lecture 2: heart Flashcards
1
Q
what is occurring in the P wave?
A
Atrial depolarization – P wave
2
Q
what is occurring in the QRS complex?
A
Ventricular depolarization – QRS complex (R and L bundle branches)
3
Q
what is occurring in the T wave?
A
Ventricular repolarization – T wave
4
Q
what is occurring for the ST segment?
A
cardiac perfusion
5
Q
describe the electrical pathway of the heart:
A
SA and AV nodes, HIS bundle, R and L bundle branches
6
Q
T/F: A fib is normal in some situations
A
FALSE
7
Q
what is an AV block?
A
AV node conduction delays
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)
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)
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)
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
12
Q
Left Ventricular Hypertrophy puts you at risk for what else cardiovascularly?
A
Heart failure
Atrial fibrillation
Sudden cardiac death
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
14
Q
Myocardial ischemia: what is it and how is it manifested on EKG?
A
Potentially reversible myocardial dysfunction
ST segment depression
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
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
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.
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)
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
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)
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)
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
23
Q
what cells are responsible for secreting renin?
A
JG juxtaglomerular cells
24
Q
where is the macula densa and what does it do?
A
in afferent arteriole, senses Na
25
what is creatine and what can elevated levels tell you?
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
26
what is "BUN"? what do elevated levels indicate?
BUN=Product of protein metabolism excreted by the glomerulus
- reabsorbed along with Na in volume depletion
- Elevated BUN=renal dysfunction or Volume depletion
27
Significant proteinuria suggests:
impaired glomerular filter
28
specific gravity test assesses:
renal concentrating ability
| A urine specific gravity test basically compares the density of urine to the density of water
29
what are some possible adverse effects of diuretics?
```
Electrolyte abnormalities (Na, K, Mg, Cl)
Volume depletion (at risk)
*Glucose intolerance
Photosensitivity / skin rash
Vertigo, fatigue
Erectile dysfunction
```
30
when are diuretics given?
HTN
| edema
31
what are 3 other clinical effects of ACE inhibs besides reducing vascular tone?
-Lower glomerular pressure in the kidney
•Renal protective (eg diabetes)
-Improve cardiac remodeling post-MI
-reduce afterload
32
besides HTN, why else might you give ACE inhib?
- Aortic regurgitation
| - Post-MI
33
one fatal potential side effect of ACE inhibs:
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)
34
T/F: if someone had angioedema on ACE inhib, should try ARB?
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)
35
functions of angiotensin 2?
Vasopressor
| Stimulates production of aldosterone: Causes Na reabsorption in kidney → ↑ volume → ↑ pressure
36
clinical indications for ca channel blockers?
Hypertension
Raynaud’s phenomenon (digital artery spasm)
Coronary artery disease
Certain arrhythmias
(Other - eg GI motility, migraine prophylaxis)
37
3 major Ca channel blockers and how strongly they affect heart
Verapamil: strongest cardiac effects
Diltiazem: medium cardiac effects
Dihydropiridines: little to no direct cardiac effects (so good Tx for HTN)
38
what are the ages where atherosclerosis is a risk factor for men and women?
Males > 45
| Females > 55
39
what are some atherosclerosis risk factors?
```
Age
Fam Hx
Adverse lipid profile
HTN
Smoking
Diabetes
(Inflammation, Obesity, Sedentary lifestyle)
```
40
```
function of HDLs:
Higher levels considered protective against:
```
Removes Excess Cholesterol (returns to liver)
| [Higher levels considered protective against CHD]
41
where is cholesterol produced?
liver
42
what is Tangier's disease?
```
deficiency of HDL (cholesterol trapped inside cells)
Orange tonsils (cholesterol deposits), corneal opacities, peripheral neuropathy
```
43
Abetalipoproteinemia:
Malabsorption of fat / fat-soluble vitamins (A, D, E, K), low cholesterol
44
what is the ideal lipid level when treating atherosclerosis
Lipid level monitoring to track compliance (no defined lipid level target!!)
45
statin side effects:
- liver function
- muscle soreness
- small risk of DM
46
what are some general guidelines for cholesterol levels?
LDL <200 is desirable
47
BP ranges for stage 1 and 2 HTN:
stage 1: 140 - 159 90 - 99
| Stage 2: ≥ 160 ≥ 100
48
Hypertensive Urgency vs Malignant Hypertension
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
T/F: heart failure has been on the decline in america?
False (increasing)
50
CO = __ X ___
CO = stroke volume x heart rate
| •CO usually between 5 and 7 L/min
51
ejection fraction is equal to ___/___
stroke volume/end-diastolic ventricular volume
| **heart doesn't completely empty with contraction
52
chronotropy=
Alterations in heart rate
53
inotropy=
Alterations in contractility
54
what does Starling's equation represent or summarize?
Inc. in EDV lead to increases in stroke work (EF)
| *more blood in heart, harder it has to work
55
How would systolic dysfuntion affect flow and ejection fraction?
Give an example of what might cause this?
-decreased ejection fraction
-Impaired forward flow and elevated filling pressures
Example: Damage to heart muscle after heart attack
56
what might cause diastolic dystfunction? (what part of heart is affected?)
reduced wall compliance -> elevated filling pressures (EF often normal)
Example: Thickened, stiff heart muscle from hypertension
57
what kind of permanent effects can afterload cause on the heart? preload?
"Pressure work” (afterload) -> Hypertrophy
“Volume work” (preload) -> Dilatation
58
Why does the diminished oxygenation from forward failure/dec CO cause region-specific arteriolar vasoconstriction?
-what is a consequence of this?
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
One of the earliest findings of left heart failure?
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
Earliest findings of right heart failure reflect:
Earliest findings reflect backward RV failure:
- “pitting” edema (ankles, legs, sacrum)
- Hepatic (liver) congestion
- Distended neck veins
61
list 4 possible causes of heart failure:
1) Cardiomyopathy
2) HTN
3) Ischemic heart disease
4) Valvular heart disease
62
how could Anemia, thyrotoxicosis trigger heart failure?
demand high output from heart
63
while treating predisposing conditions or making lifestyle changes comes first, what pharmacologic options are there for treating heart failure?
ACE inhibitors&Angiotensin receptor blockers
Diuretics
Digitalis, other inotropic agents
Beta blockers (cautiously)
(also pacemakers)
64
via what mechanism can inotropic agents like digitalis tx heart failure?
1) Inotropic activity:
Inhibits Na/K ATPase/strengthens force of myocardial contraction
2) Negative chronotropic activity:
Inc vagal tone/slows AV conduction
65
how is digitalis toxic? what side effects?
- 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
what is a secondary effect of valve stenosis?
Secondary hypertrophy of proximal chamber, also backward failure
67
what is a secondary effect of valve regurgitation?
Increased preload (volume work) from retrograde flow through leaking valve -> chamber dilatation
68
aortic stenosis affects what valve?
| when does it become symptomatic?
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
aortic stenosis causes what secondary changes to occur to the heart?
LV hypertrophy
LA hypertrophy
-reduced forward flow
70
what are a few precautions with aortic stenosis?
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
Most frequent cause of mitral stenosis?
Rheumatic Heart Disease (inf as a kid, symptoms later in life)
(moreso in women)
72
the mitral valve is between what 2 heart chambers?
LA>LV
73
what are some initial consequences of mitral stenosis?
LA dilatation results -> gives atrial fibrillation and pulmonary congestion (because the blood is backing up into the lungs)
74
list 3 meds you can give to a person with mitral stenosis
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
Mitral regurgitation is most commonly caused by:
most commonly caused by mitral valve prolapse (MVP)
| *could also be caused by anorexigenic meds or papillary muscle ischemia
76
How are end diastolic volume and end systolic volume affected in mitral regurgitation?
-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
drug therapy for mitral regurg?
- Afterload reduction: Vasodilators. ACE inhibitors
| - Anticoagulation for atrial fibrillation
78
4 possible causes of aortic regurg?
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
what effect does aortic regurg have on heart?
LV hypertrophy
80
which is worse, acute or chronic aortic regurg?
acute because happens suddenly and heart doesn't have chance to adapt, so you get ischemia and shock
81
what drugs can you use to tx aortic regurg?
Want to reduce afterload – decrease pressure so the blood can go forward
•ACE inhibitors, Ca channel blockers (nifedipine), vasodilator (hydralazine)
82
MVP occurs in what % of Marfan's pts?
80%
83
what are Marfans pts at risk for with cardiopulm system?
MVP
aortic dissection
Spontaneous pneumothorax
84
what is acute rheumatic fever?
Inflammatory syndrome that follows Group A streptococcal infection
- usually ages 4-9
- Febrile illness appears 2-4 weeks after episode of pharyngitis
85
what is the likelihood of valve involvement in rheumatic fever in decreasing order?
Mitral > Aortic > Tricuspid > Pulmonic
86
What is the progression like in chronic rheumatic valvular disease
Very slow progression -> symptoms unusual before 10-20 years
| -Chronic scarring may produce stenosis, regurgitation or both
87
List a few ocular side effects of bacterial endocarditis:
* Conjunctival petechiae
* Retinal hemorrhages (“Roth spots”), abscesses
* Papillitis, corneal precipitates, choroiditis
* Embolic occlusion of CRA or cerebral vessel(s) with stroke syndrome
88
List 3 signs of Bacterial Endocarditis you would find on skin areas:
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
3 subtypes of cardiomyopathy:
1) hypertrophic-impaired inotropy, with forward failure, arrhythmias, emboli, valvular incompetence
2) restrictive
3) dilated-combination of forward and backward failure
90
what is Pheochromocytoma?
adrenal gland tumor, releases too much adrenaline/noradrenaline, high bp
91
what is chagas disease?
parasite, common in other countries, can get conjunctivitis and lid, lacrimal swelling
92
list several of the many ocular findings associated with myotonic dystrophy:
- 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
Ocular features of Friedreich’s Ataxia:
Nystagmus, Optic disc pallor, Retinitis pigmentosa (unusual) Optic atrophy (rare)
94
T/F: A fib increases strke risk?
True
95
what scoring system is used to determine if the pt needs anticoagulation therapy if they have A FIB:
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
#1 cause of ischemic heart disease in US?
atherosclerosis
97
3 syndromes or types of ischemic heart disease:
1) Ischemia
2) Myocardial infarction (MI) or heart attack
3) Arrhythmias and sudden death
98
what is angina pectoris? what relieves it?
angina pectoris:chest pressure/pain
| Relieved by rest, nitroglycerine (sublingual)
99
what are the associated Electrocardiographic findings for angina pectoris?
ST segment depression
| T-wave inversion
100
what is the diff between Q vs non Q wave MI?
Non-Q-wave MI=Incomplete occlusion, some tissue infarction, some tissue salvageable
Q-wave MI=Infarction of all tissue beyond the occluded vessel
101
what is unstable angina?
Unstable plaque, compromised blood flow, no tissue infarction
(also new onset angina or change in pattern of previously stable angina)
102
WHat diff MI from angina pectoris?
MI is similar or identical to angina, more severe/prolonged, unrelieved by nitroglycerine
103
How can you officially diagnose MI at office?
- EKG abnormalities: ST elevation, Appearance of Q waves
| - cardiac enzyme elevation : CK-MB, troponins
104
what are a few possible MI complications?
Arrhythmias
CHF
Hypotension (cardiogenic shock)
105
what are some choices of drug therapy for anti-angina? (5)
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
how can you treat someone having an acute MI?
thrombolytic (break up clots, faster the better)
anticoag
balloon angioplasty/stent
