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CPR > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

what nerve goes anterior and which goes posterior to root of the lung

A

phrenic is anterior, vagus is posterior

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2
Q

layers of the pleura of he heart from out to in

A

fibrous pericardium
parietal serous pericardium
visceral serous pericardium = epicardium

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3
Q

ligamentum arteriosum

A

in fetal circulation, gets shunted from RV through ligament into aorta (in fetus it’s called ductus arteriosis)

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4
Q

what is the nerve that’s close to the ligamentm arteriosum

A

recurrent laryngeal nerve (branch off of the vagus) - loops under, innervates things in the larynx on the left side

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5
Q

muscular ridges in atrium

A

pecinate muscles on the wall of the base of the RA - create turbulent flow

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6
Q

muscular ridges in ventricle

A

trabeculae carnae - create turbulent flow

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7
Q

openings into right atria

A

superior (From head and neck) and inferior vena cava - dump into opening of coronary sinus

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8
Q

edge behind right atria

A

sulcus terminalis - internal change between smooth wall and pectinate muscles

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9
Q

coronary sinus

A

hole in right atrium where coronary veins dump

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10
Q

impression between inferior and superior vena cava in R atrium

A

fossa ovalis - in fetus it’s an opening - shunt from RA to LA to bypass the RV (to avoid the lungs) - patent foramen ovale if it’s still open

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11
Q

valve betwen RA and RV

A

Tricuspid valve - anterior, posterior and septal

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12
Q

valve between LV and LA

A

mitral/bicuspid - anterior and posterior

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13
Q

cordae tendinae

A

valves are anchored to papilary muscles via cordae tendinae (3 muscles in tricuspid, 2 muscles in mitral)
work with papilary muscles to prevent eversion of cusps into atria

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14
Q

moderator band

A

AKA septomarginal trabecula - specialized trabecula that forms a bridge between the interventricular septum and the base of the anterior papillary muscle of the right ventricle that carries the right purkinje fibers

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15
Q

semilunar valves

A

ventricles to pulmonary trunk or aorta - have left right and posterior leaflets

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16
Q

flow into LA

A

4 pulmonary veins

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17
Q

what is right behind LA

A

esophagus

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18
Q

pectinate muscles in LA

A

there aren’t any - internal surface is smooth

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19
Q

first branch of aorta

A

coronary arteries - can see openings for arteries behind the aortic semilunar valve

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20
Q

where do you listen to the tricuspid valve

A

over left lower end of sternum

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21
Q

where do you listen to the mitrlal valve

A

over the left fifth intercostal space at the midclavicular line

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22
Q

where do you listen to the pulmonary valve

A

over the left second intercostal space lateral to the sternum

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23
Q

where do you listen to the aortic valve

A

right second intercostal space lateral to sternum

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24
Q

right coronary artery and branches

A

travels off of aorta, supplies R atrium and ventricle, gives rise to 4 branches:

1) (60% of people)SA nodal artery
2) right marginal artier (right border of right ventricle)
3) (67% of people) posterior interventricular artery aka PDA (supplies both ventricles)
4) (85% of people) AV nodal artery

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25
Q

left coronary artery and branches

A

short, quicky branches into the following branches:

1) anterior interventricular artery/ Left anterior descending LAD - supplies both ventricles
2) circumflex artery - supplies LV and LA
3) maybe SA or AV nodes if not supplied by right

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26
Q

when you say triple bypass, what does that mean

A

means that 3 coronary arteries were blocked and had to be bypassed

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27
Q

what determines R or L dominance?

A

if the posterior descending artery comes from L or R coronary artery

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28
Q

venous drainage of heart

A

1) coronary sinus -
2) great cardiac vein
3) middle cardiac vein
4) small cardiac,

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29
Q

coronary sinus - where does it come from where does it go

A

main vein of heart, wide channel that runs in coronary sulcus that collect blood from coronary veins, opens into right atrium

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30
Q

great cardiac vein, where does it go?

A

travels with anterior interventricular and circumflex branch

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31
Q

middle cardiac vein, where does it go?

A

travels with posterior intervenricular

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32
Q

small cardiac vein, where does it go?

A

travels with right marginal and then right coronary artery

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33
Q

where is SA node located

A

in the crista terminalis in the junction of the SVC and the right atrium

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34
Q

where is AV node located

A

in the interatrial septum (Between RA and RV) near the opening of the coronary sinus - right above tricuspid valve

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35
Q

AV bundle, where do they travel

A

located within interventricular septum - branch towards apex. right bundle branch is contained in moderator band, then they ramify into purkinje fibers

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36
Q

AV bundle, where do they travel

A

located within interventricular septum - branch towards apex. right bundle branch is contained in moderator band, then they ramify into purkinje fibers

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37
Q

prevalance

A

proportion of people in a population with disease at a given time – positive and nevative predictive values are dependent on prevlanance

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38
Q

positive predictive value

A

proportion of people with positive test results who have disease – true positives

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39
Q

negative predictive value

A

proportion or people with negative result who don’t have disease – true negatives

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40
Q

precision

A

are findings consistent with repeated testing

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41
Q

accuracy

A

do they correctly predict diagnosis, compare to gold standard

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42
Q

sensitivity

A

“positive in disease” - proportion of people with disease in whom the test result is positive
– true positives

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43
Q

specificity

A

“negative in health” - proportion of people without the disease in whom the test result is negative
– true negatives

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44
Q

as sensitivity increases, what happens to specificity?

A

decreases

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45
Q

likelihood ratio

A

measure of how much more or less likely the patient is to have the disease because of the test result

some result in patient with disease/the same result in patient without disease

more extreme (over 10 or under 0.1) are more useful

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46
Q

how to use nomogram

A

plot pre-test probability and likelihood ratio, and then extrapolate to find post-test probability

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47
Q

action threshold

A

diagnostic tests are most useful when results push disease probability across a threshold (treatment or test) leading to a specific action

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48
Q

layers of endocardium

A

1) inner most layer has endothelium
2) deep to endothelium is subendothelium which is CT and SM
3) beneath subendothelial layer is subendocardial layer which is CT laer that contains Purkinje fibers and

beneath that is myocardium

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49
Q

what is at intercalated disc (3)

A

fascia adherentes
gap junctions
desmosomes

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50
Q

what’s in epicardium (4)

A

1) mesothelium (visceral serous pericardium)
2) fat
3) autonomic ganglia (vagus nerve branches)
4) coronary arteries and venules

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51
Q

cardiac skeleton componenets (4)

A

1) membranoues portion of intervertricular septum
2) 4 annuli fibrosi around big vessels around valves
3) trigona fibrosa - 2 parts (left and right)
4) heart valves

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52
Q

valve layers (4)

A

1) endothelium innermost
2) spongiosum (loose CT)
3) fibrosa (dense CT)
4) ventricularis (elastic)

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53
Q

modified myocytes in purkinje fibers as compared to regular myocytes (5)

A

1) 2x bigger
2) few myofibrils
3) more glycogen centrally
4) binucleated
5) conducts 4x faster

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54
Q

chondroid

A

similar to hyalin collagen but different and found in cardiac skeleton

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55
Q

accountable care organization (ACO)

A

ACO = group (of physicians, hospitals, insurers etc.) that assumes responsibility for quality and cost of care for a population of patients with the goal of minimizing cost of high quality care for medicare patients

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56
Q

classical conditioning

A

pavlov’s dog
phase 1: neutral stimulus (no response)
phase 2: pair neutral stimulus with unconditoned stimulus
phase 3: eventually neutral stimulus causes conditioned response

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57
Q

operant conditioning

A

1) positive reinforcement: push lever get reward - or push lever and get punishment
2) negative reinforcement: getting shock and when you push lever it stops, so you keep pushing lever
3) punishment: stop behavior because it hurts - behavior stops

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58
Q

social learning theory

A

how personal factors interact reciprocally with environmental factors - modeling what you see (violence, cigarettes etc)

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59
Q

transtheoretical model

A

stages of change:

1) precontemplation (no interest in changing)
2) contemplation (thinking but no action)
3) preparation (planning for change - scared to take the steps)
4) action
5) maintenance

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60
Q

schedule of reinforcement (options)

A

continuous
intermittent
- interval (fixed or variable)
- ratio (fixed or variable)

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61
Q

self-efficacy

A

I know I can do it

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62
Q

prazosin does what

A

selective a1 blocker

decreases BP get reflex tachycardia

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63
Q

is prazosin reversible?

A

yes

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64
Q

what does phenoxybenzamine do

A

blocks a1 and some a2

decreases BP lasts 24hours

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65
Q

is phenoxybenzamine reversible?

A

no

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66
Q

phentolamine does what

A

blocks a1 and a2 nonselectively (a1 decreaes BP, a2 prevents feedback inhibition, causing more NE released onto B1 – MORE tachycardia)

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67
Q

therapeutic use of proazosin

A

HTN

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68
Q

therapeutic use of phenoxybenzamine and phentolamine

A

pheochromocytoma management (block catecholamines)

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69
Q

phenoxybenzamine, prazosin and terazosin therapeutic use

A

benign prostatic hypertrophy - relax smooth muscle in prostate capsule

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70
Q

side effect of alpha1 blockade

A

postural hypotension
reflex tachycardia
nasal stuffiness
inhibition of ejaculation

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71
Q

epi-reversal

A

pure beta2 - just decrease BP, no “pressor” response

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72
Q

do you use beta blockers in people iwth breathing problems?

A

no

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73
Q

propranolol

A 
non-selective beta blocker
decreases HR due to beta1 block by:
- decreases cardiac output
- decreases plasma renin
- decreases sympathetic tone via effects in CNS
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74
Q

metabolic effects of non-selective beta blockers

A

no effect on glucose of normal people, but slows recovery from hypogycermia in diabetics. increased VLDL and decreased HDL

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75
Q

atenolol what does it do

A

selective beta1 blocker

  • similar cardiac effects as non-selective
  • no resp effects
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76
Q

esmolol what does it do

A

selective beta 1 with really short half life - used for emergency procedures

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77
Q

pindolol

A

partial agonist - partially activate beta receptor but block access of full agonist NE

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78
Q

acebutolol

A

partial agonist - partially activate beta receptor but block access of full agonist NE

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79
Q

what do you use for glaucoma

A

timolol - decrease acqueus humor production - via beta1

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80
Q

labetalol

A

mixed alpha and beta - blocks beta to alpha1 at 4:1 ratio

used for chronic hypertension or acute management of hypertensive crisis secondary to excessive catecholamines

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81
Q

carvedilol

A

mixed alpha and beta - blocks beta to alpha1 at ratio of 10:1

  • used for congestive heart failure
  • antioxidant
  • antihypertensive
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82
Q

beta blocker uses (10)

A 
1- hypertension
2- cardiac arrhythmia
3- angina pain
4- prophylaxis for migraine
5- may inhibit cancer progression
6- used in MI (early and after)
7- pheochroocytoma
8- glaucoma
9- heart failure
10 - performance anxiety
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83
Q

side effects of beta blockers (3)

A

1- B1 block causes decreased cardiac output, heart block and bradycardia
2- B2 block causes bronchoconstriction
3- CNS: depression and lethargy

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84
Q

guathenidine

A

works at presynaptic site
neither agonist or antagonist, but has anti-adrenergic effect
prevents storage of NE, MAO eats up NE
- originally used as antihypertensive, but has a bunch of side effects - diarrhea, postural hypotension etc.

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85
Q

risperpiine

A

doesn’t use NET - dissolves through presynaptic, binds to NE transporter and blocks storage of NE - empty vessicle

  • used to be used for hypertension
  • side effects were depression and orthostatic hypotension
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86
Q

alpha2 agnoist actions (2)

A

in brain alpha2 block sympathetic outflow and thus decrease blood pressure

at presynaptic postganglionic adrenergic neurons, alpha2 inhibit NE release and reduce tone

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87
Q

clonidine mechanism and uses (4)

A

alpha2 agonist that works directly at alpha2 receptors

  • for hypertension
  • reduce withdrawl symptoms for opioids
  • open angle glaucoma (reduce acqueus humor)
  • ADHD
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88
Q

a-methyl-dopa mechanism and uses (2)

A

alpha2 agonist that must be metabolized to alpha-methyl-NE

  • for hypertension
  • safe in pregnancy
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89
Q

side effects for alpha2 agonists (4)

A
  • dry mouth
  • sedation
  • hypertensive crisis if quick withdrawl of clonidine
  • alpha-methyldopa produces autoimmune response (positive coombs test)
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90
Q

what kind of cardiovascular diseases are associated with pestilence and famine

A

rheumatic fever - valve damage,

cardiomyopathy

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91
Q

what kind of CV diseases are associated iwth degenerative and man-made diseases

A

CHD, stroke, HTN (most deaths in this category)

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92
Q

what is fibrillation

A

re-entry

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93
Q

what would you do to give best immediate treatment for venricular fibrillation

A

shock - depolarize all cells, and first to repolarize and depolarize will be SA to re-establish normal rhythm

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94
Q

which has higher conduction rate, bundle of his or sa NODE

A

bundle of HIS

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95
Q

which has higher spontaneous discharge, buldne of his or SA node

A

SA node

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96
Q

which electrode is positive A or B

A

B is positive, A is negative

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97
Q

first thing that happens in ventricular AP, and what kind of deflection do you have as depolarization approaches B

A

calcium and sodium move into the cell (makes A more negative) B-A gives you positive deflection

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98
Q

what happens when depolarization recedes from B

A

sodium move into cell at B, makes B more negatve, makes B-A deflection negative

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99
Q

repolarization receding from B, what kind of deflection do you have

A

get potassium ion out of cell, makes B more positive- causeing B-A positive deflectioon

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100
Q

repolarization approaching B gives what kindof deflection

A

potassium ions leaving cell at A, makes A more positive, so B-A is negative deflection

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101
Q

vector of atrial depolarization

A

atrium - right side to left side and from base to apex - pointing to left leg

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102
Q

vectors of ventricular depolarization (3)

A
  1. across septum from L to R and slightly up (becuase of density of purkinje fibers)
  2. from endo to epi at apex of heart
  3. up from L ventricular wall (and to lesser extent R because of less mass) and along the septum, away from L leg
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103
Q

vector of ventricular repolarization

A

from epicardium to endocardium at apex of heart away from L leg

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104
Q

lead 2 position of electodes, and what does it pick up

A

neg electrode on R arm, pos on L leg, so can pick up depolarization along that axis (along septum more or less)

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105
Q

lead 1 position of electrodes, and what does it pick up

A

neg R arm, pos L arm (

can pick up horizontal signals

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106
Q

lead 3 position of electrodes, and what does it pick up

A

neg L arm, pos L leg, picks up signals pointing diagnoally to R leg

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107
Q

aVF what does it measure

A

augmented voltage foot, averages R arm and L arm and makes that negative, and makes L leg pos

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108
Q

aVR what does it measure

A

augmented voltage right, averages L arm and L leg and makes that negative, and makes R arm pos

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109
Q

aVL what does it measure

A

augmented voltage left, averages R arm and L leg and makes that negative, and makes L arm pos

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110
Q

what is P wave

A

atrial depoarlization - small positive deflection

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111
Q

what is QRS wave

A

3 phases of ventricular depolarization:

Q= small negative deflection (across septum L and upward)
R = large positive deflection (vector towards apex)
S = medium negative deflection (up septum and walls)
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112
Q

what is T wave

A

ventricular repolarization - from epi to endo at apex away from L leg (repolarization receding away from L leg = positive deflection)

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113
Q

what are the isopotential lines

A

1) PR segment -
through AV node
2) ST segment as everything is depolarized

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114
Q

what does ST elevation indicate

A

damaged tissue that continues to depolarize

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115
Q

einchoven’s triangle

A

lead 1 + lead 3 = lead 2

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116
Q

what do you see in first degree heart block on ECG, what causes it

A

there is a lag between P wave and QRS (elongated PR interval) (usual is 180ms, >200ms is abnormal)

goes too slowly through AV node

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117
Q

what is one big box on the time axis for an ECG

A

0.2 seconds - 5 big boxes is 1 second

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118
Q

what is one big box on voltage xis on ECG

A

0.5 mV

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119
Q

difference between interval and segment

A

segment is straight line, interval is segment plus at least 1 wave

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120
Q

what is normal PR interval

A

0.12 - 0.2 sec

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121
Q

normal QRS interval

A

0.06 - 0.1

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122
Q

normal QT interval

A

0.35 - 0.4

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123
Q

what does QT interval represent

A

from begining of depolarization to end of repolarization - full AP of ventricular cells

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124
Q

second degree heart block

A

not every P wave is followed by QRS

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125
Q

type 1 second degree heart block

A

increasing delay between P and QRS

until P doesn’t evoke a QRS

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126
Q

type 2 second degree heart block

A

no increasing delays between P and QRS, but you still have Ps that aren’t followed by QRS

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127
Q

3rd degree heart block

A

complete dissociation between atrial and ventricular depolarization - P and QRS happen independently

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128
Q

ventricular fibrillation

A

“bag of snakes squirming around”

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129
Q

ventricular tachycardia

A

ventricles are contracting at a rate greater than 100 BPM

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130
Q

sinus bradycardia

A

heart rate lower than 60 bpm - generated by SA node

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131
Q

atrial fibrillation

A
  • no distinct P waves, but still get QRS

- atria quiver, but you can live with this - can depolarize and contract ventricles

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132
Q

atrial flutter

A

looks like saw tooth waves or Zs before QRS wave

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133
Q

sinus tachycardia

A

heart rate greater than 100 bpm originating at SA

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134
Q

la place’s law for pressure in ventricles

A

P = (tension x thickness) / r

Pleft = 120
Pright = 1/6 Pleft = 20

pressure in left is about 5x right

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135
Q

kinds of cardiac hypertrophy

A
  1. concentric hypertrophy -
    pressure overload (thickness increases, volume decreases, pressure increases)
  2. eccentric hypertrophy - volume overload (radius increases, thickness decreases, pressure decreases)
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136
Q

how many microns are myocytes

A

150 microns

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137
Q

what does phosphorylation do to proteins

A

faster contraction (DHPR, Ryanodine etc.), SERCA shortens relaxation time by pumping Ca back in -reabsorption

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138
Q

treppe

A

AKA bodwitch effect. more frequent stimulation causes stronger contraction - staircase effect
less time for calcium to get transported out of cytosol

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139
Q

isometric

A

generates only force, no muscle shortening

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140
Q

isotonic

A

produces shorteining at constant load

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141
Q

preload

A

extent to which muscle is stretched before the onset of contraction (for heart, preload is end diastolic volume)

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142
Q

afterload

A

load lifted by the muscle in isotonic contraction (for heart, afterload is aortic pressure - pressure against which you’re trying to eject)

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143
Q

frank starling

A

the more you stretch, the more forecul the contraction - like rubberband

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144
Q

mechanisms for grading strength of contraction in cardiac muscle

A

a. CONTRACTILITY increased amplitude or duration of calcium transient (amount of calcium available for contraction)
b. PRELOAD - stretching the myocyte for optimal force

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145
Q

ionotropy

A

influence of agents that alter contractility - positive ionotrope (exercise allowing for more contractility and more calcium available)

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146
Q

systole phases

A

1- isovolumetric ventrical conraction (builds pressure)

2- ventricular ejection (when pressure exceeds aortic pressure)

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147
Q

diastole phases

A

1- isovolumetric ventricle relaxation

2- ventricular filling (AV valve opens)

3- atrial contraction (upon excitation - end of diastole)

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148
Q

how long does systole last

A

250-300msec

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149
Q

how long does diastole last

A

500-550 msec

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150
Q

a wave

A

measures atrial pressure during atrial contraction

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151
Q

c wave

A

measures atrial pressure during closing of AV valve during ventricular contraction, dips down once ventricular ejection occurs

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152
Q

v wave

A

measures atrial pressure during ventricular relaxation during diastole, until you open AV valve

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153
Q

x deflection

A

venous pressure during systole

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154
Q

y deflection

A

venous pressure during diastole

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155
Q

dicrotic notch or insicura - caused by what (3)

A

aortic pressure at the end of systole when the ventricle relaxes:

1) get some reguritation
2) get rebound of the valve
3) and get some back flow into coronaries

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156
Q

mean arterial pressure equation

A

at rest,

MAP = 1/3 max arterial systolic pressure + 2/3 minimal arterial diastolic pressure

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157
Q

pulse pressure

A

arterial systolic - arterial diastolic pressure

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158
Q

stroke volume equation

A

end diastolic volume - end systolic volume

120-40 = 80mL

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159
Q

ejection fraction - equation and values

A

stroke volume/end diastolic volume

80/120 = 66%
normal is 60-70%
under 30% is grave

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160
Q

S1 is closures of what valve

A

AV

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161
Q

S2 is closure of

A

semilunar

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162
Q

are chylomicrons the most dense or the least dense

A

least dense - on top

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163
Q

as you go from HDL to chylomicron, how does your protein content change

A

lots of protein in HDL, very little protein in chylomicrons

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164
Q

as you go from HDL to chylomciron, how does your cholestorl content change?

A

HDL has 2nd highest, LDL has highest, and then decreasing from there to chylomicron lowest

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165
Q

as you go from HDL to chylomicron, how does your phospholipid content change?

A

highest at HDL, lowest at chylomicron

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166
Q

as you go from HDL to chylomicron, how does your triacylglycerol content change?

A

lowest at HDL, highest at chylomicron

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167
Q

LDL does what

A

delivers membrane building materials peripherally

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168
Q

HDL does what

A

take membrane materials back to the liver

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169
Q

chylomicrons do what

A

deliver dietary fats (triglycerides)

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170
Q

relative size of lipoproteins from HDL to chylomicrons

A

chylomicrons are really big (120nm), VLDL also big (80nm) IDL is around 50nm -
none of these can diffuse through membranes - need to dock to offload

LDL is smaller, HDL is around 8nm, can diffuse into deeper tissues

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171
Q

what does apoB48 do

A

stabilizes the core

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172
Q

what does apoC do

A

helps chylomicron target a lipase so that fatty acid can get into adipose and muscle cells

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173
Q

what does apoE do

A

targets chylomicron remnant back to the liver, so it can be recycled and reused

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174
Q

relationship between cholesterol levels and chylomicron remnants

A

if you have high systemic dietary cholesterol, chylomicron remnant will get back to liver to tell it to down regulate de novo synthesis of cholesterol (at HMG-oA reductase)

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175
Q

SREBP-SCAP and cholesterol levels

A

regulates HMG CoA reductase and LDL receptor

in low cholesterol:
SREBP gets cleaved and migrates to nucleus to upregulate cholesterol synthesis and LDL receptor

in high cholesterol:
cholesterol binds SCAP, inhibiting cleavage of SREBP by binding with high affinity to SREBP - downregulation of cholesterol biosynthesis and LDL receptor

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176
Q

apoB structures in chylomicron

A

apoB48 (with membrane component solubilizing to get it into circualtory, and core stability component)
filled with triglycerides

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177
Q

apoB strucures in VLDL and LDL

A

apoB100 (more cholesterol and cholesterol ester) and antennae with lysines in it (positively charged) to bind to negatively acids (aspartic/glutamic) - bind to LDL receptor with a lot of aspartic acids

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178
Q

where is apoB100 made

A

liver (for LDL/lipid trafficking building materials to cells) - extra antennae = longer

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179
Q

where is apoB48 made

A

intestines (for dietary fat delivery through cholesterol)

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180
Q

what is IDL?

A

it’s basically VLDL remnant that eventually gets converted to LDL:

  • has apoB100 and apoE to target to the liver, procesessed IDL to LDL
  • also gets shuttled to HDL to strip it of its surface apo proteins - A C E so that you just have apoB100 left (which is LDL)
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181
Q

lipoprotein lipase (LPL) function

A

chylomicrons and VLDL will bind to it through apoC, free fatty acids go in (to muscle cell or adipose tissue), glycerol stays in circulation where it goes back to liver

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182
Q

how do fatty acids get mobilized within adipose cells

A

hormone sensitive lipase is activated by glucagon in a G-protein coupled receptor dependent fashion via activation of Protein Kinase A

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183
Q

LDL metabolism (receptor binding, delivery etc.)

A

delivery of membrane building materials to target tissue by LDL-LDL receptor interaction:
apoB100 (LDL or IDL) binds to receptor with clathrin coated pit endocytosed (receptor will either get recycled back to membrane and LDL will fuse with lysosome and apoB100 is degraded and amino acids are recycled, all other components become part of the membrane system)

most receptors are found in liver

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184
Q

PCKS9

A

protein that promotes internalization but blocks recycling - increasing circulating LDL

anti-PCSK9 IgG binds interaction of LDL receptor with PCKS9 - knocks out ability of PCKS9 to degrade receptors, scavenging circulating LDL

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185
Q

HDL metabolism (docking, cholesterol uptake)

A

when HDL docks with membrane raft with apoA1 stimulates ABCA1 transporter to pump cholesterol into HDL. free cholesterol covers surface, but in order to fill core, you need to convert to cholesterol ester, with the help of LCAT enzyme. goes back to liver where apoE endocytosis occurs

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186
Q

Fiber (types, mechanisms)

A

2 types

  • insoluble (skins)
  • soluble (metamucil - slurry)

mechanisms:

  • adsorbs cholesterol (sticks to cholesterol)
  • GI motility changes

facilitate excretion

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187
Q

Omega 3 fatty acids

A
  • increase clearance of triglyceride levels (triglycerides lead to pancreatitis)
  • anti-inflammatory response
  • eat fish, improve cardiac health
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188
Q

atorvastatin - mechanism

A

statin - lipitor

metabolized by CYP3A4

longer half life - can take whenever

more lipophilic - crosses BBB

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189
Q

pravastatin

A

statin - prevacor

metabolized by sulfation and IS NOT P450 dependent!! - fewer drug-rug

half life is lower - have to take before bed

more water soluble (more hepatoselective)

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190
Q

ezetimibe (mechanism, metabolism)

A

absorbtion blocker

inhibits Niemann-Pick C1-Like 1 (NPC1L1) transporter which decreases delivery of intestinal cholesterol to the liver which decreases cholesterol in chylomicrons/remnants, leading to increase in LDL receptors and increase clearance in LDL from plasma

not metabolized by p450s, undergoes repeated enterohepatic circulation causing long duration of drug

no adverse effects really

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191
Q

cholesteryamine (use, mechanism, adverse)

A

bile acid sequestrant/resin

used in combo with statins because it can lead to up-regulation of HMG-CoA reductase

charged - not absorbed, but bind to bile acids, metabolites of cholesterol to prevent absorption which leads to increased conversion of cholesterol to bile acids, which up-regulates LDL receptors and LDL clearance from plasma

adverse: GI effects, absorption of other drugs might be impaired

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192
Q

niacin (mechanism, metabolism, adverse)

A

nicotinamide derivative

only drug to elevate HDL- inhibits lipolysis in adipose tissue, decreases free fatty acid transport to liver (decreases VLDL synthesis in liver) and decreases triglyceride synthesis in liver
: overall effect is decreasing TGs and LDL while raising HDL

Hepatic metabolism

adverse: can cause vasodilation - flushing, hepatotoxicity and GI discomfort

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193
Q

gemfibrozil (mechanism

A

fibrate

works to lower TG levels through activating agonist for PPAR alpha receptor (a TF), which lowers TGs through increasing clearance of TG and VLDL

can cross placenta

short half life

GI discomforta, myopathy (risk with statin), many drug interactions

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194
Q

evolocumab/repatha (mechanism, adverse)

A

PSCK9 inhibitor

binds to PSCK9 protein from being able to bind and endocytose LDL receptor

has to be injected, is expensive, only causes about 15% decrease in primary endpoint,
nasopharyngitis

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195
Q

statin mechanism

A

look like HMG-CoA, binds to receptor, to reversibly inhibit cholesterol production
leading to increasing synthesis of LDL receptors in liver, which increases clearance of LDL in the circulation

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196
Q

statin adverse effects (3)

A

hepatic toxicity (more so for atorvastatin)

muscle pain and weakness (rhabdomyalisis) - caused by drug interaction with gemfibrozil which inhibits transport of statins into liver or with other cyp inhibitors (would not affect pravastatin)

small increased risk for diabetes

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197
Q

what does rheumatic fever cause/present in cardiac exam

A

atrial fibrillation - enlarged left atrium

opening snap, diastolic rumble, NO enlarged left ventricle (normal PMI) - mitral stenosis

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198
Q

gender differences with CVD

A
  • women present later in life (risk worsens after menaupause) -
  • they present with different symptoms (shortness of breath vs. pain)
  • more strokes
  • higher complications in sx
  • more reserved ejection heart failure later in life
  • more non-obstructive coronary disease - microvascualr issue
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199
Q

estrogen and stroke risk

A

increases stroke risk

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200
Q

risks for cardiovascular disease in hispanic population

A

varying ancestral mix = varying risk

  • hypertension and diabetes are high, but once controlled, no difference among ethnic groups
  • disparities in defibrillator use in hispanics
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201
Q

hydralizine

A

overall population not effective for heart failure, but for AA there is positive effect, perhaps because it’s addressing the underlying hypertension, which is overwhelming cause of HF in AA patients

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202
Q

3 phases of disparities research agenda

A
  1. detecting (define health disparities)
  2. understanding (identifying determinants at different levels)
  3. reducing (intervention, evaluation, change policy)
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203
Q

what causes murmur in man with heart failure due to uncontrolled hypertension

A

holosystolic murmur - mitral regurgitation due to dilated left ventricle

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204
Q

what causes crescendo-decrescendo systolic murmur

A

aortic stenosis - with degenerative heart disease

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205
Q

what is sternal angle vertebral level

A

T4/T5

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206
Q

which is longer, right or left brachiocephalic

A

left- because superior vena cava is on the right side of the heart, so the left brachiocephalic has to travel further

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207
Q

components of brachiocephalic vein

A

subclavian and internal jugular

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208
Q

branches off of the arch of the aorta

A
  • brachiocephalic artery
  • left common carotid
  • left subclavian
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209
Q

brachiocephalic artery branches

A

right subclavian and right common carotid

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210
Q

branches off of the ascending aorta

A
  • right and left coronary arteries
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211
Q

branches coming off of thoracic aorta

A
  • posterior intercostal arteries

- pericardial, esophageal and bronchial arteries

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212
Q

where is the left recurrent laryngeal nerve on chest film

A

in the aortopulmonary window (between arch and L pulmonary artery or trunk)

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213
Q

L vagus becomes ___ as it descends

A

anterior

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214
Q

R vagus becomes ___ as it descends

A

posterior

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215
Q

where do veins drain into on the right side?

A

right intercostal veins, hemizygous, accessory hemi all dump into azygous, azygous dumps into superior vena cava

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216
Q

where do veins drain into on the left side?

A

left hemiazygous (drains 9, 10 and 11) and accessory hemiazygous (Drains 4, 5, 6, 7 and 8 intercostal veins)

get over to the right side through shunts over to azygous at lower or upper level

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217
Q

where does thoracic duct start

A

cisterna chyli in abdomen

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218
Q

where does thoracic duct dump into

A

venous system near the union of the left internal jugular and subclavian veins

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219
Q

what structures does the thoracic duct lie between

A

the duck between two geese (the duct between azygous and esophagus)

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220
Q

which closes earlier, aortic or pulmonic?

A

aortic - delayed when you breathe in so you can hear the split, or during normal breathing when you have L ventricular problems or aortic stenosis (these people will reduce the split when breathing in)

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221
Q

aortic stenosis, what do you hear

A

narrow, more turbulence - murmur during systole

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222
Q

aortic incopetence, what do you hear

A

doesn’t completely close, so hear backflow during diastole

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223
Q

mitral stenosis, what do you hear

A

narrow, more durbulence, murmur during diastole

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224
Q

mitral incompetence, what do you hear

A

doesn’t close completely, so you hear backflow during systole

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225
Q

pressure-volume loop - describe it

A

in LV, measure pressure and volume:

starts at 120 volume and low pressure, increases pressure until aortic valve opens, then you keep increasing pressure as volume decreases, then the aortic valve closes, volume stays the same as pressure decreases, and then mitral valve opens and pressure stays low as volume increases back to 120

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226
Q

what curve on the pressure-volume loop do you look at to assess compliance

A

bottom curve - as ventricle is filling - low pressure = compliant, high pressure = not compliant

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227
Q

how do you measure stroke volume from poressure-volume loop?

A

stroke volume is the width of the curve - between two isovolumentric lines (end diastolic and systolic volumes)

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228
Q

what is the end diastolic volume on the pressure-volume loop?

A

the isovolumetric line at max ventricular filling

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229
Q

what is the end systolic volume on the pressure-volume loop?

A

the isovolumetric line at min ventricular filling

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230
Q

what is the filling preload pressure on the pressure-volume loop

A

the point at which the ventricle increases pressure without increasing volume

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231
Q

what is the aortic pressure/ afterload on pressure-volume loop

A

point at which the aorta opens and the volume starts to decrease with increasing pressure

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232
Q

what is the external work on the pressure-volume loop and what’s the equation

A

area inside the curve
external work = change in volume x change in pressure
OR
stroke volume x aortic pressure

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233
Q

how do you measure heart muscle efficiency ratio?

A

external work/ internal work

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234
Q

what is internal work on the pressure-volume curve

A

area under the curve at lower volume than end systolic volume - proportional to oxygen consumption

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235
Q

what do you see on pressure-volume loop with increased contractility

A

when you eject you reach a lower end systolic volume so you are able to eject more - more efficient pump

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236
Q

what do you see on pressure-volume loop with increased aortic pressure?

A

because you have to have higher ventricular pressure to reach aortic pressure before ejection, you hit the ESPVR curve earlier and thus your end systolic volume is higher, meaning you’re not able to pump as much blood out, creating a less efficient pump

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237
Q

if you have higher venous pressure, what do you see with pressure-volume curve

A

increased venous pressure allows a larger end diastolic volume, which in turn increases total stroke volume, making more efficient pump

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238
Q

how do left and right cardiac output compare

A

about the same

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239
Q

2 equations for cardiac output

A 
CO = SV x HR
CO = MAP / TPR
MAP = mean arterial pressure
TPR = total peripheral resistance
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240
Q

what is the average CO?

A

5-6 L/min, little less in women

proportional to tissue mass/metabolic rate

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241
Q

what are the long-term factors that can affect cardiac output (3)

A

1) ventricular geometry (Thicker/thinner, wider/narrower)
2) ventricular compliance
3) electrical coordination of contraction

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242
Q

what are the short-term factors that affect cardiac output (4)

A

1) preload
2) afterload
3) contractility
4) heart rate

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243
Q

what is the point at which increased HR does NOT increase cardiac output

A

around 180 - heart doesn’t have time to fill back up

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244
Q

chronotropic relates to

A

HR

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245
Q

dromotropic relates to

A

conduction velocity

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246
Q

inotropic relates to

A

contractility

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247
Q

pulse pressure relation to stroke volume and compliance

A

directly related to stroke volume, indirectly related to compliance

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248
Q

do we feel pressure wave or blood flow in wrist?

A

pressure wave

249
Q

what is the systolic pressure in medium sized arteries compared to aorta, and why is there this difference

A

systolic pressure is higher in the medium arteries than the aorta, because some of the flow gets deflected back (because of branching points etc) and thus the waves get summated.

250
Q

how do you measure contractility with pulse pressure

A

steeper slope of ventricular pressure as it rises to meet aortic pressure indicates higher contractility

251
Q

why does pulse pressure increase as we age?

A

because arteries are not as compliant, and thus are not able to store pressure, so the mean pulse pressure has to increase to compensate

252
Q

things that affect venous return (6)

A

1) auxillary pumps - without skeletal muscle pump activity (standing still) get pooling of blood, no venous return, and fainting, (also have aortic and respiratory pumps)
2) TPR - increased TPR shifts curve down - decreases venous return, while keeping MSFP (x-intercept) the same
3) Mean systemic filling pressure - how full is circulation if your heart stopped working (around 7mmHg) - increasing MSFP increases venous return
4) compliance of veins - decreased compliance increases venous return
5) effect of gravity - hydrostatic pressure - around 90mmHg at foot, -25 at head, 0 at heart. so at feet, arterial gauge pressure is 170, venous is 100. in the head, arterial is 65, venous is -10 (which is why air gets in if you crack skull)
6) vascular permeability - as venous pressure increases, albumin is not as able to reabsorb fluid into capillaries (starling forces) - leading to edema

253
Q

relationship between venous pressure/RA pressure and venous return

A

negative - less venous return with higher RA pressure

254
Q

how do you get mean systemic filling pressure from vascular function curve (venous return/RA pressure)

A

it’s the X intercept (around 7mmHg) - flow stops

255
Q

what is flat portion at beginning of vascular function curve

A

at venous pressure less than 0, veins collapses, flow stops.

256
Q

significance of interception of cardiac function curve and vascular curve

A

equilibrium point between both systems

257
Q

how does this graph change when you increase the volume

A

the point shifts up because the vascular curve shifts up (cardiac curve stays put) - now new equilibrium point is at higher CO and venous pressure values

258
Q

how does this graph change when you have a hemorrhage

A

your venous curve shifts down because you lose volume, but there are 2 compensatory actions:
1) you get venous constriction, so the venous curve will shift back up a bit, and

2) your cardiac curve will try to compensate with sympathetic stimulation (slope increases - increasing contractility)

259
Q

which has worse prognosis, cardiac cause or non-cardiac cause of syncope

A

worse for cardiac

260
Q

neurally mediated syncope causes (3)

A
  • vasovagal
  • carotid sinus
  • situation (cough or post-micturation)
261
Q

cardiac arrhythmia causes of syncope (3)

A
  • brady (sick sinus, AV block)
  • tachy (VT, SVT)
  • long QT syndrome
262
Q

top 3 causes of syncope

A
  1. unknown cause
  2. neurally mediated
  3. cardiac arrhythmia
263
Q

what does POTS stand for

A

postural orthostatic tachycardia syndrome (young people who can’t stand up)

264
Q

structural cardiac reasons for syncope (3)

A
  • aortic stenosis
  • HOCM (hypotrophic cardio myopathy)
  • pulmonary hypertension
265
Q

top 3 common causes of syncope for young people

A
  • vasovagal
  • situation
  • psychiatric
266
Q

top 4 common coauses of syncope for older patients

A
  • orthostatic hypotension
  • drug-induced
  • neurally mediated
  • multifactorial
267
Q

how do patients feel with cardiac syncope

A

feel fine, on the ground, feel fine after

268
Q

how do patients feel with neural syncope

A

feel bad for a few seconds or minutes, passed out for longer, feel bad for a while after

269
Q

what to check on physical exam for syncope

A

1- orthostatic changes in BP and pulse
2- cardiac exam (look for CHF or valve disease)
3- neurological exam
4- carotid sinus massage

270
Q

how to do a carotid sinus massage

A

just below thyroid cartilage, R and then L (pause between) - do for 5-10 seconds, don’t occlude

positive outcome is 3 seconds of asystole or 50mmHg fall in systolic blood pressure – carotid sinus syndrome

271
Q

what are things on an EKG that could explain syncope (7)

A
  • heart block
  • v tach
  • long QT
  • short QT
  • WPW (second electrical connection)
  • bruagda (genetic - see ST elevation, right bundle branch block)
  • Q waves (sign of MI)
272
Q

what happens in tilt table test

A

upright posture is sympathetic stimulus - makes HR and BP go up and then we correct and things level out. sometimes this causes too much sympathetic curbing and you get significant drop in both HR and BP (in orthostatic you get dropped BP and increased HR)

273
Q

san francisco syncope rule

A 
C- CHF (history of)
H- Hct <30%
E- ECG abnormality
S- Shortness of breath
S- Systolic BP <90 mmHg
274
Q

SEEDS

A

for intermediate risk patients to go to syncope clinic - screen for high or low risk

275
Q

midodrine

A

alpha agonist - works to reduce vasovagal neurally mediated syncope

276
Q

at what week of fetal development does the heart start beating

A

4 weeks (earliest system)

277
Q

does the CV system come from endoderm, mesoderm or ectoderm?

A

mesoderm

278
Q

what are angiogenic cell clusters

A

mesenchymal cells that arrange into epithelial vesicles - precursors of heart, BVs, and nucleated RBVs

279
Q

changes in orientation of atria and ventricles in early fetal development

A

atria are caudal, ventricles are cephalic - as it grows, it loops, so that atrial end bends dorsally, up and left, and the ventricular end bends ventrally, down and right (but there’s no septation between L and R atria, ventricles, or outflow tracks)

280
Q

how do atria get divided

A

flap that allows for flow from R to L as long as pressure is higher in R than L, but at birth will close off because L atria pressure increases and R atria decreases because detached from placenta

281
Q

what is ductus venosus

A

shunt through liver that hooks umbilical vein to inferior vena cava

282
Q

septum primum and secundum

A
  • septum primum is a curtain that starts at apex of atria and descends down heart -restricts interatrial orifice.
  • the hole at bottom of this curtain is ostium primum.
  • once it curtain fuses, a second hole appears above, called ostium secundum.
  • septum secundum grows down over ostium secundum and fuses with endocardial cushions, leaving a hole called foramen ovale – creating one-way valve from high pressure RA to LA
283
Q

pathway of fetal blood from RA to LA

A

from RA, throuhgh foramen ovale, between septum P and S, through ostium secundum to LA

284
Q

ventricular septation

A

thick muscular structure with 2 portions - muscular and membranous (part of cardiac skeleton - where you have defects)
downgrowth of membranous from valves, and muscular that grows up from apex and fuse

285
Q

outflow spetation

A

spiraling septum separates pulm and aortic septum

286
Q

what is the most common congenital heart defect

A

ventricular septal defects (1.4/1,000 births)

287
Q

major disorders (genetic and environmental) that lead to congenital heart defects (5)

A
  1. DiGeorge syndrome (22q11 deletion)
  2. trisomy 21
  3. turner syndrome
  4. diabetic mother
  5. congenital rubella
288
Q

what CHD does digeorge’s syndrome present with

A

(22q11 deletion) = truncus arteriosus, tetralogy of fallot

289
Q

what CHD does trisomy 21 present with

A

ASD, VSD, Atriventricular septal defect

290
Q

what CHD does turner syndrome present with

A

coarctation of aorta

291
Q

what CHD does a diabetic mother present with

A

transposition of great vessels

292
Q

what CHD does congenital rubella present with

A

PDA, pulmonary artery stenosis

293
Q

what does CHD present with

A

either:
1- congestive heart failure

or:
2- cyanosis

sometimes:
3- pulmonary hypertension

294
Q

reasons why CHD presents with congestive heart failure (4)

A

1- volume overload
2- pressure overload
3- cardiomyopathy
4- rhythm disturbances

295
Q

ventricular septal defect prevalance

A

1/4 of all CHDs

296
Q

how does a large VSD present

A

large VSD with pulmonary vascular resistance that’s lower than systemic resistance, a large amount of overflow of L side of heart to right side to the lungs will occur - causing CHF. sometimes the pulmonary vascular resistance will get so high that it equals the systemic vascular resistance and you’ll get some deoxygenated blood crossing over to the LV, causing cyanosis

297
Q

treatment for ventricular septal defect

A

if defect is in muscular part and small-ish, it can close on itself

can place surgical patch through RA

percutaneous repair - meshwork of metal with thrombin - clots off, and closes hole

298
Q

L to R shunt causes

A

increased pulmonary blood flow/ O2 content

299
Q

R to L shunt causes

A

decreased systemic O2 content (hypoxemia)

300
Q

bidirectional shunt

A

decreased systemic O2 content (hypoxemia)

301
Q

Eisenmenger’s syndrome

A

ireversible changes in pulmonary arterioles caused by pulmonary hypertension secondary to chornic volume overload from large L to R shunt (in beginning). eventually vascular damage causes increased pulmonary resistance which causes reversed shunt later on - R to L shunt

get hypoxemia, clubbing, cyanosis, polycythemia

302
Q

cyanosis - types

A

blue discoloration of skin
2 types
- peripheral (slow, reynods)
- central (CHD, greater than 5g/dL unoxygenated Hgb in arterial blood) - if you put on oxygen and it improves, it’s a pulmonary cause, not cardiac

303
Q

in what conditions do you see decreased pulmonary blood flow (2)

A
  • septal defects with severe pulmonary stenosis

- tetralogy of fallot

304
Q

in what conditions do you see increased pulmonary blood flow (4)

A
  1. transposition of great arteries
  2. mixing lesion w/o pulmonary stenosis- single ventricle
  3. mixing lesion w/o pulmonary stenosis– tricuspid atresia
  4. mixing lesion w/o pulmonary stenosis- total anomalous pulmonary venous return
305
Q

tetralogy of fallot mechanism

A

RV outflow to lung is stenonic (pulm valve stenosis) and malalignment of ventricular septum causes hypertropy of RV - R to L shunt - systemic circulation has deoxygenated blood

“tet spell” - RV outflow goes into spasm and causes crisis where not enough blood goes to lung to get oxygenated - increased R to L shunt, can cause seizure

306
Q

treatment for tetralogy of fallot

A

little kids:
palliation - BT shunt between subclavian artery to pulmonary artery

older:
can patch close defect and cut out hypertrophic pulmonary stenosis

render pulmonary valve incompetent - has pulmonary valve regurgitation now - right heart failure

307
Q

blood pressure equation

A

BP = CO x TPR

308
Q

How to decrease TPR (2)

A

1- relax resistant vessels

2- decrease symp activity

309
Q

how to decrease CO (4)

A

CO = HR x SV
SV is proportional to contractility and preload
you can change either of those things to lower BP

preload is proportional to venous tone and blood volume
you can change these things to alter BP

310
Q

hydrochlorothiazide mechanism

A

inhibits Na-Cl co-transport in the distal convoluted tubule - gets excreted with water - works to decrease blood volume, preload, stroke volume, cardiac output and thus BP

311
Q

long term effect of thiazide (positive)

A

reduce vascular resistance, thus reducing afterload

312
Q

adverse effects of thiazide (3)

A
  • sexual impotence
  • increased loss of K (increased risk of arrhythmias and fibrillation)
  • don’t use with renal issues
313
Q

amiloride

A

blocks Na+ channels in collecting duct, reducing potassium loss. given with hydroclorothiazide to minimize adverse effects of K loss

314
Q

ACE mechanism

A

ACE (angiotensin converting enzyme)

ang1 is inactive, ACE converts ang1 to ang2 which is active hormome that acts on receptors (AT1) that causes vasoconstriction, aldosterone secretion and sodium retention

ACE also breaks own bradykinin

315
Q

losartan

A

ARB (ang2 receptor blocker), decreases blood volume

316
Q

captopril effects (5)

A

ACE inhibitor -

  • decreases blood volume
  • also inhibits breakdown of bradykinin causing dry cough
  • regress LV hypertrophy
  • can prevent/delay MI and heart failure
  • slow progression of renal disease in diabetics
317
Q

in what patients do you NOT give ACE inhibitors or ARBS

A

1) pregnant ladies

2) people with bilateral renal artery stenosis (may cause decrease in GFR and possibly renal failure)

318
Q

adverse effect of ACE inhibitors

A

angioedema

319
Q

how to decrease contractility (and drugs)

A

1) use beta blockers (propranolol)

2) use calcium channel antagonists (amlodipine, verapamil)

320
Q

what are beta blockers used for? (7)

A 
1- decrease contractility (cause dephosphorylation of calcium channels)
2- decrease HR (block symp)
3- reduce renin secretion
4- reduce levels of ang2
5- treat angina and arrhytmias
6- decrease mortality after MI
321
Q

who don’t beta blockers work well for

A
  • elderly
  • African American
  • people with asthma
322
Q

adverse effects of beta blockers

A
  • erectile dysfunction
  • depression
  • insomnia
323
Q

how do calcium channels work

A

less influx of calcium, weaker contraction, less contractiltiy

324
Q

nifedipine vs verapamil effects on coronary vasodilation

A

nifedipine way way up, verpamil up

325
Q

nifedipine vs verapamil effects on peripheral vasodilation

A

nifedipine way way up, verapamil up

326
Q

nifedipine vs verapamil effects on HR

A

nifedipine increased reflex (because they have such a pronounced vasodilatory effect)
verapamil decreased HR

327
Q

nifedipine vs verapamil effects on contractility

A

nifedipine increased reflex (because they have such a pronounced vasodilatory effect)
verapamil decreased contractility

328
Q

nifedipine vs verapamil effects on rate of recovery of calcium channels

A

nifedipine has no effect on calcium channel recovery rate

verapamil decreases calcium channel recovery rate

329
Q

nifedipine vs verapamil effects on AV conduction

A

nifedipine has no change on AV conduction

verapamil slows AV conduction

330
Q

what is the risk of too much vasodilation

A

reflex HR and contractility increase and risk of MI - less risk for long acting dihydropyridine

331
Q

who could take long acting calcium channel blockers

A
  • angina
  • arrhymtia
  • elderly
  • african american
  • low renin

FYI, amlodipine is a long acting calcium channel blocker

332
Q

how to decrease total peripheral resistance (and drugs)

A

1) relaxation of resistance vessels by direct vasodilators (hydralazine, minoxidil, sodum notroprusside)
2) decrease symp activity and vasocontriction (alpha-1 blockers like prazosin)
3) decrease symp activity and vasocontriction (adrenergic inhibitors - guanethidine, reserpine)
4) decrease symp activity and vasocontriction (alpha2-agonists, methyldopa, clonidine)

333
Q

how do hydralazine and minoxidil work?

A

direct vasodilation of arterial vascular SM

334
Q

what are the adverse effects of hydralazine and minoxidil? (4)

A

1) increased HR and contractility (b/c of baroreflex)
2) increased plasma renin (b/c of baroreflex)
3) fluid retention because (b/c of baroreflex)
4) cardiac ischemia due to incrased cardiac oxygen demand

335
Q

how does prazosin work

A

alpha-1 blockers, blocking NE binding to BVs, blocking symp

336
Q

adverse effects of prazosin

A

“first dose phenomenon” –drop in BP so much that they can faint (can’t be used as monotherapy)

337
Q

who should use prazosin

A

men with prostatic hyperplasia and bladder obstruction symptoms

338
Q

how does guanethidine work?

A

gets transported in, replaces NE, depletes it, and blocks excitation-secretion coupling

(mostly post-ganglionic)

339
Q

guanethidine adverse effects (3)

A

1) postural hypotension
2) sexual dysfunction (retrograde ejaculation)
3) diarrhea

340
Q

how does reserpine work?

A

binds to NE storage vessicles, interferes with transmitter uptake and leaving empty vesicles

works more upstream (on pre-ganglionic) - central (thus CNS side effects) and peripheral

341
Q

adverse effects of reserpine (3)

A

1) sedation
2) inability to concentrate
3) severe depression

342
Q

what do methyldopa and clonidine do?

A

alpha 2 agonist that reduce activity of neurons in brainstem responsible for generating and maintaining symp activity

343
Q

adverse effects of methyldopa and clonidine (5)

A

1) immunological abnormalities (just methyldopa)
2) dizziness
3) reduced libido
4) sedation
5) depression

344
Q

what happens with sudden discontinuation of methyldopa and clonidine?

A

withdrawl syndrome with BP rising to levels above those present prior to treatment

345
Q

who should use methyldopa

A

pregnant ladies

346
Q

newer treatments for hypertension (4)

A

1- aldosterone blockers (spironolactone)
2- vasopressin antagonists
3- renal denervation
4- baroreceptor electrical stimulation devices

347
Q

firstline drug choice for uncomplicated hypertension in someone with systolic hypertension

A

diuretics

348
Q

firstline drug choice for someone with history of ischemic heart disease

A

beta blockers

349
Q

firstline drug choice for type1/2 diabetes

A

ACE inhibitor

350
Q

firstline drug choice for heart failure

A

ACE inhibitor

351
Q

firstline drug choice for cardiac hypertrophy

A

ACE inhibitor

352
Q

firstline drug choice for MI

A

beta blocker (or ACE inhibitor)

353
Q

firstline drug choice for angina

A

beta blocker (or Ca antagonist)

354
Q

firstline drug choice for fribrillation or arrhythmia

A

beta blocker (or Ca antagonist - not DHP)

355
Q

what anti-hypertensives should be avoided in asthma

A

beta blockers

356
Q

what anti-hypertensives should be avoided in depression

A

beta blockers, alpha2 agnoists

357
Q

what anti-hypertensives should be avoided in pregnancy

A

ACE and ARB

358
Q

what anti-hypertensives should be avoided in heart failure

A

Ca antagonists

359
Q

what anti-hypertensives should be avoided in bilateral renal stenosis

A

ACE and ARB

360
Q

What do you do for someone who is not getting BP reduction or is having side effect on current medication

A

switch to another drug in a different class

361
Q

what do you do if a drug is well tolerated but is not working to decrease BP

A

add a second agent from another class (esp diuretic)

362
Q

how many americans have high BP

A

1:2

363
Q

3 big bad things that happen from uncontrolled hypertension

A

CVD
Stroke
Kidney disease

364
Q

what does left ventricular hypertrophy evenutally cause

A

diastolic dysfuction and CHF

365
Q

what does MI eventually cause

A

systolic dysfunction and CHF

366
Q

pathophysiologic findings on kidney in hypertension leading to kidney disease (2)

A

1) hyaline atherosclerosis around arterioles

2) onion-skin pattern of hyperplastic ateriosclerosis

367
Q

risk for stroke increaes dramatically after what BP

A

110/75

368
Q

risk for CHD increases dramatically after what BP

A

130/80

369
Q

what defines stage 1 hypertension

A

greater than 130/80 less than 140/90

370
Q

what defines stage 2 hypertension

A

greater than 140/90

371
Q

what defines elevated BP

A

greater than 120/80, less than 130/80

372
Q

what intervensions do you give for stage 1

A

assess 10 year ASCVD risk

if above 10%, start treatment, if below, advise on lifestyle changes and reassess in 3-6mo

373
Q

what is first line for AA with hypertension but WITHOUT chronic kidney disease or heart failure

A

thiazide diuretic or calcium channel blocker

even with diabetes

374
Q

how do you assess for end organ damage for HTN in exam (6) and testing (3)

A

physical exam:
1. check BP in both arms to screen for aortic dissection or coarctation

  1. examine jugular veins for JVD
  2. auscultate for 3rd or 4th heart sounds or murmurs
  3. listen to lungs to listen for pulmonary edema
  4. look for swelling in extremities
  5. neurologic exam for localizing signs (vision changes etc.)

testing:
1. serum chemistries to look for renal problems

  1. CXR for pulm vasc congestion
  2. EKG for MI
375
Q

what happens if you bring people down too quickly from really high BPs

A

hypoperfusion of brain and watershed infarcts

376
Q

what are the only cases where you would do this - bring down super quickly (more than 25% immediately) (3)

A
  1. aortic dissection
  2. severe preeclampsia or eclampsia
  3. pheochromocytoma crisis
377
Q

most common patients seen by vascular surgeons (3)

A
  1. carotid artery disease
  2. aortic aneurysms
  3. lower extremity disease
378
Q

what diameter is considered aortic aneurysm

A

3cm (50% larger than normal)

379
Q

two types of aneurysms

A
  1. fusiform (most common, univorm dilation)

2. saccular (focal dilation)

380
Q

where does abdominal aortic aneurysm occur?

A

below the renal arteries above aortic bifurcation (right above umbilicus)

381
Q

at what diameter do you start to think about intervention for abdominal aorta aneurysm

A

5-6cm (risk of rupture is from 3-15%) - risk exceeds risk of operation

382
Q

stroke is the ___ leading cause of death in US

A

3rd

383
Q

examples of symptomatic carotid artery disease

A
  1. TIA (less than 24 hours, reversible)
  2. amaurosis fugax (temp blindness - shade coming down)
  3. stroke (neurologic deficit - brain injury)
384
Q

example of asymptomatic carotid artery disease

A
  1. bruit
385
Q

what is lower extermity arterial disease mostly due to

A

atherosclerotic occlusive disease - blood flow does not meet the tissue demands of the lower extremities

386
Q

symptoms of lower extremity arterial disease

A

75% are asymptomatic

common symptom is claudication - cramping of calves with walking

387
Q

physical exam for lower extremity arterial disease (7)

A
  1. pulse exam
  2. hair loss
  3. poor nail growth
  4. dry scaly thin skin
  5. dependent rubor (red when down)
  6. elevation pallor (white when up)
  7. ulcers or gangrene
388
Q

ankle-brachial index

A

measure ankle bp/arm bp (0.9 or higher is normal)

389
Q

3 indications for intervention for lower extremity arterial disease

A
  1. lifestyle limiting claudication
    limb-threatening ischemia:
  2. rest pain (dangle leg off of bed at night)
  3. tissue loss (non-healing ulcer or gangrene)
390
Q

lower extremity arterial disease therapeutic interventions

A
  1. endovascular therapy (angioplasty and stent)
  2. surgery (endarterectomy removal of plaque and patch, bypass procedure with great saphenous vein or prosthetic PTFE teflon or dacron graft)
391
Q

what does the ST wave do in MI versus ischemia

A

ST segment up in MI, down in ischemia

392
Q

T wave in inschemia

A

deep symmetric T wave inversions

393
Q

what do you see with toursaddes de pointes, what could it be caused by?

A

elongated QT interval (more than 400ms) -sometimes caused by meds (amiodarone, quinolones, fluconazole, methadone, tamoxifen, grapefruit juice)

394
Q

tachy vs brady

A

tachy more than 100 (less than 3 boxes), less than 60 is brady (more than 5 boxes)

395
Q

what causes sinus bradycardia (6)

A
  1. hypothyroidism
  2. sinus node dysfunction
  3. high vagal tone (athletes)
  4. Bblockers, non DHP CC blockers
  5. amiodarone, sotalol, propafenone
  6. digoxin
396
Q

what causes sinus tachycardia (8)

A
  1. fever
  2. anemia/blood loss/ orth hypo
  3. drugs (NE, Epi, cocaine)
  4. exercise
  5. pain
  6. anxiety/panic
  7. hyperthyroidism
  8. illness (PE, pneumonia, CHF)
397
Q

what is P mitrale and what does it mean

A

broad p wave in “m” shape >120msec – indicates enlarged LA (caused by mitral regurg, for example)

398
Q

what is a delta wave and what does it signify

A

short PR interval and slurred slope - delta. signifies that there’s an accessory pathway between A and V - WPW

399
Q

How do you measure LV hypertrophy

A

S wave V1 + R wave V5 > OR = 35

400
Q

what is the QT intervial = what to what

A

beginning of Q to end of T

401
Q

what is too long for QT interval

A

400ms - tourssades de point

402
Q

what causes low voltage on EKG (3)

A
  1. Fluid (pericardial effusion)
  2. air (emphysema)
  3. fat (obesity)
403
Q

what causes type 1 second degree heart block (3)

A

increased vagal tone that can affect AV conduction

  • benign, when sleeping
  • older
  • too much B blocker or CC blocker
404
Q

what causes type 2 second degree heart block (2)

A

more dangerous, associated with:

  • acute MI (look for ST elevation)
  • chagas disease (kissing bug)
405
Q

what causes 3rd degree/complete heart block

A

AV conduction doesn’t work - P waves are consistent (SA node ok) but not generating QRS consistently. can lose ventricular escape and can die
need pacemaker

406
Q

what is the R to R interval like in a fib

A

variable

407
Q

why are a fibs important to diagnose

A

cause strokes (give anticoag - warfarin, dabigatran etc.)

408
Q

what does supra ventricular tachycardia (SVT) look like? what do you do?

A

fast, narrow complex tachycardia, no p wave (buried in QRS) - AV node re-entry, get QRS at about the same time

can block AV node (adenosine, push on carotids)

409
Q

Who should get defibrillator implanted?

A

previous MI, low ejection fraction

410
Q

two types of ventricular tachycardias

A
  1. stable (BP is okay - give amiodorone)

2. unstable (BP is low - shock them)

411
Q

what does v tach look like

A
  1. wide QRS tachycaridia

2. AV dissociation (p at different rates than QRS)

412
Q

who has v tach

A

people with dilated cardiomyopathy, past infarct (causing re-entry)

413
Q

1A,B,V, 2, 3, 4 classes of antiarrhythima - what are they used for

A

1B - just VT
1C&A - mostly VT, some SVT
3 - both VT and SVT
4&2 - SVT

414
Q

examples of class 1B (2)

A

lidocaine (post MI), mexiletine (long QT)

415
Q

examples of class 1C (1)

A

flecainide (no ischemia, v fib)

416
Q

examples of class 1A (2)

A

quinidine, procainamide (a fib)

417
Q

examples of class 3 (2)

A

amiodarone (low 1st line a fib, high 1st line VT abnormal hearts), sotalol (use with defibs)

418
Q

examples of class 4 (2)

A

verapamil, diltiazem (rate control, NOT in CHF)

419
Q

examples of class 2 (1)

A

metoprolol (good post MI, symp arrhythmias)

420
Q

what classes do you worry about for long QT

A

class 1A and class 3

421
Q

what classes are used for rhythm control

A

1C, 1A, 3

422
Q

what classes are used for rate control

A

4, 2, and other

423
Q

examples of “other” class antiarrhythics (2)

A

digoxin

adenosine

424
Q

which classes block sodium channels

A

1A,B, and C

425
Q

which classes are beta blockers

A

2

426
Q

which class blocks calcium channels

A

4

427
Q

which class blocks potassium channels

A

3

428
Q

what are the properties of sodium channels that are voltage dependent

A
  1. # of excitable channels (at -80 all are excitable, at -50 only some are)
  2. time to recovery (at -80, recovery is shorter than at -50)
429
Q

effective refractory period

A

when you cannot activate the channel - time from un-activatable to activatable

430
Q

group 1A drugs that directly increase BP and directly increase contractility (4)

A

1) dobutatime
2) high dose dopa
3) high dose NE
4) high does Epi

431
Q

group 1B drugs that directly increase BP but do NOT directly affect contractility (4)

A

1) phenylephrine
2) vasopressin (ADH)
3) angiotensin 1
4) angiotensin 2

432
Q

group 2A drugs that directly decrease BP and directly increase HR (3)

A

1) low dose dopa
2) isoproterenol
3) theophylline

433
Q

group 2B drugs that directly decrease BP but do NOT directly increase HR (8)

A

1) Ach
2) charbachol
3) clonidine
4) verapamil
5) nitroglycerin
6) terbutaline
7) histamine
8) bradykinin

434
Q

drugs that cause bronchodilation (5)

A

1) terbutaline
2) theophylline
3) dopa
4) epi
5) isoproteranol

435
Q

what do you use to block the reflex caused by NE

A

ATROPINE

436
Q

interaction between physostigmine and Ach

A

potentiation

437
Q

interaction between atropine and Ach

A

competitive inhibition

438
Q

what does altering the fast sodium channel control

A

1) conduction velocity

2) effective refractory period

439
Q

what does altering the calcium channel control

A

1) AP duration

2) indirectly ERP

440
Q

what does altering the TEA type K channel control

A

1) AP duration

2) indirectly ERP

441
Q

what ion is phase 0 determined by in SA node and myocardium

A

SA - calcium

myocardium - sodium

442
Q

main causes of tachycardias (3)

A

1) reentry circuits
2) ectopic pacemakers
3) early after depolarizations (fib)

443
Q

is hypoxic tissue more or less depolarized

A

less depolarized - more positive

444
Q

do hypoxic tissues have a longer or shorter refractory periods

A

longer (more sodium channels are un-activatable)

445
Q

what do you do for rate control in A fib

A

anesthetize AV node - 10:1 block “screw the p wave”

- also consider anticoag

446
Q

what do you do for rhythm control

A

restore normal sinus rhythm - pharmacological cardioversion - gets rid of a fib

447
Q

drugs for rate control (3)

A

1) metoprolol
2) verapamil
3) digoxin

448
Q

drugs for rhythm control (2)

A

1) amiodarone

2) flecainide

449
Q

during what “states” of the sodium channel do class 1 drugs bind and what do they do (2)

A

1) open (makes them less-ecitable, slows phase 0, slows conduction velocity)
2) un-activatable (increases refractory period, takes longer to repolarize)

450
Q

How do class 1 drugs affect rhythm control

A

effect reentry:

makes effective refractory period longer than conduction time

451
Q

class 1a (effect on Na+ and K+ channels)

A
  • medium reduction in slope (medium Na+ block)

- prolonged AP (partially block K+) - long QT

452
Q

class 1B (effect on Na+ and K+ channels)

A
  • mild Na+ block, little reduction in slope

- shortened AP (paritally activating K+) - short QT

453
Q

class 1C (effect on Na+ and K+ channels)

A
  • marked Na+ block, big reduction in slope (longest effective refractory period)
  • no change in repolarization - no interaction with K+
454
Q

what do you use class 1B for

A
  • only for VT

- best post MI

455
Q

Which is more selective or sick cells, Ib or 1C

A

1B

456
Q

adverse effects for 1A (3)

A
  • torsades de pointes long QT
  • V tach (use calcium channel to slow AV node)
  • can cause asystole in incomplete heart block
457
Q

what channels do class 3 block

A
  • blocks potassium efflux during phase 3 (increase AP)

- blocks Na+ channels (increase ERP)

458
Q

amiodarone adverse effects

A

1) torsades de pointes
2) pulmonary fibrosis
3) blue man syndrome

459
Q

can you use rate control drugs in WPW?

A

no! because you have accessory pathway and can cause arrhymthmia

460
Q

major effect of class 4 drugs

A
  • blocking Ca2+ channels in AV node (slow down responsiveness)
461
Q

class 2 drug effects

A

block symp, decrease AV node conduction and decrease excitability

462
Q

when do you use adenosine

A

in supraventricular tachycardia that you think is from the AV node (would see narrow QRS), used acutely

463
Q

what drug types cause long QT

A

1A and 3

464
Q

familial hypercholesterolemia findings

A
  • tendon xanthoma
  • defect in LDL receptor
  • coronary artery disease
465
Q

what are the polar (2) and non-polar (2) parts to lipoprotein structure

A

polar:
1- phospholipid
2- free cholesterol

non-polar
1- triglyceride
2- cholesterol ester

466
Q

Friedewald Forumla

A

(LDL-C) = TC - (HDL-C) - (VLDL-C)

VLDL-C –> TG/5

467
Q

sources of error in friedwald formula (30

A
  1. super high TGs >400
  2. non-fasting
  3. errors in each individual measuremnt
468
Q

C Reactive Protein

A

as it increases, it raises risk for cardiac event - used in Reynolds Risk Score

469
Q

coronary calcium score

A

on cat scan can see calcium. high levels of calcium in coronary arteries predict levels of coronary events - MESA risk score

470
Q

if someone has clinical ASCVD and over 75 vs under 75 management

A

under 75 - high intensity statin

over 75- moderate-intensity statin

471
Q

if someone does NOT have clinical ASCVD but has baseline LDL-C >190 management

A

high intensity statin

472
Q

if someone does NOT have clinical ASCVD but has DM

A

moderate intensity statin

473
Q

if 10-year ASCVD risk is over 7.5 and age is under 75

A

moderate intesnsity statin

474
Q

PCSK9 monoclonal antibodies (2)

A

1) alirocumab

2) evolocumab

475
Q

endothelial cell injury theory

A

the endothelial cell lining undergoes some kind of insult (hypertension, toxins, lipidemia) then infusion in lipids and cells through endothelium accumulation of macrophages, that become foam cells, cytokines trigger inflammation - cytokine cascade increase acute phase reactants (CRP levels reflect atherosclerosis)

476
Q

where do lesions occur (atherosclerotic plaques)

A

aorta near branch points
lower extremities
in circle of willis
coronary arteries

477
Q

histologic changes of atheroslerosis

A

thicking of intima, accumulation of lipids under thickened intima, fibroblasts and macrophages between the two layers, fibrous cap on most intimal layer
tunica media then becomes thinned and weakened

478
Q

aortic dissection causes and pathogensis

A

hypertension, marfans, pregnancy
rip through iintima that dissects along outer 2/3 of media
more in males
presrents with chest/back pain

479
Q

aortic dissection classifications (debakey)

A 
type1 = ascending and descending = poor
type2 = just ascending = poor
type3 = desencding only = better
480
Q

mycotic aneurysm - syphillis - findings

A

associated with infection (syphillitic in aortic arch = leutic aortitis)

vaso vasorum (that are BVs to the heart itself) have predelection for syphillis - cause infarction of aortic wall - proximal ascending aorta - see grainly inflammaed appearance, see spirochetes on stain

481
Q

vascular pathology of hypertension that affects small arteries (2)

A

1) hyaline arteriolosclerosis

2) hyperplastic ateriolosclerosis

482
Q

monckeberg medial calcific sclerosis

A

medium sized muscular arteries
over 50 years old
no narrowing of lumen

483
Q

hyalien aterioloslerosis

A

pink, smooth, deep proteinaceous infiltration
associated with prolonged hypertension
narrowing of lumen
seen in kidneys often

484
Q

hyperplastic arteriolosclerosis findings

A

concentric laminated thickening of intima
cellular proliferation making onion skin appearance (consists of SM, BM)
can be associated with characteristic fibrinoid necrosis
associated with malgnant hypertension

485
Q

malignant hypertension

A

rapid, severe hypertension (200/120)

patients have headache, renal railure, retinal exudates, organ failure

486
Q

characteristics of hypertensive heart disease (5)

A
  • heart is larger than 500g
  • see concentric hypertrophy
  • LV wall is greater than 2cm
  • reduction of luman size
  • microscopically see large mycocytes, large nuclei (box car) and fibrosis
487
Q

characteristics of hypertensive changes in the brain (3)

A
  • lacunar infarcts
  • slit hemorrhage (rupture of small vessles with hemorrhage, browinish slit cavity)
  • intercerbral hemorrhage (common cause of death in people with chronic hypertension)
488
Q

characteristics of hypertensive change sin kidneys (2)

A
  • benign nephrosclerosis (hyaline arteriolosclerosis (grainy surphace), glomerulosclerosis, tubular atrophy, iinterstitial fibrosis)
  • chronic renal failure
489
Q

exercise ECG testing use (5)

A
  • measure exercise capacity and duration
  • BP respose
  • HR response
  • provoked ysmptoms (dizziness, chest pain)
  • see changes in EKG that might suggest CAD
490
Q

echocardiography use (5)

A

ultra sound

  • look at valves and chambers
  • 1st line test for LV structure and function - ejection fraction assessment
  • pericardial effusion
  • masses
  • aortic diseases
491
Q

normal ejection fraction and how is it calculated

A

> 55%
= (LVEDV - LVESV) / LVEDV
= amount pumped out of ventricle/total amount in ventricle

492
Q

nuclear cardiology indications (3)

A
  • diagnosis and assessment of CAD
  • evaluation of ventricular function
  • myocardial viability imaging (recoverability of heart)
493
Q

cardiac CT indications (3)

A
  • non-invasive anatomic assessment of CAD
  • risk stratification (coronary calcium scoring)
  • eval acute chest pain quickly
494
Q

cardiac MRI indications (4)

A
  • tissue charactization (muscle, fat, blood etc)
  • whole heart imaging
  • cardiomyopathies
  • congenital heart diseases

not so great in obese, coaustrophobic, costly, need long breath hold

495
Q

cardiac cath indications (1)

A
  • CAD
  • into fem or radial artery into ascending aorta into main coronary artery

risks of death and stroke

496
Q

SA and AV are typically supplied by

A

RCA

497
Q

when do coronary arteries fill

A

diastole

498
Q

what supplies posterior papillary muscle

A

RCA

499
Q

what supplies anterior and anteroseptal heart region

A

LAD

500
Q

what supplies anteriolateral and lateral heart region

A

L circumflex

501
Q

what supplies inferior and posterior heart region

A

RCA

502
Q

what is the first line test for evaluating CAD

A

EKG stress test

503
Q

what is sensitivity and specificity for exercise treatmill test

A

60 and 70

504
Q

what is sensitivity and specificity for stress echo

A

80 and 84

505
Q

what is sensitivity and specificity for nuclear SPECT MPI

A

90 and 75

506
Q

what is sensitivity and specificity for coronary CTA

A

95-99 and 83

507
Q

are primary tumors of the heart rare or common

A

rare

secondary tumors are 40x more common

508
Q

are primary tumors of the heart malignant or benign

A 
mostly benign (58%) usually myxoma
malignant (42%) usually sarcoma
509
Q

myxoma treatment

A

resection

510
Q

carney complex

A

familial variety (10%) of myxomas

511
Q

where do you find myxomas

A

most commonly LA, usually arising from interatrial septum, may have peduncle - obstruction in valves

the familial version can be found in multiple locations, ventricular, and recur after resection

512
Q

where do you find cardiac sarcomas

A

R side of the heart more likely, pericardial space as well

513
Q

where do you usually find metastatic cardiac tumors

A

pericardium

514
Q

does aortic stenosis cause volume or pressure overload

A

pressure overload

515
Q

at what area do you start to see symptoms with aortic stenosis

A

below 0.5-0.8 cm2

516
Q

clinical manifestations of aortic stenosis (3)

A

angina
CHF
syncope during exercize

517
Q

what do you hear on PE for aortic stenosis

A

crescendo decrescendo murmur during systole (radiates into neck)

518
Q

treatment for aortic stenosis

A

valve replaement

519
Q

benefit of mechanical valve

A

longevity

520
Q

downside of mechanical valve

A

have to take anticoag

521
Q

transcath aortic valve replacement

A

take balloon with stent with tissue valve sewn into it (bovine pericardium)

522
Q

is mitral stenosis pressure or volume overload

A

pressure (increased LA pressure)

523
Q

when do people become symptomatic with mitral stenosis (at what area)

A

less than 2 cm2

524
Q

4 cuases of mitral regurg

A

1- mitral valve leaflet disorder (marfans, rheum)
2- annulus disorder
3- chordae disorder
4- papillary muscle

525
Q

what do ou hear on PE for mitral regurg

A

parasystolic murmur

526
Q

what do you hear on PE for mitral valve prolpase

A

midsystolic clinck and late systolic murmur

527
Q

is regurg pressure or volume overload

A

volume (both mitral and aortic)

528
Q

what is classic BP for someone with aortic regurg

A

120/40 - large pulse pressure

529
Q

alpha1 adrenergic receptor (location and net effect)

A

vasculature (also some alpha2) = vasoconstriction (Gq)

530
Q

alpha2 adrendergic receptor (location and net effect)

A

CNS = synaptic transmission

531
Q

beta1

A

heart = increase HR, contractility, conduction (Gs)

532
Q

beta 2 location and net effect

A

skeletal muscle = vasodilation

bronchial SM = bronchodilation

533
Q

beta 1

A

juxtaglomerular apparatus = renin release

534
Q

leading cause of acute bacterial endocarditis and cause of death

A

staph aureus

535
Q

is the underlying valve normal or abnormal is subacute and acute bacterial endocarditis

A

normal in acute, abnormal in subacute (need turbulent flow - high to low pressure sinks)

536
Q

venturi principle

A

vegetation occurs distal/in the direction of the turbulent flow

537
Q

what are 3 examples of bacteria that are adherent

A

enterococcus
strep viridans
staph aureus

538
Q

why is treatment difficult for bacterial endocarditis

A

because they divide so slowly

539
Q

what are the etiologic agents responsible for subacute bacterial endocarditis (4)

A

strep viridans
group D step (enteroocci, strep bovis)
coag negative staph

540
Q

where do IV drug users get vegetations

A

tricuspid valve

541
Q

classic triad for clinical presentation of infective endocarditis

A
  1. fever (maybe not in elderly or uremic patients)
  2. anemia (maybe not in acute endocarditis)
  3. heart murmur (actually a changing/new regurg murmur, not always present)
542
Q

are systolic flow murmurs holosystolic or “diamond shaped”

A

diamond shaped - crescendo decrescendo

543
Q

are mitral regurg murmurs holosystolic or “diamond shaped”

A

holosystolic - same throughout

544
Q

peripheral manifestations of endocarditis 5)

A
  1. conjunctival petecchiae
  2. splinter hemorrhages
  3. osler;s nodes
  4. janeway lesions
  5. roth spots
545
Q

if you have a patient with endocarditis with PR interval heart block, what is that a clue to

A

myocardial abcess in septum, needs surgery

546
Q

do you anticoag a patient with endocarditis?

A

no, could have a mycotic aneurysm that could burst in brain and cause death

547
Q

what should you do for a patient with endocarditis and heart failure

A

surgery immediatley. don’t try to give diuretic and wait and see. go to the OR

548
Q

how much is 1 MET

A

3.5 ml/min/kg - resting

549
Q

how many mets can you get to with minimal exercise

A

20 METS

550
Q

What is respiratory quotient equation

A

CO2 production/ O2 consumption - during anaerobic metabolism, RQ is greater than 1

551
Q

O2 pulse equation

A

O2 consuption/ HR

approximation of stroke volume

552
Q

breathing reserve equations

A

max voluntary ventilation (MVV) = 35 x FEV1

breathing reserve = MVV - max exercise ventilation

553
Q

heart rate reserve equations

A

Predicted HR = 220 - age

HR reserve = (predicted HR - actual HR) x highest exercise HR

554
Q

what hapens in acute coronary syndrome

A

vasospasms episodically reduces coronary blood flow, AKA variant angina

555
Q

unstable angina is caused by what

A

rupture of atherosclerotic a plaque - must be treated to prevent MI

556
Q

what are treatments for variant angina

A

calcium channel blockers - reduce likelihood of vasospasm

557
Q

coronary blood flow equation

A

(diastolic pressure in aorta - LV pressure during diastole) / coronary vascular resistance

558
Q

nitroglycerin mechanism of action

A

converts to NO, increases guanylate cyclase, increases cGMP, dephosphorylates MLC kinase, DECREASING contractile state of SM particularly in venules (less so in arterioles) decreasing pressure in preload, increasing coronary blood flow and decreasing tension (decreasing ischemia)

nitroglycerine ALSO dilates the large epicardial arteries increasing coronary blood flow reducing coronary steal, shunting to where you need it

559
Q

what is coronary steal

A

shunting to places where you don’t need it - ubiquitous vasodilation

560
Q

do calcium channel blockers work on arterioles or venules

A

more so on arterioles

561
Q

in what patient population with angina would you ot to use beta blocker

A

someone with hypertension or prievious MI

562
Q

when would you want to give someone ranexa for angina

A

if they have not responded to the other anti-anginal drugs (nitrates, CC blockers or BBs)

563
Q

why would you give nitrate with beta blocker

A

same reason you give diuretic for antihypertension. you want to reduce preload as well

564
Q

what does Kawasaki disease do to the heart

A

autoimmune inflammatory disease that involves coronary arteries - aneurysms and ischemic changes in heart

565
Q

which part of the heart dies with occlusion of LAD

A

anterior 2/3 of septum and anterior left ventricle

566
Q

which part of the heart dies with RCA occlusion

A

posterior 1/3 of septum, posterior left ventricle

567
Q

which part of the heart dies with LCircumflex occlusion

A

lateral left ventricle

568
Q

microscopic changes from 4-12 hours

A

some wavy fibers,

some gross mottling

569
Q

microscopic changes from 12-24 hours

A

coagulation necrosis, acute inflammatory cells, neutrophils, edema, heomorrhage,

grossly see pallor and mottling

570
Q

microscopic changes from 24-72 hours

A

coag necrosis, DENSE neutrophil infiltrate, loss of nuclei and cross striations

grossly see pallor

571
Q

microscopic changes from 3-7 days

A

macrophages replace neutrophils, granuation tissue forms from periphery - at greatest risk for rupture

grossly see pallor

572
Q

changes from 7-10 days

A

yellow in center grossly

more macrophage and granulation tissue at edges

573
Q

changes from 10-21 days

A

gray collor grossly

fibrosis increasing

574
Q

6wk to 1 year changes

A

scar reaches full tensile strength at 1 year, fibrosis

575
Q

reperfusion injury

A

tissue damage breaks down BVs, even though you release obstruction of BV you might have leakage and extend area of infarction and lead to fatality (rare fatality)
see contraction bands - shocked sudden re-oxygenation causes contraction of myocardium

576
Q

what are 2 EKG findings in unstable angina

A

1) T-wave inversion

2) ST segment depression

577
Q

common cause of myocarditis

A

coxsackie A and B (enterovirus)

578
Q

common cause of pericarditis

A

rheumatic fever, uremia

or extension from myocarditis

579
Q

defifnition of cardiomypoathy

A

non-inflammatory disorder of the myocardium - can be dilated (aka congestive), hypertrophic or restricrtive

580
Q

causes of dilated cardiomyopathies (4)

A
  1. genetic (pheochromocytoma, dystrophin etc.)
  2. infectious (sequelae from viral myocarditis)
  3. post partum
  4. toxins (diabetes, hemochromatosis, alcohol, amiodarone)
581
Q

causes of hypertrophic cadiomyopathy (1)

A
  1. sarcomere protein mutations (B- myosin heavy chain, myosin binding protein C, Troponin T)
582
Q

is hypertrophic cardiomyopathy aymmetric or symmetric?

A

asymmetric (with or without obstruction)

583
Q

who gets hypertrophic cardiomyopathy

A

young adults - sudden death in kid playing basketball

584
Q

restrictive vardiomyopathy causes

A
  1. amyloidosis
  2. sarcoidosis
  3. endomyocardial fibrosis
585
Q

bugs and worms that cause infectious myocarditis (4 categories)

A

VIRAL

  1. cocksacie B enterovirus
  2. adenovirus
  3. parvovirus B19
  4. influenza
  5. herpes
  6. HIV

BACTERIAL

  1. diptheria
  2. lyme

PROTOZOA
1. trypanosoma vruzii - chagas

HELMINTH
2. trichinella spiralis (nematode)

586
Q

who gest myocarditis

A 
bimodal - young children and teenagers (get acute presentation)
older adults (insidious symptoms of dilated cardiomyopathy and heart fiailure)
587
Q

causes of infectious pericarditis (2)

A

viral: coxsackie
bacterial: TB, staph, h. flu, legionella

588
Q

what are the 4 mechanisms that can lead to heart failure

A
  1. increased blood volume (increased preload)
  2. increased resistance to blood flow (increased afterload)
  3. decreased contractility
  4. decreased filling
589
Q

3 scenarios with increased afterlad

A
  1. CHF
  2. HTN
  3. aortic stnosis
590
Q

4 scnearios with decreased afterload

A
  1. mitral regurg
  2. VSD
  3. A-V fistula
  4. septic shock
591
Q

what does aldosterone secretion do

A
  1. increases salt and water retention

2. myocardial fibrosis

592
Q

neprilysin

A

does the same thing as angiotensin 2

blocks natriuretic peptides which are helpful, so you want to inhibit it

593
Q

administration of BNP to patient with heart failure causes

A
  1. natriuresis
  2. reduced filing pressures

BNP causes decreased systemic vascular resistance and sodium excretion

594
Q

symptoms with isolated right-sided congetsion (2)

A

GI discomfort and edema

595
Q

symptoms with left-sided congestion (3)

A

orthopnea, immediate dyspnea, fatigue

596
Q

what is wedge presssure

A

back pressure from pulmonary artery wedge, no more forward flow,
should be equal to left atrial pressure (equal to LV diastolic pressure)

597
Q

wet and warm =
dry and cool =
wet and cool =

A

wet and warm = congestion (over hydrtation)
dry and cool = hypoperfusion (dehydration)
wet and cool = hypoperfuson AND congestion

598
Q

ivabradine mechanism of action

A

works on funny current i(f) in slow repolarization. no effect on contractility. reduces SA node rate

use for stable, symptomatic CHF with EF less than 35% and tachycardic

quality of life, not curative

599
Q

when do you see narrow pulse pressure

A

aortic stenosis, severe CHF

600
Q

when do you see wide pulse pressure

A

aortic insufficiency

601
Q

when do you hear S3 pathologically

A

floppy dilated heart

602
Q

when do you hear S4

A

hypertrophy stiff heart

603
Q

when do you hear opening snap

A

rheumatic mitral stenosis

604
Q

when do you hear ejection click

A

bicupsid aortic valve

605
Q

when do you hear midsystolic click

A

mitral valve prolapse

606
Q

when do you hear flow murmur (4)

A
  • normal
  • anemia
  • AV fistula
  • aortic or pulmonic (semilunar) valve stenosis
    “diamond shaped”
607
Q

when do you hear holosystolic murmur (2)

A
  • AV valve(mitral.tricuspid) insufficiency

- VSD

608
Q

when do yo have diastolic murmurs (2)

A
  • semilunar valve insufficiency (aortic or pulmonic)
  • AV valve (mitral or tricuspid) valve stenosis
    (low pitched murmur)
609
Q

when do you have continuous murmurs

A
  • abnormal connection artery and vein (AV fistula)

- abnormal connection aorta with R heart (PDA)

610
Q

high reisk statin therapy

A

atorvastatin 40-80

rosuvastatin 20-40

611
Q

moderate risk statin therapy

A

atorvastatin 10-20
rosuvastatin 5-10
simvastatin, pravastatin, lovastatin, fluvastatin, pitavastatin (all above 30/40mg)

612
Q

low risk statin therapy

A

simvastatin, pravastatin, lovastatin, fluvastatin, pitavastatin (all below 30/40mg)

613
Q

long erm complications of heart transplants

A 
acute cellular and Ab mediated rejection
osteoporosis
hypertension
DM
neuropathy
614
Q

mean pulm artery pressre equation

A

= diastolic pressure + 1/3 (sys - dias)

615
Q

pulm vasc resisyance equation

A

(mpap-pcwp)/ co

616
Q

dias pulm gradient

A

iff btw padp and pcwp

617
Q

definition of pulm hyepertension

A

mean pulm artery pressure greater than 25mmHg

618
Q

pre cap vs. post cap PH

A

pre Cap has less than 15 wedge pressure, post has more than 15

pre AND post wedge pressure more than 15, DPG more than 7

619
Q

groups for PH classification

A
  1. pulmonary arterial hypertension (plexiform lesions)
  2. PH due to left heart disease (most common)
  3. PH due to lung diseases or hypoxia
  4. chronic thrombo-embolic pulmonary hypertension (only one with cure, do VQ scan)
  5. PH with unclear/multifactorial mechanisms

CPR (3 decks)

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