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Clinical Med > lecture 2: heart > Flashcards

lecture 2: heart Flashcards

1
Q

what is occurring in the P wave?

A

Atrial depolarization – P wave

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2
Q

what is occurring in the QRS complex?

A

Ventricular depolarization – QRS complex (R and L bundle branches)

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3
Q

what is occurring in the T wave?

A

Ventricular repolarization – T wave

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4
Q

what is occurring for the ST segment?

A

cardiac perfusion

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5
Q

describe the electrical pathway of the heart:

A

SA and AV nodes, HIS bundle, R and L bundle branches

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6
Q

T/F: A fib is normal in some situations

A

FALSE

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7
Q

what is an AV block?

A

AV node conduction delays

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8
Q

V tach vs V fib

A

VT almost always symptomatic (may overlap with underlying cause e.g. MI)
VF –> cardiac arrest (will drop dead with AED)
*both are pathologicalm usually triggered by underlying cause (e.g. MI, drug toxicity)

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9
Q

list 5 possible symptoms of poor perfusion (Fast or slow rhythm)

A 
Dark, grey or blurred vision
Lightheaded, faint, fatigued
Diaphoresis
Angina (generally with underlying cardiac disease)
Syncope (collapse)
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10
Q

What is wrong in A fib? what will this present as on EKG?

A

SA node dysfunction: Disorganized atrial contractions
No P waves on EKG
Irregular heart rate (speed varies – often rapid)

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11
Q

is v tach fatal? what are some symptoms?

A

Symptoms of poor perfusion (circulatory shock, collapse)
May progress to VFib
-usually fatal if not treated

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12
Q

Left Ventricular Hypertrophy puts you at risk for what else cardiovascularly?

A

Heart failure
Atrial fibrillation
Sudden cardiac death

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13
Q

List 2 other end-organ effects of hypertension Left Ventricular Hypertrophy is associated with:

A

1) Retinal vascular changes
- Arteriolar narrowing (focal, generalized)
- AV nicking
2) Hypertensive renal disease

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14
Q

Myocardial ischemia: what is it and how is it manifested on EKG?

A

Potentially reversible myocardial dysfunction

ST segment depression

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15
Q

Myocardial infarction: what is it and how is it manifested on EKG?

A 
Irreversible death (necrosis) of myocardium
ST segment elevation
Q waves (deep) indicated previous heart attack
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16
Q

with Radionuclide injection and imaging during a cardiac stress exercise test, what do you see for a normal pt? one with ischemia? one with infarction?

A

Normal: Exercise uptake; Rest uptake
Ischemia: Exercise no/reduced uptake; Rest uptake (reperfusion)
Infarct: Exercise and rest: no uptake

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17
Q

Endocrine and Ocular side effects of sympathetic activation:

A

Endocrine (B): increase renin (increase BP)

Ocular (B): aqueous production – so B-blockers can cause dry eye.

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18
Q

list a few of the multiple clinical indications for beta blockers:

A 
Hypertension
Tachyarrhythmias 
Ischemia / angina
Post-MI (↓ risk for recurrent MI)
Congestive heart failure (selected agents used cautiously)
(Stage fright, migraine prophylaxis)
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19
Q

list 4 ways beta blockers impact the heart:

A

1) Decrease cardiac output and ↓ renin
2) Negative chronotropy [Nodal blocking (SA, AV)]
3) Negative inotropy
4) Decrease myocardial oxygen demand

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20
Q

List 4 conditions that might make beta blockers a bad drug:

A

1) Hypoglycemia unawareness (bad for diabetics maybe)
2) Bronchospasm in asthma
3) Bradycardia / heart block
4) Congestive heart failure (selective use)

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21
Q

what specific ocular adverse effect can alpha agonists have?

what is a condition in which you might want to take one?

A

IFIS (intraoperative floppy iris syndrome)
also ***Increase risk for CHF when used alone for hypertension
-Prostatic hypertrophy with bladder outlet obstruction
(blocks constriction of bladder smooth muscle)

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22
Q

How could alpha 2 AGOnists be used to tx HTN?

what are some adverse effects?

A

Activate cardiovascular control centers in the brain and decrease sympathetic outflow
Adverse effects: Orthostatic hypotension, Dry mouth, eyes, Sexual dysfunction

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23
Q

what cells are responsible for secreting renin?

A

JG juxtaglomerular cells

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24
Q

where is the macula densa and what does it do?

A

in afferent arteriole, senses Na

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25
Q

what is creatine and what can elevated levels tell you?

A

Break down product from normal muscle metabolism (Creatine Kinase)
Filtered through glomerulus: poor renal function=higher serum creatinine
**False elevation w/ increased muscle, myopathy, trauma, meds

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26
Q

what is “BUN”? what do elevated levels indicate?

A

BUN=Product of protein metabolism excreted by the glomerulus

  • reabsorbed along with Na in volume depletion
  • Elevated BUN=renal dysfunction or Volume depletion
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27
Q

Significant proteinuria suggests:

A

impaired glomerular filter

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28
Q

specific gravity test assesses:

A

renal concentrating ability

A urine specific gravity test basically compares the density of urine to the density of water

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29
Q

what are some possible adverse effects of diuretics?

A 
Electrolyte abnormalities (Na, K, Mg, Cl)
Volume depletion (at risk)
*Glucose intolerance
Photosensitivity / skin rash
Vertigo, fatigue
Erectile dysfunction
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30
Q

when are diuretics given?

A

HTN

edema

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31
Q

what are 3 other clinical effects of ACE inhibs besides reducing vascular tone?

A

-Lower glomerular pressure in the kidney
•Renal protective (eg diabetes)
-Improve cardiac remodeling post-MI
-reduce afterload

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32
Q

besides HTN, why else might you give ACE inhib?

A
  • Aortic regurgitation

- Post-MI

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33
Q

one fatal potential side effect of ACE inhibs:

A

Swelling of face, lips, tongue – potentially life threatening. Drugs must be stopped; never re-challenge (ie; never try to re-Rx it because re-exposure could be fatal)

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34
Q

T/F: if someone had angioedema on ACE inhib, should try ARB?

A

FASLE; Angioedema with ACE inhibitor may also occur with ARB use and may be life-threatening! (so never take an ARB if had angioedema with ACEi)

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35
Q

functions of angiotensin 2?

A

Vasopressor

Stimulates production of aldosterone: Causes Na reabsorption in kidney → ↑ volume → ↑ pressure

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36
Q

clinical indications for ca channel blockers?

A

Hypertension
Raynaud’s phenomenon (digital artery spasm)
Coronary artery disease
Certain arrhythmias
(Other - eg GI motility, migraine prophylaxis)

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37
Q

3 major Ca channel blockers and how strongly they affect heart

A

 Verapamil: strongest cardiac effects
 Diltiazem: medium cardiac effects
 Dihydropiridines: little to no direct cardiac effects (so good Tx for HTN)

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38
Q

what are the ages where atherosclerosis is a risk factor for men and women?

A

Males > 45

Females > 55

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39
Q

what are some atherosclerosis risk factors?

A 
Age
Fam Hx
Adverse lipid profile
HTN
Smoking
Diabetes
(Inflammation, Obesity, Sedentary lifestyle)
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40
Q 
function of HDLs:
Higher levels considered protective against:
A

Removes Excess Cholesterol (returns to liver)

[Higher levels considered protective against CHD]

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41
Q

where is cholesterol produced?

A

liver

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42
Q

what is Tangier’s disease?

A 
deficiency of HDL (cholesterol trapped inside cells)
Orange tonsils (cholesterol deposits), corneal opacities, peripheral neuropathy
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43
Q

Abetalipoproteinemia:

A

Malabsorption of fat / fat-soluble vitamins (A, D, E, K), low cholesterol

44
Q

what is the ideal lipid level when treating atherosclerosis

A

Lipid level monitoring to track compliance (no defined lipid level target!!)

45
Q

statin side effects:

A
  • liver function
  • muscle soreness
  • small risk of DM
46
Q

what are some general guidelines for cholesterol levels?

A

LDL <200 is desirable

47
Q

BP ranges for stage 1 and 2 HTN:

A

stage 1: 140 - 159 90 - 99

Stage 2: ≥ 160 ≥ 100

48
Q

Hypertensive Urgency vs Malignant Hypertension

A

Hypertensive Urgency:

  • High BP w/o acute signs or symptoms
  • Prompt but cautious reduction in BP

Malignant Hypertension: Medical emergency
just like urgency but with symptoms (papilledema, disoriented etc)
**both are: BP > 200 systolic and/or >120 diastolic

49
Q

T/F: heart failure has been on the decline in america?

A

False (increasing)

50
Q

CO = __ X ___

A

CO = stroke volume x heart rate

•CO usually between 5 and 7 L/min

51
Q

ejection fraction is equal to ___/___

A

stroke volume/end-diastolic ventricular volume

**heart doesn’t completely empty with contraction

52
Q

chronotropy=

A

Alterations in heart rate

53
Q

inotropy=

A

Alterations in contractility

54
Q

what does Starling’s equation represent or summarize?

A

Inc. in EDV lead to increases in stroke work (EF)

*more blood in heart, harder it has to work

55
Q

How would systolic dysfuntion affect flow and ejection fraction?
Give an example of what might cause this?

A

-decreased ejection fraction
-Impaired forward flow and elevated filling pressures
Example: Damage to heart muscle after heart attack

56
Q

what might cause diastolic dystfunction? (what part of heart is affected?)

A

reduced wall compliance -> elevated filling pressures (EF often normal)
Example: Thickened, stiff heart muscle from hypertension

57
Q

what kind of permanent effects can afterload cause on the heart? preload?

A

“Pressure work” (afterload) -> Hypertrophy

“Volume work” (preload) -> Dilatation

58
Q

Why does the diminished oxygenation from forward failure/dec CO cause region-specific arteriolar vasoconstriction?
-what is a consequence of this?

A

Body wants to preserve flow to heart an brain while decreasing perfusion to kidneys, skin, and gut
–Leads to a reduction in renal perfusion> Increases renal Na reabsorption, increasing blood volume (preload)

59
Q

One of the earliest findings of left heart failure?

A

LV backward failure
lungs filling with fluid and cannot oxygenate as a result
-intermittent nocturnal dyspnea from diminished circulation at night
severe=acute pulmonary edema (fluid in lungs)

60
Q

Earliest findings of right heart failure reflect:

A

Earliest findings reflect backward RV failure:

  • “pitting” edema (ankles, legs, sacrum)
  • Hepatic (liver) congestion
  • Distended neck veins
61
Q

list 4 possible causes of heart failure:

A

1) Cardiomyopathy
2) HTN
3) Ischemic heart disease
4) Valvular heart disease

62
Q

how could Anemia, thyrotoxicosis trigger heart failure?

A

demand high output from heart

63
Q

while treating predisposing conditions or making lifestyle changes comes first, what pharmacologic options are there for treating heart failure?

A

ACE inhibitors&Angiotensin receptor blockers
Diuretics
Digitalis, other inotropic agents
Beta blockers (cautiously)

(also pacemakers)

64
Q

via what mechanism can inotropic agents like digitalis tx heart failure?

A

1) Inotropic activity:
Inhibits Na/K ATPase/strengthens force of myocardial contraction
2) Negative chronotropic activity:
Inc vagal tone/slows AV conduction

65
Q

how is digitalis toxic? what side effects?

A
  • cardiac arrhythmia, GI symptoms
  • Impaired color vision
  • scotomas
  • flickering vision/glare
  • **other, rarer effects: decreased VA, retrobulbar neuritis, diplopia, photophobia, visual hallucinations, decrease IOP, EOM paresis
66
Q

what is a secondary effect of valve stenosis?

A

Secondary hypertrophy of proximal chamber, also backward failure

67
Q

what is a secondary effect of valve regurgitation?

A

Increased preload (volume work) from retrograde flow through leaking valve -> chamber dilatation

68
Q

aortic stenosis affects what valve?

when does it become symptomatic?

A

BICUSPID valve
*usually asymptomatic, symptoms develop with significantly narrowed valve area
symptoms: 15% syncope, 35% angina, 50% heart failure
(all of these symptoms have relatively high mortalities)

69
Q

aortic stenosis causes what secondary changes to occur to the heart?

A

LV hypertrophy
LA hypertrophy
-reduced forward flow

70
Q

what are a few precautions with aortic stenosis?

A

1) Do not use vasodilators / ACE inhibitors:
Drop aortic pressure>Syncope
2) Do not order a cardiac stress test
-Compromised cardiac output (especially with exertion)
-Increased myocardial oxygen demand (LVH)
-Diminished coronary circulation (increased pressure)

71
Q

Most frequent cause of mitral stenosis?

A

Rheumatic Heart Disease (inf as a kid, symptoms later in life)
(moreso in women)

72
Q

the mitral valve is between what 2 heart chambers?

A

LA>LV

73
Q

what are some initial consequences of mitral stenosis?

A

LA dilatation results -> gives atrial fibrillation and pulmonary congestion (because the blood is backing up into the lungs)

74
Q

list 3 meds you can give to a person with mitral stenosis

A

1) diuretics
2) rhythm drugs
3) anticoagulants in a-fib: these patients are at high risk of thromboembolism and you want to reduce their stroke risk

75
Q

Mitral regurgitation is most commonly caused by:

A

most commonly caused by mitral valve prolapse (MVP)

*could also be caused by anorexigenic meds or papillary muscle ischemia

76
Q

How are end diastolic volume and end systolic volume affected in mitral regurgitation?

A

-End-diastolic volume (EDV) increased
-End-systolic volume decreased
*Starling: Increases in EDV lead to increases in stroke work
Stroke volume increased but forward flow diminished
**Heart failure develops despite normal EF

77
Q

drug therapy for mitral regurg?

A
  • Afterload reduction: Vasodilators. ACE inhibitors

- Anticoagulation for atrial fibrillation

78
Q

4 possible causes of aortic regurg?

A

1) infective endocarditis
2) rheumatic heart disease: inflammatory syndrome following a group A streptococcal infection (often strep throat)
3) Anorexigenic Drugs
4) Disorders of Aortic Root: Dissection, Marfan’s, Syphilis

79
Q

what effect does aortic regurg have on heart?

A

LV hypertrophy

80
Q

which is worse, acute or chronic aortic regurg?

A

acute because happens suddenly and heart doesn’t have chance to adapt, so you get ischemia and shock

81
Q

what drugs can you use to tx aortic regurg?

A

Want to reduce afterload – decrease pressure so the blood can go forward
•ACE inhibitors, Ca channel blockers (nifedipine), vasodilator (hydralazine)

82
Q

MVP occurs in what % of Marfan’s pts?

A

80%

83
Q

what are Marfans pts at risk for with cardiopulm system?

A

MVP
aortic dissection
Spontaneous pneumothorax

84
Q

what is acute rheumatic fever?

A

Inflammatory syndrome that follows Group A streptococcal infection

  • usually ages 4-9
  • Febrile illness appears 2-4 weeks after episode of pharyngitis
85
Q

what is the likelihood of valve involvement in rheumatic fever in decreasing order?

A

Mitral > Aortic > Tricuspid > Pulmonic

86
Q

What is the progression like in chronic rheumatic valvular disease

A

Very slow progression -> symptoms unusual before 10-20 years

-Chronic scarring may produce stenosis, regurgitation or both

87
Q

List a few ocular side effects of bacterial endocarditis:

A
  • Conjunctival petechiae
  • Retinal hemorrhages (“Roth spots”), abscesses
  • Papillitis, corneal precipitates, choroiditis
  • Embolic occlusion of CRA or cerebral vessel(s) with stroke syndrome
88
Q

List 3 signs of Bacterial Endocarditis you would find on skin areas:

A

1) Osler’s nodes - painful, typically located on fingers and toes
2) Janeway’s lesions – flame-like appearing hemes, are painless, typically occurring on palms and soles of feet
3) splinter hemes: linear, red-brown, and non-blanching, occurring often under the nails

89
Q

3 subtypes of cardiomyopathy:

A

1) hypertrophic-impaired inotropy, with forward failure, arrhythmias, emboli, valvular incompetence

2) restrictive
3) dilated-combination of forward and backward failure

90
Q

what is Pheochromocytoma?

A

adrenal gland tumor, releases too much adrenaline/noradrenaline, high bp

91
Q

what is chagas disease?

A

parasite, common in other countries, can get conjunctivitis and lid, lacrimal swelling

92
Q

list several of the many ocular findings associated with myotonic dystrophy:

A
  • Bilateral ptosis, orbicularis weakness, EOM dysfunction
  • Secondary corneal ulceration
  • Blepharoconjunctivitis, hordeola
  • Cataracts: fine “irridescent dust”, brilliantly colored -subcapsular deposits are pathognomonic***
  • Miosis, macular degeneration
93
Q

Ocular features of Friedreich’s Ataxia:

A

Nystagmus, Optic disc pallor, Retinitis pigmentosa (unusual) Optic atrophy (rare)

94
Q

T/F: A fib increases strke risk?

A

True

95
Q

what scoring system is used to determine if the pt needs anticoagulation therapy if they have A FIB:

A

CHADS2 (for pts with non-valvular a-fib because if there is an underlying valve issue, there is no scoring needed to determine the pts risk – you know the pt is high risk and needs to be anticoagulated)
•congestive heart failure (1pt), HTN (1pt), age over 75 (1pt), diabetes (1pt), stroke (2pts)

96
Q

1 cause of ischemic heart disease in US?

A

atherosclerosis

97
Q

3 syndromes or types of ischemic heart disease:

A

1) Ischemia
2) Myocardial infarction (MI) or heart attack
3) Arrhythmias and sudden death

98
Q

what is angina pectoris? what relieves it?

A

angina pectoris:chest pressure/pain

Relieved by rest, nitroglycerine (sublingual)

99
Q

what are the associated Electrocardiographic findings for angina pectoris?

A

ST segment depression

T-wave inversion

100
Q

what is the diff between Q vs non Q wave MI?

A

Non-Q-wave MI=Incomplete occlusion, some tissue infarction, some tissue salvageable
Q-wave MI=Infarction of all tissue beyond the occluded vessel

101
Q

what is unstable angina?

A

Unstable plaque, compromised blood flow, no tissue infarction
(also new onset angina or change in pattern of previously stable angina)

102
Q

WHat diff MI from angina pectoris?

A

MI is similar or identical to angina, more severe/prolonged, unrelieved by nitroglycerine

103
Q

How can you officially diagnose MI at office?

A
  • EKG abnormalities: ST elevation, Appearance of Q waves

- cardiac enzyme elevation : CK-MB, troponins

104
Q

what are a few possible MI complications?

A

Arrhythmias
CHF
Hypotension (cardiogenic shock)

105
Q

what are some choices of drug therapy for anti-angina? (5)

A

1) B-blockers: Decrease myocardial oxygen demand or [Calcium-channel blockers] if asthmatic
2) ACE inhibitors: Afterload reduction (cardiac remodeling after MI)
3) Statins: Lipid lowering, plaque stabilization (?reduce inflammation)
4) Aspirin: Antiplatelet therapy
5) Nitrates: Vasodilators

106
Q

how can you treat someone having an acute MI?

A

thrombolytic (break up clots, faster the better)
anticoag
balloon angioplasty/stent

Clinical Med (10 decks)

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