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year 2 > cardio > Flashcards

cardio Flashcards

1
Q

EKG numbers

PR interval

A

P-R interval = 0.12- 0.2 seconds

3-5 teeny boxes

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2
Q

cardiac output formula

normal # for middle age sednetary person

A

Q = HR * SV

5L/min

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3
Q

why does contractility affect CO?

A

contractility of heart based on SR releasing Ca (contraction) and reabsorbing Ca (relaxing). if heart does not fully relax, it cannot take up enough blood

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4
Q

preload

A

crossbridging (max crossbridging = max preload)

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5
Q

afterload definition

A

amt of resistance heart faces moving blood forward

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6
Q

what kind of ventricular dysfunction is associated with decreased exercise tolerance? why?

A

right sided ventricular function because enough blood is not being sent to lungs to be oxygenated

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7
Q

VO2

normal number

A

oxygen consumption = 10mets =

35mL O2/kg bdy wt/ min

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8
Q

RPP
formula
why we care

A

rate pressure product
=SBP * HR
if it doesn’t increase as you exercise this should increase otherwise may be sign of ischemia

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9
Q

fatty streak (3)

A
  1. earliest visible atherosclerotic lesion
  2. do not disturb blood flow because they don’t go into the lumen
  3. from foam cells derived from lipid filled macrophages
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10
Q

fibrous plaque (2)

A
  1. more advance lesions that project into lumen => affect blood flow.
  2. these foam cells are derived from smooth muscle
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11
Q

complicated lesions (types) (4)

A
  1. calcification
  2. rupture of a fibrous plaque
  3. hemorrhage
  4. embolization
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12
Q

fibrous cap

A

extracellular C.T. embedded in smooth muscle. separates the atrial lumen from cell debris

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13
Q

calcification of fibrous plaque issues

A

result in pipelike rigidity of wall which increases fragility and decreases elasticity

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14
Q

rupture of a fibrous plaque

A

exposes thrombogenic material into circulating blood

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15
Q

embolization of fibrous plaque results in… (3)

A

can result in stroke, PE or MI

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16
Q

role of endothelial wall (3)
and what happens if injured
what happens if weak

A
  1. causes vasodilation
  2. resists formation of clots
  3. inhibits smooth muscle cell migration

if injured: if injured these things don’t happen which lead to clots on the surface

if weakened in spots vessel may burst = aneurysm which can lead to MI or tompenade

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17
Q

AHA cholesterol recommendations

  1. total cholesterol
  2. LDL if no heart disease
  3. LDL if heart disease
  4. HDL, and a positive number
A
  1. total cholesterol < 200 mg/dL
  2. LDL if no heart disease < 130 mg if no heart disease
  3. LDL if heart disease > 100mg/ dL
  4. HDL > 35mg/dL - >60 gives a beneficial result
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18
Q

classification of hypertension

  1. normal
  2. high normal
  3. stage I HTN
  4. Stage II HTN
  5. Stage III HTN
  6. Stage IV HTN

what’s considered uncontrolled HTN for normals and diabetics? and how does it affect PT?

A

SBP DBP

  1. normal - 120-129 80-84
  2. high normal 130-139 85-89
  3. stage I HTN 140-159 90-99
  4. Stage II HTN 160-179 100-109
  5. Stage III HTN 180-189 110**-114
  6. Stage IV HTN >200** >115

SBP > 200 or DBP > 110 is considered uncontrolled HTN and we do not exercise pt. (110 at exercise or rest!)
SBP >180 for diabetics is considered uncontrolled

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19
Q

how do we classify stage of HTN

A

by the highest stage - either SBP or DBP (eg 120/99 is stage I HTN because the 99)

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20
Q

during exercise- at what BP do we stop?

A

230/110***

DBP should not get above 110 during exercise or rest

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21
Q

how does diabetes affect the heart?

A

postulated that there is increased platelet adhesiveness due to diabetes

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22
Q

blood glucose levels

  1. normal fed
  2. normal fasting
  3. diabetes - fed and fasting- whats considered impaired

when do we stop diabetics from exercise?
when do we check for ketones

A
  1. normal fed - 70-110 mg/dL
  2. normal fasting - 125 mg/dL or 110 fasting

we stop diabetics at >300 mg/dL, at >260 check for ketones in urine

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23
Q

BMI formula

A

bdy wt (kg)/ height ^2

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24
Q

stable angina
description of symptoms
what we see on EKG
can we treat pt?

A
  1. chronic pattern of transient chest pain, precipitated by phsical activity, eating, or emotional upset- relieved w/i minutes
  2. transient shifts of ST segment (usually elevated)
  3. treatment is ok
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25
Q

unstable angina
description of symptoms
what happens if untreated

A
  1. increased frequency and duration of angina, after less exertion or at rest
  2. usually => MI if untreated
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26
Q

variant angina
etiology
what we see on EKG

A
  1. results from coronary artery vasospasm (vs. increased O2 demand) ** therefore more autonomic dysfunction and not exercise dependent, so happens at rest**
    vasospasm can still cause MI*
  2. associated with transient shifts of ST segment (usually elevated)
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27
Q

who is most at risk for variant angina?

A

women

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28
Q

ischemia
what happens if vessel is 70% stenosed?
what happens if vessel is 90% stenosed?

A
  1. at 70% stenosis vessel needs to be completely dilated to achieve adequate perfusion
  2. at 90% stenosis at constant ischemia, not able to meet basal requirements, hopefully collateral circulation kicks in here
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29
Q

MI

definition

A

condition of irreversible necrosis of heart muscle that results from prolonged ischemia

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30
Q 
transmural MI
 aka
 whats anatomy is affected 
 EKG 
 mortality rates
A
  1. aka Q-wave MI or ST elevation MI
  2. full thickness of myocardium- this is what increases Q wave because signal gets to heart wall then has to go all the way around to healthy tissue
  3. EKG- elevated ST
    T becomes pointy & inverts w/i days
    QRS widens permanently
  4. High because sudden change in pumping capabilities
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31
Q 
subendocaridal MI
 aka
 what anatomy is affected
 EKG
 mortality/ reinfarction rates
A
  1. aka non-Q wave MI
  2. exclusively innermost layer of muscle (which is most easily affected because it is furthest away from coronary ateries)
  3. EKG: inverted T
    depressed ST
  4. high rates of re-infarction
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32
Q

EKG - QRS duration

What does it mean if wide?

A

QRS complex = 0.04 - 0.1 seconds
1-2.5 teeny boxes

If wide- beat starts below AV node

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33
Q

QT interval duration

A

Q-T interval = 0.32- 0.4 seconds

34
Q

risk stratification for smoking
low
mod
high

A

lowest: if quit 6+ months ago
moderate: smoker if quit < 6mo ago
highest: smoker

35
Q 
LOW risk stratification for 
 fat % intake 
 dyslipidemia (LDL)
 cholesterol ratio
 triglycerides
A

diet includes 15-25% fat
LDL < 100 mg/dL,
cholesterol / HDL < 0.5
triglycerides < 100

36
Q 
MOD risk stratification for 
 fat % intake 
 dyslipidemia (LDL)
 cholesterol ratio
 triglycerides
A

diet includes 25.1-29% fat
LDL 100-129
cholesterol/ HDL 5.0-6.0
triglycerides 100-149

37
Q 
HIGH risk stratification for 
 fat % intake 
 dyslipidemia (LDL)
 cholesterol ratio
 triglycerides
A

diet inclues >30% fat
LDL > 130mg/ dL
cholesterol/ HDL >6
triglycerides > 150

38
Q

DM risk stratification (HbA1c (glycolated Hbg) and fasting blood glucose)
low
mod
high

A

lowest:
HbA1C 8% or
fasting blood glucose <180

39
Q

risk stratification for obesity (BMI)
low
mod
high

A

low: BMI < 25
mod: BMI 25.5-29.9
high: BMI > 30

40
Q

risk stratification for hypertension
low
mod
high

A

low: 120/ 80 (normal)
mod: 120-139/80 -89 (high normal)
high: > 140/ > 90 ( HTN stage I)

41
Q

risk stratification for sedentary lifestyle (kcals burned/ week)

A

low: >1500 kcal/wk
mod: 700-1499 kcal/ week
high < 700 kcal/ week

42
Q

risk stratification for depression
low
mod
high

A

low: no clinical depression
mod: mildly depressed
high: clinically depressed

43
Q

LOW risk for exercise events
functional capacity (in mets)
EF % at rest
anginal symptoms

A
  1. functional capacity > 7 mets
  2. EF% rest >50%
  3. and absence of any arrythmias or anginal symptoms
44
Q

MOD risk for exercise events
functional capacity (in mets)
EF % at rest
anginal symptoms

A
  1. functional capacity < 5 mets
  2. EF (rest) = 40 -49%
  3. angina or other symptoms
45
Q

HIGH risk for exercise events
functional capacity (in mets)
EF % at rest
anginal symptoms

A
  1. functional capacity < 3.5 mets
  2. EF (rest) < 40 %
  3. angina
    Hx heart atack
    abnormal hemodynamics during rest
46
Q 
Borg scale of perceived dypnea
 when to stop exercise on which scale and which scale
 0-10
 0-+4
 6-20
A

0-10- 6 = shortness of breath, hard breathing
0-+4 = +3 moderately severe, very uncomfortable
6-20 = 12-16, very hard breathing (start at 11- 13)

47
Q

evaluation of venous pressure
test
if late response
if early response

A

hang arm down veins will bulge. at heart level they flatten out.
if late= fluid overload
if early = dehydration

48
Q

pulses alterans
def
leads to
2 causes

A
  1. regular alteration in force of beats of pulse (weak follows strong, etc)
  2. leads to alternating stroke volume

2 causes
arrhythmia or LVD (left ventricular dysfunction)

49
Q

pulsus paradoxus
def
pathophysiology
3 conditions that can lead to it*

A

def- exaggerated decrease in pulse volume during inspiration and increase during exhalation

pathophysiology: from abnormally large decrease in SBP during inspiration

3 conditions that can lead to it:

  1. cardiac tompondae
  2. pericarditis
  3. obstructive lung disease (COPD or asthma)
50
Q

why do we see an abnormally large decrease in SBP during inspiration with pulsus paradoxus?

A

when we breathe in => increase intrathoracic pressure => compressing the inferior vena cava => decrease in preload

51
Q

asculation of heart sound- Bruits
what its caused by
sounds like..
what it means

A
  1. turbulence in arteries where they branch or where vessel is narrowed
  2. low -> med short loud -> soft sound which is unaffected by respiration
  3. means there is thinning in arterial wall, immobilize immediately** pt may bleed out
52
Q 
S1 heart sounds
 what is it
 whats happening in the heart
 where do i auscultate for it
 palpation
A
  1. defines onset of systole
  2. closure of M1 (mitral) and T1 (tricuspid) closure
  3. ascultate loudest over mitral valve (5th IC space, mid-clavicular)
  4. palpate- feel a lift in your hand =S1, as pulse pulls away = S2
53
Q 
S2 heart sounds
 what is it
 whats happening in the heart
 where do i auscultate for it
 physiological splitting S2 (when do you hear it)
A
  1. end of ventricular systole
  2. closure of A2 (aortic) and P2 (pulmonic) valves
  3. auscultate 2 IC space, l/R sternal border
  4. physiological splitting- heard at the end of inspiration
54
Q

S3
a.k.a.
caused by…

A

abnormal heart sounds

  1. ventricular gallop from 1 or both ventricles
  2. from lack of compliance in vessel => stiffness in valve secondary to ischemia
55
Q

S4
a.k.a.
caused by… (x2)
indicative of

A

abnormal heart sounds

  1. atrial gallop
  2. caused by vibrations created in ventricles as they expand in the second phase of rapid diastolic filling (when atria are contracting) which is caused by stiffness in valve, secondary to ischemia
  3. indicative of heart disease
56
Q

summation gallop

what is it/ why does it occur

A
  1. occurs when S3 and S4 sounds fuse, when HR > 120 (because diastole is so short)
57
Q

pericardial friction rub
caused by…
auscultated where?

A
  1. pts with inflammation of pericardial membrane or pleural sac
  2. auscultated over 3rd or 4th ICS at L sternal border
58
Q

heart murmurs
resultant of…
4 factors that produce murmurs

A

resultant from turbulent blood flow

4 factors:

  1. high rates of flow thru normal or abnormal valves
  2. forward flow thru constricted or irregular valve or into thin or dilated vessel
  3. backward flow thru incompent valve, septal defect or patent ductus arteriosus
  4. decreased viscosity => increased turbulance
59
Q

grading intenstiy of murmurs

I-VI

A

I: audible with concentration
II: faint, but heard immediately
III: not loud but > grade II
IV: loud, intermediate intensity, palpable thrill
V: v. loud, heard with edge of stethoscope against wall, palpable thrill
VI: heard w/o stethoscope, palpable thrill

60
Q 
total cholesterol/ HDL ratio
 men
 average risk
 2x average risk
 3x average risk

women
average risk
2x average risk
3x average risk

A

men:
5= average risk for CAD
9.55 = 2x average risk
23.39 = 3x average risk

women:

  1. 4 = average risk for CAD
  2. 05 = 2x average risk for CAD
  3. 04 = 3x for average risk
61
Q

what is considered elevated triglycerides?

A

150 mg/dL

associated with increase CHO ingestion

62
Q

Na electrolyte levels
average levels
what low/ high numbers cause
at what # do we see something bad? what do we see

A

135-145
low = hypotension, high = hypertension
180+ => at risk for seizures

63
Q

K normal levels

what happens if pt is out of normal levels?

A

3.5-5.0
significant cardiac arrhythmias on either end
- with end stage pts this can be life threatening

64
Q

Mg normal levels

what happens if pt is out of normal levels?

A

1.5-2.5
significant ventricular arrhythmias on either end
- with end stage pts this can be life threatening

65
Q 
cardiac catheterization pressure measurements
what is the test looking for?
 RA pressure
 PA pressure
 Lungs PCW (pulmonary capillary wedge)
 LA pressure
A

looking for plaque after:
heart attack, chest pain or after abnormal EKG

RA pressure = 0-8 = central venous pressure
PA pressure = 15-30/4-12
lungs pressure PCW: 1-10 (used during R sided heart surgery to represent LA pressure)
LA pressure = 1-10

66
Q

inotropic drugs
purpose
what we observe (2)

A
  1. purpose- increase ventricular contraction in failing heart
  2. decreases HR at rest and
  3. blunts HR response in exercise
67
Q

sympathetic amines (purpose)

A

work to increase release of Ca from SR (=> increase contractility)

68
Q

dopamine
low doses
high doses

A

low doses: increases BF to kidneys so they DONT retain fluid or cause vasoconstriction ==> increasing afterload

high doses: cause vasoconstriction => incrase in systemic resistance which sends all the blood to head and heart ** for people in shock*

69
Q

phosphodiesterase inhibitors

A

enhance Ca entry into cell => increase force of contraction

70
Q

IV b-type natriutretic peptide (BNP)

A

causes smooth muscle cell relaxation => decreased afterload

71
Q

ACE (angiotensin converting enzyme) inhibitors
what they do
possible side effects

A

stop angiotensin I => angiotension II (which causes increase in BV)
=> treat hypertension by decreasing arterial pressure

possible side effects- blunt exercise response, can lower BP too significantly

72
Q

Na-nitroprusside

A

potent dilators of both arteries and veins for ICU emergency settings to treat hypertension

73
Q

alpha adrenergic antagonists

A

vasodilation to treat hypertension

74
Q

calcium channel blockers

A

decrease afterload

75
Q

nitrates

A

vasodilation to treat hypertension

76
Q

beta blockers
what they do
possible side effects

A

decrease myocardial O2 demand by decreasing HR, BP, and contractility

blunt HR & BP exercise response so use Borg scale

77
Q

loop diuretics

A

acute pulmonary edema and heart failure

78
Q

lipid lowering drugs

A

statins

79
Q

what 3 drug categories can blunt exercise effects of HR and BP?
what do we do about it?

A
  1. inotropic drugs (increase contractility)
  2. beta blockers
  3. ACE inhibitors

we use Borg scale of perceived exertion

80
Q 
heart auscultation
AV        
PV        
tricuspid 
mitral
A

AV: 2nd IC space R sternal border
PV: 2nd IC space L sternal border
tricuspid : 4th IC space L sternal border (if enlarged heart, hear at 5th IC)
mitral: 5th IC space mid-clavicular

81
Q

3 types of drugs that affect Ca uptake/ release into SR (=> increased contraction)

A
  1. Inotropic
  2. sympathetic amines
  3. Phosphodiesterase inhibitors

year 2 (24 decks)

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