Perfusion: Final Exam Flashcards
Define Hypertension.
Hypertention= High Blood Pressure
Hypertension represents an elevation in the systolic and diastolic blood pressure.
Blood Pressure calculation.
Blood Pressure (BP)= Cardiac Output (CO) x Systemic Vascular Resistance (SVR)
Cardiac Output calculation.
Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)
Systemic Vascular Resistance calculation.
Systemic Vascular Resistance= Dilated artery/vessel (Low resistance), A narrow and constricted artery/vessel (High resistance)
Mean Arterial Blood pressure calculation.
MAP= 2(Diastolic) + sysolic
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What are Beta-adrenergic Blockers?
Beta-blockers decrease heart rate and cardiac output by inhibiting the binding of epinephrine onto the beta receptors found on the myocardial fibres. Reducing the number of times the heart contracts and the force it contracts; causing the blood pressure to lower.
Where are Beta-1 Receptors Found?
Beta-1 receptors are predominantly found in three locations: the heart, the kidney
Where are Beta-2 Receptors Found?
Beta-2 receptors are found in the bronchioles of the lungs, GI system, skeletal muscle
What do Beta-Blocker medications end in?
Beta-blocker medications end in ‘lol’
What are ACE inhibitors?
Angiotensin-converting enzyme inhibitor medications inhibit the conversion of angiotensin I to angiotensin II. The decrease of angiotensin II reduces its vasoconstriction effects, therefore reducing the SVR resulting in vessel dilation. Ultimately, reducing blood pressure.
Process of Angiotensinogen II Release.
- The blood pressure drops (Detected by the baroreceptors)
- The sympathetic nervous system is stimulated and sends signals to the kidneys
- Once stimulated the juxtaglomerular cells to release renin
- When angiotensinogen and renin combine they react together and transform into angiotensin I
- ACE (angiotensin-converting enzyme) is released from the endothelium of the kidneys. The purpose of the ACE enzyme is to convert Angiotensin I to Angiotensin II
- Angiotensin II is responsible for constricting the blood vessels and increasing blood volume
What Are Calcium Channel Blockers?
Inhibit the movement of calcium into cardiac and vascular smooth muscle. They have a direct myocardial effect that reduces the cardiac output through a decrease in cardiac contractility and heart rate. They also act on the vascular and arterial smooth muscles causing relaxation and dilation of the blood vessels. Further contributing to the drop in blood pressure!
What do Calcium Channel Blockers End In?
Calcium channel blockers end in pene.
How do Calcium Channel Blockers Work?
In order for the heart to contract the calcium must enter the cardiac muscle. Inhibiting the entrance of calcium inhibits cardiac contraction. Calcium channel blockers also work on the smooth muscles, causing arterial dilation!
- They promote smooth muscle relaxation
- Vasodilation
- Decrease contractility of the heart
What are Diuretics?
Decrease circulation blood volume by helping to rid the body of salt (sodium) and water. The sodium helps remove water from your blood, decreasing the amount of fluid flowing through your veins and arteries. This reduces blood pressure.
- First Line of Treatment
- Increased Urine Output
Loop Diuretics.
Blocks the re-absorption of Na+, K+, and Cl- at the loop of Henle. By blocking the reabsorption of sodium, chloride and potassium, they will excrete themselves with the waste and be removed from urine. As sodium exits the system, water will follow resulting in a decrease in blood volume, due to the increased loss of fluids.
Loop Diuretic Medications.
Furosemide (Lasix)
Thiazide Diuretics.
Work similarly to loop diuretics however block the re-absorption of Na+, K+, Cl- at the renal distal convoluted tubules. The loss of fluids will decrease the blood volume.
Thiazide Diuretic Medications.
Hydrochlorothiazide (HZTZ), Chlorothiazide (Diruil), Metolazone (Zaroxolyn)
Potassium Paring Diuretics.
Increase nephron reabsorption of potassium by interrupting sodium reabsorption in the collecting duct. Potassium-sparing diuretics block renal aldosterone, which increases sodium excretion but spares potassium.
Potassium Sparing Diuretic Medications.
Meds: Spironolactone (Aldactone)
Osmotic Diuretics.
Inhibits reabsorption of water and sodium. They pull the solvent (water) into circulation and into the renal tubules at the proximal tubule and loop of Henle
Osmotic Diuretic Medications.
Meds: Mannitol (Osmitrol) and Isosorbide
Angiotensin II Receptor Blockers (ARBs).
ARBs inhibit the binding of angiotensin onto the receptors site of the smooth muscle cells. By antagonizing the receptor site, angiotensin is unable to bind and constrict the blood vessel.
ARB’s Medications.
Meds: Losartan (Cozaar), Ibesartan (Avapro)
Adrenergic Antagonists.
Adrenergic antagonists are compounds that inhibit the action of adrenaline (epinephrine), noradrenaline (norepinephrine), and other catecholamines that control the autonomic outflow. By inhibiting the binding of catecholamines t the adrenergic receptor site these drugs play an antagonistic role which results in;
- Decreased HR
- Decreased Conduction rate
- Decresed streghth of contratility
- Vasodilation
Adrenergic Antagonist Medications.
Meds: Atenolol, Propranolol and Metoprolol
Alpha1 Receptors.
Adrenergic receptors are located on the smooth muscles of the vascular, genitourinary, intestinal, and cardiac systems. When these receptors are stimulated they cause:
- Vasoconstriction
- Increase Heart Rate
- Increase Blood Pressure
- Pupil Dilation
- Constriction of the urinary sphincter
How is Cholesterol Synthesized?
Cholesterol is manufactured in the liver by a series of enzymatic reactions! Beginning with acetyl CoA is produced from the breakdown of fatty acids
- Acetyl CoA and acetoacetyl CoA initiate HMG-CoA synthase
- The HMG-CoA is synthesized (3-hydroxy-3methyl-glutaryl-CoA=HMG-CoA)
- The HMG-CoA reductase is synthesized and creates mevalonic acid
- Which Ultimately creates Cholesterol
What are Phosphodiesterase Inhibitors?
Phosphodiesterase inhibitors prevent the phosphodiesterase enzymes from breaking down cAMP and cGMP in the cell. As a result, they increase the cAMP and cGMP, leading to a decrease in intracellular calcium, which causes vasodilation and smooth muscle relaxation.
- The production of cAMP and cGMP are regulated by a molecule called nitric oxide, and their function is to help regulate physiological processes by decreasing the levels of calcium in the cell. Ultimately, cAMP and cGMP are broken down by phosphodiesterase enzymes. Therefore, the lack of phosphodiesterase leads to the inhibition of cAMP breakdown.
Define Atrial Flutter.
caused by an electrical impulse that travels around in a localized self-perpetuation loop in the right atrium. This causes the atrial rate to be higher than the ventricular rate. It occurs when a short circuit in the heart causes the upper chambers (atria) to pump very rapidly.
Define Atrial Fibrillation.
Caused by multiple electrical impulses that are initiated randomly. These un-synchronized, chaotic electrical signals cause the atria to quiver or fibrillate rather than contract.
AV Nodal Re-entry Tachycardia.
Occurs when one or more extra electrical pathways near the Atrioventricular or AV node allow an electrical impulse to loop back on itself or short circuit. The episodes are due to an extra pathway located in or near the AV node that causes the heart to beat prematurely.
Define Ventricular Fibrillation.
Is caused by multiple weak ectopic sites in the ventricles. These un-synchronized, chaotic electrical signals cause the ventricles to quiver or fibrillate rather than contract. The heart pumps little or no blood.
