HTN Flashcards
1
Q
+New Scheme
Categories of BP in Adults
- Normal:
- Elevated:
- Stage 1 HTN:
- Stage 2 HTN:
Inidividuals with SBP and DBP in 2 categoires should be designated to the ____ BP category
Based on average of > __ careful readings obtained on > __ occasions
A
- < 120 and <80
- 120-129 and <80
- 130-139 or 80-89
- > 140 or > 90
higher
2, 2
2
Q
Hypertension
- BP is based on a mathematical equation:
- BP = ____ x _____
- Increased BP can result from either ____ in __ or ___
- Controlled by (2) systems
A
- Equation
- BP = CO x SVR (cardiac output, systemic vascular resistance)
- Increase, CO, SVR
- Sympathetic nervous system
- Renin-angiotensin-aldosterone system (RAAS)
- CO = SV/HR*
- Renal homeostasis is V important- thats why HTN is so hard to tx in those with CKD*
3
Q
Regulation of BP
BP = CO x SVR
Sympathetic nervous system:
- Works on CO by?
- Works on SVR by?
A
Sympathetic nervous system is your “fight or flight” response -> increases BP when needed
- Activation of B1 receptors on the heart
- Activation of a1 receptors on the vasculature
4
Q
Regulation of BP
BP = CO x SVR
RAAS system
- Angiotension -> Renin -> Antiotensin I -> ACE -> Angiotensin II ->
- Adrenal Cortex -> Aldosterone -> ________________
- Blood Vessels -> _____________
A
- Sodium and Water Retention
- Vasoconstriction
- Ang II is a very potent vasoconstrictor*
- So unless your in septic shock we don’t want lots of Ang II-> it’ll really boost your BP*
- Aldosterone is very CARDIOTOXIC -> so we try to target in HF*
5
Q
Determinants of BP
A
- Afterload = amount of pressure heart has to exert to get blood out*
- End diastolic volume, end systolic volume*
- EF normal = 50%, Normal SV for an adult is about 70cc*
6
Q
Regulation of BP
- Causes of increased CO
- Increased fluid _____ (____ sodium and water)
- Excess stimulation of _____
- Sympathetic nervous system ______
- Causes of increased SVR
- Excess stimulation of _____
- Sympathetic nervous system ______
A
- CO
- volume (excess)
- RAAS
- overactivity
- SVR
- RAAS
- overactivity
7
Q
+Medications Used to Treat Hypertension
(8)
A
- Diuretics
- B Blockers
- Angiotensin converting enzyme inhibitors (ACEI)
- Angiotensin receptor blockers (ARB)
- Calcium Channel Blockers (CCB)
- a1 receptor antagonists
- a2 receptor agonists
- Vasodilators
8
Q
Diuretics Patho
- Diuretics MOA are differented by?*
- Proximal tubule is were most of NA is reabsorbed HOWEVER?*
A
- Where they work in the kidneys*
- Is actually the WEAKEST! Bc other parts later in the kidney adapt/compensate , therefore diuretics that target reabsorption later in the kidneys are more effective*
9
Q
Diuretics
- Initial BP decrease:
- Decrease blood _____ -> decreases ___
- Compensatory increase in ____
- Sustained BP decrease
- Decrease SVR -> decrease in _____ content of smooth ____ cells
A
- Inital
- volume, CO
- SVR
- Sustained
- sodium content, muscle
Diuretics that are the most potent are not really used for BP, theyre reserved for ppl with HF -> ex) Loop diuretics not used for HTN
10
Q
+Diuretics
A
- SVR decreases overtime*
- CO decreases bc decreases preload*
11
Q
+Diuretic Medications
(4)
- Classificaton of diuretics are based on the MOA in the _____
A
- nephron
- Carbonic Anhydrase Inhibitors
- Loop Diuretics
- Thiazide Diuretics
- Potassium Sparing Diuretic
12
Q
Carbonic Anhydrase Inhibitors
MOA
- Inhibit_______ _______ in the _____ tubule
- Increase ________ fo HCO3 (bicarbonate)
- _____ produce potent diuresis of sodium and water
A
- carbonic anhydrase, proximal
- excretion
- Does NOT
- So they work where there is most reasorption of Na and Water -> but NOT POTENT for diuresis and HTN bc of all the distal tubules*
- Is used for altitude sickness, breathing on vents, gets rid of excessive bicarb ot help ICU pts breathe, HCO3- alkalinizies urine for icu pts*
- Causes accumulation of carbonic acid by preventing its breakdown*
13
Q
+Carbonic Anhydrase Inhibitors
(1)
A
Acetazolamide (Diamox)
14
Q
+Carbonic Anyhdrase Inhibitors
Therapeutic Uses (4)
Not effective for?
A
- Glaucoma
- Urinary alkalinization
- Metabolic alkalosis
- Acute mountain sickness
Not an effective class to use for diuresis and management of hypertension
15
Q
Carbonic Anhydrase Inhibitors
AE (5)
A
- Metabolic Acidosis
- Renal stones
- Drowsiness
- Parasthesias
- Hypersensitivity reactions
16
Q
+Loop Diuretcs
MOA
- Inhibits sodium reabsorption in the:
- Promotes up to ___ sodium and water excretion
- Increases urinary excretion of:
A
- ascending limb of LOOP OF HENLE
- 25%
- other electrolytes
- Water follows salt*
- Main problem is other electrolyte losses*
17
Q
+Loop Diuretics
(4)
A
Furosemide (Lasix)
Bumetanide (Bumex)
Torsemide (Demadex)
Ethacrynic acid (Edecrin)
- Ethacrynic = an oldie, only one that doesn’t have a sulfamoity so only really used if allergic to others -> not used bc V expensive esp the IV version*
- LASIX -> aka “Lasts six hours”*
18
Q
+Loop Diuretics
Routes
A
PO and IV
19
Q
+Loop Diuretics Dosing
- _____ is most potent*
- ________ of furosemide is not the best - we use it commonly bc its the first one, nonexpensive, however ppl get tolerant through “diuretic ______”, which is now when we ould ______ to bumetanide or torsemide*
A
- Bumetanide*
- Bioavailability, “resistance” , switch*
20
Q
Loop Diuretics
- Oral Bioavaliability
- Furosemide__-__%
- Bumetanide __-__%
- Torsemide __-__%
- Excreted by the ______
- _____ duration in renal dysfunction
A
- Bioavailability
- 10-70%
- 80-100%
- 80-100%
- Kidneys
- Prolonged
21
Q
+Loop Diuretics
- Therapeutic Uses
- States of volume ______: ____ effective for fluid _____
- _____ extensively used in the ________ tx of high BP
- Serum electrolyte ______ -> therefore sometimes also used when pts are ____ or ______
A
- Uses
- overload: very, elimination
- Less, maintenance
- imbalances ,hyperkalemic or hypercalcemic
22
Q
+Loop Diuretics
AE (8)
A
- Hypotension
- Hyponatremia
- Hypochloremia
- Hypokalemia*
- Hypomagnesemia
- Hypocalcemia
- Ototoxicity (from high IV doses)
- Azotemia = renal injury (BUN/CR > 20 -> better thing about stopping lasix, pt is dry)
23
Q
Loop Diuretics
- Loop diuretics have a “______” effect
- ____ doses do ___ further _____ diuresis
- Differ from pt to pt: ____ ____ thresholds identified clinically
- Tolerance
- _____ of distal ____/collecting ___
- ______ sodium reabsorption in ____ segments
A
- “ceiling”
- Higher, not, increase
- Patient specific
- Tolerance
- Hypertrophy, tubules, ducts
- Increased, distal
- The dose that makes them pee is uaully their max dose*
- Maladaptive process -> gotta start giving more frequently/increasing doses when resistance starts*
24
Q
+Thiazide Diuretics
MOA
- Inhibits sodium reabsorption in the:
- Promotes up to ___ sodium and water excretion
- Increases urinary excretion of:
A
- distal tubule
- 5%
- other electrolytes
Less potent than LOOP which is V potent
25
**+Thiazide Diuretics**
## Footnote
(5)
* **Hydrochlorothiazide (Microzide)**
* **Chlorothiazide (Diuril)**
* **Metolazone (Zaroxolyn)**
* **Chlorthalidone (Thalitone)**
* **Indapamide (Lozol)**
26
**+Thiazide Diuretics Routes**
## Footnote
* Hydrochlorothiazide:
* Chlorothiazide:
* Metalazone:
* Chlorthalidone:
* Indapamide:
* PO
* PO, IV
* PO
* PO
* PO
27
**+Thiazide Diuretics**
## Footnote
* Therapeutic Uses
* Treatment of:
* Allow for \_\_-\_\_ weeks for max effect on BP
* The effectiveness of diuretics is diminished when ____ falls below ___ mL/min
* Less extensively used in tx of:
* Therapeutic Uses
* HTN
* 2-4 wks
* CrCL, \<30
* Acute edema
* Commonly used ot treat BP but doesn't work well in advanced/chronic CKD*
* Thiazides are first line agents for BP, but don't work as well for Edema like Loop Diuretics do*
28
**+Thiazide Diuretics**
## Footnote
AE (8)
* Hypotension
* _Hyponatremia_
* _Hypokalemia_
* Hypomagnesemia
* _Hypercalcemia_
* _Increased uric acid_
* Increased plasma glucose levels
* Azotemia
## Footnote
* Notice its HYPERCALCEMIA -\> diff between loop and thiazide*
* Beneift: may help with bone loss in older adults bc of hypercalcemia*
* Con: increases uric acid -\> gout "The GOUCH, OUCH it hurts"*
* Slight bump in glucose levels, not significant, still given in DM pts*
29
Loops and Thiazides
* Loop diuretics block Na+ reabsorption in the ______ of \_\_\_\_\_
* Results in \_\_\_\_physiologic Na+ concentrations in _____ nephron segments
* \_\_\_\_\_/hyper-\_\_\_\_ of ____ nephron segments
* _____ NA+ reabsorption
* Reduced _____ of loop diuretics
* Use of thiazides in combo with loop diuretics:
* Sample combination regimen:
* loop of Henle
* supra, distal
* Hypertrophy/hyper-function, distal
* Increased
* natriuresis
* blocks Na+ reabsorption in distal nephron segments
* Metolazone 5-10mg PO follwed by Furosemide 80mg IVP
*The whole idea is they work in concert together (synergistic effect) - only really done in the hospital though*
30
**+Potassium-Sparing Diuretics**
## Footnote
MOA
* Acts at _\_\_\_\_\_ \_\_\_\_\_\__to inhibit sodium reabsoprtion
* Promotes up to ____ sodium and water excretion
* Blocks effects of ______ in kidney
* _collecting duct_ *(faaarrr away in very last part of nephron)*
* 2%
* aldosterone
31
**+Potassium Sparing Diuretics**
## Footnote
(2)
* **Triamterene (Dyrenium)**
* **Spironolactone (Aldactone)** *(also an aldosterone antagonist)*****
32
**+Potassium Sparing Diuretics**
## Footnote
* Therapeutic Uses
* Protect against _____ with other diuretics
* ____ \_\_\_\_ (aldosterone antagonist)
* _____ hypertension
* Therapeutic Uses
* hypokalemia
* Heart Failure
* Resistant
* Triameterene almost soley used to protect against hypokalemia*
* Spironolactone is a \* for HF*
* These drugs not really used for HTN but for SE of other diuretics*
33
**+Potassium Sparing Diuretics**
## Footnote
Routes
PO
34
**+Potassium Sparing Diuretics**
## Footnote
AE (5)
* Hypotension
* N/V, constipation, diarrhea
* Hypercalcemia
* _Hyerkalemia_
* _Gynecomastia (spironolactone)_*- (again the gynecomastia more pertinent in HF -10% of male pts get it when taking it for HF)*
35
**+B Blockers**
## Footnote
MOA
* Blocks B1 receptors in _____ muscle
* ____ HR ( negative _____ effects)
* ____ CO (negative _____ effects
* _____ release of ____ from the kidenys
* Some agents ____ activity of the _____ nervous system
* Some agents directly \_\_\_\_\_:
* cardiac
* Decrease (chronotropic)
* Decrease (inotropic) *- decreasing contractility -\> decreases CO*
* Inhibit, renin
* inhibit, sympathetic
* decrease peripheral vascular resistance
36
**+B Blockers**
## Footnote
MOA
*The main thing we care about with B-Blockers is they drop CO, and act pretty quickly after admin*
37
**+B Blockers**
## Footnote
(6)
* **Atenolol (Tenormin)** *most commonly used - convenient bc once per day*
* **Carvedilol (Coreg)**
* **Esmolol (Brevibloc)**
* **Labetalol (Trandate)**
* **Metoprolol (Lopressor, Toprol XL)**
* **Propanolol (Inderal)** - *oldest and historical gold standard*
38
B Blockers
## Footnote
* Other therapeutic uses
* _____ pectoris
* M\_\_\_\_\_ i\_\_\_\_\_
* _____ failure
* Ventricular \_\_\_\_\_\_
* ______ prophlyaxis
* _______ thyroidism
* G\_\_\_\_\_\_\_
* *Are B Blockers used for HTN ?*
* Therapeutic uses
* Angina
* MI
* Heart
* arrhythmia
* Migraine
* Hyperthyroidism
* Glaucoma (eyedrops)
* *NOT popular for HTN, 2nd or 3rd line agent, however first line for lots of ther stuff*
39
B Blockers Selectivity
## Footnote
* Pharmacological differences
* _B selectivity_
* __B1-adrenergic receptors are located in the \_\_\_\_
* B2-adrenergic receptors are located in the \_\_\_\_
* NOTE: selectivity is?
* _a1 blockade_
* __Decrease ______ stimulation causing \_\_\_\_\_\_\_
* Differences
* B selectivity
* Heart
* Lungs
* NOT ABSOLUTE
* a1 blockade
* sympathetic, vasodilation
## Footnote
*So obvs with pulmonary disease you want B1 selective*
40
B Blockers
* Pharmacological Differences
* Intrisic ______ activity (ISA)
* Causes activation of _____ receptors producing effects similar to stimulation of the _ \_ \_
* ______ solubility
* ______ agents have larger volumes of distribution
* ______ agents depend more on renal function for elimination
* Pharmacological Differences
* sympathomimetic
* adrenergic, SNS
* Lipid
* Lipophilic
* Hydrophilic
## Footnote
* Not really gonna talk about this bc we tried making a BB agonist/antagonist essentially to derease SE of BB "have my cake and eat it too" but didn't pan out*
* Lipid solubility -\> matters bc contributes to SE*
41
**+B Blockers Chart**
## Footnote
*Most important things: Beta selectivity bc of SE (don't really care about ISA)*
42
**+B Blockers**
## Footnote
AE
* \_\_\_\_tension
* \_\_\_\_\_\_\_\_\_\_\_\* related to ____ selectivity!!
* \_\_\_\_\_cardia
* F\_\_\_\_\_, exercise \_\_\_\_\_
* D\_\_\_\_, C\_\_\_\_\_, A\_\_\_\_, Ps\_\_\_\_
Cautions
* What happens with abrupt discontinuation?
* Contraindication with what type of pts?
* Hypotension
* Bronchospasm
* Bradycardia
* Fatigue, exercise intolerance
* Depression, confusion, agitation, psychosis
* Rebound hypertension
* Poorly controlled diabetic pts *(masks S/S of hypoglycemia)*
*Bc they work on sympathetic nervous system -\> fatigue, exercise intolerance -\> happens quick! "They're on a walk then boom, i get tired all of sudden -\> another reason why we don't use for HTN bc these patients obv should exercise"*
43
Angiotensin Converting Enzyme Inhibitors (ACEI)
## Footnote
MOA
* _____ RAAS by preventing conversion of ______ to ______ -\> decreased ______ -\> decreased \_\_\_
* Inhibits ______ of ______ and _____ synthesis of _____ prostaglandins
* Inhibits, angiotensin I, angiotensin II, systemic vascular resistance, BP
* degradation, bradykinin, increase, vasodilating
44
**+Angiotensin-Converting Enzyme Inhibitors (ACEI)**
## Footnote
MOA
*Some SE of ACEI related to inability of bradykinin to break down -\> lvls will go up*
45
ACEI
## Footnote
(4)
Routes
How long do they take to work?
**Captopril (Capoten)** PO
**Enalapril (Vasotec)** PO
**Lisinopril (Prinivil)** PO
**Ramipril (Altace)** PO
Several weeks to see full effect - reevaluate in 2-4 wk of starting or changing dose
*All end in pril, like other BP meds gotta give them a few weeks to work*
46
ACEI
## Footnote
* Other therapeutic uses
* _____ failure
* ____ \_\_\_\_\_\_\_\_ dysfunction
* D\_\_\_\_ n\_\_\_\_\_
* A\_\_\_\_ _____ \_\_\_\_\_
* Chronic ____ \_\_\_\_\_\_
* *\_\_\_\_\_\_\_\_\* given when pt has HTN and CKD*
* Other therapeutic uses
* Heart failure
* LV dysfunction
* Diabetic nephropathy
* Acute MI
* CKD
* *NEPHROPROTECTIVE\**
47
**+ACEI**
AE (5)
* Hypotension
* _Hyperkalemia_
* Acute renal failure
* _Cough_
* _Angioedema_
* Hyperkalemia a major problem with ACEI -\> so alway check*
* Higher levels of bradykinin cause Cough, Angioedema -\> robitussin doesn't help it, just gotta swtich to another drug*
* Long term ACEI are nephroprotective but they acutely reduce GFR -\> bc kidney relies on Ang II for renal blood flow -\> but again long term they are a slam dunk for renal protectors (ARBS are close cousins)*
48
**+ACEI**
## Footnote
Significant Drug Interactions (2)
Potassium supplements
or
Potassium sparing diuretics
49
**+ACEI**
## Footnote
Contraindications (3)
Pregnancy *(bc any drug that works on ang is teratogenic: ACE enzyme is necessary for fetal development)*
Aortic Stenosis
Renal Artery Stenosis
50
Angiotensin Receptor Blocking Agents (ARB)
## Footnote
MOA
* Used in patients that can't tolerate?
* Should probably not use if?
Selectively blocks the vasoconstrictive effects of angiotensin II by blocking binding of angiotensin II to its receptor
* ACEI due to _cough_
* not be use if angioedema on ACEI
51
**+ARB**
## Footnote
MOA
*ARBS just works a bit more ____ than ACE -\> net effect/differentiating effect is that it doesn't effect _______ so only diff is the \_\_\_*
downstream, bradykinin, SE
52
ARBS
## Footnote
(2)
Routes
**Losartan (Cozaar)** PO
**Valsartan** **(Diovan)** PO
53
**+ARBS**
## Footnote
AE (4)
* Hypotension
* _Hyperkalemia_
* Acute renal failure
* Angioedema (very rare)
*NO COUGH!! Bc doesn't influence bradykinin*
54
**+ARB**
## Footnote
Significant Drug Interactions (2)
Potassium supplements
or
Potassium sparing diuretics
55
**+ARB**
## Footnote
Contraindications
Pregnancy, Aortic Stenosis, Renal Artery Stenosis
(same as ACEI)
56
**+ACEI/ARB**
## Footnote
MOA Chart
*Pure ______ don't really effect (2) -\> which is the main way they decrease BP*
*Vasodilators, CO or Blood volume*
57
Calcium Channel Blockers
## Footnote
MOA
* Blocking calcium entry into smooth \_\_\_\_\_\_
* Results in \_\_\_\_\_\_\_
* Can also effect cardiac \_\_\_\_\_\_\_
* muscle
* vasodilation
* conduction
*Relaxes smooth muscle -\> pure vasodilators*
58
**+Calcium Channel Blockers**
## Footnote
Dihydrophyridines (3)
Non-dihydropyridines (2)
Routes
* **Amlodipine (Norvasc)** PO
* **Nicardipine (Cardene)** PO, IV
* **Nifedipine (Adalat, Procardia XL)** PO
* **Verapamil (Calan)** PO, IV
* **Diltiazem (Cardizem)** PO, IV
59
**+Dihydropyridines (DHP)**
## Footnote
MOA Chart
60
**+Non-Dihydropyridines (NON-DHP)**
## Footnote
MOA Chart
*NON-DHP has additive effect of being negative chronotrope -\> decreases HR bc works on AV node*
61
**+CCB**
## Footnote
MOA Chart
Non-DHP and DHP
Effects on BP
Effects on HR
* Amlodipine is the classic: potent, cheap!*
* The non-dhp are v potent at lowering HR not rly BP -\> thats why mostly used for arrhythmias (dilt for Afib)*
62
CCB
## Footnote
* Other therapeutic uses
* _____ pectoris
* _____ \_\_\_\_\_ disease
* _____ prophylaxis (non-DHP)
* \_\_\_\_\_\* (non-DHP)
* Other therapeutic uses
* Angina
* PVD
* Migraine
* Arrhythmia
63
**+CCB**
DHP AE (3)
NON-DHP AE (3)
* DHP AE
* Hypotension
* HA and flushing
* Peripheral edema
* non-DHP AE
* Bradycardia
* Hypotension
* Constipation (verapamil)
64
**+a1 Receptor Antagonists**
MOA
Decrease sympathetic stimulation causing vasodilation and thus reducing blood pressure
65
**+a1 Receptor Antagonists**
Agents
Blood pressure, non-selective (3) + Routes
Prostate, selective for 1A subtype (2) + Routes
* **Doxazosin (Cardura)** PO
* **Prazosin (Minipress)** PO
* **Terazosin (Hytrin)** PO
* **Alfuzosin (Uroxatral)** PO
* **Tamsulosin (Flomax)** PO
66
a1 Receptor Antagonists
## Footnote
Indication
Used as last line agent in the treatment of hypertension
## Footnote
*Another PURE VASODILATOR - salvage therapy for intoleracne to other meds or really uncontrolled HTN*
67
a1 Receptor Antagonists
## Footnote
AE (2)
* First dose phenomenon -\> decreased BP
* Chronic administration -\> water and sodium accumulation
68
**+a2 Receptor Agonists**
## Footnote
MOA
Decrease sympathetic stimulation to cause vasodilation and thus reduce BP
69
**+a2 Receptor Agonists**
## Footnote
(2)
Routes
**Clonidine (Catapres)** PO, IV, Transdermal patch
**Methyldopa (Aldomet)** PO
70
a2 Receptor Agonists
## Footnote
Indication
Used as a last-line agent in the treatment of HTN
## Footnote
*also helps with anxiety (clonidine)*
71
a2 Receptor Agonists
## Footnote
AE (2)
Sedation and HA
Abrupt discontinuation may result in rebound HTN
*Last line agents bc they have rly bad AE*
72
**+Direct Vasodilators**
## Footnote
MOA
Causes artery relaxation (vasodilation) resulting in decreased BP
73
**+Direct Vasodilators**
## Footnote
(2)
Routes
**_Hydralazine (Apresoline)_** PO, IV
Minoxidil (Loniten) PO
74
Direct Vasodilators
## Footnote
AE (2)
Requires ___ admin -\> results in:
Hydralazine -\> Tachycardia and fluid retention
Minoxidil -\> hirsutism
TID: poor adherence
75
Direct Vasodilators
## Footnote
Indication
Reserved for pts with severe hypertension
76
**+New 2017 ACC/AHA Guidelines**
*clinical ASCVD rt ASCVD calculator*
77
**+Treatment Choices Part 1**
## Footnote
1) For initation of antihypertensive drug therapy first line agents include
Thiazide diuretics
CCBs
ACE inhibitors or ARBS
78
**+Treatment Choices Part 2**
## Footnote
1. In black adults with HTN but without HF or CKD, including those with DM, initial antihypertensive treatment should include:
2. ___ or more antihypertensive medications are recommended to achieve a BP target of \< than \_\_\_/\_\_\_ in most adults with HTN, especially in ____ adults with HTN
1. thiazides or CCB
2. Two, \< 130/80, black
* Biological reasoning for not using ACE/ARBS in black patients is because they have "lower renin" -\> less reponse to ACE/ARB*
* Statistically significant: most ppl need TWO OR MORE meds*
79
**+Treatment Choices Part 3**
## Footnote
1. In adults with DM and HTN, antihypertensive drug tx should be initiated at a BP of _\>_ \_\_\_/\_\_\_ or higher with a tx goal of:
2. In adults with DM and HTN, all first line class of antihypertensive agents are (4) are useful and effective
3. In adults with DM and HTN, (2) may be considered in presence of \_\_\_\_\_\_.
1. _\>_ 130/80, \< 130/80
2. Diuretics, ACEI, ARBS, CCBs
3. ACEI, ARBS, albuminuria
80
**+Treatment Choices Part 4**
1. Adults with HTN and CKD should be treated to a BP goal of:
2. In adults with HTN and CKD (stage 3 or higher or stage 1 or 2 with albuminuria (_\>_ 300 mg/d, or _\>_ 300mg/g albumin:creatinine ratio or the equivalent in the first morning void), tx with ______ is reasonable to slow disease progression.
3. In adults with HTN adn CKD (stage 3 or higher or stage 1 or 2 with albuminuria (_\>_ 300 mg/d, or _\>_ 300mg/g albumin:creatinine ratio or the equivalent in the first morning void) treatment with an ____ may be reasonable if _______ is not tolerated.
1. \< 130/80
2. ACE inhibitor
3. ARB
*ACE or ARB still preferred agent for CKD\**
81
Select a Drug Treatment Strategy
## Footnote
* _____ first medication before adding a \_\_\_\_
* ___ second agent _____ reaching _____ dose of first medication
* Start with ___ medication classes ______ or as a fixed-dose _____ (ie not typically on an ACEI and ARB)
* Maximize, second
* Add, before, maximum
* 2, separately, combination
82
**+Hypertensive Crisis**
* _Hypertensive Urgency_
* __SBP _\>_ ____ and/or DBP _\>_ _____ without:
* _Hypertensive Emergency_
* __Presence of an ____ significantly _____ BP (often defined as SBP \> ____ and /or DBP \> \_\_\_\_) with:
* Hypertensive Urgency
* 180, 110, **without** evidence of target organ damage
* Hypertensive Emergency
* abrupt, elevated, 200, 120, **with** concurrent target organ dysfunction (brain, heart, kidneys, eyes)
*Organ dysfunction: Chest pain/other symptoms*
83
Hypertensive Crisis Goals
## Footnote
* Urgency
* lower _____ to goal or near goal within ___ hrs: oral ___ can be used
* Emergency
* lower ____ by \_\_\_% or ____ pressure to \_\_-\_\_ mmHg within \_\_-\_\_minutes
* Exceptions for (3) conditions
* Urgency
* MAP, 24hrs, meds
* Emergency
* MAP, 25%, diastolic, 100-110 mmHg, 30-60 min
* Acute aortic dissection, Acute ischemic stroke, Intracerebral hemorrhage
* Urgency = Oral meds*
* Emergency = IV meds*
84
Common IV Drugs Used in Hypertensive Emergency
## Footnote
(3)
* **Sodium Nitroprusside (Nipride)**
* **Nitroglycerin**
* **Nicardipine (Cardene)**
85
**+Sodium Nitroprusside**
MOA
* Converts to ___ \_\_\_\_ (NO) -\> activates ____ \_\_\_\_\_ (GC) -\> converts ____ \_\_\_\_ ____ (GTP) into ____ \_\_\_\_ ____ (cGMP)
* _____ preload (**\_\_\_\_\_\_\_\_**) and afterload (**\_\_\_\_\_\_ \_\_\_\_\_\_** ) to a similar degree
* ____ cardiac output and ____ heart rate
* nitric oxide -\> guanylate cyclase -\> guanosine triphosphate -\> cyclic guaninine monophosphate
* Decreases, **venodilation,** **arterial dilation**
* Reduces CO, Increases HR
* V potent vasodilator -\> drops preload AND afterload*
* Its nice bc it has a short half-life usually given as a gtt so if you go to far, just turn it off*
86
**+Sodium Nitroprusside**
How is it administered?
What is its half life?
* Continuous infusion (gtt)
* \< 10 minutes
87
**+Sodium Nitroprusside**
AE (2)
* Conversion to NO generates **_cyanide**_ -\> liver converts to _**thiocyanate_** -\> eliminated through kidneys *(Cyanide poisoning when given in v low doses over long periods of time)*
* Tachycardia
88
**+Sodium Nitroprusside**
Risk of Toxicity
* Doses \> ___ mcg/kg/min
* _____ administration
* ____ or ____ insufficiency
* \> 2mcg/kg/min
* Prolonged
* Renal, Hepatic
89
Sodium Nitroprusside
## Footnote
NOT the drug of choice for (3)
(not really on exam?)
* Acute Coronary Syndromes
* Aortic Dissection
* Increased ICP
90
**+Nitroglycerin**
MOA
* Combines with _____ groups in vascular ____ that mimics ___ stimulation of _____ \_\_\_\_ and production of \_\_\_\_
* Preferentially relaxes _____ smooth \_\_\_\_\_
* sulfhydryl, endothelium, nitric oxide's, guanylate cyclase, cGMP
* _venous_, muscles
91
**+Nitroglycerin**
## Footnote
Indications
Not as potent as nitroprusside for lowering BP
Use more for acute heart failure or ACS
92
**+Nitroglycerin**
## Footnote
Admin
Half life
Administered as continuous infusion
HF: 2-3 minutes
93
**+Nitroglycerin**
## Footnote
Disadvantages
* \_\_\_\_\_\_\_\_\_\*
* Prevention includes maintaining a "nitrate \_\_\_" interval
* Do not (2)
* Tachyphylaxis (tolerance, even within 24 hours)
* "nitrate free" interval
* DO NOT apply patches for a continuous 24hr period
* DO NOT use oral tablets or sustained release products around the clock
*Know that IV and sublingual forms act quickly, and PO/tablets are long acting which is primarily what we want depending on what we use it for*
94
**+Nitroglycerin**
## Footnote
AE (3)
Hypotension
Headache (*nitro HA are real\* very common)*
Reflex Tachycardia
95
**+Nitroglycerin**
Significant Drug Interactions
Phosphodiesterase-5 inhibitors (ie. sildenafil (VIAGRA))
## Footnote
*(ED meds)*
96
Nicardipine
## Footnote
* What is it?
* Used for what? or when ___ is no available (ie. post op)
* Normal dose \_\_-\_\_ mg/hr continuous
* Unique \_\_\_-phasic elimination, watch for \_\_\_\_\_
* Intravenous CCB
* Hypertensive emergency, PO
* 5-15 mg/hr
* Tri-phasic, accumulation
* is an IV CCB -\> given alot in CCU*
* Be mindful that it can accumulate -\> tanks BP*
