HTN Crisis - DUNN

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107 Terms

1
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What organ’s blood flow is sacrificed first in hypertensive crisis?

cerebral blood flow is sacrificed first

2
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Which organ is often the first to show damage in hypertensive crisis?

the kidney are the first to go

3
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What role does diastolic blood pressure (DBP) and systolic blood pressure (SBP) play in cerebral perfusion?

cerebral blood flow depends on mean arterial pressure, which is influenced by DBP, SBP, and time in diastole

4
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What antihypertensive is called a “repeat offender” in hypertensive crisis due to rebound hypertension?

clonidine is a repeat offender for reflex/rebound hypertension

5
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What is the first question to ask about a patient’s blood pressure in crisis?

ask what their normal BP usually is

6
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What symptoms should be specifically checked in a hypertensive crisis?

current symptoms, especially vision changes 

7
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What should be reviewed about the patient’s medications?

prescribed meds, compliance, OTC drugs, and herbals

8
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What should always be screened for in patient history during hypertensive crisis evaluation?

recreational drug use

9
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Which class of antidepressants may contribute to hypertensive crisis?

SNRIs (serotonin-norepinephrine reuptake inhibitors)

10
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What blood pressure level defines Stage 2 hypertension in the notes?

greater than or equal to 140/90 mmHg

11
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Where is Stage 2 hypertension often encountered?

outpatient settings

12
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What example BP is given in the notes for hypertensive crisis?

203/0 mmHg

13
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What should be considered if a patient is already on antihypertensive meds but presents with severe hypertension?

poor adherence, drug resistance, or secondary cause of hypertension

14
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What route of administration is recommended for acute hypertensive crisis?

parenteral therapy with continous tiratable IV infusion

15
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Which IV drug should not be used for hypertensive emergencies?

enalaprilat should not be used

16
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Why are continuous IV infusions preferred over bolus therapy in hypertensive crisis?

they allow tirtration to safely reduce BP without overshooting

17
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Which patients should avoid β-blockers during hypertensive crisis?

patients with bronchospastic airways disease

18
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What is the specific indication for β-blocker use in hypertensive emergencies?

only for rate control not ischemia management

19
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Which type of calcium channel blockers are highlighted in the hypertensive crisis notes?

dihydropyridine calcium channel blockers

20
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What comorbidity is specifically noted in relation to antihypertensive choice in crisis?

kidney failure (important consideraiton for drug selection)

21
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Which type of calcium channel blockers are highlighted in the hypertensive crisis “Sacrificed first” note refers to cerebral perfusion

brain is highly vulnerable to BP changes

22
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“Ser kidneys first to go” indicates

renal injury is an early complication

23
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Clonidine note:

commonly cause rebound hypertension if stopped suddenly or misused 

24
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Evaluation emphasis

always ask baseline BP, assess complinance, check OTC/herbals (like decongestant) and screen recreational drugs (cocaine, amphetamine, etc)

25
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Parenteral titratable infusions

are the standard of care for emergencies (nicardipine, clevidipine, nitroprusside, nitroglycerin, esmolol, labetalol)

26
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Enalaprilat (IV ACE inhibitor)

is specifically not recommended due to slow onset and unpredictable effects

27
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β-blockers

should be avoided in asthma/COPD, labetalol and esomolol maybe be used selectively. not for MI/ischemia in acute setitng.. mainly for HR control

28
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Calcium channel blockers

dihydropyridine (nicardipine, clevidipine) are preffered for rapid tirtration

29
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Kidney failure

drug clearance and renal perfusion are critical factors in crisis management 

30
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What is a hypertensive crisis?

a severe elevation in blood pressure that requires urgent or emergent medical attention

31
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What are the two major categories of hypertensive crisis?

hypertensive urgency (very high BP without acute target organ damage) and hypertenive emergency (very high BP with acute target organ damage)

32
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Which three pressure parameters are critical for cerebral blood flow regulation?

diastolic blood pressure, systolic blood pressure, and mean arterial pressure 

33
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Why is time spent in diastole important for cerebral blood flow?

because cerebral perfusion occurs largely during diastole, and prolonged uncontrolled HTN disrupts autoregulation

34
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What happens once cerebral autoregulation is exceeded?

risk of hypertensive encephalopathy, ischemia, or hemorrhage

35
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Which organs are most vulnerable in hypertensive crisis

kidneys (first to go), brain (vision changes, confusion, stroke-like symptoms), and heart/vasculature (LV strain, MI, dissection)

36
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What baseline should always be established in hypertensive crisis?

the patient’s usual or normal BP

37
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What neurologic symptoms may suggest hypertensive crisis?

vision changes, confusion, headache, seizures

38
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What cardiac symptoms should be checked?

chest pain and palpitations 

39
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What pulmonary symptom is important in assessment?

shortness of breath

40
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What common cause of hypertensive crisis is related to medications?

missed doses/non-adherenece

41
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Which OTC and herbal medications may trigger crisis?

decongestant, NSAIDs, stimulants

42
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Which recreational drugs are potent triggers of hypertensive crisis?

cocaine, amphetamines, MDMA

43
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Which antihypertensive drug is known as a “repeat offender” in hypertensive crisis?

clonidine due to rebound hypertension when abruptly stopped

44
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Which antidepressant class may increase BP and cause crisis?

SNRIs such as venlafaxine and duloxetine, especially at higher dose 

45
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List other agents that may induce hypertensive crisis.

stimulants, cocaine, amphetamine, decongestant

46
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What BP defines Stage 2 hypertension?

greater than or equal to 140/90 mmHg

47
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What BP levels are often seen in urgency or emergency?

SBP > 180 and/or BDP >120 mmHg

48
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What is the key factor distinguishing urgency from emergency?

presence or absence of acute target organ damage

49
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How is hypertensive urgency typically managed?

oral antihypertensive, gradual BP lowering over 24-48 hours, outpatient/ER follow up

50
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How is hypertensive emergency managed?

hospital admission with continous IV tiratable antihypertensives

51
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Why is enalaprilat not appropriate in hypertensive emergencies?

too long-acting and unpredictable

52
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What type of antihypertensives are preferred in emergencies?

continous, tirtatable IV infusions

53
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Which drugs should be avoided in hypertensive emergency?

enalaprilat (unpredictable, long-acting) and short-acting nifedipine (rapid BP drop which leads to ischemia)

54
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Which patients should not receive β-blockers?

those with broncospatic airway disease (asthma, COPD)

55
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What is the role of β-blockers in hypertensive emergencies?

used only for rate control (aotric dissection, tachyarrythmias)

56
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Why must drug selection be cautious in renal failure?

some vasodilators worsen kidney function; renally cleared drugs can accumualtes

57
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What organ is often the first to be damaged in hypertensive crisis?

kidney

58
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Why is clonidine a common culprit in hypertensive crisis?

some withdrawal cause rebound hypertension

59
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Why is compliance check critical in hypertensive crisis assessment?

non-adherence is one of the most common cause of crisis

60
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When is outpatient management appropriate?

only for urgenecy (not emergency)

61
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What type of therapy should never be used in emergencies?

long-acting one shot oral drugsWhat determines classification of crisis: BP numbers or organ damage? 

62
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What determines classification of crisis: BP numbers or organ damage?

end organ damage

63
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Which two organs are most vulnerable early in hypertensive crisis?

kidneys and brain

64
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Which medication withdrawal is a common cause of crisis?

clonidine

65
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Which drug classes/substances must always be considered as causes?

SNRIs, stimulants, illicit drugs, NSAIDs

66
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What is the gold-standard therapy for hypertensive emergency?

IV titratable antihypertensive

67
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How does severe hypertension (“urgency”) present?

marked BP elevation without processing target-organ damage; develops over delays weeks; managed with oral meds 

68
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How does hypertensive emergency present?

marked BP elevation with acute end-organ damage; develop rapidly (hours-days); requires immediate IV therapy

69
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Why must BP reduction be cautious in chronic hypertension patients?

their cerebral autoregulation curve is shifted upward; rapid lowering can cause hypoperfusion

70
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What is the general principle of BP reduction in emergencies?

lower BP enough to stop organ damage but avoid excessive rapid drops 

71
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What is the BP goal in aortic dissection?

reduce SBP to < 120 mmHg within 20 minutes

72
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What is the first-line drug class in aortic dissection?

beta blockers to reduce shear stress

73
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What are BP goals in acute ischemic stroke?

if candidate for thrombolysis, keeps BP < 185/110; otherwise avoid excessive lowering 

74
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How should BP be managed in hemorrhagic stroke?

lower cautiously, avoid drugs that raise intracranial pressure

75
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What therapy is used in acute pulmonary edema with systolic dysfunction?

vasodilators (nitrorpusside, nitroglycerin) + diuretics

76
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How should severe hypertension without organ damage be treated?

gradual reduction with oral therapy over hours-days 

77
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What is the MOA of nicardipine?

DPH calcium channel blocker, arterial vasodilaiton

78
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What are nicardipine’s key features?

onset 5-10 minute, long duration; side effect include reflex tachycardia, flushing, edema

79
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What is the MOA of clevidipine?

ultra-short acting DHP CCB

80
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What are clevidipine’s unique cautions?

lipid emulsion (avoid in soy/egg allergy or lipid metabolism disorder); very short onset/offset

81
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What is labetalol’s MOA?

alpha 1 and nonselective Beta-blocker leads to decrease resistance and HR

82
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When is labetalol especially useful?

emergencies including pregnancy and stroke

83
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What are labetalol’s side effects?

bradycardia, bronchospasm, heart block

84
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What is esmolol’s profile?

short-acting B1-selective blockers; half-life minutes; easily tirtratable

85
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What are esmolol’s adverse effects?

bradycardia, heart block

86
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What is sodium nitroprusside’s MOA?

potent arterial and venous vasodilator; immediate onset

87
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What are risks with nitroprusside?

cyanide/thicyanate toxicity (esp.renal/hepatic dsyfunction) increased ICP

88
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What is nitroglycerin’s primary effect?

predominantly venodilator —> reduces preload; best for ischemia and pulmonary edema 

89
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What contraindication applies to nitroglycerin?

PDE-5 inhibitor use

90
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What is fenoldopam’s MOA?

dopamine-1 receptor agonist —> arterial/renal vasodilation

91
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What is a unique adverse effect of fenoldopam?

increase intraocular pressure 

92
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What is hydralazine’s MOA?

direct arteriolar vasodilator

93
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When is hydralazine often used?

in pregnancy

94
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What are hydralazine’s adverse effects?

reflex tachycardia, headache, lupus-like syndrome 

95
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What is enalaprilat’s MOA?

is IV ace inhibitor which reduce afterload 

96
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Why is enalaprilat less favored?

it has a slower onset, unpredictable effect; contraindicated in pregnancy and bilateral RAS

97
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What is phentolamine’s MOA?

nonselective alpha blocker

98
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When is phentolamine indicated?

catecholamine excess (pheochromytoma, stimulant crisis)

99
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What are the first stabilization steps in hypertensive emergency?

airway, breathing, circulation; IV acesss, continous monitoring

100
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What rapid assessments are needed?

neuro exam, ECG, troponins, renal function, urine output