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Pharmacology > Perfusion Concept: Cardiovascular Disease > Flashcards

Perfusion Concept: Cardiovascular Disease Flashcards

1
Q

What is blood pressure?

A

Blood pressure is identified as systolic over diastolic and represents the cardiac output (the contracting and relaxation of the heart). BP= Cardiac Output X Systemic Vascular Resistance

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2
Q

What is cardiac Output?

A

The cardiac output represents the exertion being placed on the heart. It demonstrates the amount of work being placed on the heart during each contraction. CO= Stroke Volume X Heart Rate

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3
Q

What is Systemic Vascular Resistance?

A

Systemic vascular resistance represents the width of the arteries. The more dilated the artery is the less pressure/resistance. A narrow artery will increase the resistance.

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4
Q

What is the calculation for mean arterial pressure?

A

Mean arterial pressure= Systolic + 2(Diastolic) divided by 3

Double the diastolic blood pressure and add the sum to the systolic blood pressure. Then divide by 3.

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5
Q

How does Blood volume affect blood pressure?

A
  • Fluid retention will cause an increase in blood volume, increase the CO and the SVR ultimately increasing BP
  • Fluid loss will cause dehydration leading to a decrease in blood volume and decreased CO due to the low pre-load
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6
Q

How does peripheral resistance affect blood pressure?

A

When the arteries are narrowed the pressure within will increase, causing an increased resistance during blood flow. As the arteries dilate the resistance decreases as well as the pressure within the lumen.
-Angiotensin II is a hormone that is released to stimulate vascular constriction (constricting the arteries in order to increase blood pressure)

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7
Q

How does Cardiac Output affect Blood pressure?

A
  • Stroke volume identifies the preload (filling the heart with blood), the contractility of the myocardial muscles as well as the afterload (ejection of blood). If the stroke volume increases or decreases it has a direct effect on the cardiac output and will have an effect on BP
  • Heart Rate will also affect CO, the frequency of beats will determine the stress on the heart and the BP
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8
Q

What is the role of aldosterone?

A

aldosterone is a hormone released in order to stimulate the kidneys and control the retention of sodium and excretion of potassium. This controls the blood volume and has an overall effect on the BP

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9
Q

What is the Renin-angitensin-aldosterone system?

A

RAAS is to increase the BP:

  1. when the blood pressure drops below average it stimulates the initiation of the RAAS system
  2. The sympathetic nervous system is stimulated and triggers the stimulation of the kidneys, causing the release of renin
  3. The release of renin into the system causes the release of angiotensinogen by the liver
  4. The interaction between angiotensinogen and renin causes the creation of angiotensinogen I
  5. Angitensigonen I is converted into angiotensinogen II by an ACE enzyme
  6. The angiotensinogen II which is responsible for stimulating the adrenal glands
  7. The adrenal gland secretes aldosterone which stimulates the kidneys into retaining sodium, but excreting potassium (which allows for water retention) as well as causing vasoconstriction
  8. Increasing blood volume, and SVR. Causing the BP to increase.
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10
Q

How can Hypertension be treated?

A
  • Lifestyle changes such as; diet, exercise, cessation of smoking and reduced alcohol intake.
  • Medication treatment
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11
Q

What are beta-blockers? (androgenic agents)

A

Beta-blockers decrease heart rate and cardiac output by blocking the effects of epinephrine (adrenaline).
-Beta-blockers make sure norepinephrine and epinephrine CANNOT bind to the beta receptors. By blocking these receptors the sympathetic nervous system will be inhibited. Causing a decrease in heart rate, increased urination, decreased stroke volume. All these factors decreased BP

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12
Q

Where are beta-1 receptors located?

A

-They are located in the heart and kidneys

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13
Q

Where are beta-2 receptors located?

A

-They are located in the lungs, GI tracts, Bladder, uterus, Liver and blood vessels. Beta-2 receptors are responsible for smooth muscle relaxation

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14
Q

What do beta-blocker medications end in?

A

All beta-blocker names end in ‘LOL’

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15
Q

Side Effects of Beta Blockers? (Nursing Considerations)

A
  • Bradycardia
  • Heart failure
  • Asthma and COPD (patients with respiratory complications cannot use non-selective bet blockers due to bronchoconstriction)
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16
Q

What are Ace-Inhibitors?

A

They inhibit the conversion of angiotensin I to angiotensin II. Angiotensinogen II is responsible for stimulating the adrenal glands in order to release aldosterone which increases the blood volume (by allowing sodium retention but excreting potassium) as well as promotes vascular constriction. However, by inhibiting angiotensinogen II we inhibit this cascade of reactions.
*The ACE inhibitor prevents the ACE enzyme from converting angiotensinogen I into angiotensinogen II!

-Without the increase of systemic vascular resistance the blood vessels will dilate, causing a decrease in CO and ultimately a decrease in BP.

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17
Q

What do Ace inhibitors end in?

A

-ACE inhibitors end in ‘pril’

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18
Q

Side Effects of Ace inhibitors? (Nursing Considerations)

A
  • Persistent COUGH!
  • Severe Hypotension
  • Renal Failure (monitor creatinine levels, normal range is; 0.6-1.2 mg/dL)
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19
Q

What are Angiotensin II receptor blockers (ARBs)?

A

Angiotensin II receptor blockers (ARBs) inactivate the receptors that readily accept angiotensin II, so angiotensin II can’t bind to its receptors to do its job. LEading to vasodilation of vessels and decreased SVR, decreasing BP.

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20
Q

What do ARBs end in?

A

ARBs will end with “sartan”

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21
Q

Side Effects of ARBs? (Nursing Considerations)

A
  • Monitor potassium levels (hyperkalemia, the normal range is; 3.5-5 mEq/L)
  • Avoid high potassium foods
  • Assess for hypotension
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22
Q

What are Calcium Channel Receptor Blockers?

A

-They inhibit the movement of calcium ions into the myocardial and vascular smooth muscle. They work by reducing the contractility of the cardiac muscles to decrease CO.

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23
Q

What are Vascular selective drugs?

A

They target smooth muscle

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24
Q

What are Cardio selective drugs?

A

They target the cardiac muscle (myocardial cells). These medications are used to treat arrhythmias and atrial fibrillation

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25
Q

Name Two vascular-selective drugs.

A

Nifedipine (Adalat) and Amlodipine (Norvasc)

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26
Q

Name Two cardio-selective drugs.

A

Verapamil (Isoptin) and Diltiazem (Cardizem)

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27
Q

What is the Effect of calcium channel blockers?

A
  • Decreased heart rate
  • Decreased cardiac output
  • Decreased blood pressure
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28
Q

Side Effects of calcium channel blockers (Nursing Considerations)

A
  • Dizziness, flushing
  • Hypotension
  • Dysrhythmias
  • Reflex tachycardia (If blood pressure decreases, the heart beats faster in an attempt to raise it)
  • Assess for pulmonary edema
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29
Q

What is Gingseng?

A

Gingseng is a calcium channel antagonist, it is a natural health product

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30
Q

What is the therapeutic dose of ginseng?

A

20-30 mg/day

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31
Q

What are Centrally acting alpha2 adrenergic agonists?

A

These drugs stimulate the CNS alpha 2 receptors in the vasomotor center directly. The presynaptic alpha-2 receptors inhibit the release of norepinephrine

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32
Q

Side Effects (Nursing Considerations)

A
  • Hypotension

- Headache

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33
Q

What do Calcium Channel Blocker end in?

A

They end in ‘pene’

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34
Q

What is a diuretic?

A

Decrease blood volume by excreting sodium and water. decreasing the blood volume will decrease the BP and CO

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35
Q

What are the four types of diuretics?

A

Loop diuretics, Potassium sparing diuretics, Thiazide Diurectics and osmotic diuretics

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36
Q

What are loop diuretics?

A

Loop diuretics block the reabsorption of NA+, K+ and Cl- at the loop of Henle. Forcing the molecules to be excreted through the urine. This kind of diuretic is potent and is administered through IV or PO

37
Q

Side Effects of Loop Diuretics (nursing considerations)

A
  • Hypokalemia!
  • Ototoxicity
  • High PPB (stay within the blood for a long period of time before being metabolized therefore there is a high chance of drug interaction)
  • Dehydration
38
Q

What are Thiazide diurectics?

A

Thiazide diuretics inhibit the reabsorption of Na+, K+, and Cl- at the renal distal convoluted tubule! It is administered by PO

39
Q

Side Effects of Thiazide diurectics

A
  • Hypokalemia (low potassium levels)
  • Hyponatremia (low sodium levels)
  • Dehydration
40
Q

What is Potassium SparingDiuretics?

A

-Blocks renal aldosterone (Remember: Aldosterone causes Na+ retention) Untilmately doing the opposite as aldosterone by; excreting sodium and keeping the potassium

41
Q

Side Effects (Nursing Considerations)

A

-Hyperkalemia

42
Q

What are Osmotic Diurectics?

A

Osmotic diuretics pull solvents into circulation and into renal tubules and inhibits renin release

43
Q

What are Osmotic Diuretics used to treat?

A

-Cerebral edema
-Intraocular Hypertension
-

44
Q

What are direct-acting vasodilators?

A

These are used for emergency treatment during a hypertensive crisis. These drugs are administered PO, IV, parenteral

45
Q

How do Direct Acting Vasodilators work?

A

Direct-acting vasodilators act by dilating the arterioles to reduce SVR. This medication stimulates the release of Nitric oxide which activates a cycle of reactions to activate Protein Kinase G which initiate the relaxation and dilation of the blood vessels

46
Q

What are low-density lipoproteins? (LDL)

A

LDLs are low density-lipoproteins. they are composed of triglycerides, cholesterol and phospholipids. These lipoproteins carry the MOST amount of cholesterol
LDL= Bad cholesterol!

47
Q

What are high-density lipoproteins? (HDL)

A

HDLs are high-density lipoproteins, they are composed of cholesterol, triglycerides AND apoprotein!
HDL= Good cholesterol!

48
Q

What is the role/function of LDLs?

A

They transport cholesterol from the liver to the tissues and organs where it is used. The excess cholesterol is stored within the lining of the blood vessels, which contributes to plaque build-up over time.

49
Q

What is the role/function of HDLs?

A

HDL uptakes cholesterol and brings it to the liver to be processed! The cholesterol is then broken down by bile and excreted through feces.

50
Q

What is atherosclerosis?

A

The buildup of plaque within the arterial walls, causing the narrowing of the blood vessels. Ultimately leading to Hypertension as the SVR increases.

51
Q

How is Cholesterol Synthesized?

A

Cholesterol is created in the liver!

  1. Acetyl CoA and acetoacetyl CoA initiate HMG-CoA synthase
  2. The HMG-CoA is synthesized
  3. The HMG-CoA reductase is synthesized and created mevalonic acid which creates cholesterol
52
Q

What are the steps in plaque pathogenesis?

A
  1. The endothelial cells have been damaged due to exposure to risk factors (for example; hypertension, smoking, high blood glucose (hyperglycemia) All of these factors INCREASE the amount of LDLs in the bloodstream
  2. Due to cell damage, the permeability of the arterial wall is increased! (the wall is more permeable to contents) Therefore, allowing the LDL to easily enter the Tunica Intima of the artery!
  3. The damaged cells initiate a ‘healing process by producing adhesion molecules (ex. VCAM-1), these molecules CAPTURE white blood cells (WBC) such as monocytes
  4. When the monocyte attaches to the adhesion molecules, the monocyte is able to penetrate into the tunica intima of the artery
  5. WBCs are capable of producing FREE RADICALS. These radicals are responsible for the oxidation of the LDL molecules that entered the artery
  6. Once LDL is oxidized, it triggers the immune response
  7. The immune response is initiated and attracts more monocytes to the site of injury! This causes an accumulation of oxidized LDL molecules and WBCs
  8. Macrophages (a type of WBC) is brought to the tunica intima as a result of the immune response trigger and ENGULFS the oxidized LDL cells
  9. When the LDL molecules are taken up by the macrophages they are converted into FOAM CELLS
  10. The foam cells after time die (apoptosis) and leave behind lipids!
  11. This process will continue and as a result, there will be an accumulation of lipids (fat) in the arterial wall.
    The lipid accumulation will cause the formation of plaque and the plaque will harden over time ultimately narrowing the artery.
53
Q

What is angina?

A

Angina is chest pain or discomfort caused when your heart muscle doesn’t get enough oxygen-rich blood. if there is a blockage or a complication in blood flow the heart will not receive enough blood.

54
Q

Signs and Symptoms of Stable angina

A
  • Chest pain with exertion
  • Pain relieved when resting
  • Shortness of Breathe
  • Fatigue
  • Pain is relieved with Nitroglycerin
55
Q

What is Unstable angina?

A

Unstable angina is a medical emergency and is identified through severe chest pain that is not relieved after resting or after administering nitroglycerin tabs. These cases need to be treated immediately and can lead to myocardial infarction.

56
Q

How to diagnose atherosclerosis?

A
  • Blood tests: identifying LDL and HDL levels, cholesterol levels
  • EKG: asses for changes is ST segment
  • Stress Test: shows how the heart reacts to physical activity
57
Q

What is Dyslipidemia?

A

Occurs when LDL and cholesterol levels are elevated. An abnormal or excessive amount within the bloodstream. Dyslipidemia aggregates the process of atherosclerosis

58
Q

Signs and Symptoms of Dyslipidemia (Nursing Considerations)

A
  • Chest pain
  • Dizziness
  • Heart palpitations
  • Exhaustion
  • Swelling of ankles and feet
  • Yellowish fatty bumps on the skin
  • Poor diet
59
Q

How is Dyslipidemia Diagnosed?

A

it is identified through a blood test. The serum lipid levels are measured, same as HDL and LDL

60
Q

How is Dyslipidemia Treated?

A
  • Through lifestyle changes such as (exercise, healthy diet, decreasing tobacco use and decreasing alcohol consumption)
  • The first line of medical treatment are STATINS!
61
Q

What are statins and how do they work?

A

Statins act by inhibiting HMG-CoA reductase which results in the inhibition of cholesterol synthesis. As the liver makes less cholesterol, it responds by making more LDL receptors on the surface of the liver cells
The more LDL receptors sites on the liver will increase the REMOVAL of LDL from the blood.
Blood levels of cholesterol and LDL reduce

-They are administered PO

62
Q

What do statins end in?

A

All statins end in ‘Statin’!

63
Q

What is coronary artery disease?

A

Coronary artery disease is caused by plaque buildup in the wall of the arteries that supply blood to the heart. the lack of blood flow causes a lack of oxygen supply to the heart and myocardial muscles.

64
Q

What is chronic CAD?

A

Chronic coronary artery disease is the narrowing of arteries overtime, due to the accumulation of plaque within the arterial walls. A thick fibrous layer of plaque in preserving a small lipid pool within the lumen.
-Stable angina a prominent symptom is CAD

65
Q

What is acute CAD?

A

Acute coronary artery disease is the sudden reduced blood supply to the heart. This occurs when a large lipid pool within the coronary artery is coated in a thin fibrous layer. Causing a rupture of plaque and initiating an inflammatory response, resulting in the complete blockage of the artery.

  • Unstable angina is a common result. Unstable angina occurs when the heart doesn’t get enough blood flow and oxygen.
  • Medical emergency*
  • Myocardial infarction (HEART ATTACK) If the ischemia is severe it might block the artery completely and stop the blood flow to the heart.
66
Q

How to treat acute CAD?

A
  • antiplatelets

- Thrombolytics!

67
Q

How to treat chronic CAD?

A
  • Treat associated symptoms such as hypertension, dyslipidemia, dietary habits
  • Anti-coagulants
  • Antiplatelet
68
Q

What is Hemostasis?

A

Hemostasis is the mechanism that leads to the cessation of bleeding from a blood vessel. This occurs in three steps;

  1. vascular spasm
  2. platelet plug formation
  3. blood clot formation
69
Q

What is the pathophysiology of Hemostasis and Coagulation?

A
  1. A damaged blood vessel will express vWF (von Willebrand factor)
  2. vWF binds platelets to the collagen within the vessel wall
  3. As the platelets bind to vWF they activate and transform in shape
  4. active fibrinogen receptors (GPIIb/IIIa) is expressed
  5. The activated platelets begin to secrete granules to aid in the process (Alpha and dense granules)
  6. Fibrinogen binds to the Finbringoen receptors (GPIIb/IIIa) on activated platelets
  7. The activated platelets that are attached to the collagen membrane releases the Prothrombin activator
  8. The prothrombin activator stimulates the release of prothrombin (which is produced in the liver and is vitamin K dependent!)
  9. The prothrombin transforms into thrombin!
  10. the thrombin converts fibrinogen into fibrin
  11. The fibrin molecules then combine to form long threads and entangle the platelets. This will gradually harden and contract to form a blood clot
70
Q

What are antiplatelets?

A

They stop platelets from sticking together and forming a clot. By stopping the binding/linkage of platelets we inhibit the creation of ‘plug’ in the injured area and inhibit the creation of a clot!

71
Q

What are anticoagulants?

A

Anticoagulants directly affect the steps within the coagulation cascade to inhibit coagulation and inhibit blood clotting

72
Q

Unfractionated Heparin (UFH) function.

A

This anticoagulant prohibits the release of Factor Xa. Factor Xa is a serine protease that cleaves prothrombin into thrombin which allows for fibrinogen to be cleaved into fibrin. This inhibition of this process, therefore, inhibits the clotting cascade.
These are used mainly in hospitals via IV before and after surgeries

73
Q

Low molecular weight Heparin function.

A

Low molecular weight heparins are administered at home. They are less potent, however, accomplish the same task as UFHs. They inhibit the release of Factor Xa, therefore, inhibiting the formation of prothrombin.

74
Q

What are Vitamin K dependant antagonists?

A

Promothorbin relies on K+ (potassium) in order to synthesize. If prothrombin is unable to be synthesized there is no thrombin, fibrinogen or fibrin!

75
Q

What are Thrombolytics?

A

Thrombolytics are used in emergency situations in order to lyse the blood clot. The thrombolytic drug dissolves the blood clot by activating plasminogen which is cleaved into plasmin. The plasmin is capable of breaking links between the fibrin mesh. Ultimately destroying the blood clot.

76
Q

What is an Ischemia?

A

Ischemia occurs when there is a blockage within the blood vessels and results in a lack of blood flow. The lack of blood flow and oxygenation will cause cell necrosis. te lack of oxygen forces the cells to respire anaerobically (without oxygen) which over time will cause acidosis.

77
Q

Signs and Symptoms for Ischemia. (nursing considerations)

A
  • Assess pain
  • Numbness
  • SOB
  • Hypoxemia (not enough oxygen in the blood)
  • No contractility
  • Injury to myocardial cells (check for creatinine and Tropinin levels)
  • Inflammation
78
Q

What is the treatment Focus for MI? (heart attack)

A
  • Oxygenate
  • Vasodilation!
  • Return BP to normal
  • Treat obstruction
  • Treat clotting
  • Treat underlying issues/symptoms (dyslipidemia, atherosclerosis, diet, exercise etc)
79
Q

What is a Thrombus?

A

A blood clot!

80
Q

What is an embolism?

A

When a piece of a blood clot (thrombus) has been dislodged and gets stuck in another rea of the body.

81
Q

What is DVT?

A

Deep veined Thrombosis (a blood clot that is found within the deep veins)

82
Q

Pathophysiology of DVT?

A
  1. Damage to the endothelium
  2. Damaged cells vasoconstrictor and express VCAM-1 in order to initiate the clotting cascade
  3. The platelets bind to adhere to each other at the damaged site
  4. the binding of the platelets to the collagen wall cause differentiation
  5. The activated platelets form a platelet plug
    The coagulation cascade initiates
83
Q

Effects of DVT?

A
  • Decreased blood flow
  • Increased venous pressure
  • Increased blood pressure
84
Q

What is Virchows Triad?

A
  1. Slowed Blood Flow (stasis)
  2. Hypercoagulation (altered amount of clotting factors)
  3. Damage to blood vessel

All of these factors promote DVT and are risk factors

85
Q

Why is pregnancy and taking birth control increase the risk of DVT?

A

High estrogen levels affect blood clotting by increasing fibrinogen and the activity of the coagulation factors! Increased fibrinogen causes an altered amount of clotting factors and contributes the Hypercoagualation!

86
Q

What is a pulmonary embolism?

A

A pulmonary embolism is a blockage within the lungs. This is caused by a piece of a thrombus that has been dislodged and free within the circulation.

87
Q

Signs and Symptoms of a pulmonary embolism.

A
  • Shortness of breath
  • Low O2 sat
  • Chest pain
88
Q

How to diagnose Pulmonary embolism?

A

CT scan

89
Q

How to treat a pulmonary embolism?

A
  • anticoagulants

- thrombolytics

Pharmacology (27 decks)

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