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Cardiovascular Flashcards

1
Q

What is the process of atherosclerosis?

A

Plaque collects under damaged intima. Plaque collects in artery walls, causing the artery to narrow. The plaque ruptures and blood clots form.

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2
Q

What are interventions for atherosclerosis and CAD? Explain?

A

Aimed at life-style changes and early detection/intervention. Diet and lifestyle changes are tried first before medication.

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3
Q

What should fasting cholesterol level be? What are the elements of cholesterol?

A

<200 mg/dL
HDL (high-density lipoprotein)
LDL (low-density lipoprotein)
Triglycerides

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4
Q

What is the mechanism of action of statins?

What is it contraindicated in?

A

Mechanism of action is to lower LDL and triglycerides, increase the HDL, decrease synthesis of cholesterol in the liver.Contraindicated in liver disease (can cause increased LFTs). Don’t use for folks with severe muscle pain.

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5
Q

What are common potential side effects of statins?

Most serious adverse reactions?

A

Common potential side effects include abdominal cramps, diarrhea, constipation, flatus, heartburn, rash. Contraindicated in liver disease (can cause increased LFTs). Don’t use for folks with severe muscle pain.

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6
Q

What is needed to diagnose hypertension (HTN)?

A

Systolic BP consistently > or equal to 140 mm/Hg and a diastolic consistently > or equal to 90 mm/Hg on two or more different occasions.

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7
Q

What is normal BP in adults?

A

SBP is less than 120

DBP is less than 80

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8
Q

What are risk factors for secondary HTN?

A

Coarction of aorta, brain tumors, encephalitis, medications, pregnancy, renal disease, endocrine disorders

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9
Q

Early clinical manifestations of HTN?

A

Initially, asymptomatic. Headache, dizziness, fainting, vertigo, flushed face, spontaneous epistaxis, blurred vision, retinal changes

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10
Q

What occurs as HTN progresses?

A

Dyspnea, orthopnea, chest pain, leg edema, nausea, vomiting, drowsiness, confusion, numbness or tingling of extremities.

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11
Q

Very late signs and symptoms of HTN?

A

Angina, MI, heart failure, kidney changes, stroke

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12
Q

Clinical manifestations of hypertensive crisis or malignant HTN?

A

Systolic greater than 240, diastolic greater than 120. Blurred vision, severe headache, dyspnea, epistaxis, disorientation, dizziness

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13
Q

How much fluid is equal to a kilogram of pt weight when it comes to fluid loss and gain?

A

1 liter of fluid

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14
Q

What is the mechanism of action of thiazide diuretics?

A

Increased excretion of sodium and water by inhibiting sodium reabsorption in the distal tubule of kidney.

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15
Q

What is the most common potential side effect of thiazide diuretics? Serious adverse reactions?

A

Most common potential side effect is hypokalemia

Most serious adverse reaction is none

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16
Q

Nursing considerations for thiazide diuretics?

A

Nursing considerations: monitor for dehydration and hypokalemia. Usually used first as a cost-effective drug to treat uncomplicated HTN. Not used for emergency diuresis.

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17
Q

What is the mechanism of action for loop diuretics?

A

Mechanism of action is inhibited reabsorption of sodium and chloride from of Henle and distal renal tubule. Increased renal excretion of water, sodium, chloride, magnesium, potassium and calcium to promote diuresis and decrease in BP.

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18
Q

What are the most common potential side effects of loop diuretics? Adverse reactions?

A

Most common potential side effects are hypokalemia, hypomagnesemia, hyponatremia, dehydration
Most potential adverse reactions are aplastic anemia, agranulocytosis

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19
Q

What are nursing considerations for loop diuretics?

A

dehydration. Evaluate electrolytes frequently. Strict I and O. Can be given PO or IV. Used when there is an emergent need for rapid mobilization of fluid.

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20
Q

Mechanism of action for calcium channel blockers?

A

Inhibits transport of calcium into myocardial and vascular smooth muscle cells which leads to systemic vasodilation and relaxation of smooth muscles which leads to decreased BP. Acts on myocardium, SA node, and AV node.

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21
Q

Side effects and adverse effects of calcium channel blockers?

A

Side effects: Headache, facial flushing, peripheral edema, hypotension, irregular heartbeats, constipation Adverse reactions: heart block or heart failure

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22
Q

Nursing considerations for calcium channel blockers?

A

Check BP, IO, daily weight. Constipation. Teach pt to monitor bowel function. Avoid grapefruit juice. Regular dental care-may cause gingivitis.

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23
Q

Mechanism of action for ACE inhibitors?

A

blocks conversion of angiotensin I to angiotensin II. Blocks release of aldosterone which leads to decreased sodium and water retention. Antihypertensive

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24
Q

Side effects and adverse reactions for ACE inhibitors?

A

Side effects: Hypotension, cough
Adverse effects: Angioedema (swelling of tissues in lips, face, throat, tongue, and oropharynx). Emergency situation that constitutes an allergy

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25
Nursing considerations for ACE inhibitors?
Safety. Pt should remain on bedrest for the first few hours after initial dose to prevent injury related to the “first dose effect.” May cause annoying cough.
26
What is included in Virchow's Triad?
At least one of these factors is necessary for development of VTE. Endothelial damage, venous stasis, altered coagulation.
27
What is included in a venous thromboembolism (VTE)?
Deep vein thrombosis and pulmonary embolism.
28
Risk factors for DVT?
Age, prior history of DVT, surgical and invasive procedures, coagulation abnormalities, oral contraceptives, pregnancy, HF, obesity, immobility, trauma, ulcerative colitis, lupus, sepsis, advanced neoplasms
29
Clinical manifestations of DVT?
Pain in the area of thrombosis. Sudden onset, unilateral edema. Red, warm, indurated vein.
30
What's involved in the diagnosis of DVT?
Physical exam. Assess S/S. Venous duplex ultrasonography (aka venous doppler). Venogram (invasive). D-Dimer blood test that measures fibrin breakdown. It's only suggestive of DVT.
31
Treatment of existing DVT?
Rest and elevation of extremity. Do not rub or massage the area. No SCD stockings or ROM to affected extremity. Compression stockings. Anticoagulation therapy. Assess neurovascular status of extremity. IVC filter.
32
Pathophysiology of a pulmonary embolism?
Thrombus causes an obstruction of blood flow to the pulmonary circulation. There is ventilation but no perfusion.
33
Manifestations of a pulmonary embolism?
Sudden onset SOB. Sharp, stabbing chest pain. Anxiety or apprehension. Cyanosis, tachycardia, tachypnea. Cough, hemoptysis.
34
Diagnosis of PE?
Patient history. EKG, CXR to rule out other conditions. D-Dimer. V/Q scan (ventilation-perfusion). Spiral CT scans. Pulmonary angiography.
35
What are some lab tests for monitoring heparin
Activated partial thromboplastin time (APTT) Partial thromboplastin time (PTT). Therapeutic should be 1.5-2.5 the norm or 60-80 seconds Evaluate baseline labs: CBC, platelets, urinalysis, stool, creatinine
36
Who are candidates for home enoxaparin (Lovenox) therapy?
Stable DVT/PE. Reliability, low risk for bleeding, adequate renal functioning, normal vital, able to monitor and report bleeding
37
What drugs should NEVER be given concurrently?
Heparin and enoxaparin (Lovenox)
38
Lab test for warfarin (Coumadin)?
International normalized ratio (INR/PT). Hold dose of warfarin if INR is 3.0+ and consult with HCP for dosing. Seek parameters from HCP as to when to hold warfarin r/t INR level
39
How to wean a pt from heparin or enoxaparin to warfarin?
Administer warfarin & heparin OR enoxaparin concurrently for 3-5 days until INR reaches its therapeutic range of 1.5-2.5. Then maintain on warfarin w/ close monitoring of INR. Warfarin takes 48-72 hrs to affect PT/INR
40
Pt teaching for warfarin?
s/s report to HCP. Safety, labs, take as directed. Notify all HCP/dentists that you're on the med. Avoid NSAIDs, salicylates, and OTC drugs
41
Diet with warfarin?
Avoid foods high in vitamin K. Keeping diet consistent and with low amount of vitamin K is more important than trying to keep intake low. Green leafy veg, certain legumes, and veg oil are avoided.
42
A clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of the ventricles to fill or eject blood. Results in?
Heart failure resulting in inadequate CO, tissue perfusion, hypertrophy of the myocardium, pulmonary, systemic congestion
43
Types of HF and what they are?
Systolic HF, the most common. Decreased ability of the ventricle to contract. Diastolic HF, less common. Stiff, noncompliant heart muscle making it difficult for the ventricles to fill.
44
Percentage of blood volume in the ventricles at the end of diastole that is ejected during systole, measure contractility.
Ejection fraction. Normal is 55-65%. Systolic HF: decreased Diastolic HF: normal
45
What is the initial compensatory mechanism of the heart to counteract HF? Most start out as what?
Sympathetic stimulation | Left-sided
46
What is the major underlying cause of HF?
Chronic HTN and myocardial infarction (MI). Any condition that results in direct damage to the heart, ventricular overload. Constriction of the ventricles, limiting ventricular filling and decreasing stroke volume.
47
Risk factors for HF?
HTN, CAD, MI, cardiomyopathy, valve disease, cardiac infections, substance abuse, arrhythmia, diabetes, smoking, family HX, metabolic diseases
48
Left-sided heart failure?
The left ventricle isn’t pumping with enough force to eject blood during systole→↓ tissue perfusion r/t ↓ CO & Pulmonary congestion r/t ↑ pressure in pulmonary vessels CO from left ventricle ↓ than the volume of blood received from pulmonary circulation→ pulmonary congestion
49
Clinical manifestations of left-sided HF?
Relate to the respiratory system and will produce s/s related to the respiratory system as blood accumulates in the lungs.
50
s/s of left-sided heart failure?
Asymptomatic initially. Pain, exercise intolerance, unable to perform ADLs, anxiety, deceased urine output during the day, nocturne, possible edema
51
Right-sided heart failure?
The failing heart can’t pump volume of blood received from body into lungs for oxygenation; “back up” of fluid develops →to peripheral edema Right ventricular CO ↓ than volume received from peripheral circulation → edema. Right-sided HF produces s/s of vascular congestion in body
52
Right-sided HF failure risk factors?
Left-sided HF: As fluid accumulates in lungs r/t left sided HF,→↑ pressure in lungs causes ↑resistance to blood flow into lungs over time→ to right sided HF. Right ventricular MI. COPD.
53
s/s of right-sided heart failure?
Peripheral edema, decreased urine output during waking hours. Diuresis at rest, nocturia. Weight gain, hyper or hypotension. May have s/s of left-sided HF
54
Distinguishes between dyspnea of HF and dyspnea of lung disease
``` Brain natriuretic peptide (BNP) ↓100 pg/mL = none 100-300 pg/mL= present ↑300 pg/mL = mild ↑600 pg/mL = moderate ↑900 pg/mL = severe ```
55
Considered to be the best tool to diagnose HF. Used to determine cardiac ejection fraction (EF).
Echocardiography
56
Medications for HF?
Diuretics, vasodilators, ACE inhibitors, beta blockers, digoxin (Lanoxin)
57
Mechanism of potassium sparing diuretics
inhibits sodium reabsorption in kidney while saving potassium and hydrogen ions (antagonizes aldosterone receptors)
58
Side effects and adverse effects of potassium sparing diuretics
Most common side effect is hyperkalemia | Most serious adverse reaction is none
59
Considerations of potassium sparing diuretics
Nursing considerations: should not administer K+ supplements. Monitor for hyperkalemia. Strict I and O. Usually used in combination with other diuretics. Has a weak effect on its good, good synergistic effect. Used mainly to counteract K+ loss from other diuretics.
60
Mechanisms of ARBS
blocks vasoconstrictor and aldosterone producing effects of angiotensin II at receptor sires at vascular smooth muscle which leads to decreased BP, decreased release of aldosterone which leads to increased renal excretion of Na+ and water.
61
Side and adverse effects of ARBS
Side effects: Dizziness, hypotension | Adverse effects: Angioedema
62
Nursing considerations of ARBs
Monitor for angioedema and heart failure. Not as effective in black folks unless taken in conjunction with other antihypertensive. Safety: assist the pt in activities r/t potential dizziness r/t orthostatic hypotension
63
Mechanisms of beta blockers non cardio selective
Blocks stimulation of beta 1 (myocardial) and beta 2 (pulmonary, vascular, uterine) adrenergic receptor sites to decreased BP and HR. Improves cardiac output, slows progression of HF.
64
Effects of beta blockers non cardio selective
Side effects: Dizziness, fatigue, weakness, erectile dysfunction Adverse reactions: Bradycardia, heart failure, arrhythmia, orthostatic hypotension
65
Considerations of beta blockers non cardio selective
Non cardio selective BB given with care to pt with lung disorders due to possible bronchospasm. Contraindicated in asthma, chronic bronchitis, and emphysema (COPD). Assess BP and HR prior to administration. Monitor for respiratory distress.
66
Mechanisms of alpha II adrenergic agonists
Stimulates alpha adrenergic recpetors in the CNS which leads to deceased SNS inhibiting HR and vasocontriction centers to decreased BP, decreased systemic vascular resistance.
67
Effects of alpha II adrenergic agonists
Side effects: Drowsiness, dry mouth | Adverse effects: Can cause severe rebound hypertension if stopped abruptly.
68
Considerations of alpha II adrenergic agonists
Try to give at night: causes drowsiness. Can be given by transdermal patch, not to be used as a first line treatment for hypertension. Orthostatic hypotension and safety. If patch used, consult with HCP for removal of patch at night to avoid tolerance
69
Mechanisms of vasodilators
produces vasodilation and increased myocardial bloodflow
70
Effects of vasodilators
Side effects: Dizziness, headache, hypotension, tachycardia Adverse effects: Concurrent use of sildenafil, tadalafil, or vardenafil may lead to significant, potentially fatal hypotention.
71
Considerations of vasodilators
Take BP prior to administration. If systolic is less than 90, don’t administer, ask for vitals parameters and trend BP. May produce severe headaches until pt becomes acclimated to the med. May take Tylenol for it. Educate
72
Causes of PE?
DVT, air, fat, amniotic fluid, septic
73
Mechanisms for heparin?
Potentiates inhibitory effect of anti-thrombin and thrombin. Prevents conversion of prothrombin to thrombin. Prevents thrombus formation and prevents extension of existing thrombi. Used when rapid anticoagulation needed.
74
Effects of heparin?
Side effect: spontaneous bleeding (hematuria, bleeding gums, positive blood in stool, ecchymosis, petchiae) Adverse reactions: Hemorrhage, altered LOC, decreased platelets (heparin induced thrombocytopenia (HIT))
75
Considerations for heparin?
special considerations with use in thrombocytopenia, untreated hypertension, ulcer disease, spinal cord/brain injury, bleeding disorders, malignancy, use cautiously in late trimester pregnancy. Monitor for bleeding and PTT.
76
Mechanism for enoxaparin
Potentiates inhibitory effect of antithrombin on factor Xa and thrombin. Prevention of thrombus formation. Used for prevention and treatment of DVT.
77
Effects for enoxaparin
Side effects: anemia, spontaneous bleeding | Adverse: thrombocytopenia, hemorrhage
78
Considerations of enoxaparin
PTT not checked regularly because dosing of LMWH not adjusted. Monitor CBC, platelet count, stools and urine for occult blood. Assess for bleeding. If platelet is less than 150,000 may have HIT would need to d/c lovenox. Use cautiously with spinal and severe uncontrolled HTN and bleeding disorders.
79
mechanism for warfarin
Interferes with hepatic synthesis of vitamin K dependent clotting factors: II, VII, IX, and X. Prevention of thromboembolitic events.
80
effects of warfarin
Side effects: alopecia, urticaria, skin necrosis, dermatitis, fever, Gi distress, red/orange discoloration of urine Adverse: Bleeding
81
considerations for warfarin
Therapeutic effects take 3-4 days to develop. Usually on the drug for greater than or equal to 3-6 or more if indicated. Assess PT/INR daily until INR 2.0 and frequently per orders. Hold dose if INR greater than 3.0. Consistency in eating green leafy veg. Lab monitoring PT/INR
82
mechanism of alteplase
converts plasminogen to plamin which berak down fibrin clots causing a destruction of the thrombi and emboli.
83
effects of alteplase
Side effects: none | Adverse: Bleeding
84
considerations for alteplase
Long list of exclusive criteria, must be given within certain time frame, given IV. Should have all the blood draws and IV’s started prior to administering their med. Antagonist is aminocaproic acid/amicar
85
Antiplatelet meds?
Aspirin and clopidogrel/plavix. Prevents the development of thrombosis in the arteries by suppressing platelet aggregation
86
Manifestations of PVD?
Brown pigmentation of skin and legs, aching pain relieved by elevation, edema around the ankles, cyanosis, stasis ulcers
87
Mechanism beta blockers cardio selective
Blocks stimulation of bet 1 myocardial adrenergic receptors to decrease blood pressure and heart rate, decrease peripheral vascular resistance and decrease force of myocardial contractility. Cardio selective works only on cardio system. Blocks sympathetic stimulation to heart and decreases heart rate.
88
Side and adverse of beta blockers cardio selective
Side: weakness, fatigue, erectile dysfunction Adverse: bradycardia, orthostatic hypotension, HF
89
Considerations cardio selective beta blockers
Check BP and HR prior to administration. Assist prn with activities related to potential dizziness. Caution as early signs of hypoglycemia will not be seen

Basic Med-Surg (11 decks)

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