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cardio pathophys Flashcards

0
Q

What factors increase cardiac contractility?

A

Exercise
Increased SS tone
Catecholamines
Increased HR

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1
Q

LaPlace’s Law

A

Wall stress = ((pressure x chamber radius)/2x wall thickness)

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2
Q

What factors decrease contractility?

A 
Acidosis
Ischemia
SS blockade (Beta Blocker)
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3
Q

What is concentric hypertrophy?

A

Seen w/ high BP
increase in number of sarcomeres laid in parallel -> decreased cavity size and increased wall thickness -> decreased wall stress w/ preserved contractility

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4
Q

What is eccentric hypertrophy?

A

Occurs w/ chronically elevated preload
Increased sarcomeres in series -> increased chamber size + increased wall stress -> increased sarcomeres in parallel
proportional increases in cavity size and wall thickness

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5
Q

What is concentric remodelling?

A

Reversible, physiologic LV hypertrophy seen in athletes.

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6
Q

4 ways that IC Ca++ is recovered after cardiomyocyte contraction

A

1: SERCA - in SR, ATP dependent
2: Na/Ca exchanger - uses Na gradient to move Ca out
3: Plasma membrane Ca++ -ATPase
4: Mitochondrial Ca++ uniporter

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7
Q

What is preload?

A

Passive tension in cardiac myocyte at rest - length of cell prior to contraction

Greater length -> stronger contraction

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8
Q

What is afterload?

A

The force that a muscle cell must overcome in order to contract

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9
Q

What is isometric contraction?

A

Afterload > contraction force

sarcomere does not shorten

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10
Q

What is contractility?

A

contractility = inotropy
intrinsic ability of cardiac myocyte to alter ability to contract independent of preload and afterload

due to changes in biochemical environment of myocyte
due to increased actin-myosin interractions.

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11
Q

Stroke Volume

A

EDV - ESV = SV

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12
Q

Ejection Fraction

A

EF = SV / EDV

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13
Q

3 phases of ventricular filling

A

Early rapid filling
Slow mid-diastolic filling
Rapid filling from atrial contraction

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14
Q

2 factors that influence Preload

A 
Venous return (blood volume, venous tone, posture, pericardial constraint, atrial contraction efficacy)
Ventricular compliance
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15
Q

What is normal EF? What EF %s indicate mild, moderate, severe dysfunction?

A

Normal: 55-65%
Mild LV dysfunction: 45-54%
Moderate LV dysfunction: 30-44%
Severe LV dysfunction: <30%

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16
Q

2 methods of measuring CO

A

Thermodilution: most common - cath inserted, cold saline injected in RA, measured in PA, CO is calculated

Fick method: tedious
equation: CO = O2 consumption / AV O2 difference

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17
Q

What is a Wood Unit (WU)?

A

Used in calculations of TPR

WU = (dyne . sec . cm^-5) / 80

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18
Q

How is TPR calculated? Normal values?

A

measure of afterload
Mean pressure difference across vascular bed / mean blood flow
Systemic VR = (MAP - MRAP)/CO. Normal = 13-16 WU
Pulmonary VR = (MPAP - PCWP)/CO. Normal = 0.5-11 WU

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19
Q

What is initial treatment for STEMI?

A

PCI, CABG

If not immediately possible - thrombolytics

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20
Q

what anti-ischemic treatments are recommended for early hospital care of ischemic heart disease?

A

1: oxygen (maintain O2 sat >90%)
2: nitrates (SLx3 or IV for ongoing ischemia, HF, HTN)
3: Oral B-blocker in 1st 24 hrs if no contraindication
4: NDHP Ca++ channel blocker if B-blocker contraindicated
5: ACE inhibitor in 1st 24 hrs for HF or EF <40%
6: Statin

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21
Q

What are contraindications for Nitrate use?

A

Hypotension (present or likely)
Right ventricular infarct
Severe aortic stenosis
PDEi taken in last 24 hours

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22
Q

What are indications for Beta blocker use in Ischemic heart disease and what are the preferred agents?

A

Ongoing chest pain, hypertension or tachycardia not caused by HF

Metoprolol or atenolol are preferred

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23
Q

Should a patient w/ MI precipitated by cocaine use be treated with a beta-blocker?

A

No

Blockade of B2 mediated vasodilation may precipitate coronary artery spasm

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24
Q

What patients may receive IV beta blocker?

A

Patients with ischemic heart disease and significant hypertension
Afib with RVR

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25
Q

Contraindications for beta-blocker use

A

active bronchospasm
hypotension, bradycardia, heart block, pulmonary edema
MI assoc. w/ cocaine use

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26
Q

What is the recommended statin in treatment of ischemic heart disease?

A

Atorvastatin, 80mg / day

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27
Q

What studies demonstrated the efficacy of statin treatment in treatment of ischemic heart disease?

A

PROVEIT-TIMI 22 and MIRACL

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28
Q

What is class III therapy for ischemic heart disease?

A

Contraindicated therapy

  • Nitrates if Systolic pressure <90
  • Nitrates if Sildenafil or Tadalafil w/in 24 hrs
  • Immediate release Ca Channel blockers w/o B-blocker
  • IV ACEi
  • IV B-blocker if AHF, low output, long PR, 2nd or 3rd deg heart block, asthma or reactive airway disease
  • NSAIDs and COX-2 inhibitors
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29
Q

What is the mechanism of aspirin’s anti-platelet activity?

A

inhibition of Thromboxane A2 (stimulates platelet aggregation)

Aspirin irreversibly inhibits COX inhibiting PGI2 and TxA2 production.

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30
Q

What is the recommended dosing for aspirin?

A

Initially: 325 mg non-coated, chewed
Prophylaxis: 75-100 mg/day inhibits TXA2 w/o significant impairment of PGI2

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31
Q

Name 4 P2Y12 receptor blockers and differentiate

A

Clopidogrel
Ticlopidine: worse side effect profile - not used
Prasugrel: greater anti-platelet activity, increased risk of bleeding
Ticagrelor: reversible blockade. greater anti-platelet activity

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32
Q

What is recommended anti-platelet therapy for a patient w/ ACS?

A

1 year of dual anti-platelet therapy: aspirin + P2Y12 receptor blocker

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33
Q

Clopidogrel dosing for pt. w/ NSTEMI ACS

A

300mg loading dose

75mg/day maintenance

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34
Q

Prasugrel vs. Clopidogrel

A

Prasugrel: faster onset, higher degree of platelet inhibition, effective for more patients (20-25% of pts are clopidogrel resistant)

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35
Q

What are contraindications for Prasugrel?

A

Hx of TIA or stroke

> or = 75 yoa

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36
Q

What are 2 classes of P2Y12 receptor blockers?

A

Thienopyridine - clopidogrel

Cyclopentyltriaolopyrimidines - ticagrelor

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37
Q

In treatment of ACS what patients are given GIIbIIIa inhibitors?

A

Those receiving early invasive therapy

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38
Q

examples of GIIaIIIb inhibitors

A

eptafibatide - preferred
abciximab
tirofiban - lowest preference

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39
Q

What are the anticoagulants of choice for ACS patients undergoing early invasive treatment? what about conservative treatment?

A

early invasive: bivalirudin or UFH

conservative: enoxaparin or fondaparinux

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40
Q

What ACS patients should receive fibrinolytic therapy?

A

STEMI patients w/in 12 hours of onset w/ no contraindications for whom reperfusion therapy cannot be performed w/in recommended timeframe.
Patients presenting after 12 hrs but before 24 hrs of symptom onset for whom reperfusion therapy is not available

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41
Q

3 fibrinolytics and differences

A

Alteplase (tPA)
Reteplase (rPA) - sim to tPA, longer half-life
Tenecteplase (TNK-tPA) - sim to tPA, lower incidence of noncerebral bleeding and easier to use, longer half-life

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42
Q

When is Ranolazine used and what is the dose?

A

Used in patients receiving max-dose of long acting nitrates with persistent symptoms. Decreases frequency of anginal events.
Dose: 500 mg bid (1000 mg bid w/ persistent symptoms)

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43
Q

Contraindications for Ranolazine

A

pre-existing QT prolongation
hepatic disease
use of diltiazem or verapamil

Note: inhibits degradatory path for simvastatin and digoxin - lower doses needed.

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44
Q

What is Cardiac X syndrome? Treatment?

A

Angina-like chest pain w/ exertion, positive ECG (ST depression during stress test), normal coronary angiography, no inducible vasospasm.

Treatment: reassure stable patients. B-blockers help, Nitro helps. Calcium channel blockers not very helpful.

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45
Q

What is the use of CRP in understanding risk of a CV event?

A

independently of questionable use, but can be used for stratification w/in risk groups

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46
Q

What inflammatory cells are primarily involved in atheromatous plaque formation?

A

Monocytes and Tcells (CD4)

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47
Q

What are two main causes of endothelial injury precipitating atheromatous plaque formation?

A

hemodynamic stress: HTN, turbulent flow

chemical / physical agents: hypercholesterolemia, smoking (free-rad and toxins), chronic inflamm, homocysteine

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48
Q

How do foam cells form in atherosclerotic plaques?

A

endothelial damage -> increased adhesion molecules (VCAM-1) and increased permeability -> increased lipid infiltration, cholesterol deposition and monocyte infiltration
local free radicals -> oxidized LDL -> activated macs phagocytosis of oxidized lipid via SCAVENGER RECEPTOR-> foam cells

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49
Q

How are smooth muscle cells recruited to atherosclerotic plaques?

A

PDGF from platelets, macs, endothelium, and other sm.m. cells
FGF and TGF-a

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50
Q

What are the most common sites of atherosclerosis?

A

Large elastic and medium sized muscular arteries

abdominal aorta, coronary aa., popliteal, carotid aa.

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51
Q

What is a fatty streak?

A

Pre-atherosclerotic lesion. Present in childhood, may not lead to atherosclerosis.
Aggregate of lipid filled macrophages w/in intima.

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52
Q

What is an atheroma and what are its components?

A

An uncomplicated fibrofatty plaque

fibrous cap
lipid core
inflammation at periphery - Tcells and macs, granulation tissue

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53
Q

What is hypertension?

A

Elevation of arterial BP that results in adverse health effects
Generally: systolic >140 or diastolic > 90

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54
Q

4 targets of Angiotensin II

A
  1. Vasculature -> vasoconstriction
  2. Post. Pituitary -> Vasopressin (ADH) production
  3. Kidney -> Na+ and H2O retention
  4. Adrenal glands -> Aldosterone release
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55
Q

What are the underlying causes of Primary Hypertension?

A

Poorly understood:

1) genetic predisposition - multifactorial, familial hx
2) environmental influences - stress, obesity, Na+ intake

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56
Q

Potential mechanisms of primary HTN

A

Genetic defects in

1) renal Na excretion -> increased CO
2) vascular sm. muscle Na / Ca transport -> increased peripheral vascular resistance

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57
Q

5 major causes of Secondary HTN

A
  1. Renal disease (renal artery stenosis)
  2. Pheochromocytoma
  3. Endocrine disorder
  4. Aortic coarction
  5. Pregnancy
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58
Q

What is the mechanism underlying renovascular HTN?

A

Reduction in renal perfusion due to atherosclerosis (or other process) -> persistent activation of renin-angiotensin-aldosterone system

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59
Q

What is fibromuscular dysplasia?

A

Irregular thickening of the intima and most often the media of the renal artery -> renal artery stenosis
Most common in young women (30-40s)

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60
Q

2 types of arteriolosclerosis

A
  1. hyaline: endothelial damage -> leakage of plasma protein and sm. m. matrix synth -> luminal narrowing
  2. hyperplastic: malignant HTN. concentric thickening of vessel walls - sm. m w/ thickened reduplicated basement membrane
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61
Q

What defines malignant HTN?

A

Diastolic pressure >130

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62
Q

What is the pathogenesis of hyperplastic arteriolosclerosis?

A

endothelial damage -> plasma protein leakage (esp. fibrinogen) and thrombosis -> PDGF -> intimal hyperplasia and luminal narrowing -> deceased renal perfusion -> increased renin production -> vasoconstriction and exacerbation (self-perpetuating cycle)

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63
Q

What kind of necrosis is associated with hyperplastic arteriolosclerosis?

A

fibrinoid necrosis - vessel walls replaced by smudgy fibrin deposits.

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64
Q

Where is cerebral hemorrhage most likely to occur secondary to HTN?

A

Putamen, thalamus, pons

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65
Q

What are 2 changes that can occur to the kidney due to HTN

A

1) benign nephrosclerosis - normal w/ aging, exacerbated w/ HTN, diabetes: fibroelastic hyperplasia of larger aa, hyaline arteriolosclerosis, ischemic changes in parenchyma (fibrosis), mild reduction of GFR
2) malignant nephrosclerosis - malignant HTN: “flea-bitten” kidneys, hyperplastic arteriolosclerosis, infarction, ischemic atrophy, papilledema, encephalopathy, cardiac complications, proteinuria, hematuria, acute RF

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66
Q

What are the differences between flame shaped and dot shaped retinal hemorrhages in the setting of HTN?

A

flame: closer to the inner limiting membrane (more superficial) - due to nerve fiber lying parallel to membrane
dot: deeper

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67
Q

What are cotton wool spots seen on retinal exam?

A

Cytoid bodies: due to arteriolar occlusion (vascular damage / HTN related) swollen dammaged axons distal to occlusion

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68
Q

What is a macular star and what is it associated with?

A

Due to intraretinal lipid deposition in plexiform layer due to breakdown or blood-retinal barrier
Seen in malignant HTN +/- increased intracranial pressure

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69
Q

What cardiac cells produce “fast response” action potentials and what is the respective conduction velocity of each?

A

Regular atrial and ventricular cardiomyocytes: 0.3-1 m/s

Purkinje fibers: 1-4 m/s

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70
Q

What cells produce “slow response” action potentials and what is the respective conduction velocity of each?

A

Pacemaker cells in the SA and AV nodes: 0.02 - 0.1 m/s

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71
Q

4 phases of fast myocyte AP cycle and ion flow associated w/ each

A

0: inward Na+ (depolarization)
1: Na+ close, outward K+ open
2: inward Ca++ balance outward K+ (plateau)
3: Ca++ close, outward K+ (repolarization)
4: Na+/K+ ATPase restores normal [ion] (resting membrane potential)

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72
Q

If measuring EKG deflection in terms of voltage, what is the scale?

A

1mV = 10mm vertically

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73
Q

What is the time scale on EKG paper?

A

Small square = 1mm = 0.04s
Large square = 5 small squares = 5mm = 0.2s
5 large squares = 25 mm = 1.0s

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74
Q

What is Einthoven’s Triangle?

A

Orientation of EKG leads I - III
I: RA (-), LA (+)
II: RA (-), LL (+)
III: LA (-), LL (+)

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75
Q

What are the lateral leads on 12 lead EKG?

A

I and aVL

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76
Q

What are inferior leads in 12 lead EKG?

A

II, III, aVF

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77
Q

What is placement of the precordial leads?

A 
V1: 4th intercostal, R of sternum
V2: 4th intercostal, L of sternum
V3: between V2 and V4
V4: 5th intercostal, mid clavicular line
V5: between V4 and V6
V6: 5th intercostal, mid axillary line
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78
Q

What areas of heart do the precordial leads look at?

A

V1 and V2: Right
V3 and V4: septal
V5 and V6: Left

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79
Q

What does a biphasic deflection on EKG indicate?

A

Wave of depolarization is moving perpendicularly to (+) electrode

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80
Q

What is the normal rate of sinus rhythm?

A

60 - 100 bpm (sinus rhythm - set by SA node)

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81
Q

What is the normal amplitude of a P wave on EKG?

A

<2.5mm

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82
Q

What leads record a biphasic Pwave?

A

III and V1

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83
Q

What leads record positive and negative P waves?

A

Positive: I, II, V6
Negative: aVR

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84
Q

What structures insulate the ventricles from electrical activity of the atria?

A

Atrio-ventricular valves (tricuspid and mitral)

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85
Q

What does the PR interval represent?

A

Delay between the onset of atrial depolarization and ventricular depolarization.

Beginning of P wave -> beginning of QRS

Normal: <0.2 s

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86
Q

What structures are composed of Purkinje fibers?

A

Bundle of His
L and R bundle branches
Terminal Purkinke filaments

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87
Q

What is a QS wave?

A

Depression missing an R wave. R wave divides and defines Q and S waves, so minus the R it appears as a single depression. Generally considered a Q wave.

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88
Q

What do the components of the QRS complex represent?

A

Q: Septal depolarization
R: Apical ventricular depolarization
S: Basal (near valves) ventricular depolarization

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89
Q

What is the directionality of septal depolarization?

A

Right, Forward, and Down

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90
Q

What is the directionality of early ventricular depolarization?

A

Left, down, forward

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91
Q

How is early ventricular depolarization seen on EKG in each lead?

A

Frontal: positive R wave in I and II, negative QS in aVR
Horizontal: positive R wave w/ progressive intensity from V1-6

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92
Q

What is the directionality of late ventricular depolarization?

A

Left and upward

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93
Q

How is late ventricular depolarization seen on EKG?

A

Frontal: positive in I and aVL -> increased R wave amplitude, negative in aVF -> S wave
Horizontal: negative in V1 and 2 (S) and positive in V5 and 6 (+R)

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94
Q

What is the R wave Transition Zone?

A

in precordial leads, the point at which the positive R amplitude = negative S amplitude.
Usually in V3 or 4

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95
Q

In what leads should the Q wave be most apparent?

A

aVL and I

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96
Q

What is a normal QRS duration?

A

0.06 - 0.1 s

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97
Q

What is the direction of the ventricular repolarization vector?

A

Right and up

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98
Q

How is the T wave seen on EKG?

A

Frontal: positive in I, II, aVF; negative in aVR
Horizontal: positive V6, negative V1

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99
Q

What is a normal QT interval? What is it used for clinically?

A

0.30 - 0.44s (0.45 in women): at normal HR, < 1/2 of R-R interval.
Majority of QT is ventricular repolarization - clinical indicator of this.

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100
Q

What is QTc?

A

QT corrected for HR. > 0.44 is considered prolonged.

QTc = QT/sq. rt (R-R)

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101
Q

What are the rates of 3 ectopic pacemakers?

A

atrial: 60-80
junctional (w/in AV node): 40-60
ventricular: 20-40

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102
Q

What is a normal mean QRS vector?

A

0 - +90 degrees

Right deviation: > 90
Left deviation: < 0

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103
Q

In what settings are vertical and horizontal mean electrical axi seen?

A

Vertical: axis is vertically downward - heart is shifted toward right - variant of normal seen in tall, slender, healthy people

Horizontal: axis is leftward horizontally - apex of heart is pressed up by diaphragm in obese individual

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104
Q

What two settings could a deviated MEA be seen on EKG?

A
  1. Ventricular hypertrophy: increased electrical activity of hypertrophied ventricle dominates
  2. MI: infarcted area is dead. Deviation away from infarcted region.
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105
Q

What leads are used for evaluation of atrial enlargement?

A

V1: perpendicular to wave -> biphasic EKG tracing
LII: parallel -> positive deflection

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106
Q

What is normal P wave amplitude?

A

<2.5mm

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107
Q

What are signs of RV hypertrophy seen on EKG?

A

Precordial: Large R wave on V1, rightward movement of transitional point, shrinking R wave from V1-6 w/ persistence of S wave in 5 and 6.

Limb: Right MEA axis deviation.

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108
Q

What signs of LV hypertrophy can be seen on EKG?

A

Precordial: V1: deep S, V5: tall R
Sokolow Index: depth of S in V1 (mm) + height of R in V5 > 35mm - diagnosis of LVH

Limb: Lewis Index: LI R (mm) + LIII S (mm) > 25mm - diagnosis of LVH

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109
Q

What is an indication of ventricular strain seen on EKG?

A

Usually coupled w/ LVH:

Inverted T wave in V5 and V6 w/ gradual down slope and rapid upslope.

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110
Q

3 Stages of EKG changes seen in STEMI

A

1: Large T wave peaks followed by symmetrical inversion
2: ST elevation
3: Q wave emergence (pathological Q waves longer than 0.04s and at least 1/3 the amplitude of R wave of same complex)

ST and T wave changes may disappear w/ time, but Q wave will remain and is a marker of previous MI

T

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111
Q

What is seen on EKG in acute anterior infarction?

A

ST elevation and Q waves in V1-4

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112
Q

What is seen on EKG in lateral infarction?

A

ST elevation and Q waves in LI and aVL

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113
Q

What is seen on EKG in inferior infarction?

A

ST elevation and Q waves in LII, LIII, and aVF

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114
Q

What is seen on EKG in acute posterior infarction?

A

Large R waves and ST depression in V1, 2, and sometimes 3

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115
Q

What are 2 methods of EKG evaluation to assist in cases of suspected posterior infarction?

A

Transillumination: flip EKG paper and hold in front of a strong light - if what originally looked like ST depression looks like ST elevation, supports posterior MI.
Mirror test: look at tracing in a mirror.

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116
Q

Is EKG diagnosis of infarction valid in a patient w/ left bundle branch block?

A

Naw, bitch!

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117
Q

What modifiable risk factors have a causal relationship to CAD?

A

Elevated LDL

Hypertension

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118
Q

What effect does raising HDL levels have on CAD risk?

A

Does not reduce risk

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119
Q

What is positive remodeling in CAD?

A

Expansion of vessel wall outward to accommodate growing plaque and maintain vessel integrity.
After this process exhausts -> luminal narrowing

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120
Q

At what point does a fixed coronary obstruction become critical? What happens at this point?

A

70% diameter stenosis
90% reduction in cross-sectional area
1. resistance vessels are maximally dilated at rest
2. O2 supply threshold reached - if demand exceeds -> symptoms

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121
Q

3 factors that determine myocardial O2 demand:

A

HR
Contractility
Wall stress (preload, LV hypertrophy)

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122
Q

Formula for approximating myocardial O2 demand

A

Rate Pressure Product

HR x SBP

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123
Q

2 factors determining myocardial O2 supply

A

Coronary BF

O2 carrying capacity (Hgb)

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124
Q

How is pre-test probability for Angina determined?

A

Clinical history

Other tests to confirm or refute (ECG, Stress test +/- imaging, coronary angiography)

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125
Q

How is a stress test w/ imaging performed?

A

Thalium or Technetium injected at peak exercise and hours later at rest.
Isotope concentrates in metabolically active cells.
Cells that are ischemic w/ exercise do not concentrate isotope.
Perfusion defect w/ exercise compared to rest.

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126
Q

Gold standard for diagnosis of CAD

A

coronary angiography

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127
Q

Treatments for chronic stable Angina

A

Pharm: TNG, B-blocker, Ca++ channel blocker
Mechanical: PCI, CABG

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128
Q

Most important components of chronic stable angina treatment

A 
ASA (anti-platelet)
HMG-CoA reductase inhibitor (statin) - treats causal factor
BP control - treats causal factor
Diabetes control
Smoking cessation
Diet and exercise - lower LDL
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129
Q

What is the pathophysiology of ACS?

A

Thrombus overlying disrupted plaque obstructs blood flow

-transient or persistent

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130
Q

What are the clinical symptoms of ACS?

A

Prolonged chest discomfort at rest, radiation
-variable between pts.
Dyspnea, diaphoresis, N/V, HTN, hypotension

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131
Q

Who is more likely to have atypical symptoms of ACS?

A

Elderly, diabetic, females, history of CABG

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132
Q

Symptoms of proximal LAD occlusion

A

hypotension, reciprocal tachycardia
S3 - increased LVEDP
S4 and rales - pulmonary congestion (decreased diastolic compliance)

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133
Q

Exam findings suggestive of RCA occlusion

A 
hypotension, tachycardia
JVP elevation
No pulmonary congestion, no S4
bradycardia, variable heart block
murmur of mitral valve regurgitation
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134
Q

Primary diagnosis of STEMI

A

Persistence of ST elevation - indicates occluded epicardial artery or distal embolization obstructing microvascular perfusion

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135
Q

What is seen on NSTEMI EKG? How is NSTEMI diagnosed?

A

No ST elevation - may be ST depression (ischemia). Chest pain persists at rest.
Diagnosis: biochemical markers - elevated Troponins

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136
Q

What are the two main causes of cardiovascular disease related deaths?

A

Coronary Heart Disease: >50%

Stroke: ~20%

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137
Q

According to the Framingham study, what are the major risk factors for cardiovascular disease?

A 
Smoking
Elevated total or LDL cholesterol
HTN
Low HDL
Family history (male:  1st deg <65 yoa)
Age (men 45, women 55)
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138
Q

What BMI is considered obese? What is abdominal obesity?

A

30+
25-29 = overweight
Abdominal obesity: men: waist 40+; women: waist 35+

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139
Q

What patients should have a 10-year risk assessment for CHD?

A

Those with 2+ major risk factor.

Not required for those with fewer than 2, most have 10 year risk of <10%.

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140
Q

What factors are considered in Framingham CHD risk assessment?

A

Age
Total Cholesterol
HDL
Systolic BP
Smoking Status
After 10 points (men), risk grows rapidly from 6%
After 18 points (women), risk grows rapidly from 6%

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141
Q

What are primary, primordial, and secondary disease prevention?

A

Primary: prevention of disease onset in asymptomatic
Primordial: prevention of causative risk factors to prevent disease
Secondary: preventing recurrence or death in symptomatic pts.

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142
Q

How do gerontologists define “old”?

A

Young old: 60-74
old-old: 75-85
very old: >85

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143
Q

How do the WHO and US Task Force define old?

A

WHO: >60

US Task Force: >65

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144
Q

What is the leading cause of death in the elderly?

A

CVD

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145
Q

What is the most frequent hosiptal discharge diagnosis in older adults?

A

CHF
Usually diastolic dysfunction w/ preserved EF
More common in women

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146
Q

What are the 4 most common chronic medical conditions seen in addition to CVD in older adults?

A 
Arthritis
Cancer
Diabetes
Dementia (13% @65, 40% @80)
**50% of pts >80 have at least 2 other chronic conditions
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147
Q

What CV parameters increase w/ aging?

A 
Systolic BP
Pulse Pressure
PWV
LV mass
incidences of CAD and afib
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148
Q

What CV parameters decrease w/ age?

A

early diastolic filling (EF more dependent on atrial contraction)
max exercise HR
max CO
max aerobic capacity and O2 consumption
HR response to B agonist
Vasodilator response to endothelium dependent vasodilators

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149
Q

What causes changes in PWV changes w/ age and what is the end effect?

A

Arterial stiffening -> increased PWV (from 5m/s in youth - 12 m/s in elderly)
young: reflected wave augments diastolic pressure -> increased coronary perfusion
Old: reflected wave augments systolic pressure -> high systolic BP and pulse pressure

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150
Q

What changes in cardiac Ca++ handling occur w/ aging?

A

L-type receptor: reduced and delayed inactivation
Decreased and delayed SERCA reuptake
Reduced and delayed outward K+ rectifier current
-> prolonged AP, prolonged contraction, prolonged relaxation

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151
Q

What 3 factors are considered in the Unifying Hypothesis of Age Related Changes in CV Function?

A

Cumulative oxidative stress from increased superoxide anions
Inflammatory cell response to stress / infection
Programmed cell death

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152
Q

What type of HTN is particularly prevalent in the elderly population and what medication is it most responsive to?

A

Isolated systolic HTN

Responds to diuretics

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153
Q

In an older patient w/ diabetes, what HTN med is recommended?

A

ACE inhibitor to delay nephropathy

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154
Q

What causes post-prandial hypotension?

A

Shunting of blood to digestive tract. Occurs 30-120 min after meal.
May be symptomatic in elderly pop.

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155
Q

What % of elderly population may have silent cardiac ischemia and why?

A

25-50% due to decreased pain perception, dementia, memory impairment.

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156
Q

How do PCI and CABG compare in elderly?

A

PCI: better procedure survival rate, lower post-procedure stroke rate
CABG: better survival after 6mos.

157
Q

What effect does revascularization have in the setting of stable angina in an elderly population?

A

No survival benefit over optimized medical therapy - symptomatic treatment

158
Q

What is the link between influenza vaccination and cardiac death in the elderly?

A

Flu vaccine decreases risk of cardiac death in elderly

Also prevents CHF hospitalizations

159
Q

What defines systolic CHF? What are common causes in the elderly? How are elderly treated?

A

EF improved survival

160
Q

What causes diastolic HF and what are effective treatments for elderly pts?

A

Diastolic HF (preserved EF) caused by stiff ventricles - abnormal relaxation
No treatment improves survival in elderly
HF w/ PEF has better survival in younger pop, same as systolic CHF in elderly.

161
Q

How do BNP levels compare in older and younger patients w/ CHF?

A

4x higher in older population

162
Q

Examples of medications that may require weight based dosing in elderly

A 
Digoxin
Certain antiarrhythmics
Warfarin
UFH
LMWH
163
Q

Are drugs metabolized by glucuronidation, sulfation, and methylation affected by age?

A

No

ex: methyldopa, diazepam, procainamide

164
Q

Is the P450 pathway affected by aging?

A

Yes - slows down
drugs affected: a-blockers, B-blockers (meto, propan), CCB, statins
may increase side effects.

165
Q

3 factors affecting Warfarin activity

A 
CYP2C9 polymorphisms may increase effect (12% of dose variations)
Vitamin K epoxide reductase  complex polymorphism may increase or decrease sensitivity (25% of dose variation)
Increased age (40% of dose variation)
166
Q

What happens in cocaine induced MI?

A

Vasospasm

Do not give B-blocker - may worsen.

167
Q

In the course of MI, how long from time of onset to irreversible myocyte injury? How long until total infarct size determination?

A

30 minutes of ischemia -> irreversible damage

6 hours - total infarct size determination

168
Q

Sequence of morphological changes in MI

A

12-24 hrs: Dark red, mottled
1-3 days: pale, tan region
3-10: well defined, soft, tan, red hyperemic border
10 days - 2 mos: red - gray -> gray - white, changes from periphery to center
2+ mos: rubbery white scar

169
Q

What is myocytolysis?

A

reversible ischemic injury - hydropic change - swelling of cells

170
Q

Sequence of microscopic changes post MI

A

4-24 hours: coagulative necrosis - ghost cells, hypereosinophilia, pinknotic nuclei
2-3 days: invasion of inflammatory cells (macs and neutrophils), interstitial edema
3-7 days: tissue disintegration by phagocytosis
1-2 weeks: gradual replacement by granulation tissue (capillaries and fibroblasts
2 weeks - 2 mos: increased collagen, decreased fibroblasts and capillaries with ensuing aggregate of dense collagen

171
Q

What is myocardial stunning?

A

Temporary decrease in contractility following reperfusion therapy

172
Q

3 features of reperfusion injury

A

1) myocyte death (free-radicals)
2) microvascular injury (endothelial cell swelling
3) arrhythmias

173
Q

2 labs evaluated in MI timing of changes

A

Troponin (I and T): elevation 2-4 hrs, peak in 48 hrs, remain elevated 7-10 days

Creatine Kinase MB (CK-MB): elevation 2-4 hrs, peak in 24, return to normal in ~3 days

174
Q

At what point is fibrinous pericarditis seen in MI patients?

A

2-3 days after a transmural MI

175
Q

When is the greatest risk for myocardial rupture after MI?

A

4-5 days post MI (maximal tissue disintigration)

  • usually older women
  • -> hemopericardium and tamponade, rarely -> false aneurism
176
Q

What is the pathological characterization of chronic ischemic heart disease?

A

LVH + dilation
Severe coronary atherosclerosis
Multiple areas of myocardial fibrosis
Subendocardial myocytolysis

177
Q

3 causes of serous pericarditis

A

Uremia (CKD)
Autoimmune (SLE)
Viral infection

178
Q

Etiology of fibrinous pericarditis

A 
Uremia
Autoimmune
Post MI
Post surgery
Radiation
Early bacterial infection
179
Q

Characteristic finding in fibrinous pericarditis

A

pericardial friction rub

180
Q

Causes of hemorrhagic pericarditis

A

metastatic malignancy (cancer -> angiogenesis)
infection (TB)
coagulopathy
status post cardiac surgery

181
Q

What is adhesive pericarditis?

A

Sequela of serous or fibrinous pericarditis

Strands of fibrinous CT between visceral and pericardial surfaces

182
Q

What are soldiers plaques?

A

Chronic pericardial disease
Benign
Pericardial thickenings that may become calcified.

183
Q

4 forms of chronic pericarditis

A

Adhesive (sequela of serous / fibrinous)
Soldier’s Plaques - benign thickening
Constrictive - sequela of purulent or caseous
Adhesive mediastinopericarditis - complication of radiation, surgery, purulent, or caseous
-

184
Q

What is Carney Syndrom?

A

Autosomal Dominant condition characterized by multiple myxomas

185
Q

What condition is rhabdomyoma occasionally associated with?

A

Tuberous sclerosis

186
Q

What kind of tumor is rhabdomyoma?

A

Hamartoma

Most common cardiac tumor in children

187
Q

What tumors spread to the heart?

A

carcinomas (lung, breast)
melanoma
WBC malignancies (leukemia, lymphoma)

188
Q

Three complications resulting from tumor derived mediators

A
  1. Non Bacterial Thrombotic Endocarditis - assoc. w/ mucinous adenocarcinomas
  2. Carcinoid heart disease (serotonin secreting neuroendocrine tumor of GI w/ hepatic metastasis)
  3. Amyloidosis: excessive Ig production
189
Q

Drug toxicity linked to decreased myocardial contractility and CHF

A

Doxorubicin

190
Q

3 Etiological causes of CHF

A
  1. decreased contractility
  2. increased resistance to ventricular filling or ejection
  3. systemic disease (severe anemia, hyperthyroidism)
191
Q

What are “heart failure cells”?

A

Intra-alveolar macrophages filled w/ hemosiderin - indication of CHF chronicity

pulmonary congestion -> microhemorrhage -> phagocytosis of RBCs

192
Q

Role of the kidney in CHF

A

decreased renal perfusion -> activation of renin - angiotensin - aldosterone system -> retention of Na+ and H2O -> worsening pulmonary edema

193
Q

How much pericardial fluid is typically present?

A

15-50 mL

194
Q

What EKG changes are seen in acute pericarditis?

A

Stage 1: elevated, concave ST, and early PR depression in all leads except aVR
Stage 2: J point normalizes and decrease in T wave amplitude
Stage 3: T wave inversion
Stage 4: EKG resolution

195
Q

3 components of pericardial friction rub as heard in acute pericarditis

A
  1. Mid-systolic: V. contraction
  2. Mid-diastolic: Rapid V. filling
  3. Late-diastolic: A. contraction
196
Q

What lab abnormalities are seen in acute pericarditis?

A

elevated WBC (11-13,000) w/ mild lymphocytosis (viral / idiopathic)
elevated ESR
elevated CK, CK-MB, Troponin (inflamm of neighboring myocardium)

197
Q

What infections are associated with pericarditis?

A

Viral: Echo, Coxsackie, Adeno, CMV (HIV pts)
Bacterial: Pneumococcus, Strep, Staph
Mycobacterial: TB, Avium intracellulare
Protozoal

198
Q

What is the most common precursor to bacterial pericarditis?

A

Surgery (often w/ endocarditis and bacteremia)

Used to be pneumonia

199
Q

What is Dressler’s Syndrome?

A

Acute pericarditis weeks or months after MI
Autoimmune etiology - sensitization following necrosis
Anti-myocardial Ab
Often self-limited
Treat w/ NSAIDS or steroids

200
Q

Prognosis in pericarditis secondary to malignancy. Treatments?

A

Poor - limited survival. Marker for extensive disease.

Percutaneous drainage or surgical “window” in pericardium

201
Q

What kind of pericarditis can radiation produce?

A

Constrictive or Restrictive - drainage may not relieve symptoms

202
Q

4 drugs associated with pericarditis

A

Minoxidil
Hydralizine
INH (isoniazid)
Cyclosporin

203
Q

What is treatment for endocarditis?

A

No standard treatment
Symptomatic: NSAIDS (2 weeks of indomethacin or ibuprofen)
Steroids - second line following NSAID failure
Colchicine - alternative to steroids

204
Q

What is Ewart’s sign and what is it indicative of?

A

Dullness, decreased breath sounds, egophony over posterior left lung
Due to lung compression by large pericardial sac
Suggests large pericardial effusion

205
Q

How does pulsus paradoxus affect stroke voume?

A

increased right sided filling shifts interventricular septum left -> compression of LV -> decreased SV

206
Q

PE findings in case of cardiac tamponade

A

Pulsus Paradoxus
Tachycardia
Increased JVP
Hypotension

207
Q

Most common cause of constrictive pericarditis?

A

Post cardiac Sx

208
Q

What is Kussmaul’s sign and what does it indicate?

A

Increase in venous pressure during inspiration.

Seen in constrictive pericarditis - not tamponade

209
Q

What is treatment for constrictive pericarditis?

A

Palliative - diuretics and salt restriction

Surgery - only definitive treatment - difficult procedure

210
Q

What heart sound is heard in constrictive pericarditis?

A

Diastolic knock following S2 (higher pitch than S3)

Sudden cessation of filling due to constriction

211
Q

Differentiate an Ejection Click and Opening Snap.

A

Ejection click: follows S1: bicuspid aortic valve/ aortic stenosis
Opening snap: follows S2: mitral stenosis

212
Q

Differences between S3 and S4

A

S3: systolic HF
S4: diastolic HF

213
Q

What are the components of the cardiovascular physical exam?

A

Inspect: JVP, precordium
Palpate: Pulses, precordium
Auscultate

214
Q

Where is the usual point of maximal impulse (PMI) on cardiac exam?

A

4th or 5th IC space, mid clavicular line

215
Q

What causes palpable “thrills” on cardiac exam?

A

Obstruction to LV outflow
Assoc. with loud murmurs
usually felt over L sternal border

216
Q

Where is S1 splitting audible and considered normal?

A

Lower left sternal border: Tricuspid closes after mitral valve

217
Q

What is paradoxical splitting?

A

splitting of S2 heard during expiration - delay in closure of aortic valve so P2 precedes A2

218
Q

What are the histologic layers of a cardiac valve?

A

Valvular fibrosa: faces outflow chamber
Valvular spongiosa: central core of loose CT w/ proteoglycans
Elastin-rich layer: inflow surface (atrialis or ventricularis)
Endothelial covering

219
Q

2 categories of valvular insufficiency

A

Primary: abnormality of valve cusps (myxomatous degeneration, infective endocarditis, rheumatic heart disease)
Secondary: abnormality of surrounding structures (chordae tendineae, papillary muscle, ventricular enlargement)

220
Q

Clinical manifestations of calcific aortic stenosis and who is affected.

A

CHF, syncope, angina
Presents in older adults in 70-80s w/ previously normal valves
50s and 60s w/ bicuspid valve

221
Q

What are some complications of Mitral Annular Calcification?

A

Usually benign, but can -> regurgitation, stenosis, arrhythmia (irritation of underlying ventricle),

222
Q

What is another name for mitral valve prolapse and how is it usually detected?

A

Myxomatous Degeneration of the Mitral Valve

Usually detected as mid-systolic click in young woman

223
Q

What genetic disorder is Mitral Valve Prolapse associated with?

A

Marfan

224
Q

What is seen microscopically in mitral valve prolapse?

A

Expansion of spongiosa layer and loss of collagen in fibrosa layer of valve

225
Q

What is the pathogenesis of Rheumatic Heart Disease?

A

Cross-reacting antibodies induced by B-hemolytic GAS (S.pyogenes) pharyngitis

226
Q

What is a microscopic indicator of Rheumatic Heart Disease?

A

Aschoff Bodies: (granulomas) areas of fibrinoid necrosis within heart muscle. Degenerating collagen, lymphocytes, plasma cells, activated macs (Caterpillar cells: nuclear chromatin is disposed into central wavy ribbon)

227
Q

What pericardial disorder is assoc. with rheumatic heart disease?

A

Fibrinous pericarditis

228
Q

What are indicators of chronic rheumatic heart disease?

A

Neovascularization and fibrotic valvular deformities - fusion of cusps and chordae tendineae, fishmouth stenosis

usually left sided

229
Q

What antibodies can be found in a patient with acute rheumatic fever?

A

anti- streptolysin O and DNAase B

230
Q

Major criteria of Acute Rheumatic Fever

A

Acute pancarditis (friction rub, arrhythmia, weakening, dilation)
Migratory polyarthritis of large joints (adult)
Subcutaneous nodules
Erythema marginatum
Sydenham chorea

231
Q

What are the primary organisms associated with infective endocarditis?

A 
Strep viridans (other oral flora) (50-60% of cases, requires prev. valve damage)
Staph aureus (IV drug use)
Coagulase neg. staph (S. epidermidis) (prosthetic valves)
232
Q

What is Marantic Endocarditis?

A

Nonbacterial Thrombotic Endocarditis (NBTE)

233
Q

2 pathologies that can -> NBTE

A

1) Hypercoagulability assoc w/ debilitating illness (mucinous adenocarcinoma of the spleen, sepsis)
2) Endocardial injury (IC cath)

234
Q

What areas of the heart are affected by carcinoid syndrome?

A

Right side valves - lungs break down serotonin to inactive byproduct.

Usually caused by hepatic metastasis of carcinoid tumor

235
Q

Which ventricle better tolerates volume overload?

A

Right

236
Q

When does congenital valve stenosis typically?

A

May see symptoms w/ closure of ductus arteriosus.

Mostly seen in pediatrics

237
Q

What is the equation for estimation of pressure gradient?

A

P2-P1 = 4(V2^2 - V1^2) where V=velocity

238
Q

What mitral valve area is considered stenotic?

A

<2cm^2

239
Q

What differentiates moderate and severe mitral valve stenosis?

A

Moderate: AV pressure gradient is 6-12 mmHg (normal 13

CO: subnormal at rest, may fall w/ exertion

240
Q

Sounds heard in mitral valve stenosis

A 
Loud S1 (valve closing - high LV pressure needed to overcome AV pressure gradient -> sharp closing)
Opening Snap (after S2)
Diastolic rumble
241
Q

What is the most common EKG finding with mitral stenosis?

A

P-mitrale

wide, notched p-wave (2 side by side p waves) - reflective of increased time required for depolarization of enlarged LA

242
Q

What are indications for mitral valvotomy?

A

Pulmonary HTN
Symptoms w/ moderate stenosis
Systemic embolization
Asymptomatic female desiring pregnancy (Hx of symptoms)

243
Q

Key PE findings in case of aortic stenosis

A 
Narrow pulse pressure
DOE
Syncope
Sudden Death
Pulsus tardus and parvus (slow and weak)
Systolic Ejection click (can disappear w/ worsening stenosis)
S4
Paradoxical S2 splitting
Ejection murmur / thrill
244
Q

Physical exam findings with mitral valve prolapse

A

Midsystolic click, late systolic murmur if regurgitant.

Click moves away from S1 w/ increased preload (increase LV volume), and nearer w/ decreased preload.

245
Q

Key physical exam findings in mitral regurgitation

A

Hyperdynamic percordium
High frequency systolic regurgitation murmur
Diastolic rumble

246
Q

Differential in Mitral regurgitation

A

Acute: Endocarditis, papillary muscle/ chordal rupture, trauma
Chronic: Congenital heart disease, mitral prolapse, rheumatic fever, hx of endocarditis, annular calcification, hypertrophic / dilated cardiomyopathy, hx of MI, radiation

247
Q

Indication for surgery in Mitral regurgitation

A

Symptoms
Recent onset afib and pulmonary HTN
Asymptomatic: significant LV dilation / dysfunction

248
Q

Differential Diagnosis in aortic regurgitation

A

Valve leaflet disease
Aortic root / surrounding apparatus disease: fibromuscular aortic ridge, prolapsed aortic leaflet, syphillis, hypertrophic cardiomyopathy, aortic root dilation, HTN, retrograde aortic dissection

249
Q

Mechanical vs. Bioprosthetic replacement valves

A

Mechanical: durable, but req. chronic anticoag therapy and may -> endocarditis

Bioprosthetic: anticoag not needed, but less durable: tears and calcification

250
Q

When is rheumatic fever’s onset?

A

2-3 weeks post Strep A pharyngitis

stenotic valve disease 10-30 years later

251
Q

what organs are affected by rheumatic fever?

A

brain, heart, skin, joints

252
Q

Rheumatic fever diagnosis according to Jones criteria

A

Evidence of prior GAS infection and either 2 major ot 1 major and 2 minor of:
Major: Polyarthritis, erythema marginatum, carditis, chorea, subcutaneous nodules
Minor: Fever, acute phase proteins (ESR, CRP), arthralgia, prolonged PR interval

253
Q

3 exceptions to Jones criteria

A
  1. Chorea may be the only sign
  2. Carditis may be the only sign if detected late
  3. Lower threshold for diagnosis of current rheumatic fever
254
Q

Differential Diagnosis in Rheumatic disease

A 
arthritis
lupus
connective tissue disease
serum sickness
leukemia
255
Q

What is the prognosis in acute rheumatic disease?

A

Dependent on severity of cardiac involvement at presentation
Valvular disease resolves in 25%
Worse cardiac disease w/ recurrent disease
Prophylaxis (penicillin) aids in resolution

256
Q

What are the most common causes of native valve infective endocarditis?

A

Strep species and S. aureus

257
Q

What is the organism most frequently seen in prosthetic valve infective endocarditis?

A

Staph epidermidis

258
Q

What is a mycotic aneurysm?

A

Aneurysm caused by bacterial infection of arterial wall. Septic embolus from infective endocarditis may cause.

259
Q

How do streptococcus organisms adhere to thrombi?

A

Dextran in cell wall adheres to thrombus -> vegetation

260
Q

What are Janeway lesions and what organism is most often associated?

A

Non-tender lesions on palms and soles caused by septic emboli embedded in dermis.
Most often S. aureus

261
Q

What are Roth Spots?

A

Retinal hemorrhages caused by emboli - seen in infective endocarditis, but also DM, leukemia, pernicious anemia

262
Q

What is the cause of petechiae in infective endocarditis?

A

Immune complex deposition in small vessels.

263
Q

Osler’s Nodes

A

Painful raised bumps, usually on pads of fingers and toes, associated with bacterial endocarditis.
Caused by immune complex deposition w/ acute inflammation

264
Q

What lab abnormalities are seen in infective endocarditis?

A

Elevated WBC
Anemia: normochromic, normocytic
Elevated CRP and ESR
Elevated Rheumatoid Factor (50%)

265
Q

How is endocarditis treated?

A

High dose, long duration ABX (6-8 wks, often 2 abx)

Removal of prosthetic material

266
Q

Indications for surgery in native valve endocarditis?

A

Persistent infection despite 7-10 days of abx treatment
-persisting fevers, + blood culture, elevated WBCs

Annular or aortic abscess
Recurrent emboli
Refractory CHF due to valvular dysfunction
Fungal endocarditis

267
Q

What are Duke Criteria?

A

For diagnosis of infective endocarditis
Major: 2 positive blood cultures (typical organisms)
1 positive culture for Coxiella burneti or antiphase I IgG Ab
titer >1:800
Evidence of endocardial involvement (+ echo, new regurg
murmur)

268
Q

According to Duke criteria, what is needed for definite diagnosis of infective endocarditis?

A

2 major criteria
1 major + 3 minor
5 minor

269
Q

At what point is a widened QRS considered a danger?

A

Widened by 20-25%

Class I antiarrhythmic: adjust meds if this occurrs

270
Q

Primary uses for 1A antiarrhythmics

A

SVT, AF, VT

271
Q

What drug is “a pill in the pocket” for afib?

A

Flecainide: For afib patients who have exacerbations a few times / year, taking flecainide PRN rather than daily dosing is useful

272
Q

What is the most potent agent for Afib and Vtach?

A

Amiodarone

nota FDA approved for afib

273
Q

Amiodarone drug interactions

A

Warfarin (cut in half if amio added), Digoxin, Quinidine, Procainamide, Flecainide

274
Q

What are the characteristics of a syphilitic aortic aneurism?

A

Fusiform dilation of aortic arch and thoracic aorta
White, folded intima
Adventitia: narrowed vasa vasorum w/ lymphocytes and plasma cells
Media: patchy loss of sm. muscle cells w/ inflammation and fibrosis

275
Q

What is a double-barreled aorta?

A

Aortic dissection that re-ruptures into the lumen

276
Q

What is seen microscopically in aortic dissection?

A

“Cystic” degeneration of the media: Fragmentation and loss of elastic tissue replacement by pale, amorphous ECM

277
Q

2 classifications of aortic dissection

A

Type A: more severe - requires immediate surgery: proximal +/- descending aorta
Type B: descending only

278
Q

What is ANCA? 2 examples

A

Anti-neutrophil cytoplasmic antibody
c-ANCA (cytoplasmic) anti-proteinase 3
p-ANCA (perinuclear) anti-myeloperoxidase

279
Q

What antibody is present in Kawasaki disease?

A

Anti-endothelial cell Ab

280
Q

What antibody complex has been associated with polyarteritis nodosa?

A

Hep B surface Ag

281
Q

What Ab-Ag complex is associated with Henoch-Schonlein purpura?

A

Anti-IgA immune complex

282
Q

How are ANCAs pathogenic?

A

initial insult -> immune activation (neutrophil expression of antigens such as PR3 and MPO) -> production of ANCA -> binding of ANCA to neutrophil and degranulation -> vascular injury

283
Q

What is seen in temporal arteritis?

A

intimal thickening, granulomatous inflammation, focal destruction of internal elastic lamina in temporal artery -> painful, palpable, nodular temporal artery

treat w/ steroids

284
Q

What is Takayasu arteritis?

A

“Pulseless Disease”
Mononuclear inflammation of aorta and major branches
Young women w/ neurologic or visual defects, HTN, weak or absent pulses of extremities.

285
Q

Wegener granulomatosis

A

involves c-ANCA, affects middle-aged men, responds to immunosuppressive therapy
classic triad:
1) necrotizing granulomatous inflammation of respiratory tract
2) necrotizing granulomatous inflammation of small vessels (esp. of respiratory tract)
3) necrotizing proliferative glomerulonephritis -> hematuria, proteinuria, renal failure

286
Q

What organs are effected by polyarteritis nodosa?

A

Small- medium vessels of kidney, GI, heart (NOT lung)

287
Q

Features of polyarteritis nodosa

A

Regions of fibrosis, necrosis, thrombosis, aneurism -> tissue ischemia
Young adults w/ fever, malaise, myalgia
Assoc. w/ HTN, GI bleeds, GI infarct
Responds to immunosuppresives

288
Q

Features of Kawasaki disease

A

Young children:
fever, mucosal erythema, desquamating rash, edema, cervical lymphadenopathy, cardiovascular complications (coronary aa involvement)

289
Q

Features of microscopic polyantiitis

A

p-ANCA, no granulomas - usually onset after exposure to new antigen: Drug, malignancy
hemorrhagic skin lesions
Effects small vessels - capillaries, arterioles, venules
Fragmented neutrophils
Similarly aged lesions

290
Q

Henoch-Schonlein purpura

A

Childhood systemic vasculitits, usually follows URI
Necrotizing vasculitis w/ IgA immune complexes and C3
Effects skin, GI, kidneys (hypercellular mesangium)

291
Q

What is Buerger’s Disease?

A

Thromboangiitis Obliterans
Seen in heavy smokers >40 yoa
Distal ulcers and gangrene
Medium sized and small arteries - thrombosis, acute and chronic inflammation (stenotic corkscrew vessels)

292
Q

What is Churg-Strauss Syndrome?

A

p-ANCA, middle-aged adults

1) allergic rhinitis, sinusitis, asthma
2) peripheral hypereosinophilia
3) extravascular and vascular necrotizing granulomas involving lungs, skin, PNS, CNS, heart, GI, kidney, musculoskeletal ss.

293
Q

Do varicose veins predispose to thromboembolism?

A

No

Thrombosis - yes, but not embolism

294
Q

What is nevus flammeus?

A

Birth mark, type of vascular ectasia
Regresses w/ time

Port wine stain - subtype that enlarges w/ growth

295
Q

What is spider telangiectasia associated with?

A

Elevated estrogen (pregnancy, cirrhosis)

296
Q

What is Kaposi’s Sarcoma?

A

STI: HHV-8 or KSHV -> vascular proliferation
Classic: distal extremities of older, eastern-euro and mediterranean men
Endemic: aggressive - involves lymph nodes. Africa.
Immunosuppression assoc: AIDS and post-transplant. multi-organ

297
Q

What is angiosarcoma and what are risk factors?

A

Aggressive malignancy of endothelial cells - often breast, liver
mass often contains multiple hemorrhages
Risk: radiation exposure, chronic lymphedema, vinyl chloride, thorotrast, arsenic

298
Q

What are normal O2 saturations in the heart?

A

Left side: 100%
Right side: 75%
Coronary sinus: lowest sat in the heart - drains myocardium

299
Q

What are causes of CHF in the newborn?

A 
A-V malformation
Truncus
Single Ventricle
Severe valvular insufficiency (usually AV valve)
Myocarditis, arrhythmia, asphyxia
300
Q

What is the main cause of CHF in the first 3-7 days of post natal life?

A

PDA dependent circulation:
Systemic (shock): Severe AS, Severe CoA, HLHS
Pulmonary (cyanosis): Pulmonary atresia, Severe PS

301
Q

What are causes of CHF in the first 1-4 months of life?

A

L-R shunting
Anomalous origin of L coronary artery from pulmonary artery
SVT
Acute HTN

302
Q

When does cyanosis become apparent?

A

5g/dL desaturated hemoglobin (normal is 2 g/dL)

303
Q

What is a hyperoxia test?

A

Usually done on an infant to determine whether cyanosis is due to lung disease or circulation
Failure to elevate pO2 to 150 mmHg after 15 mins breathing 100% O2 suggests cyanotic congenital heart disease

304
Q

In the case of a mixing lesion what is “ideal” saturation?

A

80%

Higher that 85% indicates excess pulmonary blood flow.

305
Q

What is the most common risk factor for stroke in an infant w/ cyanotic heart disease?

A

Iron deficiency anemia -> RBCs that do not deform when passing through vessels

306
Q

What is the most common cyanotic congenital heart disease?

A

Tetralogy of Fallot

307
Q

What is the most common congenital shunt lesion?

A

VSD

308
Q

What CHD is associated with trisomy 21?

A

VSD

309
Q

What CHD is associated with Turner’s (XO)?

A

Coarctation of aorta

310
Q

What CHD is associated with Trisomies 13 and 18?

A

VSD

311
Q

What CHD is associated with Di George?

A

Tetralogy of Fallot
Transposition
Truncus

312
Q

How is ASD usually detected? When are most ASDs repaired? What is a consequence of not reparing?

A

Usually found as an asymptomatic murmur.
Repaired at 2-5 years of age.
w/o repair: pulmonary vascular disease may develop in 4th decade or later.

313
Q

Two most common locations of ASD

A

1: Secundum
2: Primum

314
Q

Why does ASD produce a L-> R shunt?

A

Low pulmonary resistance and high RV compliance.

315
Q

In VSD, when does shunting develop, what causes the shunting, and when do CHF symptoms appear?

A

Shunting develops w/ drop in pulmonary resistance below systemic (with first breaths)
CHF symptoms appear in 1st 6 mos.

316
Q

What are systemic responses to VSD?

A

Inadequate systemic flow:
Increased SNS activity -> tachycardia
Aldosterone -> fluid retention
RAS -> vasoconstriction

317
Q

How does the size of a VSD relate to the intensity of a murmur sound?

A

Inverse relationship

318
Q

What is Eisenmenger Syndrome?

A

L->R shunt -> elevated pulmonary flow and pressure -> pulmonary vascular disease and increase in pulmonary resistance.
If pulmonary resistance exceeds systemic, shunt reverses to R->L
-> cyanosis.
Usually occurs in 2nd decade.

319
Q

In what patient population is AV Septal Defect most common?

A

Trisomy 21: 40% w/ CHD, 40% of those w/ AVSD

50-60% of all AVSD have Trisomy 21

320
Q

What extent of narrowing is considered significant in aortic coarctation?

A

50% or greater narrowing of lumen

321
Q

Where does aortic coarctation occur?

A

distal to L Subclavian branch, opposite ductus arteriosus

322
Q

What is the clinical effect of aortic coarction and how is it treated?

A

Closing of ductus arteriosus -> proximal HTN and decreased flow to lower limbs.
Give prostaglandin to maintain patency of ductus until surgery.

323
Q

What genetic syndromes are associated with Tetralogy of Falot?

A

22q11 deletion
Trisomies 13,18, 21
Alagille syndrome w/ associated biliary atresia (Jagged-1 deletion, 20q: Notch ligand)

324
Q

Components of ToF

A 
Tetralogy of Fallot (PROVe)
Pulmonary Stenosis  (RVOTO)
Right Ventricular Hypertrophy  (RVOTO)
Overriding Aorta
Ventricular Septal Defect
325
Q

What is blue TET vs pink TET

A

Determined by degree of pulmonary stenosis
Pink TET: equal flow to lungs (minor pulmonary stenosis)
Blue TET: decreased flow to lungs -> cyanosis

326
Q

When are Tet spells typically first observed in a child with Tetralogy of Fallot?

A

3-6 months.

327
Q

What is a typical murmur heard in a patient with Tetralogy of Fallot? What happens to the murmur during a Tet spell?

A

Murmur: 1) RVOT systolic murmur (pulmonary stenosis) 2) Holosystolic murmur from VSD (R->L shunt)

PS murmur fades due to increased systemic BF

328
Q

Management of Tet spell

A 
Knees to chest
Oxygen
Morphine
Volume expansion
Acid-base correction
Vasoconstrictor (epi)
329
Q

When is ToF typically repaired?

A

1-6 mos

Complicated patients may be 1-3 years

330
Q

What does ToF repair consist of ?

A

VSD patch repair

Relief of RVOTO

331
Q

What is the most common cyanotic lesion that presents in the neonate?

A

Dextro-Transposition of the Great Arteries

332
Q

What secondary heart defect is essential to survival in cases of TGA?

A

Septal defect allows mixing of oxygenated and desaturated blood.
Otherwise, 2 circulations in parallel -> death

333
Q

3 procedures for correction of TGA

A
  1. Atrial switch (Mustard, Senning): largely abandoned
  2. Rastelli: sometimes used: repair of VSD (graft connects Aorta to LV); closure of PA and implant of shunt to RV
  3. Arterial switch (Jatene): switch arteries, connect coronaries to new aorta.
334
Q

4 types of Persistant Truncus Arteriosus

A

I: one pulmonary artery branches from main trunk -> 2 lateral pulmonary aa.
II: two posterior / posterolateral pulmonary aa from main trunk
III: two lateral pulmonary aa. from main trunk
IV: pulmonary aa. do not arise from main trunk, but distal to L. subclavian a. no longer considered a form of TA.

335
Q

What occurs in tricuspid atresia?

A

Unequal division of the AV canal -> complete occlusion of tricuspid valve and underdevelopment of RV.
Systemic venous return must pass through PFO
VSD allows communication from LV -> PA
High mortality in first weeks of life

336
Q

What is a Blalock-Taussig shunt?

A

Create communication between R. subclavian and R. pulmonary arteries.
Increases pulmonary ciruclation.

337
Q

What are the steps in correction of Hypoplastic Left Heart Syndrome?

A
  1. Norwood: supply systemic cicrulation: Pulmonary aa. disconnected from Pulmonary Trunk, and Trunk connected to ascending aorta providing systemic circulation. BT or Sano shunt to provided circulation to Pulmonary aa.
  2. Hemi-Fontan / Bi-directional Glenn: Pulmonary artery shunt removed and SVC re-routed through pulmonary arteries (reduces load on RH while maintaining pulmonary circulation under venous pressure).
  3. Total Caval Pulmonary Anastamosis: IVC connected to pulmonary circulation (further reduces load on right heart, all systemic return routed through pulmonary circulation)
338
Q

What is the timeline for correction of Hypoplastic Left Heart Syndrome?

A

Step 1: Ensure pulmonary and systemic ciruclation, protect pulmonary aa: Neonatal
Step 2: Connect SVC -> pulmonary: 6 mos
Step 3: Connect IVC -> pulmonary: 18-24 mos

339
Q

Degrees of hypothermia

A

Normal: 37C
Mild: 32-36
Moderate: 25-31
Profound: 18-24 (at 18C, up to 45 min circulatory arrest safe)

340
Q

What are the effects of hypothermia?

A

Decreased metabolic rate
Reduced O2 consumption
Allows flow reduction

341
Q

What is Atrioventricular septal defect and how is it repaired?

A

Combination of ASD and VSD with single atrioventricular valve.
Correction includes patching the septal defects and making the single valve into two - will never be normal, will always leak, and almost always requires future 2nd surgery.

342
Q

What is increased in AVSD (flow, volume, resistance)?

A

pulmonary BF
All chamber volumes
pulmonary vascular resistance

343
Q

When is ASVD surgery usually done and why?

A

3-6 mos.

Valve leaflets are too thin at neonatal stage - will not hold a suture.

344
Q

What is a hybrid stage 1 procedure in treatment of hypoplastic left heart syndrome?

A

Branch pulmonary artery bands
Stenting of PDA
Balloon atrial septostomy (separate procedure)
avoids heart and lung machine

345
Q

Formula to determine Qp/Qs and normal ratio.

A

Qp/Qs = (Arterial sat - mixed venous sat) / (pulmonary vein sat - pulmonary artery sat)
Normal 2.5 : 1

346
Q

What happens to Qp/Qs in a single ventricle setting?

A

Qp/Qs = (Arterial sat - mixed venous sat) / (pulmonary vein sat - pulmonary artery sat)
Single ventricle: Sa = 82; Smv = 65; Spv = 100; Spa = 82
Ideal value reduced to 1 : 1

347
Q

Should a patient with a single ventricle and 80% arterial sat be given O2?

A

NO!

Will unbalance Qp/Qs (normal is 1, will increase vastly) -> critical decrease in systemic blood flow

348
Q

How can Pulmonary blood flow be increased?

A

Decrease pulmonary vascular resistance: O2, decrease pCO2, sedate, lower MAP, Milrinone, Nipride, NO

Increase Systemic vascular resistance: alpha agents: neosynepherine, NEpi, Epi

349
Q

How can pulmonary blood flow be decreased?

A

Increase pulmonary vascular resistance: increase pCO2, decrease FiO2, PEEP

Decrease systemic vascular resistance: Morphine, Nipride, Milrinone

350
Q

Causes of dilated cardiomyopathy

A

Idiopathic
Genetic (1/3 of cases): usually AD (cytoskeleton, mitochondria, nuclear membrane, sarcomere)
Toxicity: ETOH, drug tox
Thiamine deficiency: wet beriberi
Post myocarditis (due to enteroviruses)
Pregnancy-related (peripartum): hemodynamic changes

351
Q

What is Arrhythmogenic Right Ventricular Cardiomyopathy?

A

Form of dilated cardiomyopathy in which Right Ventricular myocardium is replaced by fat and fibrous tissue -> Right HF and arrhythmias
Inherited - AD

352
Q

Another name for hypertrophic cardiomyopathy

A

Idiopathic Hypertrophic Subaortic Stenosis

353
Q

What percent of hypertrophic cardiomyopathy cases have an underlying genetic cause?

A

100%

354
Q

Causes of myocarditis

A

Infection
a) enterovirus (coxsackie A and B, echovirus), CMV, HIV
b) bacteria (Borellia Burgdorferi - Lyme)
c) fungi (Candida)
d) parasites (T.cruzi (Chagas), T.gondii)
Immunologic disorder: drug hypersensitivity, autoimmune (acute rheumatic fever, SLE)
Idiopathic

355
Q

Name 2 drugs known for cardiotoxicity

A

Cyclophosphamide (alkylating agent): vascular toxicity -> cardiac hemorrhage
Doxorubicin (DNA binding): myocyte toxicity -> myocyte vacuolation and lysis -> dilated cardiomyopathy

356
Q

What is a cause of contraction band necrosis?

A

Catecholamine toxicity

pheochromocytoma, cocaine abuse

357
Q

What is present in senile cardiac amyloidosis?

A

Transthyretin

358
Q

2 forms of systemic amyloidosis that can effect the heart

A

primary (AL): Ig light chain

secndary (AA): serum amyloid associated protein

359
Q

What is isolated atrial amyloidosis?

A

ANP deposition

360
Q

What stain is used in diagnosis of amyloidosis?

A

Congo red -> yellow / green birefringence

361
Q

What is the most common cause of CHF?

A

Ischemic heart disease secondary to coronary artery atherosclerosis

362
Q

What is the 1 year mortality for patients with NYHA class IV heart failure?

A

almost 50%

363
Q

3 gene mutations associated with dilated cardiomyopathy

A

SERCA
Phospholamban
Sarcomeric contractile machinery

364
Q

When does peripartum cardiomyopathy usually occur?

A

last month of pregnancy up to 6 mos post partum

365
Q

What is seen microscopically in peripartum cardiomyopathy?

A

Lymphocytic infiltrate in myocardium

366
Q

What is Takotsubo Cardiomyopathy?

A 
Broken Heart Syndrome
Stress related increase in catecholamines -> acute dilated cariomyopathy
Contraction band necrosis is visible
Reversible w/ proper support
EKG:  may look like MI
No CAD
367
Q

What is high output heart failure and what are some causes?

A

Normal heart under excessive burden -> failure
A-V fistula: decreased systemic resistance, shunt from A->V, inadequate perfusion
Renal retention of Na and H2O -> expanded volume + elevated R and L pressures

Thyrotoxicosis, severe Paget’s of bone, severe anemia

368
Q

What are the functions of BNP?

A

Opposes Renin-Angiotensin-Aldosterone system
Peripheral vasodilation
Renal Na excretion
Inhibits renin secretion

369
Q

How does Digoxin work?

A 
Inhibits Na/K ATPase -> decreased intracellular Na++ -> decreased activity of Na/Ca exchanger -> elevated IC Ca++
increased contractility
slowed AV conduction
increased filling time
decreased myocardial O2 demand
370
Q

What defines chronic kidney disease?

A

GFR 300 mg/d

200 mg/g spot urine

371
Q

What pressures are diagnostic for HTN?

A

140 systolic or 90 diastolic

If diabetic or renal insufficiency: 130/80

372
Q

What are stage 1 and stage 2 HTN?

A

Stage 1: 140-159 systolic or 90-99 diastolic

Stage 2: 160+ or 100+

373
Q

What race has lowest BP control rates?

A

Mexican American

374
Q

What is resistant HTN?

A

BP above goal when taking 3 meds of different classes, one being a diuretic
OR
BP below goal when taking 4 meds of different classes, one being a diuretic

375
Q

What is the most frequently used drug in treatment of HTN emergency?

A

Clonidine

376
Q

How quickly should BP be reduced in the setting of hypertensive emergency?

A

10-15% in the first few hours
25% in first 24 hrs

If aortic dissection must lower more quickly and to greater extent

377
Q

3 causes of secondary HTN

A

1) primary aldosteronism
2) renovascular
3) pheochromocytoma

378
Q

How does HTN caused by unilateral and bilateral renal artery stenosis compare?

A

Unilateral: renin dependent - very responsive to ACEi and ARB
Bilateral: plasma volume expansion - little response to ACEi and ARB - diuretic responsive

379
Q

What is the best screening test for pheochromocytoma?

A

Plasma metanephrines

380
Q

What percent of patients with pheochromocytoma present with HTN and what are other symptoms?

A

50% have HTN
Other symptoms: Headache, sweating, anxiety, tachycardia
Pallor, orthostatic hypotension, nervousness, weight loss

381
Q

On average, what is the difference in systolic BP between blacks and whites w/ HTN? What is the impact of equalization?

A

7 mmHG

Equalizing: decrease stroke deaths: 2,190 ; Heart disease deaths: 5,480

382
Q

How to calculate MAP

A

MAP = [2(DBP) + SBP] / 3

MAP = SV * HR * PVR

383
Q

What are EKG criteria for RBBB?

A

QRS prolongation of 0.12s +
Slurred S wave in I and V6
RSR’ in V1

384
Q

What is EKG criteria for LBBB?

A

1: QRS wide: 0.12 +
2: I and V6: wide monomorphic R waves w/ no Q
3: V1: broad monomorphic S, may have small r.

385
Q

How does SBP and PP differ between the aorta and brachial artery?

A

Increased by 10-15 mmHg in brachial due to reflected wave. Diastolic is same (thus widened PP)

386
Q

In a normal person, how does BP differ between day and night?

A

Night is 10-20% lower

387
Q

What strategy eliminates racial differences in BP lowering effects of drugs?

A

Addition of a diuretic or CCB to ACEi/ ARB therapy.

  • ACE/ARB less effective than diuretics or CCB in African American
  • ACE/ARB less effective in African American than in white
388
Q

How does the effectiveness of hydrochlorothiazide compare to clorthalidone?

A

Clorthalidone lowers BP more effectively than HCTZ (and requires lower dosing)

389
Q

At what point should combination therapy for HTN be considered?

A

When SBP >20 or DBP >10 above goal pressure - monotherapy is frequently insufficient at these pressures

M2 (19 decks)

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