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רהב לב > Midterm > Flashcards

Midterm Flashcards

1
Q

Cardiac Output equation

A

Q = HR X SV

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2
Q

What 4 factors influence cardiac output?

A

HR
Contractility
Preload
Afterload

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3
Q

VO2 Equation

what is absolute and relative VO2

A

VO2 = CO X (arterialO2-VenousO2)

relative is divided by LBM

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4
Q

MVO2
-what is it
-what is it correlated with
-

A
  • cardiac oxygen consumption

- highly correlated with RPP and with heart rate

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5
Q

RPP Equation

A

SBP X HR

if does not increase with work then risk of ischmeia

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6
Q

Pulse Pressure

-what makes it increase and decrease

A

PP = SBP - DBP

minimal difference we want is 20!!!

Exercise: PP should increase where there is a larger difference as SBP increases and DBP does not

-Narrow: SBP not increasing, DBP comes up since not enough volume to pump-tamponode

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7
Q

Heart Rate

A

speed at which the heart is beating

to increase CO, HR increases (SV is limiting factor)

60 bpm: 1/3 systole, 2/3 diastole

120bpm: 1/2 systole, 1/2 diastole
180bpm: 2/3 systole 1/3 diastole

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8
Q

Contractility

A
  • ionotropic effect
  • ability of heart to contract depends on sarcoplasmic reticulum releasing/pulling back calcium so the heart can contract and relax

impact SV (and thus CO)

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9
Q

Preload

A

ventricular end-diastolic volume or pressure

Increased preload increases stroke volume, whereas decreased preload decreases stroke volume by altering the force of contraction of the cardiac muscle.

impact SV (and thus CO)

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10
Q

Afterload

A

“load” that the heart must eject blood against

–decreases with diuretics, BP lowering medications,

impact SV (and thus CO)

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11
Q

Poor activity tolerance with what part of heart?

A

Right ventricle because it sends blood to the pulmonary system to get oxygen

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12
Q

Dysarythmia with what part of heart?

A

Left ventricle

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13
Q

Atherosclerosis Process

A
  1. Fatty Streaks: foam cells, lipid in machrophages
  2. fibrous plaque: advanced lesions, can project into lumen, can reduce BF, intimal layer most affected. Damaged endothelium cannot send signaling ie NO, tissue factors, heparin. Debris of cholesterol + foam cells + lipid –>under the smooth muscle
  3. fibrous cap: extracellular connective tissue embedded in smoothe muscle cells
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14
Q

Complicated Lesions in Atherosclerosis (5)

A

Calcification: cannot dilate, can break

Rupture of Fibrous Plaque: thrombosis

Hemorrhage: hematoma will narrow lumen, bld clot

Embolization: fragment can cause stroke, PE, MI

Weaken of Vessel Wall: ruptured vessel

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15
Q

Role of Endothelial Wall (4)

A
  1. Barrier that contains circulating blood in the lumen
  2. resists formation of clots due to antithrombotic surface molecules
  3. secretes vasoactive substances that change contraction of smooth muscle in medial layer of the vessel wall
  4. inhibit smooth muscle cell migration and proliferation
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16
Q

modified response to injury

A
  1. endothelial cells injured–>atherosclerosis
  2. endothelial wall integrity needed to prevent clots forming on surface/ vessel dilation /prevent smooth muscle migration
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17
Q

injury to endothelial cell (5)

A
  1. increase permeability to endothelial layer
  2. antithrombotic properties lost
  3. reduced secretion of vasodilators
  4. secretion of mitogenic substances–smooth muscle goes into intima
  5. secretion of chemotactic factors to attract cells to intima (monocytes)
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18
Q

Cardiac Risk Factors

  1. Modifiable
  2. Unmodifiable
A
  1. tobacco, smoking, HTN, Dyslipidemias, Diabetes, Obesity, Sedentary Lifestyle, Stress, Depression
  2. age, gender, family history
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19
Q

Dyslipidemias
Cholesterol
LDL
HDL

Cardiac Ratio

A

Cholesterol: 40mg/dl
if above 60mg/dl, it is a negative risk factor

Cardiac Ratio:
total cholesterol / HDL
Men: 5.0
Women: 4.4

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20
Q

Smoking

who is a smoker
what causes the risk
what is the relative risk

A

risk of coronary heart disease gone if stop smoking for 6 months or longer since lose adhesive properties, but still other effects

RR: 1.35-2.4 in smokers, 1.43-3.5 heavy smokers

  • decreased HDL
  • stimulate SNS
  • CO displaces O2 on hemoglobin
  • platelets more adhesive
  • endothelial dysfunction
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21
Q

HTN

Normal:

High Normal:

Stage 1:

Stage 2

Stage 3:

Stage 4:

A

Do not exercise if:
DBP > 1110
SBP > 200

Stop exercise if
DBP >110
SBP > 250

Normal: 120-129/80-84

High Normal: 130-139/85-89

Stage 1: 140-159/90-99

Stage 2: 160-179/100-109

Stage 3: 180-199/110-114

Stage 4: > 200/ > 115

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22
Q

Diabetes
Hemaglobin A1c:
Non fasting Glu:
Fasting Glu:

Diagnosed as:
non fasting glu:
fasting glu

do not exercise if:
fingerstick

check for ketones in urine if:
fingerstick

A

Hemaglobin A1c: 5-7
Non fasting Glu: 70-110
Fasting Glu: 125
fasting glu >110

do not exercise if:
fingerstick >300mg/dl

check for ketones in urine if:
fingerstick >260 mg/dl

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23
Q

Obesity

A

20% above ideal body weight increases risk of heart disease

BMI in kg/m squared

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24
Q

Sedentary

A

exercise increase HDL, decrease BP in HTN, normalize blood glucose, increase fibrin breakdown, decrease platelet aggregation

Not sedentary: 30 minutes of moderate intensity most days of the week

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25
Q

Stress

A 
related to platelet activation
increases catecholamines (and we see more platelet secreted proteins)
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26
Q

Age

A

> 65

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27
Q

Gender

A

male

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28
Q

Family History

A

If a first-degree male relative (e.g. father, brother) has suffered a heart attack before the age of 55, or if a first-degree female relative has suffered one before the age of 65, you are at greater risk of developing heart disease.

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29
Q

BP
Do not exercise if:
DBP >
SBP >

Stop exercise if
DBP >
SBP >

A

Do not exercise if:
DBP > 110
SBP > 200

Stop exercise if
DBP >110
SBP > 250

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

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30
Q

Homocysteinemia

A

AA correlated with MI

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31
Q

Angina Pectoris

A

ischemic heart disease (lack O2 to heart muscle)

“Strangling in chest”

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32
Q

Stable Angina

A

chronic pattern of transient chest pain–happens with exercise, emotional upset, eating–relieve in a few minutes by resting

33
Q

Unstable Angina

A

pattern of increased frequency and duration of anginal episodes

produced by less exertion or may occur at rest

high frequency can progress to MI if left UNTREATED
-emergent situation, send to cardiologist to manage

34
Q

Variant Angina

A

at rest get anginal symptoms but not ischemia to myocardium–> it is instead due to
CORONARY ARTERY VASOSPASM

tx Beta blockes (has ST elevation during episodes)

35
Q

MVO2 Supply and Demand

A

Supply O2:
1. diastole perfusion pressure

  1. coronary vascular resistance– external compression, intrinsic regulation, neural innervation
  2. O2 carrying capacity

Demand:

  1. wall tension increases
  2. HR
  3. Contractility
36
Q

Myocardial O2 Supply

A

diastolic perfusion pressure
coronary vascular resistance
O2 carrying capacity

37
Q

Myocardial O2 Demand

A

Wall tension
HR
Contractility

38
Q

Process to ischemia, when does vessel need to be fully dilated to achieve adequate perfusion?

A

stenosed by 70%

if stenosed 90% probably cannot get enough O2 to meet basal requirements and see ischemia and asynchrony

39
Q

Silent Ischemia

A

no sx but can be seen on EKG
myocardial ischemia
(common in DM)

40
Q

Syndrome X

A

angina sx but no evidence of coronary artery disease (some show CAD on exercise tolerance test)

41
Q

MI

A

myocardial infarction

prolonged ischemia causes condition of irreversible necrosis of the heart muscle

42
Q

Transmural MI

  • EKG findings and reasoning
  • when more likely to die
A

Q Wave MI
ST Elevation MI

–span thickness of myocardium bc of prolonged occlusion of epicardial coronary artery

–wide Q wave forever life (signal need to go around the dead tissue)

-initial hospital mortality is higher–sudden change in ability for heart to pump–then

43
Q

Subendocardial MI

  • EKG findings and reasoning
  • when more likely to die
A

Non Q Wave MI
NON ST Elevation MI

-involves only innermost myocardium (farthest from blood supply, greatest risk of ischemia here as wall tension develops)

do not have Q wave widen because can still travel on surface

–less die in hospital but more likely to have mortality post hospital

44
Q

Tx Given for Ischemic Heart DIisease

A

NOAM

  • nitrates: decr afterload to help BF
  • oxygen: so not ischemic
  • aspirin: decr platelet agr
  • morphine: pain so not incr BP

B-blockers
ACE Inhibitors
(thrombolytic therapy)

45
Q

Interventions for Ischemia:
cardiology
surgical

A 
PTCA (percutaneous coronary angioplasty: balloon)
Intracoronary Stent
Rotablader (Ca plaque)
Impella (propellar)
Aortic Valve replace

CABG: coronary artery bypass graft (laminal to head instead of pulsitile, cause cogn issues)

off pump CAB: on beating heart

46
Q

Primary Mitral Valve Regurgitation

A

disruption mitral valve annulus, leaflet, cordae tendinae, papillary muscle (blood ventricle –> atrium)

47
Q

Secondary Mitral Valve Regurgitation

A

disease causes ventricle dilate and malalignment or dysfunction papillary

48
Q

Mitral Valve Prolapse

A

leaflet buckles into left atrium during systole and not pulled taut (becomes regurgitation eventually)

49
Q

Acute vs. Chronic Mitral Valve Regurgitation

A

acute: rupture chordae tendinae suddenly overwhelms L atrium and high fatal
chronic: congenital

50
Q

mitral valve replace vs repair

A

replace: mechanical lasts longer than tissue but tissue need to take anticoagulants
repair: sutured
annuloplasty: annulorepair

51
Q

Aortic Stenosis

A

Narrow aortic valve–most common valve to replace caused by congenital endocarditis, aortic dissection, HTN, trauma…

CHF because low CO
Syncope: lose consioussness

prosthetic valves:

bioprosthesis: low risk, only 10 yrs
mechanical: need to take anticoagulants but last more than 10 years

52
Q

elevated TG

A

150mg/d

53
Q

Prothrombin time

A

look if someone on coumadin or warfarin (note diet effects)

11.8-15.0 seconds

therapeutic for DVT/PE if it is 1.5 X 2 of the reference range to prevent clot

anticoagulation levels

54
Q

Partial Prothrombin Time

A

for heparin (IV and low MW)

21.7-34 seconds
therapeutic for DVT/PE if it is 1.5 X 2 of the reference range to prevent clot

anticoagulation levels

55
Q

why draw labs q6-8 hrs on regular IV heparin?

A

check that reference range 68 seconds because not absorbed uniformly as low MW heparin is

56
Q

INR

A

international normalized ration

to compare anticoagulation levels across institutions

INR of 1 is a 1 normal solution (so x2 is 2)

57
Q

Electrolyte Levels

Sodium
Potassium
Magnesium

BUN

creatinine

BUN/Cr

A

Sodium: 135-145

Potassium: 3.5-5.0

Magnesium: 1.2-2.5

BUN: 10-30 (if elevated, nonvolitile acids cause altered mental status)

creatinine: 0.6-1.6

abnormal BUN/Cr >15

58
Q

blood glucose levels
normal
contraindicate exercise
risk of ketoacidosis

A

normal: 70-110

contraindicate exercise >300mg/dl

risk of keto-acidosis >400

59
Q

Pressure Measures

  1. RA
  2. RV
  3. PA
  4. Wedge
  5. LV
  6. LA
A

RA pressure: 0-8mmhg

RV: 15-30/0-8

PA: 15-30/4-12

Pulmonary Capillary Wedge: 1-10

LA: 1-10

LV: 100-140/3-12

aorta: 100-140/60-90

60
Q

*Right Atrial Pressure

what are we worried about if low/high

A

0-8mmHg

Low: decrease preload, BLEEDING or lost volume (hypovolemic)

High: FLUID overload to R side of heart: head doesnt drain well, liver enlarge

61
Q

*Pulmonary Artery Pressure

which sided heart failure

A

Systole: 15-30
Diastole: 4-12

high: pulmonary HTN, RIGHT SIDED HEART FAILURE (cannot get blood to lungs)

62
Q

*Pulmonary Capillary Wedge Pressure

which sided heart failure

A

1-10

high: LEFT sided HEART FAILURE
if 12 and above

pressure measured by wedging a pulmonary catheter with an inflated balloon into a small pulmonary arterial branch

balloon to take pressure
indirect measure of the left atrial pressure.

63
Q

Fick method: Measure BF or CO

equation

A

based on the fact that:

VO2 = CO x (arterial O2 - venois O2)

CO = VO2 / (arterial O2 - venois O2)

64
Q

Pulmonary Vascular Resistance Equation

A

PVR = (MPAP - LAP/CO) X 80

mean pulmonary arterial pressure

mean left atrial pressure

cardiac output

65
Q

Systemic Vascular Resistance

A

evidence of afterload

SVR = (MAP-RAP/CO) X 80

mean arterial pressure
mean right atrial pressure
cardiac output

66
Q

dipyridamole

A

dipyridamole is a pharmacological success, but a therapeutic failure because of the coronary steal phenomenon.

an alteration of circulation patterns lead to a reduction in the blood directed to the coronary circulation

Coronary steal is also the mechanism in most drug-based cardiac stress tests; When a patient is incapable of doing physical activity they are given a vasodilator that produces a “cardiac steal syndrome” as a diagnostic procedure. The test result is positive if the patient’s symptoms reappear or if ECG alterations are seen.

67
Q

anuerism

A

“dilation”, from, aneurynein, “to dilate”) is a localized, blood-filled balloon-like bulge in the wall of a blood vessel.

if aorta can erode into vertebral bodies and get back pain

68
Q

dissection

A

endothelial layer splits from medial layer–makes a channel–if acute is lethal

69
Q

Bioavailablity:

A

how much will be available to target tissue when it gets there

70
Q

Distribution:

A

general or restricted, depending on ability of drug to traverse cell membranes (BBB corss)

71
Q

Clearance

A

rate of elimination of drug by all routes relative to concentration of the drug in any biological fluid:
A. Kidney
B. Liver
C. Pulmonary
D. But some patients with organ failure may not clear the drugs as rapidly, doses can become toxic more easily

72
Q

Half-Life:

A

the time takes for the plasma concentration of the drug to be reduced by 50%. The longer the half life, the longer the action of the drug.
A. If has short half life, and the patient has continuous infusion pack that is failing, the drug will metabolize out of the pt quickly.

73
Q

Inotropic drugs:

A

drugs used to increase the force of the ventricular contraction when the myocardial systolic function is impaired. Thought to work by increasing the intracellular calcium concentration.

Improving contractiility

74
Q

Beta Blockers

A

A. Blunt HR and BP response at rest and with exercise
B. Contraindicated for the pulmonary population, especially with asthma
i. Adrenergic blockers potentially exacerbate someone asthmatic and can precipitate intubation because they are beta adrenergic blockers so they are blocking the adrenaline response:
ii. Blocks the bronchodilation response resulting in bronchospasm
C. Effect both beta receptors even though supposed to be selective – may be specific or non specific
D. They decrease O2 demand of the heart: decrease HR, decrease BP and to some extent decrease the contractility
E. Standard of care in cardiac patients. Seen routinely given for patients with heart failure because they decrease O2 demand.
i. Not all heart failure patients tolerate this well since it lowers blood pressure
ii. Try to keep systemic BP low because do not want to have an added afterload for the heart
iii. Do not give a beta blocker to someone with low blood pressure already
F. Decrease myocardial O2 demand by decreasing HR, BP, and contractility

75
Q

Toxicity/Side effects of beta blockers:

A

i. fatigue is found with taking beta blockers in some patients
ii. bronchospasm: non selective agents can worsen pulmonary condition, bronchospasm in asthmatic
iii. conduction blocks: lowered contractility and pressure: perfusion pressure to coronaries drops
iv. vasospasm: in someone with peripheral vascular disease can precipitate arterial vasospasm in persons with PVD
v. abrupt withdrawal causes upregulation of receptors and cause reflex tachycardia
1. If there is not activity on a receptor may get up-regulation of the receptors and get reflex tachycardia
vi. If heart rate below 40 is a toxic effect (bradicardiac, call doctor, nt enough blood flow for tissue metabolism), will lower the cardiac output (even though lowering O2 demand, this would be a bad outcome of beta blocker toxicity)
vii. Cholesterol: Reduces HDL, elevate triglycerides because of tissue metabolism effects—may need cholesterol reducing medications
viii. Younger patients may have some HR response, in geriatric see almost no response in the heart rate change when exercise. Measure values on BORG to see what is ok when exercise to see how difficult something is for them in exercise.

76
Q

ACE Inhibitors

A

A. Angiotensin converting enzyme is inhibited preventing the conversion of angiotensinI to angiotensinII
B. Can blunt HR and BP response in some but not in others
C. One of the biggest issues is that pts develop is in changing position, sit to stand, should do it slowly
D. Toxicity not very common
E. Side effects: hypotension, hyperkalemia, renal insufficiency ((metabolized through kidneys so if kidney failing take off it), cough (nonproductive cough)

77
Q

Sodium Nitroprusside:

A

has a quick effect, used in someone who already has failing organs so half life may vary
A potent dilator of both arteries and veins used to treat hypertensive emergencies

78
Q

Beta Agonists:

Bronchodilators

  • epinephrine
  • albuterol
A

a. Non selective beta agonists:

Epinephrine: causes bronchodiltion but drive up heart rate rapidly, so in a cardiac patient the increased HR can drive up O2 demand (given in case of asthmatic attack)—first line in asthma attack

Beta 2 agonists: rescue inhaler

Albuterol: for asthma attack bronchodilation but HR elevation can drive up O2 demand

i. Note: Beta 1 receptors primary in cardiac
ii. Note: Beta 2 receptors primary in pulmonary

79
Q

Bronchodilator, Anti-cholenergic medications: Atrovent

-atrovent

A

Atrovent: bronchodilation

i. nebulizer treatment or meter dose inhaler
ii. meter dose inhaler should be given as open mouth technique and not put directly into mouth and goes to back of the throat and not to the lungs, held a space of 4-5 inches away, inhale and hold for 10 seconds. If patient has a hard time then can be given spacers and inhale the medication that way

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