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OPT 537 - OWN > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Heart failure

A

Disorders that lead to the inability of the heart to meet the needs of the peripheral organs or its inability to meet those needs without compensatory mechanisms

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2
Q

Risks for HF

A

NUMBER ONE RISK FACTOR: ISCHEMIC CARDIAC MYOPATHY! Sex (in younger age M are more at risk but equalizes as you age), smoking, Alcohol abuse, obesity (poor diet, lack of exercise), DM especially with retinopathy, HTN, Dyslipidemia, Poor dental health (periodontal disease) and high sensitivity C-reactive protein-suggest an inflame process).

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3
Q

Most common causes of HF

A
  1. Ischemic heart disease (35-40)-loss of blood to tissue. Will have pain and claudication (loss of strength). Eventually tissue won’t work.
  2. Cardiomyopathy (dilated)-ventrical dilated and less efficient
  3. HTN
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4
Q

Less common causes of HF

A

Cardiomyopathy(hypertrophic, restrictive)

Valvular heart disease, congenital heart disease, high output states (anemia and thyrotoxicosis)

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5
Q

Clinical syndromes of HF

A

There can be right vs left side of the heart but both will eventually fail. Include left ventricular systolic disfunction, right ventricular systolic disfunction, or diastolic heart failure

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6
Q

Left ventricular systolic dysfunction: left HF

A

Common to fail as high pressure. Commonly result of IHD, HTN, or valvular disease.

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7
Q

Right ventricular systolic disfunction: Right HF

A

Commonly result of LVSD, pulmonary dz, or tricuspid valve disease.

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8
Q

Diastolic HF

A

Problem with heart relaxing and filling. Commonly caused by decreased L ventricular wall compliance (don’t expand to fill blood). More common in elderly HTN patient, and cardiomyopathy (hypertrophic, infiltrative, restrictive). Can also be due to failure of relaxation (transfer of calcium)

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9
Q

Symptoms of HF

A
  1. dyspenia with ordinary exertion
  2. dyspenea at rest
  3. orthopenea-SOB when laying down.
  4. paroxysmal nocturnal dyspnea-wake up with SOB when sleeping
  5. Cerebral symptoms from hypoxia-confusion, anxiety, nightmares, memory loss, dizziness, delirium.
  6. Fatigue (muscles aren’t getting enough oxygen)
  7. Nocturia-pee at night. Kidney not getting enough blood so release renin which increases water and NA retention. Once patient goes to bed the blood isn’t shunted to skeletal muscle and kidney releases there is a big blood volume.
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10
Q

Signs of HF

A
  1. Severe pulmonary edema-pulmonary congestion and rales or nocturnal cough that may recover bloody sputum.
  2. tachycardia
  3. anorexia
  4. Hepatomegaly
  5. Peripheral edema and cyanosis
  6. Cardiomegaly (dilation of ventricles or hypertrophy of ventricles)
  7. Gallop rhythm (S3 and or S4)
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11
Q

Signs of HF

A
  1. Sever pulmonary edema (congestion, rales, or nocturnal cough-bloody sputum)
  2. Anorexia
  3. Tachycardia
  4. peripheral edema and cyanosis
  5. hepatomegaly
  6. cardiomegaly (dilation or hypertrophy)
  7. Gallop rhythm (S3 and or S4)
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12
Q

S1 sound

A

Beginning of systole. Mitral and tricuspids close. Associated with the pulse so you can identify.

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13
Q

S2 Sound

A

End of systole. Closing of aorta and pulmonic valves.

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14
Q

S3 sound

A

Ventricular gallop. Early diastolic sound during rapid filling phase i.e. mitral and tricuspid close too soon (not sure why we get it) Associated with enlarged ventricle but can be normal in healthy young patients (below 33) or during pregnancy. Lub-dupa. An extra sound after the dub sound.

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15
Q

S4 sound

A

Atrial gallop. Late diastolic. Associated with loss of compliance of chamber walls i.e. ventricular hypertrophy. Ventrical tries to fill with blood during diastole and the ventricle is full put atrium has more to give so ti pushes and it causes it to hit ribs and creates S4 sound. ALWAYS PATHOLOGICAL! Ta lup dup. A sound before the lup sound.

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16
Q

Diagnosis of HF

A
  1. EKG-helpful if HF caused by MI. Ambulatory 24 hour monitoring if arrhythmias suspected
  2. Chest radiograph for enlargement and lung congestion
  3. Echocardiogram and/or cardiac catheterization for chamber abnormalities, valve disease, and blood flow abnormalities.
  4. Maybe body order or breath test for acetone levels
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17
Q

Stages of Heart Failure

A

A,B,C,D

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18
Q

Stage A of HF

A

Patient with risk factors but without structure heart disease or symptoms.

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19
Q

Stage B

A

Patients with structural heart disease but no signs or symptoms.

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20
Q

Stage C

A

Pt. with current or past symptoms of heart failure such as shortness of breath. Also has structural changes.

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21
Q

Stage D

A

Pt. with refractive heart failure (hard to treat with meds) who might be eligible for specialized treatment

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22
Q

Treatment for all stages of HF

A

Patient and family education, correct underlying cause (HTN, DM, dyslipidemia), Statin drugs to reduce inflammation and sympathetic stimulation. Vaccination against pneumococcal dz and influenza, dietary salt restriction, adequate rest with some regular exercise.

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23
Q

Treatment for Stage B

A
  1. ACEi-starting drug as cheap and well tolerated. Lower systemic vascular resistance and venous pressure. Decrease circulation levels of catecholamines (drugs end in april)
  2. ARB or A2RB-more expensive but used on those who can’t handle ACEi. Similar to ACEi but no cough (drugs end in Sartan)
  3. Can add a beta blocker if the above drugs aren’t working-slow heart rate and allows it to fill more with blood to increase output.
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24
Q

Therapy for stage C

A
  1. ACEi and beta-blockers in all pt. (olol or carvediol)
  2. diuretics-will decrease edema and help with breathlessness. Start with thiazide and move to loop if symptoms persist. Aldosterone antagonist (spironolaction-breasts, eperlonene) decrease mortality
  3. Cardiac glycoside to increase contractility in certain pt. (digoxin-marks entry into stage D)
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25
Q

Therapy for Stage D

A
  1. Ionotropes (increase contraction)-Beta-adrenergic agonist (dobutamine) which is used as a bridge for transplantation or dopamine
  2. Biventricular pacemaker-for pt. with conduction defects and not responding to tX
  3. implantable cardioverter-defibrilation-for arrhythmias
  4. parachute device for infarction induced LV dilation-stop blood for traveling where dead
  5. Left ventricular assist device (LVAD) as bridge to transplantation-blood attached to pump and circulates
  6. Cardiac transplantation
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26
Q

Importance of atherosclosis

A

Important cause of death in those greater then 45. Can cause ischemic HD, MI, stroke, and increased risk of dementia.

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27
Q

First step of atherosclerosis

A

Endothelial damage is done. Can be due to

  1. elevated sheer stress (at bifurcation and curved areas or raised BP)
  2. Biochemical abnormalities-elevated ldl(impact release of NO from endo) or DM (advanced glycosolated end products get into endo and grab Ldl coming by)
  3. inflam-infection or smoking
  4. advanced age
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28
Q

Second stage in atherosclerosis formation

A

Atheroma formation

  1. increased perm. of vessel wall to LDL-endo with oxidize ldl and recruit macrophages by cytokines. Oxidized ldl stop NO activity
  2. LdL-macrophages called foam cells which progress to form fatty streaks
  3. Growth factors released by platelets and macrophages cause migration and proliferation of smooth muscle cells which grow a fibrous cap.
  4. plaque growth results in remodeling
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29
Q

Positive (outward) remodeling

A

Occurs in areas where there is a lot of sheer stress. Arterial wall bulges out preserving lumen size. Not hemodynamically significant until it occupies 50% lumen size. More commonly associated with unstable lesion (softer atheromatous core and less developed cap and more likely to cause acute coronary disease). May progress to negative remodeling.

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30
Q

Negative (iNward) movement

A

There is a decrease in lesion size. More stable and less likely to rupture though. Associated with stable angina.

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31
Q

What makes a plaque vulnerable

A
  1. shoulder region-where the cap meets the healthy vessel wall. This is where it is weakes
  2. High macrophage activity-they secret proteolytic E that break down cap
  3. More breakdown in Areas of high stress.
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32
Q

How does a plaque cause a thrombus?

A
  1. There can be superficial endo break down that exposes subendocardial CT matrix. Plateletes adhere to collage and thrombus adhere to surface. Can block flow
  2. There can be a deep endothelial fissuring tearing cap and blood enters plaque and thrombus forms within plaque. This is extremely large!
    Both result in acute coronary syndrome.
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33
Q

Signs of atherosclerotic dz

A

Early dz often has no symptoms. First symptoms often on exertion (oxygen need greater then supply and intermittent claudication in tissues with limited oxygen)
More advanced diz…
1. peripheral vascular dz, MI, kidney dz, aneurysm, angina, sudden death, stroke.

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34
Q

Imaging for diagnosis of atherosclerotic dz

A
  1. coronary angiography when considering CABG-cornary a. bypass graft or PCI-percutaneous coronary intervention
  2. Ultrasonography, CT, MRI, OCT.
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35
Q

Lab test for atherosclerotic dz

A
  1. Measure fasting total serum cholesterol and HDL in all adults over 20 q 5 y
  2. Evaluation of serum highly sensitivity C-reactive protein in patients with 10 year CHD risk of 10% or more.
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36
Q

What is the normal values for Highly sensitive C reactive protein

A

2 is normal

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37
Q

Values for cholesterol

A

HDL 50+
LDL 100-
TG 150-
Total 200-

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38
Q

management for atherosclerotic dz

A
  1. Prevention
  2. meds for chol. and inflammation
  3. surgery
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39
Q

Atherosclertoic prevention

A

Control risk factors, lose weight, modify diet, increase activity

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40
Q

What drugs would you use to lower LDL cholestorol levels?

A
  1. Statin medication-first line (will lower ldl, decrease inflame, and harden ap)
  2. Bile acid binders (sequestrant)
  3. Nicotin acid (niacin_
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41
Q

What drugs would you use to lower TG and increase HDL

A
  1. Fibrates-PPAR agonist. Gets lipids into cell

2. Niacin

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42
Q

Statin optometric consideration

A

Increase retinal blood circulation. May be useful for ischemic retinal dz, or protect against AMD. May decrease diabetic neuropathy. Must caution prescribing erythromycin and clarithromycin.

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43
Q

Bile acid binders optometric consideration

A

May interfere with absoprtions of other drugs. Vitamins may be necessary.

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44
Q

Fibrates optometric consideration

A

Decrease chance of diabetic neuropathy and decrease need for lasers with diabetic retinopathy

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45
Q

Nicotinic acid consideration

A

Can cause macula edema or toxic amblyopia

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46
Q

Ischemic Heart DZ major cause

A

Atherosclerosis.

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47
Q

Ischemic HD

A

Imbalance between the cardiac need for oxygenated blood and its supply

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48
Q

Who is more likely to have CHD M or W

A

In younger years it is more likely in M but the prevalence is equal in older years. however, women are less likely to survive and MI and more women then men die each year from CHD

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49
Q

What are the pathophysiology reasons ischemic HD differs between M and W?

A

Women have smaller coronary arteries and so endo damage in smaller a. has a greater impact as there are fewer endo. cells and there will be dramatically less No produced. Also women are more likely to have positive remodeling (not sure why)

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50
Q

Most common prodromal symptoms for Ischemic HD in women

A

Women will have fatigue, sleep disturbance, and dyspnea (happens more at sleep as you have more ach released). Often they have no history of heart pain. Men frequently get chest pain.

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51
Q

How should women be tested for ischemic Heart dz

A

Need a greater test of endothelial function as have greater disfunction.

  1. Give the pt. acetycholine which causes vasoconstriction of coronary a but itself but stim. release of NO which overpowers acetycholine and causes vasodilation. If pt. has endo damage won’t get vasodilation
  2. stress echocardiogram and stress thalium.
  3. Intravascular ultrasonography
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52
Q

Angina pectoris

A

Chest pain that results from transient myocardial ischemia. May also have referred pain in neck and jaw. Often caused by exertion

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53
Q

Lavigne Sign

A

Clenching of fist in front of chest. Often occurs with angina pectoris.

54
Q

Stable or typical angina

A

Fixed atherosclerotic narrowing that decrease blood supply when demand is increased (a continuous result of continous neg. remodeling). Usually provoked by exercise or emotional stress. Presents over a few seconds or minutes. Lasts 5-15 minutes. Releives with rest or sublingual Nitroglycerine (a potent vasodilator). Predictable.

55
Q

Prinzmetal or variant angina

A

Angina caused by vasospams. More common in W (less endo function and NO) more common at night or early morning. Associated with cigarette smoking. Pt. may exhibit other signs of arterial hypersensitivity such as migraines or raynauds. Fixed with NTG or CCB (dilation)

56
Q

General management of angina pectoralis

A

Activity guidelines and weight loss. Educate patient to seek help if pain not relieved with 2-3 NTG given 5 minutes apart. Control of risk factors: HTN, DM, Hyperlipidemia, Smoking. Treat underlying conditions: Anemia, thyroid disease.

57
Q

Medical management of angina pectoris

A
  1. baby aspiring 81 mg
  2. Nitrates for dilation-sublingual, oral, transderm, and iv
  3. Beta-blockers to decrease cardiac demand
  4. Ca channel blockers to prevent spasms and for vasodilation
  5. Ranolazine if AP still occurs with combo of other meds (used with patients with stable angina to increase blood flow)
58
Q

Surgical management of AP

A
  1. Percutaneous coronary intervention (PCI)-less invasive. Put a catheter up into heart and place a stent. Glycoprotein IIB/IIA inhibitors to inhibit platelet aggregation
  2. Coronary artery bypass grafting (CABG)-used over PCI with more complex vessels. Transplanted vessels bypass blockage. Use internal thoracic artery over saphenous v. Repat procedure in 5 years for 5-10 %
59
Q

What does Acute Coronary Syndrome Include?

A
  1. Unstable angina
  2. Non-ST elevation MI
  3. St-elevation MI
    Which one you get is just chance
60
Q

Common mechanism to all ACS?

A

Rupture of cap–>platelet aggregation and adhesion–>thrombus formation –>embolization.

61
Q

Unstable or crescendo angina

A

Unpredictable and study. Can have rest pain. Fibrous cap erosion with non-occlusive thrombus of coronary branch. No detectable release of troponin associated with myocardial necrosis. Considered pre-MI. AT a high risk for MI. Can dissociate from MI by looking to see if troponin elevated.

62
Q

Non-ST elevation Myocardial infarction

A

Less severe from of MI. Partially occluded coronary artery. No elevation of the ST segment. Differentiated from unstable angina as has cardiac enzymes (troponin I and T, CK, and CK-MB). There is still pain here!

63
Q

St elevation Myocardial infraction

A

More severe MI. EGG change shows large amount of heart damage. Total occlusion of coronary artery. Myocardial necrosis occurs within 15-30 minutes. Will get elevation and enzymes!

64
Q

MI signs and symptoms

A

Sudden onset of pericardial pain that may radiate to left arm and jaw. Pain lasts >30 min and not relieved with NTG. Nausea, diaphoresis, and dyspnea common. Patient in pain and apprehensive. Hypotension and tachycardia may be present.

65
Q

How many AMI are thought to be mild or silent

A

40-60%

66
Q

MI immediate therapy

A 
MONAHAG
M-orphine sulfate for pain relief
O-xygen
N-itroglycerine
A-SA. Chew 150-300
H-hypo. induce. 91.4 for 12-24 hours
A-ntiarrhythmic therapy (lidocaine) prn
G-P IIB/IIIa inhib. and PCI with stent within 90 min
67
Q

MI therapy for STEMI only

A
  1. thrombolysis with tissue-type plasminogen activator (Alteplase). Given within 3 hours of pain. Improves outcome for STEMI patients
  2. Low molecular weight heparins (enoxaparin) to enhance affects of t-PA.
68
Q

MI adjunctive therapy

A
  1. Beta-blocker to reduce arrhythmias and risk of reinfaraction
  2. ACEi-reduce post infraction remodeling
  3. Statins-stabilize plaques
  4. Anticogulatnts like heparin may be needed
  5. Antiplatletes (ASA 81 to prevent second attack, Prasugrel-used instead of clopidogrel. Tricagrelor-new anti plat. with shorter half life. Clopidogrel-added to aspirin to decrese risk for 2nd MI)
69
Q

MI Complications

A
  1. Acute arrhythmias and conduction defects. Can be fatal
  2. HF-when greater then 30% infarcted
  3. Chamber wall defects-ventricular septal defect, ventricular aneurysm, cardiac rupture.
70
Q

Stenosis

A

Constriction or narrowing of an orfice

71
Q

Regurgitation

A

Return of blood throughout heart valve

72
Q

Prolapse

A

A sinking down or protrusion of a tissue. Floppy or billowing valve.

73
Q

Aortic stenosis epidemiology

A
  1. Senile Calcified aortic stenosis-number one cause. Occurs with age
  2. Congenital defects (aortic valve has bicuspid instead of tricuspid) Calcium deposits occur sooner and more common in M
  3. Rheumatic Heart disease-not as common in industrialized nations
74
Q

Pathophysiology of aortic stenosis

A

Pressure overload on LV leads to LV hypertrophy. Hypertrophy results in relative ischemia with angina and LV failure.

75
Q

Signs of aortic stenosis

A

Carotid pulse is of small volume and slow rising. Systolic ejection murmur (as blood passes through it is screaming). Soft S2 sound because aortic component is absent leaving only pulmonic component. Development of S4 from hypertrophy.

76
Q

Aortic stenosis symptoms

A

None until moderately severe. Angina occurs in 50% pt. 50% die in 5 years if valve not replaced. Syncope (passing out) with exercise-2-3 survival if valve not replaced. HF: 50% die in 1-2 years if stenosis not corrected.

77
Q

Mitral stenosis Etiology

A

Almost all cases secondary to rheumatic heart disease. Other cases are those experienced by W during pregnancy

78
Q

Mitral stenosis Pathophysiology

A

Mitral stenosis impedes left ventricular filling. Elevated left atrial P is referred to the lungs and causes pulmonary congestion. Increased effort required by right ventricle to propel blood and can result in HF.

79
Q

Mitral Stenosis Signs and Symptoms

A

Progressively severe dyspnea (dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea). Hemoptysis from rupture of small bronchial v. Atrial enlargement can lead to fibrillation (re-entry chances increased), Emboli due to stagnant blood, Hoarsness if large left atrium impinges on laryngeal n. Diastolic murmur.

80
Q

Murmurs with stenosis

A

Will get a murmur when the blood is normally going through the valve. I.e. will get systolic with as and diastolic with mitral synopsis.

81
Q

Aortic Regurgitation Etiology

A
  1. Idiopathic aortic root dilation-number one cause. Possible in HTN but usually w/ advancing age.
  2. Rheumatic Heart dz
  3. Collagen vascular dz-SLE, scleroderma
82
Q

Aortic regurgitation Paraphysiology

A

Regurgitation of part of ventricular volume during diastole. Requires greater stroke volume to compensate. Can lead to left ventricular dysfunction. leads to decreased diastolic pressure and increased pulse pressure (difference between systolic and diastolic pressure)

83
Q

Symptoms of Atrial regurgitation

A

Generally don’t occur until there is HF. Palpitations (can hear heart sounds), LVF resulting in dyspnea, orthopnea, or paroxysmal nocturnal dyspnea. Syncope. Angina from reduced coronary flow

84
Q

Signs of atrial regurgitation

A

Increased left ventricular size, Quincke’s sign-capillary pulsation in nail beds (huge pulse pressure). De Musset’s sign-yead bobbing with each heart beat.

85
Q

Mitral Regurgitation Etiology

A
  1. Mitral valve prolapse-number one caused. Caused by redundant chord tindineae. Usually benign syndrome.
  2. Rhuematic heart disease
  3. Coronary artery disease-damage causes chordae tindinae to not be correct
  4. Ruptured chordae tendinae
  5. Ventricular enlargement
86
Q

Mitral Regurgitation Pathophysiology

A

Increased left atrial P with decreased forward cardiac output.

87
Q

Mitral regurgitation Signs and symptoms

A

Systolic murmur.
S3 as blood rushes back into dilated L ventricle. L and eventually left ventricular failure (dyspnea, orthopnea, paroxysmal nocturnal dysfunctions) Palpitations from increased stroke volume. Atrial fibrillation. Systemic embolization.

88
Q

Murmurs with Regurgitation

A

Will be reverse of stenosis. Will heart murmur when blood coming into wrong place. i.e. with mitral valve get systolic murmur and with aortic valve get diastolic.

89
Q

Diagnosing Valvular Disfunction

A
  1. EGG for hypertrophy or arrhythmias
  2. Echocardiaography of suspected valves. Timing of murmurs
  3. Catheterization to assess valves and chambers
  4. Chest radiography for enlargement.
90
Q

Diagnosing Valvular Disfunction

A
  1. EGG for arrhythmias or hypertrophy
  2. Echocardiogram for valves
  3. Catheterization for valves
  4. Chest radiograph fro enlargement
91
Q

Meds for valvular dz

A

Not cannot medically treat valves so this is to stop complications and HF

  1. Diuretics to decrease volume overload
  2. Digoxin for contraction and arrhythmias
  3. Anticoagulants if risk for embolization
  4. Vasodilators to reduce outflow resistance
92
Q

Valve dysfunction Surgery

A
  1. Homograft or allograft-for those under 55. Replace with a human valve
  2. Autograft-Pulmonic valve to aorta and homograft for homograft
  3. Mechanical valve (55-75)-Transcathetar aortic valve implantation (TAVI) with a stent in disfunction valve
  4. Hetograft-normally animal. Durability is limited (>75)
  5. Mitraclip for mitral reguritation
  6. Commissurotomy for mitral valve stenosis
  7. balloon valvuloplasty for mitral stenosis.
93
Q

What is infective endocarditis

A

Infection of endocardial surface and the valves

94
Q

Sources for infective endocarditis?

A

Many possible sources-nosomial (from hospital), IV drug use, prosthetic use.
Bacteria: staph. aureus is most common
Fungi: Candida albicans is most common

95
Q

Infective endocarditis acute presentation

A

Fever and a new or changed heart murmur

96
Q

Infective endocarditis subacture presentation

A

Malaise, murmurs, cardiac failure, splinter hemorrhages of conj, roth spots (hemorrhage on retina. doesn’t only occur in those with endocarditis)

97
Q

Diagnosis of endocarditis

A
  1. Blood culture for infection-3 draws 24 hours between at different sites
  2. Echocardiography showing valve disfunction
  3. Supporting evidence-fever, high CRP, history of events that lead to IE, emboli, hemorrhage, Janeway lesion-on hands and feet. Non-tender macular lesions. Immune complexes in body.
98
Q

Prognosis for infective endocarditis

A

Very high without treatment

99
Q

Treatment for infective endocarditis

A
  1. IV AB and hospital care-can take as long as 6 weeks.

2. Surgery if extensive valvular damage present

100
Q

Prophylaxis and Infective endocarditis

A

Must give AB before any invasive procedures for pt. with history of valvular dz. Amoxicillin 2-3 g po 1 hour before surgery or Clindamicin 600 mg po 1 hr before procedure

101
Q

Dilated Cardiomyopathy

A

Ventrical dilation that is not due to a compensatory rxn. Due to some intrinsic heart muscle problems. Can have to do with genetics or we can have no idea why

102
Q

Contributory history to dilated cardiomyopathy

A
  1. idiopathic-frequent familial basis
  2. Previous viral endocarditis
  3. alcohol abuse
103
Q

Symptoms of Dilated cardiomyopathy

A

Similar to HF

104
Q

Dilated cardiomyopathy therapy

A
  1. Remove any contributing agents
  2. salt restriction
  3. High dose fish oil-omega3
  4. Diuretics, vasodilators, beta-blockers, digitalis
  5. Surgical ventricular restoration-piece of dacron to strengthen dilated ventricle
  6. Cardiac transplantation
105
Q

Dilated Cardiomyopathy

A

Ventrical dilation that is not due to a compensatory rxn. Due to some intrinsic heart muscle problems. Can have to do with genetics or we can have no idea why. inappropriate contraction without pressure overload

106
Q

Hypertrophic cardiomyopathy

A

Inappropriate hypertrophy. Decreased ventricular volume and hyper contracting heart

107
Q

Contributary history for hypertrophic cardiomyopathy

A

Most often in young adults with a strong family history

108
Q

Clinical manifestations of hypertrophic cardiomyopathy

A
  1. exertional dyspnea
  2. syncope after exercise
  3. angina at rest
  4. SCD possible after exercise
109
Q

Medical therapy for hypertrophic cardiomyopathy

A
  1. Beta-blockers-slows heart and decrease contraction. Prevents back flow
  2. Digitalis only in end stage of disease when dilation has occurred
110
Q

Hypertrophic cardiomyopathy

A

Inappropriate hypertrophy. Normally in the septum. Decreased ventricular volume and hyper contracting heart

111
Q

Surgery for hypertrophic cardiomyopathy

A
  1. Myomectomy to reduce thickness of septum
  2. Pacemaker and defibrillator implantation
  3. intentional septal infarction to reduce obstruction
  4. cardiac transplantation
112
Q

Acute Pericarditis

A

Inflammation of the sac that is around the heart. Sac is inflamed and doesn’t allow for smooth motion anymore.

113
Q

Etiology of acute pericarditis

A

Post-MI, viral infection, SLE, infectious endocarditis, malignancy, Radiation drugs

114
Q

Features of acute pericarditis

A

Inspiratory chest pain on left side. Friction rub during systole and diastole.

115
Q

Therapy for acute pericarditis

A

Treat underlying disorder. Nsaids, steroids, colchicine. Asprin if post MI.

116
Q

Pericardial Effusion Etiology

A

Commonly the result of inflammation from acute pericarditis.

117
Q

Pericardial Effusion features

A

left heart pain with inhalation, pain during systole and diastole rub. Heart sounds become softer

118
Q

Therapy for effusive pericarditis

A

Treat pericarditis (Nsaid, steroids, colchine. Treat underlying disease). May involve aspiration of fluid

119
Q

Cardiac tamponade Etiology

A

Rapid accumulation of fluid from pericarditis that compresses heart and inhibits cardiac filling. Life threatening.

120
Q

Symptoms of Cardiac Tamponade

A
  1. decreased systolic pressure during inspiration

2. shock-failure of peripheral circulation

121
Q

Therapy for cardiac tamponade

A

Emergency pericardiocentesis

122
Q

Therapy for cardiac tamponade

A

Emergency pericardiocentesis. Drain the heart.

123
Q

Constrictive Pericarditis

A

Thickened pericardium in response to previous inflammation

124
Q

Symptoms of constrictive pericarditis

A

Dyspnea on exertion and orthopnea. Edema, ascites (fluid in cardio sac), and hepatic tenderness with jaundice

125
Q

Therapy for constrictive pericarditis

A

Pericardiectomy-remove pericardium. May not get relieve for 6 w.

126
Q

Lower limb ischemia

A

Peripheral a. dz. Usually the result of atherosclerosis but also due to thrombosis or embolism.

127
Q

Symptoms of lower limb ischemia

A

Pain and limping with walking, pallor, paralysis, pulselessness. Hair loss. Increased risk of HF with decreased exercise tolerance. Diabetic foot and raynauds disease.

128
Q

Patient education for lower limb ischemia

A

Avoid trauma, careful toe and foot hygiene, stop smoking, supervised exercise

129
Q

Treatment for lower limb ischemia

A

Treat underlying HTN and DM. Anticogulants-ASA, clopidocril. Angioplasty with stent. Bypass surgery.

130
Q

Varicose Veins

A

Peripheral venous dz. Dilated, tortuous superficial v. in lower legs. Pain usually with periods of standing.

131
Q

Cause of varicose veins

A

Inherited defect…could be due to defective valves or veins wall weakness. Occurs from increased venous pressure from prolonged standing.

132
Q

Treatment for Varicose Veins

A

Nonsurgical-support stockings, feet elevation, limit activities involving long periods of standing
Surgical-sclerotherapy and compression, removal of varicosity, endogenous laser therapy, radio frequency ablation.

OPT 537 - OWN (2 decks)

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