2 - Cardiovascular I Flashcards by Joanna Brown

What percentage of blood is in arteries at any given time?

What percentage is in veins?

Only 20% is in arteries

64% of the blood is in veins, venules, and venous sinuses

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What is systemic filling pressure?

The force returning blood to the heart

Think of it as the degree to which blood is returning to the heart

Normal is about 7 mmHg. Constriction of veins increases the SFP, increasing the amount of blood returning to the heart

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If the EF of the LV is 45%, what is the EF of the RV?

In a normal heart, they are always the same

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What determines arterial pressure?

Peripheral resistance x CO

An increase in either peripheral resistance or Cardiac Output will increase BP

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Under normal circumstances, Arterial Pressure is regulated by three systems:

In abnormal circumstances it is regulated by four:

The ANS

RAAS

Kidneys

Also controlled by natriuretic peptides in abnormal situations

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ANP is produced by:

BNP is produced by:

CNP is produced by:

ANP: myocytes of the atria

BNP: myocytes of the ventricles (and a little bit in the brain)

CNP: cells of the vascular endothelium

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What do ANP and BNP do?

Increase vascular permeability - moves fluid out of vasculature and into interstitial spaces
Cause diuresis and Natriuresis in the Kidney
Dilate arterioles and veins by suppressing SNS output from the CNS

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Diuretics work primarily by interfering with _______

Reabsorption

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Most diuretics share the same basic MOA:

blockade of sodium and chloride reabsorption

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The increase in urine flow that a diuretic produces is directly related to:

the amount of sodium and chloride reabsorption that it blocks

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Furosemide MOA

Blocks Na and Cl reabsorption in the Thick Ascending, preventing passive reabsorption of water

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Why is Lasix helpful in patients with severe renal failure?

Unlike thiazides, it can promote diuresis even when RBF and GFR are low

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What kind of diuretic should be used in a patient taking digoxin?

Potassium sparing

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Name the four loop diuretics:

Lasix

Ethacrynic acid

Bumetanide

Torsemide

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What is the MOA of Hydrochlorothiazides?

blocks reabsorption of Na and Cl in the early segment of the distal tubule

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What is the primary indication for Hydrochlorothiazide?

Essential HTN

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What class of diuretics is spironolactone in?

potassium sparing Aldosterone antagonists

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What is the MOA of spironolactone?

Blacks the actions of aldosterone in the distal nephron

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What are some side effects of Aldactone?

High K, obviously

But it is a steroid derivative, so it can have some steroid side effects: gynecomastia, menstrual irregularity, impotence, hirsutism, deepened voice

Which drugs should be avoided in patients taking spironolactone?

ACE inhibitors

ARBs

Direct Renin Inhibitors

All of these suppress aldosterone, and can elevate potassium levels

Spironolactone carries a black box warning for:

being tumorigenic in rats

What are the three potassium sparing diuretics?

Spironolactone

Triamterene

Amiloride

Triamterene and Amiloride carry a black box warning for:

Hyperkalemia

What is the preferred drug treatment for HTN in pregnant women?

Methyldopa

Labetalol

Which BP medications cannot be continued during pregnancy?

ARBs ACEIs DRIs Anything that messes with aldosterone messes with the baby

What are the direct actions of Angiotensin II?

1. Vasoconstriction (acts directly on vascular smooth mm) primarily in arteries 2. Synthesis and Release of Aldosterone from the Adrenal cortex

What are the indirect actions of Angiotensin II?

1. Promotes NE release by the SNS 2. Promotes Epi release from the adrenal medulla 3. increases CNS SNS outflow to blood vessels

What effect does Angiotensin II have on the heart and vasculature?

May cause hypertrophy and remodeling by: 1. Causing hypertrophy of Vascular Smooth muscle cells 2. Increasing VSM cells' production of the extracellular matrix 3. Hypertrophy of cardiac myocytes 4. Increased production of ECM by cardiac fibroblasts

What are the direct actions of Aldosterone?

Acts on distal tubule to cause retention of sodium and water AND excretion of potassium and Hydrogen

What are the cardiovascular effects of Aldosterone?

Promotes cardiac remodeling and fibrosis Dysrhythmogenic (decreases NE reuptake in the heart) Promotes vascular fibrosis Disrupts the baroreceptor reflex

What triggers renin release?

Decreased BP Decreased volume Decreased RBF Sodium Depletion Beta ONE stimulation

Where is ACE located?

In the luminal surface of all blood vessels, BUT the lung's vasculature is especially rich in ACE

ACE is an enzyme that acts on which substrates?

Angiotensin I BUT ALSO BRADYKININ When its acting on Angiotensin I it's called ACE When it's acting on Bradykinin it's called Kinase II

Where is Angiotensin II produced?

It's produced in the blood, but it's also produced in individual tissues So that they can perform local autoregulation It's inhibition of this local Angiotensin II production by ACEs that causes a lot of its side effects

What are the most prominent adverse effects of ACE inhibitors?

Cough Angioedema First dose hypotension Hyperkalemia

Anytime an ACE inhibitor is used the amount of _____ decreases and the amount of ______ increases

Angiotensin II increases BUT bradykinin increases, because it's no longer being broken down into its inactive form

Why do ACE inhibitors cause coughing and angioedema?

Because of the increased bradykinin levels

A decrease in circulating Angiotensin II causes:

Vasodilation Decreased blood volume Decreased cardiac and vascular remodeling Potassium Retention Fetal Injury

All ACE inhibitors are excreted by:

the kidney

What are some advantages to using ACE inhibitors for HTN? (5)

1. They don't mess with CV reflexes, unlike A&B blockers. This means people can still exercise etc. 2. Can be used safely in asthmatics 3. Don't cause hypokalemia, hyperuricemia, or hyperglycemia (unlike thiazides) 4. Rarely induce lethargy or sexual dysfunction 5. *Reduce the risk for CV mortality cause by HTN*

Which patients absolutely cannot receive ACE inhibitors?

1. During 2nd and 3rd trimesters 2. In patients with bilateral renal artery stenosis

Why do ACE inhibitors cause renal failure in patients with renal artery stenosis?

Efferent arteriole constriction is the only this keeping the kidney going if it's main supply is cut off, and that's achieved through Angiotensin II If you cut out Angiotensin II, the kidney can't compensate and fails

What is the MOA of ARBs?

block access of Angiotensin II to its receptors in blood vessels, adrenal gland, and other tissues

What is the primary difference between ACE inhibitors and ARBs?

ARBs do not increase levels of Bradykinin in the lungs

Which patient should receive an ARB post MI?

Only one who can't tolerate ACE inhibitors. They are not as cardioprotective

If a patient has angioedema with an ACE inhibitor, will they have the same reaction to an ARB?

Only about 8% will

ARBs carry a black box warning for:

fetal injury during 2nd and 3rd trimester (just like ACE inhibitors)