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KC Cardio Module-1 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

HTN increases the RR 2-4 fold for developing:

A
  • CAD
  • HF
  • Stroke
  • AF
  • CKD
  • PAD
  • dementias (vascular/AD)
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2
Q

HTN in general can shorten one’s lifespan an average of __________

A

5 years

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3
Q

HTN risk factors (9)

A

1- advancing age
2- genetics: 2x as common in people w/ 1-2 first degree relatives
3- DM and dyslipidemia
4- AA (more severe and 10+ years earlier than whites)
5- CKD: higher staging—> more difficulty controlling HTN
6- etoh: >2 drinks/day on average
7- high sodium diet: >3gm/day
8- lifestyle: sedentary lifestyle and weight gain
9- personality traits (hostile, impatient, depressed)

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4
Q

Minimal diastolic pressure:

A

70-80 mmHg

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5
Q

Maximum systolic pressure:

A

110-120 mmHg

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6
Q

Lowest risk of CV and renal complications associated with a BP of:

A

115/75

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7
Q

Regulation of normal BP is dependent upon:

A

Cardiac output: sodium intake, renal fx, mineralcorticoids

Peripheral vascular resistance: dependent upon the SNS, humoral factors, and local vasculature autoregulation

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8
Q

MAP calculation and goal:

A

Goal: >70 mmHg
Calculation: (DBP*2)+SBP/3

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9
Q

Heart Failure Drug line tx:

A

1- ace/arb
2- beta-blocker
3- thiazide
4- aldosterone antagonist

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10
Q

Post-MI drug line treatment:

A

1- Beta-blocker
2- Ace/arb
3- thiazide or CCB (this line not mandatory; one 1 and 2 required)

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11
Q

High coronary disease risk drug line treatment:

A

1- Beta-blocker
2- Ace/arb
3- thiazide or CCB

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12
Q

Diabetes drug line tx:

A

1- ace/arb
2- thiazide/CCB
*unless AA pt—> then put on thiazide/CCB 1st line

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13
Q

CKD drug line tx:

A

1- ace/arb
2- thiazide/CCB
*AA benefit from ace/arb first line over CCB/thiazide

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14
Q

Recurrent stroke prevention drug line tx:

A

1- ace/arb

2- thiazide/CCB

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15
Q

Factors that affect Cardiac output

A

Renal function
Mineralcorticoids
Sodium

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16
Q

Factors that affect peripheral vasculature:

A

Humoral
SNS
Local vasculature autoregulation

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17
Q

One measurement of BP w/ this value—> hypertension diagnosis and requires treatment

A

SBP>180

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18
Q

Blood pressure guidelines:

A
  • empty bladder
  • take 3 times B/L (throw out 1st one and average last 2; always take highest reading if disparity)
  • no caffeine or smoking 30 minutes prior
  • have pt sit for 5 minutes w/ feet flat of floor and back support
  • appropriate BP cuff size
  • can test orthostatic HTN in elderly adult—> rotating 1-3 mins after standing
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19
Q

Preferred BP measurements taken:

A

Automated 3-6x, unattended

—> eliminated white coat effect; increased BP reproducibility and accuracy

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20
Q

Normal BP

A

<120/<80

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21
Q

Prehypertension

A

120-139/80-89

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22
Q

Stage 1 HTN:

A

> 140-159/>90-99

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23
Q

Stake 2 HTN

A

> 160/>100

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24
Q

BP definitions only apply to adults:

A
  • not acutely ill

- not on BP meds

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25
Q

Hypertensive urgency

A

> 180/120 w/ no end organ damage

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26
Q

Hypertensive emergency

A

BP >180/120 w/ end organ damage

—> may rq neuro, renal, opthamology, or CV teams for acute organ damage

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27
Q

Acute end organ damage in hypertensive emergency may include:(12)

A 
Neuro: 4
- HTN encephalopathy
- CVA
- SAH/ICH
Cardio: 4
- aortic dissection
- acute pulmonary edema
- MI/Myocardial ischemia
- Acute left ventricular dysfunction 
Renal: 1
- acute renal failure/insufficiency 
Opth: 1 
- HTN retinopathy 
Others: 2
-preeclampsia
-microangiopathic hemolytic anemia
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28
Q

Screening guidelines:

A
  • anyone >18
  • preferred ambulatory monitoring prior to dx
  • likely beneficial for @ home measurements
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29
Q

Increased CV risk seen in

A
  • non-dippers
  • young w/ diastolic BP
  • adults and elderly w/ isolated systolic BP (normal diastolic and wider pulse pressures—> peripheral vasculature non-compliance)
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30
Q

AA patients and hypertension:

A
  • occurs at younger age
  • more severe HTN
  • more responsive to: sodium, obesity, and diet
  • 3-5x more likely—> end-stage kidney disease
  • MC w/ strokes and hypertensive KD
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31
Q

What is resistant HTN?

A

HTN >140/90 while on 3 meds including thiazide and BP wont decrease
MC w/ secondary

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32
Q

What are the 6 compelling indications for treating HTN?

A 
#1: HF
2- post MI
3- high CAD risk
4- DM
5- Recurrent stroke prevention
6- CKD
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33
Q

HF drug treatment line-up:

A 
1- ace/arb
2- beta blocker
3- diuretic
4- aldosterone antagonist
*want to get all on board; preferred low dose of all
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34
Q

Post-MI drug treatment line-up:

A

1- beta blocker
2- ace/arb
*try to get both on board

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35
Q

High CAD risk drug line-up:

A

1- beta blocker
2- ace/arb
3- CCB or thiazide
Do not need all on board if BP therapeutic

36
Q

Diabetes drug line-up:

A

1- ace/arb

2- CCB or thiazide

37
Q

Stroke drug line-up:

A

1- ace/arb

2- CCB or thiazide

38
Q

CKD drug line-up:

A

1- ace/arb

2- CCB or thiazide

39
Q

ACE,ARB,CCB can be used in:

A

Gout, urinary incontinence, SSRI rx, hyponatremia

40
Q

Thiazides, ace, arb, and CCB can be used in:

A

No gout, urinary incontinence, SSRI rx, hyponatremia

41
Q

Acceptable medications in pregnancy:

A
  • CCB, BB, or thiazides :)

- NEVER ACE/ARB

42
Q

Short term BP regulation:

A
  • neural control

- humoral control

43
Q

Long term BP control:

A
  • predominantly regulated by the kidney via widespread arteriole vasoconstriction and hydrostatic pressure
44
Q

Secondary HTN etiologies: (8)

A 
1- CKD (MC)
2- Polycystic kidney disease
3- Renovascular HTN (Renal artery stenosis)
4- Coarctation of the aorta
5- Thyroid dz (hypo- or hyper-)
6- Pheochromocytoma
7- Primary hyperaldosteronism
8- Meds
45
Q

Renovascular HTN seen in:

A
  • arteriosclerosis in old men w/ CAD RF’s

- women <50 w/ fibromuscular dysplasia

46
Q

Renovascular HTN w/u:

A

1- renal artery ultrasound
2- CT or MR angiography of renal vessels
3- invasive angiogram

47
Q

Consider Renovascular HTN if pt presents w/:

A
  • abdominal bruit
  • refractory HTN
  • recurrent flash pulmonary edema
  • AKI w/ initiation of ACE/ARB
48
Q

CKD w/u for secondary HTN:

A

Renal U/s: small shrunken kidneys

49
Q

Suspect CKD for secondary HTN if pt:

A

GFR >60 and proteinuria

50
Q

Polycystic kidney disease w/u for secondary HTN:

A
  • Renal U/S: large, cystic kidneys
51
Q

Coarctation of the aorta w/u for secondary HTN:

A

1- Screen test: Chest xray

2- Diagnostic test: CT of the chest w/ contrast

52
Q

Suspect Coarctation of the aorta if pt:

A
  • abdominal bruit
  • UE pulses stronger than LE pulses
  • rib notching on chest xray
53
Q

Thyroid disease w/u:

A

TSH to screen

54
Q

Pheochromocytoma dx:

A

1- Labs: urine metanephrine and vandyllamanilic acid levels

2- Adrenal CT or MRI w/ contrast

55
Q

Pheochromocytoma presents w/:

A
  • pallor, diaphoresis, paroxysms of HTN, palpitations
56
Q

Primary hyperaldosteronism presents w/:

A

metabolic alkalosis and persistent hypokalemia

- sxs: generalized weakness

57
Q

Primary hyperaldosteronism etiology:

A

adrenal adenoma or hyperplasia

58
Q

Meds contributing to secondary HTN:

A

E’s:

  • ethanol (chronic use is a major contributor to HTN)
  • eating black licorice
  • ephedrine/pseudoephedrine
  • exciting drugs: cocaine/meth
  • estrogens
59
Q

Natural Hx of HTN:

A

1- prehypertension: increased CO and BP
2- early HTN: increased PR
3- established HTN: vasculature remodeling and progressive damage
4- Complicated HTN: end organ damage

60
Q

Pathophysiology of essential HTN: (6)

A
  • Overactive SNS (overactive sympathetic tone leads to increased vascular tone and HTN)
  • Genetics (2x more likely)
  • Sodium intake (increased naturiesis)
  • Reduced adult nephron mass (genetic, fetal, and postnatal factors– hypoxia or malnutrition)
  • immunologic (renal infiltration of immune cells)
  • cardiac malformation (abnormal development of aortic elasticity and reduced development of the microvascular network in fetal life)
61
Q

Contributors to essential HTN: (9)

A

1- obesity (increased intravascular volume, increased CO, increased RAAS activation and increased sympathetic outflow)
2- Sleep apnea (increased oxygen is good)
3- Smoking (increases nor and CV RF)
4- alcohol (increases blood catecholamines)
5- exercise (aerobic in sedentary; active- aerobic may not benefit)
6- immune system activation
7- Polycythemia (increased viscosity)
8- Sodium (increased sodium and low potassium)
9- NSAIDs (inhibit prostacyclins and increase 5 mmHG)

62
Q

Chronic HTN leads to..

A

1- increased arterial wall stiffness
2- increased SBP’s
3- widened pulse pressures

63
Q

the vasculature remodeling associated w/ chronic HTN leads to:

A
  • decreased coronary perfusion pressures
  • increased myocardial oxygen consumption
  • LVH of myocytes
64
Q

Cardiac Pathophysiology of HTN:

A
  • myocardium structural changes (in response to increased afterloads)
  • hypertrophied cardiac myocytes
    1- diastolic dysfx: impaired passive relaxation of left ventricle secondary to hypertrophy
    2- leads to increased LV end-diastolic pressures
    3- leads to increased left atrial pressures
    4- systolic dysfx w/ LVH impinging on the heart cavity and limiting diastolic filling and SV
65
Q

Cardiac involvement in HTN manifests as: (6)

A
  • LVH/diastolic HF
  • systolic HF
  • left atrial enlargement
  • aortic root dilation and valve incompetance
  • atrial and ventricular arrhythmias
  • ischemic HD and cardiomyopathy
66
Q

LVH is associated w/:

A

increased risk of premature death and morbidity

67
Q

Patho of HTN in the CNS: w/ chronic HTN

A
  • cerebral autoregulation: to maintain constant cerebral blood flow
  • CNS adapts to elevated perfusion pressures via increased cerebral vascular resistance
  • decreases in blood flow induce cerebral ischemia
  • very dangerous to drop blood pressure rapidly, requires slow taper over weeks
68
Q

Patho of HTN in the CNS: w/ acute rise in BP

A
  • leads to hyperperfusion and increased cerebral blood flow

- causes increased ICP and cerebral edema (end organ damage)

69
Q

Patho of HTN in the Kidney:

A
  • chronic HTN damages small BV of kidney (endothelial cell dysfunction and impaired vasodilation)
  • impaired autoregulation of blood flow to glomerulus
  • intraglomerular pressure changes w/ SBP
  • volume expansion is the MAIN CAUSE of HTN in pts w/ glomerular dz
  • overactivation of the RAAS is the MAIN CAUSE of HTN in pts w/ vascular damage
  • Both are MAIN CAUSES of HTN in pts w/ chronic renal failure
70
Q

Renovascular HTN resultant of:

A
  • complete or partial occlusion of the renal artery

- + RAAS; hyper-reninemia; severe vasoconstriction and aldosterone release

71
Q

Renovascular HTN w/ one healthy kidney:

A

can handle sodium and water retention so volume does not contribute to HTN

72
Q

Renovascular HTN w/ significant CKD or one solitary, ischemic kidney:

A

volume contributes to HTN

73
Q

Screening for HTN rqs. asking about these events: hx and (6)

A

Hx: CAD/ACS, MI, revascularization

  • HF
  • PAD
  • sleep apnea
  • CKD
  • stroke/TIA
  • DM
74
Q

Screening for HTN rqs. end organ damage assessment:

A
  • eye: Retinopathy
  • Vasculature: PAD
  • CKD
  • brain: cerebral atrophy, dementia
  • heart: LVH, diastolic/systolic dysfx, wall motion abnormalities
75
Q

Assessment of pt’s CV risk status: (9)

A
  • tobacco use
  • LDL/HDL levels
  • DM
  • obesity
  • exercise?
  • age: >55 men/>65 for women
  • estimated GFR <60 (CKD stage 3)
  • microalbuminuria: spot urine ACR
  • Fam hx of premature CAD (>55 men/>65 for women)
76
Q

Secondary causes of HTN: (6)

A
  • OTC meds, OCs, etoh or illicit drugs
  • CKD
  • Pheochromocytoma
  • thyroid
  • sleep apnea
  • hyperaldosteronism
77
Q

Diagnostic w/u in HTN: (6)

A 
1- urinalysis
2- CBC
3- A1c or fasting blood glucose
4- Fasting Lipid panel
5- electrolytes
6- Baseline EKG
78
Q

Causes of drug-induced HTN: (12)

A 
Prescription drugs: (5)
- high dose OC's
- NSAIDs
- Pseudoephedrine
- migraine meds
- psych meds: SSNRIS, TCAs)
Situations w/ RX: (1)
- beta-blocker w/o an alpha-blocker first in tx: pheochromocytoma or cocaine-induced HTN
Foods: (2)
- ethanol
- sodium
Street drugs: (4)
- cocaine
- cocaine withdrawal
- St. John's wort
- narcotic withdrawal
79
Q

Screen for Secondary HTN:

A
  • new onset HTN <30 y.o.

- resistant HTN

80
Q

Screening for Secondary HTN rqs. and typical lab features include:

A
  • clinical suspicion

- hypokalemia, epigastric bruits, episodic HTN/flushing/palpitations, different BP in b/l arms

81
Q

Recommended BP goal in DM and CKD:

A

<130/80

82
Q

Recommended BP goal w/ age >80:

A

<150/90

83
Q

Recommended BP goal in general population:

A

<140/90

84
Q

In diagnosing HTN: Visit #1

A

BP>180/110=HTN
BP<140/90= pt is fine!
BP= 140-180/90-110; requires out of office assessment

85
Q

Out of office assessment for HTN f/u prefers:

A

1- Ambulatory BP monitoring
2- home BP monitoring
3- 3 f/u visits over 1 month

86
Q

Describe BP monitoring over 3 f/u visits over 1 month:

A

*only if ABPM and HBPM not available
Visit A: SBP>140 or DBP>90 then go to..
Visit B: SBP>160 or DBP>100–> dx HTN; if <160/100 then go to..
Visit C: SBP>140 or DBP>90–> dx HTN; if <140/90, no HTN!

87
Q

In diagnosing HTN: Visit #2

A
  • daytime ABPM or HBPM: >135/85 or ABPM (night) >130/80

- also if HTN 3 f/u visits w/ average BP>140/90

KC Cardio Module-1 (7 decks)

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