Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

* DIT each session > Day 6.2 Cardio > Flashcards

Day 6.2 Cardio Flashcards

1
Q

EKG P wave

A

atrial depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

EKG PR interval

A

conduction delay through AV node

usu < 200msec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

EKG QRS complex

A

ventricular depolarization

usu <120 msec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

EKG QT interval

A

mechanical contraction of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

EKG T wave

A

ventricular repolarization

T-wave inversion indicates recent MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why isn’t atrial repolarization on an EKG?

A

it’s masked by QRS complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

EKG ST segment

A

isoelectric, ventricles are depolarized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

EKG U wave

A

can be caused by hypokalemia or bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

On EKG: what waves are up, what are down?

A 
P is up
Q is down
R is up high
S is down
T is up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the PR interval?

A

From the beginning of the P wave to the start of the QRS complex (so until the Q wave)

Prolonged in AV block. Prolonged means >200 msec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Torsades de pointes

A

Ventricular tachycardia, see shifting sinusoidal waveforms on EKG.
Can progress to v-fib
Anything that prolongs the QT interval can predispose to TdeP
Rx: Mg2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What drugs prolong the QT interval (and therefore predispose to TdeP)?

A 
Macrolides (erythromycin)
Antimalarials (chloroquine, mefloquine)
Haloperidol
Risperidone
Methadone
Protease inhibitors (HIV)
Anti-arrhythmics (Class 1A, Class III)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Congenital long QT interval

A

usu due to defects in cardiac Na+ chnls or K+ chnls.

Can px w severe congenital sensorineural deafness (Jervell and Lange-Nielsen syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Wolf Parkinson White

A

Ventricular pre-excitation syndrome.
Accessory pathway (bundle of Kent) from atria to ventricle, which bypasses AV node
So, ventricles partially depolarize earlier–>
classic delta wave on EKG.
Can result in reentry current, leading to SVT
Rx procainamide or amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where is a delta wave?

A

After P wave, right at start of QRS should be.
It’s leading up to the R, you don’t really see a Q
Classic WPW.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where is the ST segment?

A

After QRS until the beginning of T wave

So from end of S wave to T.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

EKG Segment vs Interval

A

Segment = flat part bt 2 waves

Interval = includes one segment (flat part) and at least one wave.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How many leads are on an EKG? What are they?

A

12 leads:
aVR, aVL, aVF
I, II, III (bipolar)
V1,2,3,4,5,6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

aVR

A

points from heart to right arm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

aVL

A

points from heart to left arm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

aVF

A

points from heart to foot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

limb lead I

A

points from right arm to left arm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

limb lead II

A

points from right arm to foot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

limb lead III

A

points from left arm to foot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Normal net electrical signal

A

Down and to the left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

aVR net signal

A

negative deflection of QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

aVL net signal

A

positive deflection of QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Limb lead I net signal

A

positive deflection of QRS

means that signal is going to left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Limb lead II net signal

A

positive deflection of QRS

means that signal is going down and left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

T/F you can combine limb leads I and II and their overlap is the direction that the signal is going

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Positive QRS deflection in aVL and in aVR

A

Left axis deviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Causes of left axis deviation

A 
Interior wall MI
Left anterior fasicular block
LVH (sometimes)
LBBB
High diaphragm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Positive QRS in limb lead III

A

Right axis deviation (probably)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Causes of right axis deviation

A

RVH
Acute R heart strain (ex massive pulm embolism)
Left posterior fascicular block
RBBB
Dextrocardia (heart pointed toward right/on right side of body)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Quickest way to know if heart has normal axis

A

Look at limb leads I and II

If they both have positive QRS then it’s normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Positive deflection in aVR

A

almost always abnormal- completely the opposite way of where the heart should be pointing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

EKG: amt of time in 1mm (little) box

A

0.04sec (40msec)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

EKG: amt of time in 5mm (big) box

A

0.2 sec (200 msec)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Length of normal PR interval

A

Beginning of P wave to start of QRS complex should be less than 200 msec (1 big box)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Length of normal QRS

A

the ventricular depolarization should happen to both ventricles at the same time, so it should be quick- less than 120 msec (3 tiny boxes).
If both ventricles are depolarizing at the same time, it will take longer. This could be a ventricular rhythm- one that is originating from the ventricles rather than the AV node.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What ion do T waves give info about?

A

Potassium levels
Peaked T waves = hyperkalemia
Flat T waves = hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Speed of conduction- which places have fast conduction? Slow conduction?

A 
Fastest to slowest:
Purkinje (v fast)
Atria
Ventricles
AV node (v slow)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the pacemaker? What serves as the pacemaker if it stops working?

A

SA node.
If no SA, then AV node
If no AV, then bundle of His & purkinje fibers
^These will all cause normal narrow QRS. If ALL fail, then ventricles will take over- and will have wide QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Atrial fib

A

Irregularly irregular
No distinct P waves

No pattern to how often there is a QRS, can’t see P waves bt QRS.
No distinct SA nodes. (A-fib is common if there is atrial enlargement.)
No coordinated atrial contraction (that’s why there are no distinct P waves)
Can result in atrial stasis and lead to stroke (pooling of blood leads to clots –> pulm embolism, or if patent FO, then anywhere in body –> stroke)
Predisposes to SVT
>300bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Rx for A-fib

A

If new A-fib ( drugs- K+ chnl blockers (sotalol or amiodarone)

Prophylax against thromboembolism w warfarin/coumadin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Atrial flutter

A

Sawtooth
Rapid identical back-to-back atrial depolarization waves- do have distinct P waves, just a lot of them!
220-300bpm (once it’s >300 it’s A-fib)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Rx for atrial flutter

A

Try to convert to sinus rhythm

Use Class 1a, 1c, or III anti-arrhythmics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

1st degree AV block

A

Prolonged PR interval
PR should be <200 msec, so this is more than that- aka greater than one big box.
Asymptomatic, benign- but more likely to go into 2nd degree block.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What organism can cause 1st degree AV block?

A

Borrelia burgdorferi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

2nd degree heart block: what are the types?

A

Mobius Type 1 = Wenckebach

Mobius Type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Mobius Type 1 (2nd degree heart block)

A

Wenkebach.
Progressive lengthening of the PR interval until a beat is dropped- there is a P wave which is NOT followed by a QRS.
Usu asymptomatic, benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Mobius Type 2 (2nd degree heart block)

A

Dropped beats that are NOT preceded by a change in length of PR interval (so no warning, just have a missed QRS all of the sudden)
The abrupt non-conducted P waves result in a pathologic condition.
Often found as 2:1 block, where there are 2 P waves for every 1 QRS response.
Can progress to 3rd degree AV block, so treat w pacemaker to prevent this.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

3rd Degree heart block

A

Atria and ventricle beat completely independently of each other- so have both P waves and QRS, but no connection between the two.
SA node is not communicating w AV node
Atrial rate (P waves) is faster than the ventricular rate (QRS).
Usu treated w pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What disease can cause 3rd degree heart block?

A

Lyme dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Ventricular fibrillation

A

Completely erratic rhythm w no identifiable waves.

Fatal arrythmia w/o immed CPR and defibrillation.

56
Q

Sinus bradycardia

A

Rate <60
Count the boxes- 5 big boxes is 60
(300, 150, 100. 75, 60, 50)- count from e.g. peak of QRS to peak of next QRS.

57
Q

Paroxysmal SVT

A

Narrow QRS w fast rhythm

58
Q

Monomorphic V-tach

A

Wide QRS w fast rhythm

59
Q

Ventricular premature beats

A

See QRS w/o a P wave. (on top of normal P QRS T, P QRS T rhythm)
Wide QRS

60
Q

How does an MI change w time on EKG?

A

Acute: ST elevation
Hours: ST elevation + R wave is decreased + Q wave appears
Day 1-2: Deeper Q wave + T wave inversion (plus ST elev, decrsd R wave from before)
Days later: ST normal, R back up high, T wave still inverted, still have Q wave
Weeks later: ST normal T wave normal, still have Q wave (every thing looks normal except for Q)

61
Q

Where is angiotensinogen released from?

A

Liver

62
Q

Where is renin released from?

A

JG cells of kidney

63
Q

What causes renin rls?

A 
Decreased BP (sensed by JG cells)
Increased Na+ delivery (sensed by MD cells)
Increased sympathetic tone
64
Q

What is the role of renin?

A

Converts angiotensinogen from liver to AT I

65
Q

What converts AT I to AT II?

A

ACE from the lungs and kidneys

ACE also breaks down bradykinin

66
Q

What does AT II do (6 things)?

A 
Acts on ATII receptors on smth musc
Constricts eff arteriole of glomerulus
Causes aldosterone secretion (from adrenal gland)
Causes ADH secretion (from post pit)
Increases proximal tube Na+/H+ activity
Stimulates hypothalamus
67
Q

When AT II acts on receptors of vascular smooth musc, what is the effect?

A

AT tenses angios!

It causes vasoconstriction, which elevates BP

68
Q

When AT II constricts the efferent arteriole of the glomerulus, what is the effect?

A

It increases the filtration fraction to preserve renal fn (GFR) in low-volume states
eg when RBF is decreased

69
Q

When AT II causes aldo rls from adrenal glands, what is the effect?

A

Aldo causes increased Na+ chnl and increased Na+/K+ insertion into principle cells.
It enhances K+ and H+ excretion by upregulating principle cell K+ chnls and intercalated cell H+ chnls

Together, these create a favorable Na+ gradient for Na+ and H2O reabsorption.
When more Na+ and H2O stay in the body, blood prs is increased!

70
Q

When AT II causes ADH rls from the post pit, what is the effect?

A

ADH causes insertion of H2O chnls in principle cells, which leads to increased H2O reabsorption

71
Q

When AT II causes increased proximal tubule Na+/H+ activity, what is the effect?

A

H2O reabsorption

can permit contraction alkalosis

72
Q

When AT II stimulates the hypothalamus, what is the effect?

A

Increased thirst

73
Q

AT II affects barocepter function- what is the result of this?

A

It limits reflex bradycardia.

Normally, when there is increased BP, the HR will go down. This dampens that effect.

74
Q

ANP

A

Released from atria in response to increased blood volume in atria
Can act as a check on renin-AT-aldo system

Relaxes vascular smooth musc via cGMP, causing increased GFR and decreased renin.

75
Q

ADH

A

Primarily regulates osmolarity (inserts water channels), but also reacts to low blood volume, which is more imp than osmolarity.

76
Q

Aldosterone

A

Primarily regulates blood volume.

In low-vol states, both ADH and aldo help out.

77
Q

Bradykinin

A

Vasodilator, lowers BP
Bradykinin is broken down by ACE.
ACE-inhibitors are used for HTN bc they stop ACE and therefore stop the breakdown of bradykinin- meaning it can vasodilate like it normally does.

78
Q

ACE and Bradykinin

A

ACE breaks down bradykinin

79
Q

What is the “long term” way to fix a decreased MAP?

A

JGA senses decreased MAP
Renin-AT system is activated
AT II causes vasoconstriction, which increases TPR, plus Aldo increases blood vol, which increases CO.
MAP is increased d/t increased TPR and CO

80
Q

What is the “short term” way to fix a decreased MAP

A

Baroreceptor fires less often, this is sensed by the medullary vasomotor center
Causes increased sympathetic activity in heart and vasculature
B1: increased HR and contractility lead to increased CO
alpha1: venoconstriction means greater venous return, which increases CO
alpha1: arteriorlar vasoconstriction increases TPR
MAP is incrsd d/t increased TPR and CO

81
Q

When is ANP released? What does it do?

A

Diuretic, rlsd from atria in response to increased bld vol and increased atrial prs.
Causes general vascular relaxation.
Constricts efferent renal arterioles, but dilates afferent arterioles.
Involved in “escape from aldosterone” mechanism.

82
Q

Where are the baroreceptors?

A

Aortic arch and carotid sinus

83
Q

How does the baroreceptor on the aortic arch transmit info?

A

Transmits via vagus nerve, to medulla

ONLY responds to INCREASED BP, not decreased.

84
Q

How does the baroreceptor on the carotid sinus transmit info?

A

Transmits via glossopharyngeal nerve, to the solitary nucleus of the medulla.
Responds to both increases and decreases in BP.

85
Q

When there is hypotension, how do baroreceptors sense it, and what do they do?

A 
Carotid sinus (only) senses decreased arterial prs bc there is decreased stretch, and therefore decreased afferent baroreceptor firing (to glossopharyngeal)
This causes increased efferent sympathetic and decreased efferent parasympathetic.
The increased symp means alpha1 vasoconstriction, B1 increased HR and contractility, so increased BP
Overall this is a short term mechanism, but it's imp in response to severe hemorrhage.
86
Q

How does carotid massage change the heart rate?

A

Increased prs on carotid artery means increased stretch- this means increased afferent baroreceptor firing (glossopharyngeal nerve), and so decreased HR.

87
Q

How does glossopharyngeal nerve firing relate to HR?

A

decreased nerve firing means HR will increase (as in hypotensive response)

increased firing means HR will decrease (as in carotid massage)

88
Q

When is carotid massage performed?

A

SVT.
But, not in elderly/in ppl w plaques, bc could dislodge plaque.
If massage doesn’t work, use adenosine for SVT.

89
Q

Where are the peripheral chemoreceptors?

A

on carotids and aortic arch.

90
Q

What do the peripheral chemreceptors have a response to?

A

Carotid bodies and Aortic bodies respond to decreased PO2 (<60mmHg)- that is, the amt of O2 dissolved in blood (nothing to do w Hb).
They also respond to increased PCO2 and to acidosis (decreased pH of blood).

91
Q

What do central chemoreceptors respond to?

A

Centrals respond to chgs in pH and PCO2 not of blood in arteries, but in the brain interstitial fluid. (The pH and PCO2 in the brain are influenced by arterial CO2 tho.
They do NOT respond directly to PCO2.
Responsible for Cushing triad.

92
Q

What is the Cushing triad?

A

HTN, bradycardia, and respi depression

Increased ICP constricts arterioles, leading to cerebral ischemia, which leads to HTN (sympathetic response), leading to reflex bradycardia.

93
Q

Pc

A

capillary prs
pushes fluid out of capillary (it’s the fluid inside tho, that’s pushing out)
higher at beginning of capillary (w force of heart/aorta behind it)

94
Q

Pi

A

interstitial fluid prs
pushes fluid into capillary (it’s the fluid outside that’s pushing in)
higher at end of capillary

95
Q

TTc

that was supposed to be pi

A

plasma colloid oncotic prs
pulls fluid into capillaries
(proteins in blood)

96
Q

TTi

that was supposed to be pi

A

interstitial fluid colloid osmotic prs
pulls fluid out of capillaries
(proteins in interstitial fluid)

97
Q

What is the net filtration prs eqn?

A

Pnet = (Pc - Pi) - (TTc - TTi)

So, (prs d/t fluid inside - fluid outside), minus (pressure d/t proteins inside - proteins outside)

98
Q

What is edema?

A

Excessive fluid outflow into interstitium. Can be pitting (excess fluid w/o colloid) or non-pitting (lots of colloid in interstitium, so fluid comes to balance it)

99
Q

4 common causes of edema

A
  1. increased capillary prs (Pc)- typically at end of capillary (it’s already big at beginning). see in heart failure
  2. decreased plasma proteins (TTc) d/t nephrotic syndrome (peeing them out) or liver failure (not making enough)
  3. Increased capillary permeability (Kf) caused by toxins, infection, burn, septic shock. histamines and bradykinin cause capillaries to be leaky.
  4. increased interstitial fluid colloid osmotic prs (TTi) d/t lymphatic blockage
100
Q

Net fluid flow eqn

A

Pnet x Kf

101
Q

What is Kf?

A

filtration constant (aka capillary permeability)

102
Q

What is PCWP (wedge prs) a good estimate of?

A

LA prs.
(also LV end diastolic prs)
Measure w a Swan-Ganz catheter, which goes thru R heart and into pulm artery.

In mitral stenosis, PCWP > LV diastolic prs.

103
Q

What factors determine autoregulation of perfusion prs in the heart?

A

Local metabolites- O2, adenosine, NO

if O2 decreases, coronary arteries dilate
adenosine is a potent vasodilator
NO dilates the coronary arteries

104
Q

What factors determine autoregulation of perfusion prs in the brain

A

local metabolites: CO2 (regulates pH)

105
Q

What factors determine autoregulation of perfusion prs in the kidneys?

A

myogenic and tubuloglomerular feedback

106
Q

What factors determine autoregulation of perfusion prs in the lungs?

A

Hypoxia causes vasoconstriction

This is the opp of the rest of the body, but for good reason: don’t want to perfuse areas that are poorly oxygenated, bc it means the blood that goes to that area won’t take up much O2- and then you will be delivering O2-poor blood to the body.

107
Q

What factors determine autoregulation of perfusion prs in the skeletal musc

A

local metabolites- lactate, adenosine, K+

108
Q

What factors determine autoregulation of perfusion prs in the skin?

A

Sympathetic stimulation is the most imp mech- esp for temp control.

109
Q

Normal prs in heart (RV, LV, etc)

A 
RA = &lt; 10 (the 10 is PCWP)
LA = &lt;130 / 90
110
Q

Dx: HTN + paroxysms of increased SNS tone: anx, palpitations, diaphoresis

A

Pheochromocytoma

111
Q

Dx: HTN, onset bt 20-50yo

A

Primary/essential HTN

112
Q

Dx: HTN + elevated serum creatinine and abn urinalysis

A

Renal dz

113
Q

Dx: HTN + abd bruits

A

Renal artery stenosis

114
Q

Dx: HTN + BP in arms > legs

A

Coarctation of aorta

115
Q

Dx: HTN + fam hx of HTN

A

Primary/Essential HTN

116
Q

Dx: HTN + tachycardia, heat intolerance, diarrhea

A

Hyperthyroidism

117
Q

Dx: HTN + hyperkalemia

A

Renal failure

118
Q

Dx: HTN + Episodic sweating and tachycardia

A

Pheochromocytoma

119
Q

Dx: HTN w/ abrupt onset in pt 50, and depressed serum K+ levels (hypoK+)

A

Hyperaldosteronemia

high aldo in blood

120
Q

Dx: HTN + central obesity, moon-face, hirsutism

A

Cushing’s syndrome

121
Q

Dx: HTN + normal urinalysis, normal serum K+

A

primary/essential HTN

122
Q

Dx: HTN + young pt w acute onset tachycardia

A

stimulant abuse (cocaine, meth)

123
Q

Dx: HTN + hypokalemia

A

Hyperaldosteronism

Or, renal artery stenosis

124
Q

Dx: HTN + proteinuria

A

Kidney failure

125
Q

HTN features and risk factors

A

BP > 140/90
PreHTN BP >130/85

90% is primary/essential and related to increased CO or increased TPR
other 10% is secondary to renal dz.
Malignant HTN is severe and rapidly progressing.

Risk: increased age, obesity, diabetes, smoking, genetics, black>white>asian

126
Q

What does HTN predispose to?

A 
Atherosclerosis
LVH
stroke
CHF
renal failure
retinopathy
aortic dissection
127
Q

LVH

A

early form of end-organ dz caused by HTN
causes stiffened LV – so hear S4 heart sound
as musc size increases, it chgs the inside (not outside) of heart- affects the luminal diameter, so LV can’t fill as well.
Precursor to L-sided heart failure, precursor to MI

128
Q

Rx for essential HTN

A

Diuretics (hydrocholorthiazide)
ACE inhibitors
ARBs
Ca2+ chnl blockers

129
Q

T/F Beta blockers are contraindicated in decompensated CHF.

A

True.

You can only use B-blockers for STABLE heart failure.

130
Q

What 4 BP drugs can be used in pregnancy?

A

Hydralazine
Nifedipine (Ca2+ chnl blocker)
Labetalol
Alpha-methyldopa

131
Q

Hydralazine

A

Used to treat severe HTN, CHF. First-line for HTN in prego (w methyldopa).
Increases cGMP, causing smooth musc relaxation.
Vasodilates arterioles more than venuloes (unique!) so causes reduction in afterload.

132
Q

Why is hydralazine often given along w a beta-blocker?

A

To prevent reflex tachycardia.

Any time you vasodilate, you can get reflex tachycardia

133
Q

Toxicity of Hydralazine

A 
Compensatory tachycardia (contraindicated in angina/CAD. give beta-blocker).
Fluid retention
Nausea, headache
Angina
Lupus (sHipp)
134
Q

Minoxidil

A

Used for severe HTN.
K+ chnl opener- hyperpolarizes and relaxes vasc smth musc.
Tox: Hypertrichosis (it’s Rogaine!), pericardial effusion, reflex tachycardia (use a B-blocker), angina, salt retention.

135
Q

Need to read p277

A

ca chnl blockers,
nitro
malignant HTN rx

* DIT each session (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions