HTN Flashcards
1
Q
What makes up BP
What makes up CO
A
CO and SVR
HR and SV
2
Q
What makes up SV
What makes up preload
A
Contractility and preload
Venous tone and intravascular volume
3
Q
What makes up SVR
A
Direct innerv, circulating and local regulators
4
Q
What effects venous tone: 4
A
A1 antagonists, ACEI, ARB, NTP
5
Q
What affects na and h20 retention, upstream effect
A
Diuretics, acei, arb. Intravascular volume, preload, and SV
6
Q
Direct innervation SVR
A
A1 antagonists, A2 agonists
7
Q
Circulating BP regulators
A
A1 antag, A2 agonist, ACEI, ARB
8
Q
Local BP regulators
A
Endothelin antagonist, ntp, acei, arb
9
Q
DM or renal disease pts do specifically well on which drugs
A
ACEI or ARB, target RAAS and improve vascular flow to kidneys (underlying atherosclerosis)
10
Q
Renin secreted by what
Results in what
Synergistic with what
A
Juxtaglomerular apparatus
Vasoconstriction and na retention
SNS inc release of noradrenaline
11
Q
What controls ang I to II conversion
What leads to dry cough and which drugs impact this/dont
A
Renin
Bradykinin, relaxes smooth muscle w ACEI but not ARB
12
Q
Angitotensin II effects: 4
A
Adrenal cortex- aldosterone- inc nacl reabs
Renal proximal tubule- inc nacl reabs
Renal efferent arterioles vasoconstriction
Hypothalamus- thirst and inc ADH
13
Q
Acei first line therapy for 3, delays progression in what
A
Htn, CHF, mitral regurg. Renal disease (esp in DM pts)
14
Q
Ang II vasoconstricts where, inc ___ secretion
Mediated mainly at which receptor
A
Arterial smooth muscle
Aldosterone
AT 1 > AT2
15
Q
AT 1 receptor effects 4
A
Generalized vasoconstriction (esp afferrent arterioles)
Inc norepi release
Prox tubule reabs of na
Secretes aldosterone renal cortex
16
Q
ACEI MOA
A
Blocks conversion Ang I to II in vasc endo by interact w zinc ion of ACE (Peptidyl-dipeptidase). Thus prevents vasoconstriction, na retention, and SNS stim
17
Q
ACE: highly ___, minimal __ __, good patient __
A
Potent, SE, compliance
18
Q
ACEI:
Pharm fx: fall in 2
Clinical uses: 5
A
Arterial pressure, cardiac work load
Htn, HF, post MI, diabetic neuropathy, CRI
19
Q
ACEI SE: 6
A
Prolonged hypotension intra op, granulocytopenia, angioedema, proteinuria, persistent cough, hyperkalemia
20
Q
ACEI contraindications: 2
A
Pregnancy, renal artery stenosis (aCEI causes efferent arteriole constriction)
21
Q
Captopril
Onset
1/2 life
Decreases __, doesnt affect __ __
A
15 min
2 hrs
SVR, SNS outflow
22
Q
Captopril
SE: 4
Drug interaction: main 1
A
Rash, loss of taste, hyperkalemia, angioedema
NSAIDs antagonize its effects
23
Q
Enalapril
Route
What it has that makes it special why
A
IV
No sulfahydryl group, no rash or renal ins caused by it
24
Q
Lisinopril
Excretion
A
Unchanged in kidney
25
Ace prodrugs and what it means
Enalapril and ramipril, longer onset
26
Ace effects __ system more than ___ system
Arterial, venous
27
ARBs
| Antagonizes which receptor/MOA
Ang II AT1 receptor, competitive binding to inhib ang II at receptor. Doesnt affect ACE. Results in Less peripheral vasoconstriction
28
Contra ARB: 2
Renal artery stenosis, pregnancy
29
Arterial vasodilator: 2
Minoxidil, hydralazine
30
Hydralazine
| MOA
Activates guanylate cyclase, directly relaxes vascular smooth muscle. Arteries > veins. Alters ca trans into smooth muscle
31
Hydralazine
Dose
Peak
Duration
2.5-10 mg IV
10-20 min peak
6 hrs
32
Hydralazine
Metabolism
1/2 time
When in kidney
Extensive hepatic 1st pass
3 hrs
After IV <15% unchanged in kidney
33
Hydralazine SE
| Many
Reflex tachycardia, DBP reduced >SBP, dec SVR, inc HR/SV/CO, tachyphylaxis, na and h20 retention, angina w ekg changes
34
Hydralazine
| Clinically used with __ and __ to limit what
BB and diuretic, inc SNS activity
35
Minoxidil
MOA
Route
Directly relaxes arteriolar smooth muscle, little venous effect. PO
36
Minoxidil
Clinical uses: 3
Used with what
Severe htn due to: renovascular disease, renal failure, transplant rejection
BB and diuretic
37
Minoxidil
| MOA cellular level
K channel opener leading to hyperpolarization and vasodilation
38
```
Minoxidil
Absorption
Peak
E 1/2
What in urine
```
90% abs in GI
1 hr
4 hrs
10% unchanged in urine
39
Minoxidil SE (many)
Inc HR and CO, inc NE and renin leads to: na and h20 ret, wt gain, edema, hypertrichosis, pulm htn, pericardial effusion/cardiac tamponade
40
Minoxidil EKG effects
Flat or inverted T wave, inc voltage of QRS- due to altered K conductance in heart
41
Peripheral vasodilator
| Uses: 3
Facilitate forward LV flow in AR/MR/CHF, control htn in OR, tx htn crisis
42
Peripheral vasodilator: 4 main ones we use
Ntp, SNP, isorsorbid, adenosine
43
SNP
Action
Lacks effects where
Direct, nonselective peripheral vasodilator (art and vein SM). Lacks effect non vascular SM and cardiac muscle
44
SNP
| MOA
Interact w oxyhemoglobin- dissociation to methemoglobin- releases NO and cyanide. NO activ guanylate cyc- inc cGMP- inhib Ca entry into vasc SM, inc Ca uptake into smooth ER. Vasodilation via NO
45
SNP metab
4 leftover cyanide ions metab in liver and kidney to thiocyanate
46
SNP toxicity occurs due to what
Leads to 3
Caution in
High conc thiocyanate. Occurs at rates >2 mcg/kg/min. Pt develops resistance at high rates. Can precipitate tissue anoxia, anaerobic metab, lactic acidosis. Caution in preg.
47
SNP toxicity tx
D/c med. 100% o2. Na bicarb- acidosis. Na thiosulfate 150mg/kg over 15 min. Na nitrate 5 mg/kg if severe.
48
Na thiosulfate action
| Na nitrate action
Sulfur donor- converts cyanide to thiocyanate
| Converts hgb to methgb which converts cyanide to cyanomethgb
49
Thiocyanate toxicity
Toxicity/occurance compared to cyanide
Symp: 10
Rare (to kidney clearance), less toxic
| Nv, tinnitus, fatigue, hyperreflexia, confusion, psychosis, miosis, seizure, coma
50
Methemoglobinemia
| What it is
Rare, differential dx in pts w imp oxygenation despite good CO and arterial oxygenation
51
Phototoxicity of SNP
| Why
In light SNP converted to aquapentacyanoferrate, released hydrogen cyanide
52
SNP
Dose
When toxic dose risk
Onset, duration, req what
0.3 mcg/kg/min-10.
>2. >10 min max dose.
Immediate, short.
Gtt and a line
53
SNP CV effects
Inc:
Dec:
Inc: HR, contractility, intracoronary steal and MI damaged areas, venous capacitance
Dec: venous return, SBP, PVR, SVR
54
SNP Fx
CNS
Pulm
Blood
Inc CBF and ICP
Attenuates hypoxic vasoconstriction
Inc cGMP- inhibits plt agg
55
SNP clinical uses, dose if applicable
```
Controlled hypotension (0.3-0.5 mcg/kg/min)
Htn crisis (1-2 mcg/kg bolus then gtt)
Cv disease: dec LV afterload and good for MR, AR, CHF
```
56
Ntg
What it is
Acts on
Organic nitrate
| Venous capacitance vessels and large coronary arteries
57
Ntg MOA
| E 1/2
Generates NO thru glutathione dependent pathway (glut S transferase). Stim cGMP to cause vasodilation. 1.5 min
58
NTG
| What tox can lead to/tx
Methemoglobinemia. Caution in high doses. Methylene blue 1-2 mg/kg over 5 min, reconverts methgb to hgb
59
NTG cv effects
Venodilation, dec: venous return, R/L ventricular end DBP, CO. No change HR or SVR. Inc coronary BF
60
NTG tolerance
Limits use, present after 24 hr of sustained tx
61
NTG Fx
CNS
Pulm
Vasodilation and inc ICP HA
| Dec PVR, bronchial dilation, inhib hypoxic pulm vasoconstriction
62
Ntg fx
Coag
Gi
Prolongs bleeding time, inhib plt agg
| Relaxes smooth musc of GI tract
63
Ntg clinical uses
```
Angina (reduces RVEDP and LVEDP, reduces myo 02 reqs)
Cardiac failure (dec preload, relieves pulm edema, limits MI damage)
```
64
NTG
| Clinical uses: 2 and doses
Controlled hypotension: 4-5 mcg/kg/min (not in cranial sx until dura open)
Sphincter of oddi spasm: 200 mcg/1 ml bolus
65
Isosorbid
Indic, route, abs, duration
Works predom where
Angina, PO, GI in 6 hrs
SL- 2 hrs
Venous
66
Isosorbid SE
| More active form
```
Orthostatic hypotension,
active metabolite (isosorbid 5 mononitrate) > than parent compound
```
67
Trimethaphan
| Actions
Ganglionic blocker, peripheral vasodilator. Blocks ANS, relaxes vessels. Lowers CO, BP, SVR. Inc HR from PNS block.
68
Trimethaphan
Route
SE
IV, need gtt
| Mydriasis, dec GI activity, urinary retention
69
Ca ch blockers
| 3 main and action overall
Verapamil- SA/AV/V tissue > vessels
Diltiazem- heart and vascular tissue
Nifedipine- more smooth muscle in vessels
70
Ca ion channels present where
| 6
Cell membrane in skel muscle, vascular smooth musc, cardiac musc, mesenteric musc, neurons, glandular cells
71
Ca ch blockers action cell level
Bind to receptor on voltage gated ca ions maintaining channels in inactive or closed state
72
Which ca ch are we targeting w blockers, what it does
L type imp in vascular tone and cardiac contractility. Decreased ca keeps intracellular ca low
73
Ca ch blockers
| Classifications 3 based on structure
Phenyl alyl amines- av node
1,4 dihydropuridines- arterial beds
Benzothiazepines- av node
74
Nifedipine
Verapamil
Dilt
What they do at binding site
N- allosteric modulation at site
V- pore blocker at site
D- not sure
75
Ca ch blockers
| Cardiac/vascular effects
Dec: contractility, activity at sa node, rate of conduction of impulses at AV. Relaxes vasc SM: dec SVR and BP arterial >venous
76
Ca ch blockers SE
| 4
Cancer, cv depression, prolonged bleeding (ca mediated plt func), constipation
77
Ca ch blockers
Drug interactions
W/: IA, NMB, bb, la
IA- myocardial dep and vasodilation
Potentiated NMB
Contraindicated w bb (verapamil)
Inc risk LA toxicity (verapamil)
78
Ca ch blockers drug interac
Dantrolene
Dig
H2 antag
D: hyperkalemia, slows inward k, cv collapse
Dig: inc conc dig by decreasing its clearance
H2: ranitidine and cimetitine alt hepatic enzymes, could inc Ccb
79
Ca ch blockers
| Toxicity rx
IV calcium or dopamine
80
Vascular uses ca ch blockers 5
Systemic htn, pulm htn, cerebral arterial spasm, raynauds, migraine
81
Non vascular uses ca ch blockers 4
Bronchial asthma, esophageal spasm, dysmenorrhea, premature labor
82
Verapamil
Primary sire of action
Cardiac actions
AV node
| Depresses AV node, negative chronotropic effect SA, negative inotrope, moderate vasodilation coronary/systemic arteries
83
Verapamil
Clinical uses
6
SVT, vasospastic angina, htn, hypertrophic cm, maternal/fetal dysrhythmias, premature labor
84
Verapamil
| Protein binding, what inc its activity
Highly. Lidocaine, diazepam, propranolol
85
```
Verapamil
Metabolism
Excretion
Peak
E 1/2
```
Almost entirely thru first pass, almost no drug unchanged in urine
30-45 min, iv 15 min
6-12h
86
Ca ch blockers
Nifedipine
Uses
Primary site of action
Angina and htn
| Peripheral arterioles
87
```
Nifedipine
Cv effects
Comp to verapamil
No effect where
Other: 4
```
Coronary and peripheral vasodilation stronger than verapamil. No effect sa or av. Dec SVR and bp. Reflex tachycardia. Myo dep in LV dysfunc or bb
88
Nifedipine
Routes
Onset and peak oral
IV, oral, SL
| 20 min, 60-90 min
89
```
Nifedipine
Protein binding
Metabolism
Excretion
E 1/2
```
90% protein bound, hepatic metab, urine excretion
| 3-7h
90
Nifedipine SE
| 8
Vertigo, HA, flushing, hypotension, paresthesiass, muscle weakness, can induce renal dysfunc
Coronary vasospasm w abrupt D/C
91
```
Dilt
Primary action where
Main Indication
Strength compared to others in class
Minimal what
```
AV node
SVTs
Intermediate strength b/w verapamil and nifedipine
Cv depressant effects
92
Diltiazem
Clinical uses
Sim to:
3
Verapamil
| Vasospastic angina, hypertrophic cm, fetal/maternal dysrhythmias.
93
Diltiazem
Routes
Doses
Gtt
Po or iv
.25-.35 mg/kg over 2 min, repeat in 15 min
10mg/hr gtt
94
Diltiazem
Po onset, peak
Protein binding
15 min, 30 min
| 70-80% protein bound
95
Diltiazem
Excretion
E 1/2
Decrease dose in who
Bile and urine, inactive metab
4-6hr
Liver disease
96
Centrally acting agents
| MOA
Reduce sns outflow from vasomotor center in brain stem. Selective partial alpha 2 adrenergic agonist
97
Centrally acting agents
Drug name
Clinical uses 5
Clonidine
| Htn, induce sedation, dec anesthetic reqs, improve periop hemodynamics, analgesia
98
Clonidine
Effects
Warning w abrupt stop
BP reduction from decreased CO d/t dec hr and peripheral resistance
Rebound hypertension
99
Centrally acting agents
SE
9
Bradycardia, sedation, dry mouth (zerostomia), imp concentration, nightmares, depression, vertigo, EPS, lactation in men
100
Centrally acting agents
Routes
Metab/exc
PO or transdermal
| 50/50 hepatic metab and renal excretion
101
```
Centrally acting agents
Withdrawal syndrome
Occurs how, when
Duration
Tx
```
Doses >1.2 mg/day, 18hrs after acute d/c. 24-72 hour length
| Tx rectal or transdermal clonidine
102
Preop med continue
| Continue which and why
Bb (Reduces periop MI risk)
Cc (benefits outweigh risks unless LV dysfunc)
NO: ACE, withhold 1 dose
103
Htn crisis
What it is
Goal
Tx
>120 DBP, end organ failure
Goal dec DBP 100-105 asap
Ntg, ntp, labetolol
