HF
ECG- blocks

333
Q

What type of diagnostic info is used for making a Dx of ARF

A

GAS pharyngitis infection
+ throat culture
+ rapid strep Ab test
Elevated/rising strep Ab test- ASA, Anti-DNase B, or Antistreptozyme

334
Q

How many major/minor criteria are needed from Jones Criteria to make a Dx

When can a presumptive Dx of ARF be made?

A

Two major or,
One major and two minor criteria

Chorea as only manifestation
Indolent carditis- PTs failing to seek early Tx
Recurrent RF PT w/ Hx of ARF are presumed to have recurrence w/ any manifestation

335
Q

What are the DDx of RF

A 
Bacterial endocarditis- painful nodules
Viral myocarditis- cultures, low myocytes/lymphocytes
Lupus
Serum Sickness
RA
Infectious arthritis
336
Q

What part of ARF can’t be treated/slowed?

What are the major goals of treatment

A

Valve damage

Relief of acute Sxs
Eradication of GAS
Prophylaxis from future GAS infections
Most PTs are admitted

337
Q

How is ARF Treated?

A

ABX- PCN x 10 days regardless of pharyngitis presence
HF management and anti-inflammatory- ASA 80-100mg kids/4-8g in adults
Therapy is continued until all Sxs are gone and/or ESR/CRP are normal
Bed rest

338
Q

How is ARF Carditis treated?

How is the rash treated?

A

HF and Blocks Tx w/ conventional therapy
Valve repair/replacement for non-reponsive HF

No specific Tx needed

339
Q

What ABX are used for treating ARF

A 
Therapy x 10 days 
Kids under 27kg= Penicillin VK 250mg b/tid
\+28kgs= Penicilin VK 500mg b/tid
Bicillin LA IM- once in lieu of PO PCN
Kids- 600K units
Adults 1.2M units

PCN Allergic- Azithromycin, Clarithromycin, Clindamycin (Macrolides)

340
Q

What is RF prevention therapy

A

Primary= Dx and ABX Tx of GAS tonsillopharyngitis

Secondary= Hx of Dx increases PTs risk, limit Dz severity w/ prophylaxis

341
Q

How long after illness does it take RF TPs to develop heart issues?

A

10-20yrs
Mitral stenosis- most common
Aortic valve
Rarely Tricuspid

342
Q

What is Carvallo’s sign?

What are the 3 Diastolic murmurs

A

Pansystolic murmur that is louder w/ inspiration and helps distinguish from MR

Austin AR MS at rest

343
Q

Large P wave over 2.5 in lead 2 more than 4mm in height is due to ?

What are the 4 atypical MI presenters

A

Cor pulmonale- chronic from COPD, acute from PE. PTs presents w/ edema, fatigue and signs of R sided HF

DM, Old, Female, CHF

344
Q

Dx HTN

What decreases after load but can be treated with?

A

3 separate visits of 140/90

Dantrolene

345
Q

Difference Pitting and Non-Pitting edema

What is the difference between a low and high output HF

A

Pitting- CV cause
Non- lymph

High- due to high metabolic state or shunting of blood that inc O2 demand- hyperthyroid, Beriberi, AV fistula, Paget’s, Anemia, Pregnancy

Low- depressed Ejection Fraction; dilated cardiomyopathy, chronic HTN, Valvular HDz

346
Q

What are the four stages of HF Staging/Classification

A

A- high risk w/out Sxs or Dz
B- structural Dz w/out Sxs
C- structural Dz and Sxs
D- refractory HF

347
Q

What are the 4 classifications of the New York Heart Association?

A

1- ASx
2- Sx w/ ordinary activity
3- ASx only at rest
4- Sxs at rest

348
Q

What are the JNC 8 Guidelines of HTN?

A

Under 60 or Diabetic= 140/90
Over 60= 150/90

Tx: 1st line always lifestyle mod.
Non Af.Am.= Thiazide, ACEI, or ARB or CCB
Af.Am= Thiazide or CCB
CKD, with or w/out DM= ACEI or ARB

349
Q

For HTN PTs, when are the re-evaluated, referred and what are not used together?

What PE finding proves a PT has renal artery stenosis?

A

Titrate up or add therapy after 1mon if not at goal
Don’t combine ACE/ARB
If more than 3 drugs are needed= referral to HTN specialist

Bruis

350
Q

PTs presenting w/ MI Sxs need to have what drug use r/o prior to giving nitro?

Other than inferior MI, what other cardiac issue needs to avoid Nitro use?

A

Phosphodiesterase inhibitors (Viagra) in past 24hrs

RV Infart and Severe Aortic stenosis

351
Q

All PTs with ACS get ? med despite lab baseline levels?

A

High intensity statin (Atorva/Rivustatin)- LDL +190 or ASCV risk +7.5%

352
Q

Long term STEMI care

How are aneurysms seen?

A

ASA/Clopidogril
Warfarin- large Anterior MI

TEE, Echo

353
Q

What risk does the combo of smoking and contraceptives have?

What HTN emergency drug is metabolized into cyanide?

A

Venous thrombosis

Sodium Nitroprusside

354
Q

Caution before giving Clarithromycin (macrolide ABX) to PTs taking what class of medication?

Class 1A/B/C, 2 3 and 4 drugs

A

Statins- QT prolongation and hearing loss

355
Q

Rebound HTN emergencies occur w/ sudden d/c of what anti-HTN drug?

Imaging choices for suspect DVT?

A

Clonidine/Methyldopa

Duplex US to Venography

356
Q

What two murmurs increase w/ valsalva?

How can HOCM present and be confused for something else?

A

HOCM, MVP

Large amplitude QRS
Deep na`rrow Q in inf/lat leads mimicking lat/inf MI
Tall R in V1-V2 mimicking post MI/RVH

357
Q

PACs can be signs of ?

Do you stop CPR to place AED?

A

Atherosclerosis

Yes

358
Q

PT with anemia, low Hct/Hgb and is suffering from MI has what type of MI?

If PT is getting hypoglycemia on BBs, what diuretic can be given to counteract the effect?

A

High out put

Thiazide diuretic

359
Q

Which diuretic causes Ca to go up?

PT w/ MI and HTN emergency, EKG shows ST elevation in V2-4, what drug can be used for HTN?

A

Thiazide- up
Loop- down

Nitro
Avoid Enalaprilat

360
Q

PTs w/ LV failure need to receive Enalaprilat, how do you know it’s LVF?

What is the DOC for aortic dissections?

A

Rales/crackles, leg edema, no JVD, fatigue, dyspnea, EJF <40%

Esmolol

361
Q

What drug is the DOC for excess catecholamine excess states such as phenochromocytoma?

If troponin is greater than ___ it’s always a MI

A

Phentolamine; Pts presents Sx/transient HTN for 10-15m then self resolves

10

362
Q

What blood thinner can be used in STEMIs?

What class drug is not used in UA?

A

UFH

CCBs

363
Q

Statin use is contraindicated for use in ? PT population?a

What time of day is it used?

A

Pregnant/feeding

At night, when cholesterol synthesis is highest

364
Q

What are the 3 bile acid sequestrants?

Don’t use them if ? is normal in the PT

A

Cholestyramine
Colestipol- must use w/ statin

In PTs w/ normal TG levels

365
Q

How are PSK9 inhibitors administered?

What drug can be given to PTs for asthma/steroid reasons but may reverse anti-HTN med effects?

A

IM only

Naprosyn

366
Q

What causes RAD?

Hypo K causes ? ekg findings?

A

LPFB, RVH, Lateral MI, PE, COPD

U waves, ST depression, Flat T wave

367
Q

What drugs are likely to causes orthostasis and present with warning of first dose syncope?

Criteria for HTN urgency/emergency

A

A1 blockers- Doxa/Terazosin

368
Q

RF causes what type of heart murmur?

Squatting/hand grips effect on murmur

A

Mitral stenosis

> ???

369
Q

Valsavla effect on murmurs

ECG finding of L atrial enlargement

A

AS dec w/ valsalva
HOCM inc

Greater negative deflection/at least 1mm wide and deep in V1

370
Q

Factor 5 Layden

A

Pregnant

Not contraindicated in fibrolytics

371
Q

R sided HF Tx

Which mechanism best explains why excess adipose tissue leads to atherosclerosis?

A 
BiPap
Nitrate
Furosimide
Dobutamine- not in shock
NorEpi- shock

Production of proinflammatory cytokines

IPAP (212 decks)

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