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Cardio Block - CPR > General, Week 2 Cardio > Flashcards

General, Week 2 Cardio Flashcards

1
Q

what do patients with restrictive cardiomyopathy present with?

A

congestive heart failure or sudden death

decreased filling, back up

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2
Q

what do you see in histo of:

viral myocarditis
transplant rejection myocarditis
hypersensitivity myocarditis
fungal/TB myocarditis:
bacterial myocarditis:
A

viral myocarditis: lymphocytes
transplant rejection myocarditis: lymphocytes
hypersensitivity myocarditis: eosinophils
fungal/TB myocarditis: giant cells
bacterial myocarditis: neutrophils

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3
Q

will the RV hypertrophy in a VSD?

what will happen?

A

no, blood doesn’t stay in for long enough

pulmonary hypertension, L heart dilatation

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4
Q

what is natriuretic peptide ? what does it do?

A

a peptide hormones secreted from the atria

promotes salt and water excretion and lowers blood volume, lowers blood pressure

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5
Q

Vasopressin

receptor(s)
effect

use

A

Vasopressin 1 (V1) on blood vessels

vasoconstriction –> increase SVR –> increase MAP

can add to NE for septic shock

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6
Q

in what congenital heart defects do you see early cyanosis?

general concept
specific names (5):
A

R to L shunts

Tetralogy of Fallot
Transposition of the great vessels
patent Truncus arteriosus
Tricuspid atresia
Total anomalous pulmonary venous connection (TAPVC)
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7
Q

what myopathy has a dilatation of the R ventricle and fatty deposits in the RV?

A

arrythmogenic cardiomyopathy

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8
Q

why does the resting HR decrease in an athlete?

A

after training, there is an increase in heart mass (LVH), allowing for increased contractility, HR can decrease

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9
Q

what do you see on histology of the L ventricle in hypertrophic cardiomyopathy?

high yield

A

disarrayed myofibers with hypertrophy

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10
Q

name the equation for blood flow (Q) to an organ:

A

Q = perfusion pressure/resistance

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11
Q

vascular ________ receptors are more sensitive to epinephrine than _______ receptors

thus, at low levels, epi release causes ____________
at high levels, epinephrine release causes __________

A

beta-2, alpha-1

vasodilation
vasoconstriction

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12
Q

what is the treatment for an AVSD?

A

fix by 1 year of age

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13
Q

what three organs get the greatest blood flow/gram?

A

kidneys, then heart, then brain

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14
Q

systemic reduction in tissue perfusion resulting in decreased tissue oxygen delivery

A

shock

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15
Q

what problems do you see in dilated cardiomyopathy?

in terms of electrical
valves
output

A

electrical - arrhythmias due to stretching

valves: pull down, tricuspid and mitral regurgitation
output: decrease, can’t contract as strongly
- -> biventricular heart failure

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16
Q

Preload = EDV, ______ pressure

A

wedge

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17
Q

in tricuspid atresia/single ventricle, what happens to the L ventricle?

A

hypoplastic L ventricle

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18
Q

in an organ that shows autoregulation, if the perfusion pressure falls, the vascular resistance must _______ to maintain flow

A

fall

vasodilation

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19
Q

what is the murmur in a PDA?

A

continuous, machine-like murmur

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20
Q

initial emergent treatment for the transposition of great arteries (2):

long term?

A
  1. give prostaglandin E (keep PDA)
  2. balloon atrial septostomy (rip open - make ASD)

switch surgery is long term (including coronary arteries)

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21
Q

what are the ABCDEFG’s of reading a radiograph

A

A – airway – should be in midline (trachea)
B – bones
C – cardiac silhouette (heart size, less than half of angle-angle)
D – diaphragm (should have nice curve)
E – edges of heart (pneumonias will obliterate certain edges)
F – lung fields
G – gas bubble (below L diaphragm)

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22
Q

coartaction of the aorta is most commonly seen with what other CHD:

A

bicuspid aortic valve

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23
Q

benazepril

what is this?
adverse effects

A

ACE-I

cough, angioedema, TERATOGEN, hypotension, hyperkalemia, renal failure

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24
Q

sodium nitroprusside

use
mechanism
hemodynamics
side effects

A

hypertensive emergencies

release NO (cGMP - vascular smooth muscle relaxation)

Balanced arteriolar and venous dilation (decrease in preload and SVR)

hypotension, possible cyanic and thiocyanate intoxication

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25
Q

myogenic theory:

When blood pressure in arterioles increases, SMCs _________, causing an ___________ in vascular resistance, which decreases the blood flow.

When blood pressure in arterioles decreases, SMCs _______, causing a ________ in vascular resistance, and increase in blood flow

A

contract, increase

relax, decrease

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26
Q

what explains the phenomenon flow induced vasodilation?

A

shear stress activating endothelial cells to release NO, relaxation/dilation

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27
Q

in isolated aortic valve stenosis (CHD) what do you see in the heart structure?

A

LVH
mitral regurgitation
LA dilitation

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28
Q

Filling pressure (volume) = wedge pressure = pre-load estimation of ____

A

EDV

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29
Q

major side effects (2) of the diuretics (chlorthalidone):

drug-disease effect:

drug-drug interaction:

A
  1. hypokalemia
  2. electrolyte imbalance

increases risk of gout

NSAIDs

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30
Q

why is there cyanosis in tricuspid atresia/single ventricle?

A

because there is one pump for the whole body, the RA must give deoxy blood to LA, and LV.

in the common ventricle, all of the blood mixes

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31
Q

drugs that end in “-pril” are -

A

ACE inhibitors

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32
Q

what is the most important factor in pulmonary vascular smooth muscle tone?

A

local metabolic control (intrinsic)

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33
Q

in aortic valve atresia with intact ventricular septum, what do you see in the heart?

A

PDA needed to live

mitral valve, ascending aorta, LV all hypoplastic

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34
Q

how do patients with myocarditis present?

A

with arrhythmia, heart failure, fever, dyspnea, fatigue

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35
Q

during exercise, what is the most important factor in vascular smooth muscle tone?

A

local metabolic control

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36
Q

when a left to right shunt shifts to right to left because of pulmonary hypertension, this is called _________ syndrome. What do you note about the color of the patient?

A

Eisenmenger

turns acyanotic to cyanotic

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37
Q

what is the most common ASD?

A

esteem secundum type

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38
Q

list the 5 classes of 1st line antihypertensives:

A
  1. Thiazide type diuretics
  2. ACE-I
  3. Angiotensin receptor block
  4. Calcium channel blocker
  5. Beta blocker
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39
Q

in an organ that shows autoregulation, if the perfusion pressure increases, the vascular resistance must _______ to maintain flow

A

increase

vasoconstrict

(think about equation)

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40
Q

a MAP < _______ means hypotension

A

[MAP] <65 mmHg

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41
Q

what are the features of a partial AVSD?

A

primum type ASD, mitral valve cleft (mitral regurgitation)

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42
Q

drugs that end in “-olol” are:

A

beta blockers

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43
Q

amlodipine

use/class
mechanism 
hemodynamic effect
A

antihypertensive, dihydropyridine calcium channel blocker

Bind to L-type Ca++ channel, decrease amount of calcium available for vascular smooth muscle and cardiac muscle contraction.

vasodilation, decrease SVR, increase BP

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44
Q

the net result of direct sympathetic input to the heart results in what tone of the coronaries? why?

A

vasodilation

the alpha and beta counteract, the local metabolites due to the increased rate and force of the heart (sympathetic input) predominate

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45
Q

IMAGING: a term that you lose a portion of the anatomy or visualization of the normal structure since there is an adjacent disease

A

silhouette sign

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46
Q

Phenylephrine

receptor?
function?

A

alpha-1 purely.

vasoconstriction, increase SVR, increase BP

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47
Q

what is the most common comorbidity (of CHD) in people with a coarcted aorta?

A

bicuspid aortic valve

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48
Q

to regulate how much blood flow an organ gets, what is changed at the organ level?

A

vascular resistance (at arteriolar level)

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49
Q

what do you see on microscopic examination of hypertensive heart disease?

grossly?

A

increased myocyte diameter with increase in nuclear size nuclei often appear “squared off” or “box-car” shaped

L ventricular hypertrophy

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50
Q

what is the characteristic primary physiologic derangement of disruptive shock

A

afterload increase

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51
Q

in hypertrophic cardiomyopathy, what is the main finding grossly?

is the problem systolic or diastolic? why?

A

massive hypertrophy of LV ventricular septum

diastolic - decreased LV compliance, decreased filling, decreased CO

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52
Q

when first line antihypertensive drugs fail or can’t be used, __________ is used

A

hydralazine

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53
Q

what are some examples of metabolites that locally affect blood vessel diameter?

A

K+, H+, lactate, adenosine, CO2

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54
Q

metropolol

use/class
mechanism
hemodynamic effect
A

antihypertensive (first line only in special cases)

cardioselective beta blocker

decrease cardiac output (HR and contractility), decrease renin secretion, decrease in BP

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55
Q

what organs show autoregulation of vessel tone?

A

brain, kidneys, heart, skeletal muscle

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56
Q

what are the three things to look for when determining a chest x-ray quality? how do you check them?

A

R - rotation (is the spinner process between the clavicular heads?)
I - inspiration (5-6 anterior ribs)
P - penetration (should perceive spine behind the heart, and descending aorta)

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57
Q

Turner syndrome is associated with what two congenital heart defects?

A

coarctation of the aorta

bicuspid aortic valve

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58
Q

tricuspid atresia/single ventricle what do you need in order to live?

A

ASD/VSD or PDA

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59
Q

chlorthalidone

use/class
mechanism 
hemodynamic effect
A

antihypertensive
thiazide type diuretic

Blocks the Na+/Cl- cotransporter of the distal convoluted tubule of the kidney. Increased secretion of water.

Over time, lower TPR for the long term hypotensive effect

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60
Q

compelling indications for beta blockers

A

Heart failure with reduced EF mortality After myocardial infarction

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61
Q

the Swan-Ganz catheter measures _____ _____ pressure. This is the “wedge pressure”. Wedge pressure = __________ pressure

A

left atrial

filling

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62
Q

what are the two most important factors in local control of the coronary artery vascular tone?

A

adenosine, hypoxia (decreased O2)

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63
Q

why does metabolic acidosis occur in shock?

A

with hypoxia, can’t get sufficient ATP from aerobic respiration

produce lactate through the utilization of anaerobic respiration

64
Q

what organ gets the most cardiac output?

A

liver, then kidneys

65
Q

how do you diagnose myocarditis?

A

RV sample (biopsy)

66
Q

what would you find in terms of preload (central venous pressure measurement), pump function (cardiac output) and after lad (SVR) in HYPOVOLEMIC SHOCK

A

preload decreases
cardiac output decreases
afterload increases (increased SVR as a reflex)

67
Q

what septal defect is most commonly found in patients with Down syndrome?

A

AVSD

68
Q

what factors dominates vascular tone in skeletal muscle at rest?

A

the sympathetic input - tends to vasocsontrict

69
Q

what do histamine and bradykin do?

to arteries/veins
permeability

A

arteriolar vasodilation, venous constriction

increase in permeability

70
Q

define a cardiomyopathy:

A

myocardial disease leading to cardiac dysfunction

abnormality of cardiac muscle cells

71
Q

list some humeral factors? (4)

A

circulating catecholamines (indirect from the ANS)
Nitric Oxide
Vasopressin
Angiotensin 2

72
Q

what is the most important factor in skin vascular smooth muscle tone?

A

sympathetics - ANS (extrinsic)

73
Q

what is the main feature of restrictive cardiomyopathy grossly? secondary problems?

what does this mean hemodynamically? diastolic or systolic?

A

increased wall stiffness, biatrial dilation

limits ventricular stretch - causes decreased filling
DIASTOLIC dysfunction

74
Q

explain the basis of the myogenic theory: what happens when a vessel is stretched?

A

when vascular smooth muscle is stretched, it contracts

75
Q

Norepinephrine

receptor(s)?
function?

most commonly used to treat:

A

alpha-1 and beta-1 adrenergic receptors

potent vasoconstriction as well as an increase in cardiac output (HR, force)

septic shock

76
Q

what is the most common finding in the sudden death of a young athlete?

what would you find on autopsy? grossly, histo

A

hypertrophic cardiomyopathy (genetic)

hypertrophy LV septum
disarray of muscle fibers on autopsy pathology

77
Q

what are the two key findings in a NORMAL lateral CXR

A
  1. The clear triangles (should be clear in a normal patient)
    Retrosternal
    Retrotracheal
    Retrocardiac
  2. The spine should become more visible towards the diaphragm
78
Q

what happens to the heart anatomy with an ASD over time?

lungs?

A

RV hypertrophy, RV/RA dilatation (right heart enlargement)

could cause pulmonary vascular occlusive disease

79
Q

what could cause blunting of the costophrenic angles seen on chest x-ray?

A

PLEURAL EFFUSIONS

80
Q

why does cardiac output increase during exercise?

A

HR and SV increased significantly

81
Q

the formation of NO is stimulated by two things, what are they?

A
  1. Agonists (Ach, bradykinin, thrombin, substance P)

2. Shear stress

82
Q

what are the (2) methods to help prevent formation of pulmonary edema?

A

1) starling forces favor fluid resorption in lung (oncotic pressure high)
2) significant lymphatic system

83
Q

what is the largest problem in the persistent truncus arteriosus after the baby is born?

A

since the circulations are mixed, the decreasing pulmonary resistance in the lungs after birth makes all the blood flow there

early CHF

84
Q

what are the findings grossly of arrhythmogenic cardiomyopathy?

is it a systolic or diastolic finding?

A

fibrosis and fatty replacement of ventricles, especially the R ventricle! R ventricular dilatation

systolic - decreased contractility with arrhythmias, can result in sudden death at a young age

85
Q

what would you find in terms of preload (central venous pressure measurement), pump function (cardiac output) and after lad (SVR) in CARDIOGENIC SHOCK

A 
preload increases (backup of blood)
cardiac output decreased (impaired heart function)
afterload increases (SVR increased as a reflex)
86
Q

list the 5 common features of shock:

A
  1. hypotension
  2. cold/clammy skin
  3. oliguria
  4. change in mental status
  5. metabolic acidosis
87
Q

vasopressin (ADH) does what (2)?

what releases it?

A

released by posterior pituitary

acts on collecting ducts to decrease secretion water, also a potent vasoconstrictor

88
Q

how does a child compensate for coarctation of the aorta if they survived infancy (2)?

what physical findings (3)?

A

LV hypertrophy
collateral flow

hypertension in arms, decreased femoral pulses, rib notching

89
Q

K+, H+, lactate, adenosine, CO2

tend to cause:

A

smooth muscle relaxation - vasodilation

90
Q

calcium channel blockers

adverse side effects
DDI

A

hypotension, headache (vasodilation), constipation, heart failure, AV block
DDI - with drugs acting on AV node (do not take diltiazem and a beta blocker or digoxin for example)

91
Q

what is the primary way by which the coronary blood flow is regulated?

A

local metabolic control

92
Q

when severe, pulmonary hypertension can cause _____________ syndrome

A

Eisenmenger

93
Q

what would you find in terms of preload (central venous pressure measurement), pump function (cardiac output) and after lad (SVR) in DISTRIBUTIVE SHOCK

A 
preload (less or equal)
cardiac output (increases to try to make up for decreased SVR)
afterload decreases (SVR decreased significantly)
94
Q

the __________ (diastolic, systolic) cardiomyopathies generally result in arrhythmias

A

systolic

dilatation!

95
Q

in dilated cardiomyopathy, what is the main finding grossly?

is the problem systolic or diastolic? why?

A

massive dilation of all 4 chambers (BIG HEART)

systolic - unable to contract as strongly, biventricular heart failure

96
Q

in TAPVR - total anomalous pulmonary venous return, what is the problem?

A

there is no connection between pulmonary veins and L atrium

atrium does not get oxygenated blood (obligate R to L shunt - CYANOSIS)

97
Q

what are the most common causes/associations of restrictive cardiomyopathy?

A 
amyloidosis (50%) - lodge in myocardium - stiff
blood eosinophilia (35%)
sarcoidosis

NOT necessarily familial

98
Q

what are the features of a complete AVSD?

A

ASD, VSD, and a COMMON AV valve (batman logo)

99
Q

what is the most important factor in cerebral vascular smooth muscle tone?

A

local metabolic control (intrinsic)

100
Q

what is the most important factor in coronary vascular smooth muscle tone?

A

local metabolites (intrinsic)

101
Q

what are the main cause(s) of arrhythmogenic cardiomyopathy?

A

familial

102
Q

why does stroke volume increase during exercise?

A

sympathetic input to beta-1, increased contractility, decreased ESV

increased venous return (many mechanisms), increased EDV

103
Q

what are the most common causes of hypertrophic cardiomyopathy?

A

GENETIC (100%) in cardiac sarcomeric proteins

104
Q

what is the most important factor in renal vascular smooth muscle tone?

A

local metabolic control (intrinsic)

105
Q

what is the characteristic primary physiologic derangement of cariogenic shock

A

decrease in pump function

106
Q

what is the murmur in pulmonary valve stenosis?

A

harsh, systolic ejection murmur

107
Q

Dobutamine

receptor(s)
effect

A

beta-1 agonist (selective)

increase HR and force

108
Q

what determines the prognosis in tetralogy of fallot?

A

degree of sub-pulmonic stenosis

109
Q

what are the two key findings in a NORMAL lateral CXR

A
  1. The clear triangles (should be clear in a normal patient)
    Retrosternal
    Retrotracheal
    Retrocardiac
  2. The spine should become more visible towards the diaphragm
110
Q

what is the incidence of Eisenmengers syndrome in atrial septal defects?

Large VSDs? Small VSDs?

A

10% - ASD

100% - large VSD

0% small VSD

111
Q

who should you NOT give beta blockers to? (6)

5 - conditions
1 - drug adverse reaction

A

people with asthma, COPD, AV block, severe unstable heart failure, occlusive peripheral vascular disease

OR anyone that is taking drugs that impair AV conduction (digoxin, some Ca channel blockers)

112
Q

what blood vessel has the most amount of vascular basal tone?

A

skeletal muscle

113
Q

hydrazine

use
mechanism
hemodynamics
adverse effects

A

antihypertensive - second line

Mechanism: Direct relaxation of smooth muscle by actions that are not well understood.
Hemodynamics: Decrease in SVR.
Adverse effect: Reflex tachycardia lupus-like syndrome.

114
Q

how is the microcirculation of the heart designed to most efficiently extract O2 from blood? (2)

A

the capillary density of the heart is much greater

the cardiac muscle cells are smaller

decreased travel distance –> increased efficiency

115
Q

in what types of shock is administration of fluids the initial treatment needed?

next line?

A

hypovolemic and distributive shock

vasopressors (sympathomimetics)

116
Q

what are the main problems and outcomes of hypertrophic cardiomyopathy?

A

decreasing filling because of decreased LV compliance, ventricular arrhythmias can cause sudden death at a young age

ALSO can block outflow track (syncope with exercise)

117
Q

pulmonary hypertension is seen most common with what congenital heart defect?

what histo changes can be seen due to the increased blood pressure in lungs?

A

ventricular septal defects

hypertrophy, plexiform lesions

118
Q

Blood flow in coronary arteries ________ during heart contraction. why? (2)

A
  1. the arteries are compressed (increased resistance, decreased flow)
  2. the aortic valve flaps up against the openings
119
Q

what kind of murmur would you hear with a AVSD?

A

a systolic ejection murmur at the pulmonic valve

increased flow

120
Q

drug for hypertensive emergencies:

A

sodium nitroprusside

121
Q

which has a higher basal tone? kidney or skeletal muscle?

why?

A

skeletal muscle, there is a greater vasodilatory reserve

122
Q

what is the ebstein anomaly?

A

displacement of tricuspid valve leaflets downward into RV

Associated with tricuspid regurgitation and right HF.

123
Q

what is the initial problem in embryology leading to transposition of the great arteries??

A

the conotruncal septum does not spiral. it divides but does not spiral

124
Q

define the blood pressures for hypertension

A

systolic > 140, diastolic > 90

125
Q

name three general mechanisms in which to change the basal tone of a vessel:

A
  1. direct autonomic control (sympathetics)
  2. humeral factors
  3. local myogenic and metabolic factors
126
Q

on histology, you find inflammatory cells in the myocardium, causing myocyte damage. What is this disease?

A

myocarditis

127
Q

how does NO (once formed) cause vasodilation?

A

produces cGMP, activating the phosphatase to dephosphorylate myosin, relaxation

128
Q

what are causes of myocarditis? (4)

A
  1. infectious (viral, bacterial, etc)
  2. autoimmune reactions (SLE, drug reactions)
  3. rejection of heart transplant
  4. idiopathic (i.e. sarcoidosis)
129
Q

what is the treatment for a patent ductus arteriosus?

A

indomethacin - decreases prostaglandin E, which closes the shunt

130
Q

diltiazem

use/class
mechanism
hemodynamic effect
A

antihypertensive, non-dihydropyridine calcium channel blocker

Bind to L-type Ca++ channel, decrease amount of calcium available for vascular smooth muscle and cardiac muscle contraction.

ALSO decreases AV node and contractility.

vasodilation, decrease SVR, increase BP

131
Q

what is the prevalence of Eisenmengers in PDA? what does it cause?

A

80%, causes lower extremity cyanosis

132
Q

losartan:

use/class
mechanism 
hemodynamic effect
A

antihypertensive

angiotensin receptor blocker

decreases SVR (heart rate and output unchanged), decreasing BP

133
Q

do not take a calcium channel blocker (L-type Ca channels) and a medication that decreases _________ firing, such as:

A

AV node firing

a beta blocker, digoxin

134
Q

what happens to blood pressure in a trained individual? why?

A

it decreases due to more compliant large arteries

135
Q

what are the 4 things you see in tetralogy of fallot?

A
  1. Sub-pulmonic valve stenosis
  2. R ventricular hypertrophy
  3. VSD
  4. overriding aorta
136
Q

benazepril

use/class
mechanism 
hemodynamic effect
A

antihypertensive, ACE-I

inhibits angiotensin converting enzyme (ACE) to reduce formation of angiotensin 2 and aldosterone, also inhibits lysis of bradykinin

decreases SVR, decreasing BP

137
Q

what is the main goal of surgery in tricuspid atresia/single ventricle

A

separate the pulmonary and systemic circulations

138
Q

Dopamine

low dose
medium dose
high dose

A

Low dose: dopamine-1 receptors in the renal, mesenteric, cerebral, and coronary beds, resulting in selective vasodilation

Moderate dose: beta-1 adrenergic receptors and increases cardiac output (HR, force)

High doses, alpha-1 receptors –> vasoconstriction with an increased SVR.

Dopamine may be used in hypotension due to sepsis or cardiac failure, but is not a first line drug for either

139
Q

NO is released by __________ cells and promotes ________

A

endothelial cells

vasorelaxation

140
Q

what does bradykinin do?

what breaks it down?

A

vasodilator - releases NO

ACE

141
Q

metropolol

what is it
adverse effects

A

cardioselective beta blocker

aggravation of severe HF, aggravation occlusive arterial disease, slows AV conduction

142
Q

what are the most common causes of dilated cardiomyopathy?

what is the treatment?

A

familial (60%)
alcoholism
pregnancy
previous myocarditis

transplant

143
Q

why is the baby cyanotic in persistent truncus arteriosus?

A

the oxygenated and deoxygenated blood are mixed in the common trunk before getting to their circulations

144
Q

what do patients do in response to cyanotic spells (tet spells) when they have tetralogy of fallot?

A

they squat

kink femoral arteries, increase SVR, decrease the R to L degree of shunting

145
Q

what is the characteristic primary physiologic derangement of hypovolemic shock

A

decreased preload

146
Q

sympathetic direct innervation will cause vasoconstriction at the ______ receptors and vasodilation of vessels that have ______ receptors

A

alpha-1 - vasoconstriction

beta-2 (skeletal muscle)

147
Q

in pulmonary valve atresia with an intact ventricular septum, what do you need? what do you find in the heart secondarily?

A

need intact PDA

hypoplasic tricuspid valve and RV

148
Q

what cardiomyopathy is unique in mainly affecting the Right Ventricle?

A

arrythmogenic cardiomyopathy

fibrosis, fatty replacement, and dilatation of RV

149
Q

in a sedentary person vs an athlete, what is the difference in CO? why?

A

there is no difference in CO

the HR decreases and SV increases in an athlete

150
Q

in isolated pulmonary valve stenosis (CHD), what are the secondary cardiac findings?

A

RVH
tricuspid regurgitation
dilatation pulmonary artery RA

151
Q

Epinephrine

receptor(s)
function (low dose/high dose)

uses

A

beta-1, beta-2, alpha-1

Low doses: increase CO (beta-1), vasoconstriction (alpha-1) is offset by the vasodilation (beta-2).

Higher doses, the alpha-1 effect predominates beta-2 producing an increase in SVR in addition to an increase in CO.

anaphylaxis

152
Q

drugs that end in “-sartan” are:

A

angiotensin receptor blockers

153
Q

losartan

what is it?
adverse drug effects

A

a angiotensin receptor blocker

TERATOGEN, renal failure, hyperkalemia
*less of a cough and less angioedema than ACEI

154
Q

is the ability of the organ to maintain its blood supply in the face of changing perfusion pressure
(without even help from innervation - an extrinsic factor)

A

autoregulation

155
Q

the difference between what two things is vascular tone?

A

basal flow to maximal flow

156
Q

how (molecularly) is NO activated?

A

shear stress or an agonist opens calcium channels on the surface of endothelial cells

calcium –> nitric oxide synthase –> NO formed –> smooth muscle

157
Q

what is the initial problem in embryology leading to tetralogy of fallot?

A

the conotruncal septum deviating anteriorly

Cardio Block - CPR (6 decks)

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