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ACE Inhibitors and Angiotensin Receptor Blockers Beta blockers CCBs Nitrates Diuretics


Renin Angiotensin Aldosterone System

What does RAAS do?

A hormone system that regulates blood pressure and water (fluid) balance.
When blood volume is low, juxtaglomerular cells in the kidneys secrete renin directly into circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I. Angiotensin I is subsequently converted to angiotensin II by ACE found in the lungs. Angiotensin II is a potent vaso-active peptide that causes blood vessels to constrict, resulting in increased blood pressure. Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of fluid in the body, which also increases blood pressure.

Action of renin

Proteolytic enzyme, converts angiotensinogen to angiotensin 1 ( inactive)


Angiotensin Converting Enzyme
(A1 to AII)

ACE degrades ...

Bradykinin (potent vasodilator, lowers BP)

Angiotensin I

Inactive, formed from angiotensinogen by ACE

Angiotensin II

Active, formed from angiotensin I by ACE

Angiotensin II action

Causes systemic vasconstriction to push the blood to vital organs and secretes aldosterone (causes sodium and water retention),

ACE Inhibitors

Blocks ACE enzyme,also blocks angiotensin II and bradykinin. Lowers blood pressure.
Avoid with: potassium-sparing diuretics, BP lowering meds, any drug that raises potassium (hyperkalemia)
Side effects: "Ace" cough, hyperkalemia, tetrogenesis, angioedema, 1st dose hypertension
The 'pril' drugs (enalapril, captopril)


Angiotensin Receptor Blockers. These lower blood pressure. Blocks angiotensin II access to receptors on blood vessels- not affect bradykinin!!!
Avoid with: ACEi's (choose a class!), with another hypotension drug
Side effects: tetrogenesis, angioedema (very rare with this drug!)
**This is tetrogenic
The 'sartans' (Losartan, Candesartan)

Theoretical ARB benefits over ACEs:

Less drug interactions, less adverse effects, doesn't cause bradykinin accumulation.
This is a very well-tolerated drug.

Classes of drugs reduce cardiac AFTERLOAD (resistance)

Beta 1 adrenergic blockers
Calcium channel blockers (CCB's)


The RESISTANCE a muscle overcomes to contract in the aorta

Beta 1 blockers

Blocks cardiac beta receptors
Reduces: contractility, HR, CO, SV
This drugs slows the heart down so that it can rest.
Avoid with: beta inhaler, Non-dihydropyridines (CCB), insulin (hypoglycemia)
Side effects: bradycardia, broncochonstriction, blocks glyconeogenesis, fatigue, tired, depression from decreased cardiac output, Diabetecs should try and avoid this drug
Suffix "-olol" (Metroprolol)

Selective beta blockers

Block only beta-1 (cardiac)

Non-Selective beta blockers

Block all betas (heart and lungs)

Dihydropyridines (CCB)

Works on vascular smooth muscle
Side effects: Reflex tachycardia, flushing, dizziness, headache, edema
** This works well with Beta blockers (to control the tachycardia)
Drug name: suffix "-dipine" (Amlodipine)

Non-dihydropyridines (CCB)

Works on vascular smooth muscle and the heart
Side effects: Bradycardia, flushing, dizziness, headache, edema
*Do NOT use with Beta blockers, and do NOT use with digoxin (toxicity increased)
Drug name: Verapamil, diltiazam, Cardizem

Nitrate (Nitroglycerin)

Systemic vasodilator, mainly works on veins, but do impact the arteries. Decreases BOTH afterload and preload. Decreases demand and workload but does NOT decrease O2 demand or blood volume.
Avoid with: Phosphidiasterase 5 inhibitors (viagra/cialis)
Good with: CCB's and Beta blockers
Side effects: Reflex tachycardia (beta blocker helps this), edema (diuretic), orthostatic hypotension, headache, tolerance, hypertrichosis

RAAS inhibiting drugs

1) ACEi- Blocks ACE enzyme
2) ARB's- blocks Angiotension II
access to receptors

Class of drugs to decrease cardiac PRELOAD

Diuretics (3 kinds)


The amount of STRETCH or tension applied to a muscle prior to contraction

High ceiling diuretics

Block sodium reabsorption in the ascending loop of Henle. Reduces edema and fluid overload, decreases BOTH preload and afterload, kidney disease
Avoid with: other BP lowering meds, other ototoxic meds,
Do not use with Digoxin!!!
Good with: Potassium sparing diuretics
Side effects: dehydration, hypotension, ototoxicity, hyponatremia, hypokalemia, hyperuricemia
** Not known to be tetrogenic
Drug name: Furosemide


Blocks sodium chloride reabsorption in the distal convoluted tubule. Reduces edema and hypertension.
Avoid with: other BP lowering meds, pregnancy and breastfeeding, Do not use with Digoxin!!!
Good with: Potassium sparing diuretics
Side effects: tetrogenesis, hyponatremia, hypokalemia, hyperuricemia
**This is tetrogenic
**Not ototoxic, well tolerated

Spironolactone (Potassium sparing diuretic)

Blocks aldosterone in the distal nephron, sodium and water loss without losing potassium
Avoid with: ACEi's (also raises potassium)
Good with: other diuretics
Side effects: Hyperkalemia (too high)
This drug gets combined with other diuretics (high ceiling and thiazide) to prevent potassium loss
Drug name: Aldactone

Triamterene (Potassium sparing diuretic)

Disrupts potassim/sodium exchange in the distal nephron, sodium and water loss without losing potassium
Avoid with: ACEi's (also raises potassium)
Good with: other diuretics
Side effects: Hyperkalemia (too high), leg cramps
This drug gets combined with other diuretics (thiazide) to prevent potassium loss

Physiological regulators of blood

1) Sympathetic nervous system
3) Kidneys

Cardiac output

Amount of blood expelled by the ventricles of the heart per minute, determined by heart rate, contractility, blood volume, and venous return, 5L per minute (healthy)
CO = HR x SV

Stroke volume (SV)

Amount of blood expelled in one heartbeat

Myocardial contractility

How well the muscle is working (force)

Blood pressure

Cardiac output x Peripheral resistance

Peripheral resistance

Resistance against vasculature
Determined by arteriolar constriction

The relationship of afterload (AF) and stroke volume

Indirect relationship
high AF (resistance) = low SV (blood from one heartbeat) (has to work harder against more resistance to pump)
low AF (resistance) = high SV (blood from one heartbeat)

The relationship of preload (PL) and stroke volume

Direct relationship
high PL (stretch)= high SV (blood from one heartbeat)

Cardiac remodeling

Cardiacs response to injury is changing in size and shape, heart becomes stretched out and loses some function


A steroid hormone whose overall effect is to increase reabsorption of ions and water in the kidney -- increasing blood volume and, therefore, increasing blood pressure.


Swelling of the dermis under the skin, capillaries leak, tongue swells, can be fatal


A medical emergency due to the risk of potentially fatal abnormal heart rhythms (arrhythmia).


a metabolic condition in which there is not enough sodium (salt) in the body fluids outside the cells

Hyperuricemia (Gout)

a kind of arthritis that occurs when uric acid builds up in blood and causes joint inflammation

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