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Adult Health > Cardiovascular Conditions Section 2 > Flashcards

Cardiovascular Conditions Section 2 Flashcards

1
Q

Which wave on an EKG represents depolarization of the atria and the firing of the SA node?

A

P wave

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2
Q

On an EKG, what represents depolarization of the ventricles? (AV node to ventricles)

A

The QRS complex

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2
Q

On an EKG, what may represent repolarization of the Perkinje fibers or a hypokalemia?

A

U wave

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3
Q

On an EKG, what represents repolarization of the ventricles?

A

T wave

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4
Q

What is cardiac output?

A

The amount of blood pumped by each ventricle in 1 minute

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5
Q

How do you calculate CO?

A

Stroke volume x HR per minute

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6
Q

What is the range of cardiac output for a normal adult at rest?

A

4-8L/min

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7
Q

What are the main factors influencing BP?

A

Cardiac Output x SVR (systemic vascular resistance) = BP

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8
Q

What is SVR?

A

Systemic Vascular Resistance; force opposing movement of blood in within vessels

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9
Q

What is the principal factor that determines SVR?

A

Radius of small arteries and arterioles

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10
Q

What happens when a-adrenergic receptors are stimulated by noepinephrine?

A

Vasoconstriction

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11
Q

What kind of receptors do blood vessels have?

A

a-adrenergic and b2-adrenergic

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12
Q

Where are b1-adrenergic receptors found?

A

In the heart

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13
Q

What neurotransmitter stimulates the b2-adrengergic receptors? What happens?

A

Epinephrine; vasodilation

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14
Q

Name where each adrenergic receptor is found and what happens when activated

A

a1:
- vascular smooth muscle; vasoconstriction
- heart; more contractility

a2:
- vascular smooth muscle; vasoconstriction
-presynaptic nerve terminals; inhibition of norepinephrine release

b1:
- Heart; Increased contractility and heart rate and conduction
- Kidney; Renin secretion

b2:
- Smooth muscle in blood vessels in heart; vasodilation

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15
Q

How does sodium contribute to blood pressure?

A
  • Sodium attracts water
  • Increases ECF volume
  • This increases venous return to the heart and stroke volume
  • Cardiac Output and Blood Pressure increase
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16
Q

What hormones secreted by the renal medulla have vasodilator effects?

A

Prostaglandins

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17
Q

What does Aldosterone do?

A

Stimulates kidneys to retain sodium and water

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18
Q

What is primary hypertension?

A

Elevated blood pressure without a known cause

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19
Q

What is secondary hypertension?

A

Elevated blood pressure with a cause that can be identified and corrected

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20
Q

What are 8 common causes of secondary hypertension?

A

1) Cirrhosis
2) Genetic defect of narrow artery
3) Drugs
4) Endocrine problems
5) Neurological problems
6) Pregnancy
7) Renal disease
8) Sleep apnea

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21
Q

What is the hemodynamic hallmark of hypertension?

A

Persistently increased systemic vascular resistance

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22
Q

Describe the different risk factors for hypertension?

A

Age

Alcohol: 2 drinks per day for males and 1 for females

Diabetes

Ethnicity: Higher in blacks

Sodium Intake

Family history

Gender: More common in men in young adulthood and middle age. More common in women after 64 years

Serum lipids: More common in pts with high cholesterol, triglycerides, and hyperlipidemia

Obesity

Sedentary Lifestyle

Socioeconomic Status: More common in poor and low educated populations

Stress

Tobacco

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23
Q

What does angiotensin do to the body?

A

Narrows blood vessels

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24
Q

Name the different types of antihypertensive drug classes, drugs, and nursing considerations

A

1) Central-Acting a-Adrenergic Agonists

a) clonidine; withdrawal syndrome if you suddenly stop taking it (hypertension, tachycardia, headache, tremors, apprehension, sweating)

b) guanfacine (same as above)

c) methyldopa May cause sedation so don’t drive and stuff

2) a1-Adrenergic Blockers

a) doxazosin; take at bedtime to reduce risk that comes with orthostatic hypotension

b) prazosin; (same as above)

c) phentolamine

3) b-Adrenergic Blockers (monitor pulse and BP regularly; use caution in patients with diabetes because it could hide tachycardia from low blood sugar; less effective in black patients)

a) all the drugs that end with -olol

4) ACE Inhibitors; Aspirin and NSAIDs may decrease effectiveness; adding a diuretic enhances effect but shouldn’t be used with potassium-sparing; can increase serum creatinine; may cause dry, hacking cough

a) benazepril

b) captopril

c) enalapril

d) fosinopril

e) lisinopril

5) Angiotensin II Receptor Blockers; may take 3-6 weeks to see full effects; should not be used with ACE inhibitors for patients with kidney disease

a) azilsartan

b) candesartan

c) irbesartan

d) losartan

e) olmesartan

f) telmisartan

g) valsartan

6) Calcium Channel Blockers; (A-B) use with caution in patients with heart failure; avoid grapefruit juice; avoid in patients with AV block & left ventricular systolic dysfunction. (C-I) more potent vasodilators; serious adverse events have occurred; IV nicardipine is effective for hypertensive emergencies

a) diltiazem

b) verapamil

c) amlodipine

d) clevidipine

e) felodipine

f) isradipine

g) nicardipine

h) nifedipine

i) nisoldipine

7) Direct Vasodilators

a) fenoldopam; IV used for hypertensive emergencies; use cautiously in patients with glaucoma; lay flat for 1 hour after admin

b) hydralazine; IV used for hypertensive emergencies; not used by itself due to side effects; Do not use in patients with CAD

c) minoxidil; reserved for use of severe hypertension combined with renal failure and resistance to other therapy

d) nitroglycerin; IV use for hypertensive emergencies with myocardial ischemia

e) sodium nitroprusside; IV use for hypertensive emergencies; Arterial BP monitoring recommended; wrap IV solutions in material to protect from light; metabolized to cyanide and then thiocyanate so you have to monitor thiocyanate levels

8) Aldosterone Receptor Blockers; monitor for hypokalemia and orthostatic hypotension; do not combine with potassium sparing and potassium supplements; use caution with ACE inhibitors;

a) Eplerenone

b) Spironolactone

9) Loop Diuretics; monitor for orthostatic hypotension; monitor for electrolyte values; less effective for hypertension

a) bumetanide

b) furosemide

c) torsemide

10) Potassium-Sparing Diuretics; monitor for orthostatic hypotension; monitor for hyperkalemia; contraindicated in patients with renal failure; use with caution in patients using ACE inhibitors or Angiotensin blockers; avoid potassium supplements

a) amiloride

b) triamterene

11) Renin Inhibitors; may cause angioedema in face, extremities, and in mouth; contraindicated in pregnant patients

a) aliskerin

12) Thiazides; monitor for orthstatic hypotension, hypokalemia; sodium restriction; NSAIDs can cause decrease effects and cause renal problems; each potassium-rich foods

a) chlorothiazide

b) chlorthalidone

c) hydrochlorothiazide

d) indapamide

e) metolazone

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25
Q

What is the preferred first-line therapy for patients with stage-1 hypertension?

A

Thiazide diuretic, a calcium channel blocker, and an ACE inhibitor

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26
Q

What classifies as resistant hypertension?

A

failure to reach BP goal in patients that are taking full doses of a 3-drug treatment that includes a diuretic

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27
Q

Should a patient double the dose of their anti-hypertensive medication if a dose is missed?

A

No

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28
Q

List the stages of hypertension

A

Normal: 120/80
Elevated: 120-129/<80
Stage 1: 130-139 / 80-89
Stage 2: 140+ / 90+

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29
Q

What are the 3 stages of atherosclerosis deevelopment?

A

1) Fatty streaks: lipid-filled smooth muscle cells found in coronary arteries

2) Fibrous plaque: plaque made up of lymphocytes, macrophages, and smooth muscle develops in inner walls of blood vessel

3) Complicated Lesion: plaque breaks up and forms a blood clot

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30
Q

Where do HDLs carry lipids? What is the process called?

A

Away from the arteries to the liver for metabolism; process is called reverse cholesterol transport which helps prevent lipid accumulation in artery walls

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31
Q

Why are LDLs considered the bad lipoproteins?

A

They are attracted to artery walls and contain more cholesterol than any of the other lipoproteins

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32
Q
A
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33
Q

What is Prinzmetal’s Angina?

A

Rare form of angina that occurs at rest without any increased physical exertion

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34
Q

What is refractory angina?

A
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35
Q

What is EECP and its benefits?

A

Enhanced External CounterPulsation; BP cuffs around the calves that inflate during diastole and deflate during systole to:

  • Promote venous return
  • Augment diastolic BP
  • Increase coronary perfusion
  • Improve LV filling
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36
Q

What is unstable angina?

A
37
Q

What is ventricular remodeling?

A
38
Q

How does ventricular fibrillation cause death?

A
39
Q

What are the key signs of acute pericarditis?

A

Mild to severe chest pain that increases with inspiration, coughing, and movement of upper body. Often relieved by sitting forward

40
Q

What is Dressler Syndrome?

A

Pericarditis and fever that develops 1-8 weeks after MI

41
Q

What is the most common form of HF?

A

Left-sided heart failure

42
Q

What are the two classifications of left-sided heart failure?

A

Systolic heart failure (HFrEF; reduced)
Diastolic heart failure (HFpEF; preserved)

43
Q

What does LVEF stand for and what is a normal percentage?

A

Left ventricular ejection fraction; 55%-65%

44
Q

How does HFrEF cause heart failure?

A
  • Left ventricle does not generate enough pressure to eject blood through aorta
  • Left ventricle dilates and hypertrophies
  • Weakens heart which then cannot generate enough stroke volume causing cardiac output to decrease
  • Blood backs up into left atrium causing fluid accumulation in the lungs
45
Q

Describe HFpEF

A
  • Ventricles are stiff and unable to relax and fill during diastole
  • Decreased filling volume leads to decreased stroke volume and cardiac output
  • Fluid accumulates in the body
46
Q

What is the most common cause of right-sided HF?

A

Left-sided HF

47
Q

What are the main compensatory mechanisms of HF?

A

1) Neurohormonal responses (renin-angiotensin -aldosterone system & sympathetic nervous system

2) Ventricular dilation

3) Ventricular hypertrophy

48
Q

How does the renin-angiotensin-aldosterone system try to maintain homeostasis?

A

Goal is to increase preload and ventricular contractility to maintain cardiac output

  • Kidneys sense falling CO
  • Kidneys release renin which is converted to angiotensin I and then angiotensin II
  • Angiotensin II vasoconstricts
  • Stimulates water and sodium retention
  • Stimulates aldosterone release which further retains sodium and water
    -Sodium and water retention leads to higher blood pressure leading to increased cardiac output
49
Q

Does does the sympathetic nervous system compensate for HF?

A
  • Baroreceptors sense low arterial pressure
  • Epinephrine & Norepinephrine are released which stimulate b-adrenergic receptors
  • This increases HR and contractility
50
Q

What is the Frank-Starling Law?

A

The strength of the heart’s contraction is directly proportional to its diastolic stretch

51
Q

How does dilation compensate for heart failure?

A

The heart’s chamber become bigger. If they are bigger, they can hold more blood. When there is more blood, there will be more contraction to force the blood out. This will improve CO and maintain BP.

52
Q

What is ADHF? What are the symptoms?

A

Acute Decompensated Heart Failure

Symptoms are similar to pulmonary congestion & edema and fluid overload

53
Q

Describe the AHA stages of HF

A

A) High risk but no heart disease or symptoms

B) Heart disease is present but there are no signs or symptoms

C) Heart disease is present with prior or current symptoms

D) Advanced heart disease with continued HF

54
Q

Describe the NYHA stages of HF

A

I: No limitation in physical activity

II: Slight limitation of physical activity. Comfortable at rest but ordinary activity results in symptoms

III: Marked limitation of physical activity. Comfortable at rest but less than ordinary activity causes symptoms

IV: Inability to do physical activity without discomfort. Symptoms may be present at rest

55
Q

What are the symptoms of pulmonary edema?

A
  • Dyspnea
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Coughing
  • Pale and/or cyanotic
  • RR 30+
  • Use of accessory respiratory muscles
  • Pink, frothy sputum
  • Wheezes and crackles
  • S3 or S4 heart sounds
  • Cool extremities
56
Q

How are patients with ADHF categorized?

A

Dry-Warm
Wet-Warm
Dry-Cold
Wet-Cold

57
Q

Describe what it means for a patient with ADHF to be Wet and Warm

A

Wet: Volume overload
Warm: Adequate perfusion

58
Q

What is the most common presentation in a patient with ADHF? (Warm, Cold, Wet, Dry)

A

Wet and Warm

59
Q

What are the signs of Right-Sided HF?

A
  • Right ventricular heaves
  • Increased heart rate
  • Extreme general edema
  • Ascites
  • Hepatomegaly
  • Jugular Vein Distention
  • Murmurs
  • Weight gain
60
Q

What are the symptoms of Right-Sided HF?

A
  • Anorexia
  • GI Bloating
  • Fatigue
  • Nausea
  • RUQ Pain
61
Q

What are the signs of Left-Sided HF?

A
  • Left Ventricular Heaves
  • Increased HR
  • S3 and S4 heart sounds
  • Decreased PaO2
  • Confusion, Restlessness
  • Dry, Hacking cough
  • Crackles
  • Pleural Effusion
  • Shallow respirations up to 32-40/min
  • Frothy, pink-tinged sputum
62
Q

What are the symptoms of Left-Sided HF?

A
  • Anxiety, Depression
  • Dyspnea
  • Fatigue, weakness
  • Nocturia
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
63
Q

What does PAWP stand for?

A

Pulmonary Artery Wedge Pressure

64
Q

What value is considered a normal PAWP?

A

6-15 mmHg

65
Q

What medication is first-line therapy for treating patients with fluid overload?

A

Diuretics

66
Q

What is an inotropic drug?

A

A drug that affects the strength of the heart contraction

67
Q

How do we measure the effectiveness of inotropic drugs?

A

Assess for:

-Improved cardiac output
- Blood pressure
- Urine output
- Reduced filling pressures

68
Q

What are symptoms of Digoxin toxicity?

A
  • Nausea, vomiting, diarrhea
  • Yellow/Green visual discoloration, blurry vision, blind spots
  • Bradydysrhythmias (less than 60 bpm), palpitations, dyspnea
69
Q

What are major side effects of Ace Inhibitors?

A
  • Hypotension
  • Persistent dry cough
  • Hyperkalemia
  • Angioedema
70
Q

What are major side effects of ARBs?

A

Similiar to Ace Inhibitors minus cough

71
Q

Which 3 beta-blockers decrease mortality in patients with HFrEF?

A

1) Metoprolol Succinate
2) Bisoprolol
3) Carvedilol

72
Q

What is a chronotropic drug?

A

A drug that changes the heart rate and rhythm

73
Q

What is cor pulmonale?

A

Enlarging of the right ventricle due to lung problems

74
Q

What is the difference between preload and afterload?

A

Preload: Stretching and filling of ventricles during diastole
Afterload: Pressure to pump against during systole

75
Q

What are the main risk factors for Infective Endocarditis?

A

1) History of infective enfocarditis
2) IV drug use
3) Having a prosthetic valve
4) Infection from doctors putting in intravascular device
5) Renal dialysis

76
Q

What are the 3 stages that infective endocarditis can develop into?

A

1) bacteremia
2) adhesion
3) vegetation

77
Q

What are the manifestations of infective endocarditis?

A

1) Fever
2) Chills
3) Weakness
4) Fatigue
5) Anorexia
6) Splinter hemorrhages
7) Petechiae on conjunctivae, lips, buccal mucosa, palate, ankles, feet, and antecubital/popliteal area
8) Osler’s nodes on fingertips and toes
9) Systolic murmur

78
Q

What is the Duke Criteria for the diagnosis of infective endocarditis?

A

0 major, 5 minor
1 major, 3 minor
2 major, 1 minor,

79
Q

What are considered major criteria for the diagnosis of infective endocarditis?

A

1) Positive blood cultures
2) Typical microorganism for IE from 2 different blood cultures
3) Evidence of endocardial involvement
4) New valvular vegetation

80
Q

What are considered minor criteria for the diagnosis of infective endocarditis?

A

1) Predisposing heart condition
2) IV drug use
3) Vascular phenomena
4) Immunologic phenomena
5) Microbiologic evidence
6) echocardiographic findings

81
Q

What are some clinical manifestations of pericarditis?

A

1) Progressive, severe, sharp chest pain; often worse with deep inspiration and when lying flat; sitting up and leaning forward relieves the pain; pain may radiate to neck, arms, left shoulder, or trapezius muscle (makes it hard to know if it’s angina)

2) Dyspnea from trying to not breathe in too hard

3) Pericardial friction rub

82
Q

How do you listen for a pericardial friction rub?

A

Lower left sternal border with the patient leaning forward. Ask the patient to hold their breath (since it is hard to tell a pericardial friction rub from a pleural friction rub)

83
Q

What is pulsus paradoxus?

A

A large decrease in systolic BP during inspiration

84
Q

Where is the most common site of PAD for patients without diabetes? Patients with diabetes?

A

Without: Femoral popliteal area
With: Below the knee

85
Q

What is the classic symptom of PAD in the lower extremities?

A

Intermittent Claudication: Lactic acid buildup that causes pain during exercise, resolves within 10 minutes, and is reproducible

86
Q

If someone has PAD in the iliac arteries, where would you expect pain?

A

Butt and thighs

87
Q

What is a segmental BP done for and how is it done?

A

Done to diagnose PAD; a sphygmomanometer is placed at the knee, thigh, and ankle to measure a difference in BP using a Doppler

88
Q

What are the 6 P’s of clinical manifestations of Acute Arterial Ischemia?

A

Pain
Pallor
Pulselessness
Paresthesia
Paralysis
Poikilothermia

89
Q

What is poikilothermia?

A

When the limb adapts to the environmental temperature;

90
Q

What is the first line treatment of Raynaud’s phenomenon?

A

Sustained-release calcium-channel blockers

91
Q
A

Adult Health (12 decks)

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