1A: Dt 6-2

Front 1

aVR vs aVF vs aVL:
Vectors

Back 1

aVR: heart to right arm
aVF: heart to feet
aVL: heart to left arm

Front 2

Lead I vs Lead II vs Lead III:
Vectors

Back 2

Lead I: Right arm to left arm
Lead II: Right arm to left leg
Lead III: Left arm to left leg

Front 3

Left Axis Deviation:
EKG signs
Causes

Back 3

Positive QRS in aVL and aVR

Causes:
Inferior wall MI
Left anterior fascicular block
L BBB
LVH (sometimes)
High diaphragm

Front 4

Right Axis Deviation:
EKG signs
Causes

Back 4

Positive QRS in limb lead III

RVH
Acute right heart strain (massive pulm embolism)
R BBB
Dextrocardia

Front 5

Quick way to determine normal axis.

Back 5

Positive QRS in Limb Lead I and II

Front 6

1 tiny box =
1 big box =

Back 6

1 small box = 0.04 s
1 big box = 0.2s

Front 7

How wide is a normal QRS complex?
What if it's longer?

Back 7

3 small boxes

If longer-->ventricular-generated rhythm

Front 8

Peaked T wave indicates _____

Back 8

High potassium levels

Front 9

Flat T wave indicates ______.

Back 9

Low potassium levels

Front 10

Torsades de Pointes:
What is it?
Cause
Risks

Back 10

Ventricular tach that can progress to V-fib

Cause: anything that prolongs QT interval

Very fast, wide QRS

Front 11

What drugs place patients at risk of Torsades de pointes?
How?

Back 11

These drugs prolong QT interval can can cause Torsades

Marolides (thromycin)
Chloroquine, methoquine
Haloperidol
Risperidol
Methadone
Proteas Inhibitors

Front 12

Torsades de pointes:
Treatment

Back 12

Mg2+

Front 13

Back 13

Torsades de pointes--
Rapid sinusoidal waveforms
Prolonged QT interval

Front 14

Wolff-Parkinson-White Syndrome:
Pathophys
EKG characteristics
Risk
Treatment

Back 14

Accessory conduction PW from atria to ventricle (bundle of Kent), bypassing AV node.

Thus, ventricles begin to partially depol earlier, giving rise to characteristic delta wave on ECG.

Tx: amiodarone, procainamide

Risk: Supraventricular tachycardia

Front 15

Back 15

WPW delta wave

Front 16

Back 16

WPW delta wave

Front 17

Atrial fibrillation:
Predisposing factors
Risks
Treatment

Back 17

Enlarged atria, SA nodes depolarize at different times-->irregularly irregular rhythm

Blood can pool-->clots-->emboli

Tx:
If less than 48 hours-->cardiovert (defib)
If over than 48 hours-->do not cardiovert (risk of embolus):
-Heparin
-Clot assessment
-Rate control (digoxin, beta-blockers, CCB)
OR
-Rhythm control (sotalol, amiodarone--K+ blockers)

Front 18

Back 18

Atrial fibrillation--irregularly irregular

Front 19

Back 19

Atrial flutter--sawtooth pattern

Front 20

1st degree AV block:
EKG characteristics
Cause

Back 20

PR interval >.200sec

Borelli burgdorferi (Lyme)

Front 21

2nd Degree Heart Block:
Mobitz I vs II--
EKG Characteristics

Back 21

Mobitz I: Progressive lengthening of PR until beat is dropped (P wave not followed by QRS)

Usually asyx

Mobitz II: Dropped beats not preceded by change in length of PR interval; can progress to 3rd degree heart block

Front 22

3rd Degree Heat Block:
EKG Characteristics

Back 22

Atria and ventricles beat independently of each other

Both P and QRS are present, although P waves bear NO RELATION to QRS complexes

Usually treated with pacemaker; can by caused by Lyme dz

Front 23

How do you determine rate on EKG?

Back 23

Count big boxes:
300, 150, 100, 75, 60, 50

Front 24

Back 24

Front 25

Back 25

Front 26

Back 26

Front 27

Back 27

Front 28

Back 28

Front 29

Back 29

Front 30

Back 30

Front 31

Back 31

Front 32

Back 32

Front 33

Back 33

Front 34

Back 34

Front 35

Back 35

Front 36

Back 36

Front 37

Back 37

Front 38

Back 38

Front 39

Describe the JGA response to low BP

Is this a long-term or short-term response?

Back 39

JG releases Renin
Renin converts angiotensinogen (from liver) to AgI
ACE from lungs: Ag1-->Ag2

Ag2-->
-vasoconstriction at vasc SM
-adrenal production of aldosterone-->favorable gradient for Na+ and H2O reabsorption (retention)

LONG TERM RESPONSE (takes a while to retain water and sodium)

Front 40

Baroreceptors:
Location
Stimuli and Effects

Back 40

Located in carotid sinus (glossopharyngeal, responds to dec'd and inc'd BP) and aortic arch (vagus; detects inc'd BP only)

Baroreceptor:
1) Hypotn-->dec'd arterial pressure-->dec'd stretch-->dec'd afferent firing to medulla (via vagus)

Results in inc'd efferent symp firing and dec'd efferent parasymp stimuln

Results in vasoconstriction, inc'd HR, inc'd contractiliy, inc'd BP

Important for response to hemorrhage!

2nd stimulus:
Carotid massage-->inc'd pressure on carotid artery-->inc'd stretch-->inc'd afferent firing-->dec'd HR

Front 41

Chemoreceptors:
Location
Stimuli and Effects

Back 41

Located in carotid sinus (glossopharyngeal, responds to dec'd and inc'd BP) and aortic arch (vagus; detects inc'd BP only)


1) Peripheral stimulus (detected by ABG)--carotid and aortic bodies respond to PO2 <60mmHg, inc'd PCO2, and dec'd pH of blood

2) Central stimulus--respond to changes in pH and PCO2 of brain interstitial fluid (influenced by arterial CO2). Doesn't directly respond to PO2.
Inc'd intracranial pressure constricts arterioles-->cerebral ischemia-->HTN (symp response)-->reflex bradycardia and respiratory depression

Front 42

Pulmonary Cap Wedge Pressure:
Approximates what?
Example of an abnormal finding

Back 42

Measures LA pressure

If PCWP>LV diastolic pressure-->Mitral stenosis

Front 43

Describe how the following factors affect the Starling forces of fluid movement through capillaries.
Heart failure
Liver failure
Infections and toxins
Lymphatic blockage

Back 43

Heart failure: build up of fluid (?) osmotic pressure??

Liver failure: dec'd oncotic pressure due to lack of proteins

Infections, Toxins: Increase cap perm

Lymphatic blockage:: protein retention in capillaries, draw fluid in (nonpitting edema)

Front 44

What are the two different types of second degree AV block and how do they differ?

Back 44

Mobitz 1: progressive prolonged PR intervals, dropped beat

Mobitz 2: Dropped beat without progressive elongation of PR interval

Front 45

What are normal BPs in the right and left ventricles?

Back 45

RV:
Systolic <25, diastolic<5

LV:
Systolic <130, diastolic <10

Front 46

What substances act on smooth muscle myosin light-chain kinase?

How does this affect blood pressure?

Back 46

CCBs
Epinephrine at beta-2 receptors
PGE2

All will relax vascular SM

Front 47

Describe the chain of events by which hypotension causes a reflex tachycardia.

Back 47

Carotid sinus senses low BP (aortic arch doesn't sense despression)
Results in less stimuln of baroreceptor at carotid sinus
Less stimuln of glossopharyngeal nerve

Glossoph signals to solitary tract of medulla, resulting in dec'd inhibition of sympathetic output; less excitation of psymp

Results in reflex tach

Front 48

What is pre-hypertension?

Back 48

BP >130/85

Front 49

Leading cause of HTN.

Back 49

Primary causes (essential--familial); related to inc'd CO and inc'd TPR

Front 50

Left Ventricular Hypertrophy:
Cause
Associated heart sound
Effects

Back 50

Caused by chronic HTN

Requires more oxygen, becomes stiffened
S4 heart sound

LV can't fill as well (les volume bc thickened muscle takes up space)

Can lead to MI

Front 51

Cause of HTN:
Paroxysms of increased sympathetic tone
Anxiety
Palpitations
Diaphoresis

Back 51

Pheochromocytoma

Front 52

Cause of HTN:
Age of onset between 20 and 50

Back 52

Primary or essential HTN

Front 53

Cause of HTN:
Elevated serum Cr
Abnormal urinalysis

Back 53

HTN due to renal dz

Front 54

Cause of HTN:
Abdominal bruit

Back 54

Renal artery stenosis

Front 55

Cause of HTN:
BP in arms>legs

Back 55

Coarctation of aorta

Front 56

Cause of HTN:
Family history of HTN

Back 56

Primary or essential HTN

Front 57

Cause of HTN:
Tachycardia
Heat intolerance
Diarrhea

Back 57

Hyperthy

Front 58

Cause of HTN:
Hyperkalemia

Back 58

renal failure

Front 59

Cause of HTN:
Episodic sweating and tachycardia

Back 59

pheo

Front 60

Cause of HTN:
Abrupt onset in patient younger than 20 or older than 50
Suppressed serum K+ levels

Back 60

Hyperaldosteronism

Front 61

Cause of HTN:
Central obesity
Moon facies
Hirsutism

Back 61

Cushing's

Front 62

Cause of HTN:
Normal urinalysis
Normal serum K+

Back 62

Primary or essential HTN

Front 63

Cause of HTN:
Young individual with acute onset tachycardia

Back 63

Stimulant abuse: coke, amphetamines

Front 64

Cause of HTN:
Hypokalemia

Back 64

Hyperaldost or Renal Artery Stenosis

Front 65

Cause of HTN:
Proteinuria

Back 65

Renal Dz

Front 66

Essential HTN:
Treatment

Back 66

First line:
HCTZ or thiazide (retain Ca2+, can redue risk of osteoporosis, prevents calcium renal stones)
Or ACE-i

Front 67

CHF:
Treatment

Back 67

Loop diuretics (lose Ca2+, inc'd Ca2+ in urine): Furosemide
ACE-inhibitor, aldosterone antagonist, beta-blockeres (if compensated)

Front 68

DM HTN:
Treatment

Back 68

ACE-i or ARB
CCB
Diuretics, beta-blockers BUT CAN MASK SIGNS OF HYPOGLYCEMIA

Front 69

Hydralazine:
MOA
Use

Back 69

Inc'd cGMP-->SM relaxation
Vasodilation of arterioles > veins
Afterload reduction

Use: Severe HTN, HTN crisis, safe in pregnancy

Front 70

Which anti-hypertensive drugs are safe in pregnancy?

Back 70

Hydralazine
Nifedipine
Labetalol
Methyldopa

Front 71

Dihydropyridine CCBs:
Examples
Use
How do they differ from verapamil?

Back 71

-dipines (nifedipine, amlodipine, etc)

Act like nitrates; dilate veins, dec'd preload

verapamil does not do this!

Used in HTN, angina,

Front 72

Which calcium channel blockers act at vascular smooth muscle?

Back 72

Nifedipine>Diltiazem>Verapamil

Front 73

Which calcium channel blockers act at the heart?

Back 73

Verapamil > diltiazem > nifedipine

Front 74

Nitroglycerin:
MOA
Other drugs with same MOA
Use

Back 74

Vasodilate by releasing NO in smooth muscle, causing inc'd cGMP and SM relaxation

Dilate veins >> arteries; dec preload

Other drugs: isosorbide, dinitrate

Use in angina

Front 75

Nitroprusside:
MOA
AE
Use

Back 75

Short acting inc cGMP via direct release of NO for both veins and arteries

Can cause cyanide toxicity

Use in malignant HTN

Front 76

Which anti-hypertensive drug:
First dose orthostatic hypotension

Back 76

alpha-1 blockers (zosin)

Front 77

Which anti-hypertensive drug:
Ototoxic, especially with aminoglycosides

Back 77

Loop diuretics

Front 78

Which anti-hypertensive drug:
Hypertrichosis

Back 78

Minoxidil--Rogaine

Front 79

Which anti-hypertensive drug:
Cyanide toxicity

Back 79

Nitroprusside

Front 80

Which anti-hypertensive drug:
Dry mouth, sedation, severe rebound HTN

Back 80

Clonidine

Front 81

Which anti-hypertensive drug:
Bradycardia
Impotence
Asthma exacerbation

Back 81

beta-blockers

Front 82

Which anti-hypertensive drug:
Reflex tachycardia

Back 82

nitrates
hydralazine
dihydropyridine CCBs

Anything that vasodilates!

Front 83

Which anti-hypertensive drug:
Cough

Back 83

ACE-i (excess bradykinin)

Front 84

Which anti-hypertensive drug:
Avoid in patients with sulfa allergy

Back 84

Loop and thiazide diuretics are actually sulfa drugs

Front 85

Which anti-hypertensive drug:
Possible angioedema

Back 85

ACE-i (bradykinin)

angioedema = swollen face; lips to larynx

Front 86

Which anti-hypertensive drug:
Possible development of drug-induced lupus

Back 86

Hydralazine

Front 87

Which anti-hypertensive drug:
Hypercalcemia, hypokalemia

Back 87

Thiazide (HCTZ)

Front 88

Which antihypertensives are safe for use in pregnancy?

Back 88

Methyldopa
Labetalol
Hydralazine
Nifedipine

Front 89

While on an ACE inhibitor, a patient develops a cough.

What is a good replacement drug and why doesn't it have the same side effects?

Back 89

ARB (sartan)
Not inhibiting enzyme, they're inhibiting receptor; bradykinin is broken down