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CV PHAR 152 > HTN > Flashcards

HTN Flashcards

1
Q

What would happen if the cells in the SA node slowed down their frequency of depolarization over time?

A

they would have sick sinus

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2
Q

What are Sx of sick sinus?

A

dizziness
fatigue
low HR (42)
common in elderly

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3
Q

What is a treatment for sick sinus

A

pacemaker

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4
Q

more Ca entry =

A

stronger contraction
(inotropy/contractility)

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5
Q

faster Ca entry =

A

faster contraction
(chronotropy/HR)

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6
Q

Parts of ECG to look at

A

ST elevation
QT prolongation
QRS
QT prolongation

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7
Q

What is OBPM

A

in the office
attended for BP reading

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8
Q

What is AOBP

A

office automated (unattended)

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9
Q

What is ABPM?

A

Ambulatory BP monitoring

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10
Q

What is HBPM?

A

home BP monitoring

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11
Q

What to consider when taking BP?

A

conditions
timing
duration

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12
Q

Primary HTN

A

chronically increased BP results from multiple factors, no single factor predominates
also commonly associated with the metabolic syndrome

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13
Q

Secondary HTN

A

HTN is caused by significant dysfunction of a single system

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14
Q

Treatment resistance

A

usually defined as lack of BP control despite a combination of 3 HTN medications, one of which being a diuretic

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15
Q

What is masked HTN?

A

home will be high
office will be normal

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16
Q

What is white coat HTN?

A

office will be high
home will be normal

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17
Q

CV Risk Factors Non-Modifiable

A

Age > 55 years
Male
Family History of Premature CV

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18
Q

CV Risk Factors Modifiable

A

sedentary lifestyle
poor dietary habits
abdominal obesity
Dysglycemia
smoking
dyslipidemia
stress hypertension

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19
Q

HTN urgency

A

Situations where BP should be reduced within hours
BP ≥180 / ≥130 AND
papilledema or other target organ changes

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20
Q

HTN Emergency

A

Situations that require immediate BP reduction
E.g. hypertensive encephalopathy, intracranial bleed, unstable angina/MI, acute heart failure

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21
Q

Jugular venous pressure (JVP)

A

indirect assessment of right atrial pressure

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22
Q

Edema

A

swelling or accumulation of fluid in a tissue

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23
Q

How does BP increase from NSAIDs

A

inhibition of renal Pg production
lowers renal perfusion

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24
Q

How does BP increase from steroids

A

mineralocorticoid effects

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25
Q

How does BP increase from hormonal contraceptives

A

triggers angiotensinogen production from liver

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26
Q

How does BP increase from decongestants

A

SNS activity

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27
Q

How does BP increase from alcohol

A

in excess only. Impairs ADH + other mechanisms likely important

28
Q

Goal for HTN low risk

A

140/90

29
Q

Threshold for HTN low risk

A

160/100

30
Q

Goal for HTN moderate

A

140/90

31
Q

Threshold for HTN moderate

A

140/90

32
Q

Threshold for Diabetes mellitus

A

130/80

33
Q

Goal for diabetes mellitus

A

130/80

34
Q

Goal for high HTN

A

120

35
Q

Threshold for high HTN

A

130

36
Q

First line for uncomplicated

A

TZD
ACEI
ARB
long acting CCB

BB >60 years old

37
Q

How long until it should see full effect?

A

1 month

38
Q

How much will each med lower BP?

A

10/5

39
Q

What treatment resistance HTN?

A

3 antiHTN drugs used in combo
one of the drugs is diuretic
non adherence is ruled out

40
Q

Isolated Systolic HTN

A

stuff arteries do not accommodate systolic pressure
creates a high “pulse pressure” (SBP-DBP)

41
Q

What to use isolated systolic HTN?

A

TZD
ARB
long acting DHP CCB

42
Q

What is each of the diuretics best for?

A

TZD - best for BP reduction
Loop - best for fluid excretion
K sparring - K+ supplement

43
Q

What is a common consequence of diuretic therapy?

A

hypokalemia

44
Q

What is low K interpretation?

A

<3 –> always undesirable
3-3.5 -> usually treated
3.5-4 –> action may be taken

45
Q

Alternatives for Low K

A
  • general measures
    switch to another diuretic
    discontinue diuretic if K seriously low
    add K sparring drugs
    add K supplement
46
Q

Hyperkalemia

A

increase K is also potential cause of serious harm

47
Q

Patient factors associated with hyperkalemia

A

CrCl <60ml/min
Baseline K>4.5 mmol/L

48
Q

First line for Diabetes and HTN

A

ACEi or ARBs

without renal - ACEi, DHP CCB or TZD

49
Q

CKD with diabetes

A

ACEi or ARBs

50
Q

CKD

A

ACEi
adding diuretics

51
Q

HTN Pregnancy

A

labetalol
methyldopa

clonidine
hydralazine

52
Q

Pre-eclampsia

A

high BP with proteinuria
after 20 weeks

53
Q

Gestational HTN

A

high BP without proteinuria after 20 weeks

54
Q

Chronic HTN and pregnancy

A

HTN was present before pregnancy began

55
Q

What are the 3 main vasodilators classes?

A

Alpha blockers
DHP calcium channel blockers
smooth muscle relaxants

56
Q

When combining HTN drugs list them in the two categories?

A

TZD or DHP CCB

BB
ARB
ACEi

57
Q

When should ACEi and ARBs be used in CKD

A

they should be used near the end
they work better the worst the pt is

58
Q

What does the HOPE trial show?

A

Showed that ACEi has cardio protection

59
Q

What is first line for Vasodilators in uncomplicated HTN

A

DHP CCB

60
Q

ACEi in HTN and CV disease

A

Most pt at high risk for CV events are put onto ACEi even if their BP is normal

61
Q

What does accomplish trial show?

A

showed the ACEi have cough
fluid retention is dangerous

62
Q

What does SPRINT trial show?

A

BP meds help lower the risk for life threatening events

63
Q

What does RENAAL trial show?

A

ARB can help protect the kidney
works better on worst CKD at baseline

64
Q

What does IDNT trial show?

A

ARB can help protect the kidney
works better on worst CKD at baseline

65
Q

What to monitor for ACEi or ARBs?

A

Kidney function -> renal harm is possible from the drugs
lowering glomerulus pressure can be bad for the kidney too

66
Q

What should happen to monitor for renal safety for ACEi and ARBs?

A

obtain SCr and K within 1-2 wks
should not be less than 20-25% changes
BP and edema should get better not worst

67
Q

What should be monitored for all BP drugs?

A

Dizziness/headache/hypotension
orthostatic hypotension
Erectile Dysfunction

CV PHAR 152 (4 decks)

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