Antihypertensives Flashcards

1
Q

What are some drugs to reduce cardiac output?

A

Beta blockers

Ca2+ channel antagonists

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2
Q

What are some drugs that reduce plasma volume?

A

Diuretics

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3
Q

What are some drugs that reduce total peripheral resistance?

A

Vasodilators
Alpha1-adrenergic receptor antagonists
ACE inhibitors

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4
Q

Sympathetic activation during the induction of anesthesia can cause?

A

Sympathetic activation during the induction of anesthesia can cause:

  • -Blood pressure to rise by 20 to 30 mmHg
  • -Heart rate can increase by 15 to 20/min in normotensive individuals

These responses may be more pronounced in patients with untreated hypertension in whom the systolic blood pressure can increase by 90 mmHg and heart rate by 40/min.

Patients with preexisting hypertension are more likely to experience intraoperative blood pressure lability, which may lead to myocardial ischemia.

Blood pressure and heart rate slowly increase as patients recover from the effects of anesthesia during the immediate postoperative period.

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5
Q

Patients with untreated severe hypertension, what kind of response can you expect with induction of anesthesia or noxious stimuli??

A

Patients with untreated severe hypertension (mean systolic and diastolic pressure of 211 and 105 mmHg, respectively) have exaggerated hypotensive responses to the induction of anesthesia and marked hypertensive responses to noxious stimuli (for ie, emergency surgery)

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6
Q

A history of hypertension preoperatively is the MOST important risk factor for BLANK

A

A history of hypertension preoperatively is the MOST important risk factor for “postoperative hypertension”

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7
Q

MOA of ACEi

A

Inhibit (slow) the activity of the enzyme ACE which decreases the production of angiotensin II.

As a result:
Blood vessels enlarge (dilate) and BP is reduced.

Angiotensin II normally binds to a specific cell membrane receptor (AT1) that ultimately leads to increased release of calcium from sarcoplasmic reticulum to produce vasoconstriction.

Decreased generation of angiotensin II due to the administration of an ACE inhibitor results in REDUCED vasoconstrictive effects.

Plasma concentrations of aldosterone are decreased resulting in less sodium and water retention.

Block the breakdown of bradykinin, an endogenous vasodilator substance, which contributes to the antihypertensive effects of these drugs.

Ace inhibitors, like statins, reduce activation of low-density lipoprotein (LDL) receptors and thus decrease plasma concentrations of LDL cholesterol.
If the concentration of LDL cholesterol is already sufficiently low, ACE inhibitors may no longer be effective in reducing the rate of cardiovascular events.

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8
Q

MOA of ARB

A

Mechanism of Action:
Need to understand how Angiotensin II works

By blocking the conversion of angiotensin I to angiotensin II, ACE inhibitors prevent angiotensin II-mediated vasoconstriction and stimulation of the sympathetic nervous system

RELAXES BLOOD VESSELS AND HELPS TO REDUCE THE AMOUNT OF WATER REABSORBED BY THE KIDNEYS!!!

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9
Q

When do we use ACEi?

A

Most effective in treating:
Systemic HTN secondary to increased renin production

First line therapy in patients with:

  • Systemic HTN
  • CHF
  • Mitral Regurgitation
  • Safer in diabetics (beta blockers mask this)
  • Delay the progression of diabetic renal disease
  • Provide a survival benefit inpatients who have suffered a MI and CHF
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10
Q

Side effects of ACEi

A

-Cough
-Upper Respiratory Congestion
Accumulation of bradykinin in the lung, drug induced inhibition of peptidyldipeptidase activity
-If respiratory distress develops:
Prompt injection of epinephrine, 0.3 to 0.5 mL of 1:1,000 dilution subcutaneously.
-Angiodema
Life threatening!!!!
-Decreased GFR
Use with caution in patients with preexisting renal dysfunction or renal artery stenosis.
-Hyperkalemia
Possible due to decreased production of aldosterone
-May increase insulin sensitivity and cause hypoglycemia

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11
Q

What is the preoperative management of ACEi?

A

The current consensus on ace inhibitor therapy is to discontinue all such drugs until surgery and to reinitiate therapy as soon as possible postoperatively.**

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12
Q

MOA of ARB?

A

—Produce antihypertensive effects by blocking the vasoconstrictive actions of angiotensin II without affecting ACE activity.
-NameDrugs:
Losartan (Cozaar)
Candesarta
Valsartan
–Do not inhibit breakdown of bradykinin (one of the benefits of Ace Inhibitors)
–Do not cause a cough
–Not given in pregnancy, fetal death
–Active metabolite is 10-40 times more potent than the parent drug
–First pass hepatic metabolism after oral administration

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13
Q

What does inhibition of PDE cause?

A

Inhibition of PDE causes vascular smooth muscle relaxation

PDE III inhibitors:
Positive Inotropy on intracellular calcium mobilization

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14
Q

What do Phosphodiesterase Inhibitors do?

A

A broad family of 11 isoenmyzes which inhibit the breakdown of intracellular cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP).

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15
Q

What are some Phosphodiesterase Inhibitors ?

A
Drugs:
Amrinone
Milrinone, reduced side effect profile over amrinone
Sildenafil
Tadalafil
Vardenafil
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16
Q

What is the MOA of Milrinone?

A

Breakdown of cAMP and cGMP are inhibited in myocardial cells and vascular smooth muscle by this enzyme.

Positive inotropic and vasodilator actions make it an ideal drug in the short term treatment of heart failure.

17
Q

What is Dopamine?

A

Dopamine:
—Synthesized locally in the epithelial cells of the renal tubules and exerts its effect directly.

Low concentrations:
Acitivation of dopamine receptors, D1 receptors in the Proximal Renal Tubule and in the Loop of Henle increases cyclic adenosine monophosphate formation, resulting in inhibition of the Na+ H+ exchange and Na-K+ ATPase pump.
D1 receptors mediate an increase in renal blood flow leading to a small increase in GFR.

High concentrations:
Sympathetic activation begins to dominate
Increased inotropy
Increase CO
Increase in systemic blood pressure
Even higher doses, alpha activation prevails, leading to vasoconstriction

18
Q

What is Fenoldopam?

A
  • -Fast acting IV HTN
  • -Short half-life 10 minutes
  • -Used in Short-term treatment of patients with severe hypertension
  • -Selective D1 receoptor agonist with moderate affinity to x2 receptors.
  • -No effect on D2, B or X1 receptors.
  • -Increased renal blood flow and decreases SVR.
  • -Both dopamine and fenoldopam have poor availability after oral intake and are administered IV.