Bsom Cardiovascular Janz 2010 Part 3

Front 1

TL #3

Shock

what is shock

Back 1

Failure to maintain adequate tissue perfusion

impaired tissue perfusion and
impaired O2 delivery

Front 2

what is the formula for the delivery of O2 to system

Back 2

DO2 = 1.39 x Hgb x SaO2 x CO

Front 3

list the 3 stages of shock

Back 3

1st Nonprogressive stage

2nd Progressive stage

3rd Irreversible stage

Front 4

Name the stage of shock

Baroreceptor reflex stimulation

sympathetic nervous system
catecholamines released

Alpha-/beta- receptor stimulation

most pronounced in large vascular beds

Back 4

1st Nonprogressive stage

Front 5

name the stage of shock

Increased renin release (R-A-A system)- sodium/water reabsorption vasoconstriction

Precapillary/postcapillary constriction- “transcapillary refill”

Back 5

1st Nonprogressive stage

Front 6

fill in the formula

BP = CO x ___

Back 6

Systemic vascular resistance

Front 7

In the first stage of shock, non progressive, how does the body compensate

Back 7

tries to maintain BP= CO X SVR by:

1. increase CO- Increase preload, heart rate & contractility

2. maintain MAP-Increase CO & afterload

Front 8

what 4 major events happen in progressive shock

Back 8

1st- Reduced CO & BP leading to tissue hypoperfusion

2nd Aerobic to anaerobic metabolism glycolysis = lactic acid production which leads to ATP depletion and then organelle/organ failure

3rd. Humoral/vasoactive agents released like adenosine, nitric oxide, serotonin, etc.

4th Lactic acid + agents = vasodilatation, which increased capillary permeability and reverse “transcapillary refill”

Front 9

list 3 features that are ascribed to irreversible shock

Back 9

1. Vascular decompensation
resistant to therapy

2. Toxic free-oxygen radicals

3. Profound vasodilatation
“vascular collapse”

Front 10

what 4 criteria are used to clinically diagnose shock

Back 10

1. Hypotension- sBP < 90 mmHg or > 30% reduction from baseline (if know it)

2. Urine output < 0.5 cc/kg/hr

3. Metabolic acidemia
(lactic acidemia)

4. Tissue hypoperfusion

Front 11

how can you tell a tissue is hypoperfused

Back 11

Skin- pallor, diaphoresis, cyanosis, mottling

Cardiovascular- increased HR, SVR, contractility
myocardial, ischemia/dysfunction or
arrhythmias

Brain
restlessness, confusion, coma

Kidney
ischemia, dysfunction, acute renal failure

Liver- dysfunction/injury

Lungs- altered V/Q matching
hypoxemia respiratory center stimulation tachypnea, hyperventilation

Front 12

what do most people with shock die of

Back 12

RESPIRATORY FAILURE

Front 13

what are the 4 types of shock

Back 13

1. Hypovolemic

2. Cardiogenic

3. Distributive

4. Obstructive

Front 14

describe the type of shock and the signs and symptoms associated (which parameters increased or decreased)

Loss of circulating blood volume

Decreased CO from reduced preload

caused by : whole blood loss,
plasma loss, or protein-free fluid loss

Back 14

hypovolemic shock

Skin: cool, pale, clammy

Decreased parameters:
BP, CVP, PAP, PAWP, CI, SVI

Increased parameters:
HR, SVR

Front 15

what is the first line of treatment for hypovolemic shock

Back 15

replace what pt lost. if lost blood give blood, if lost plama give plasma.

reverse hypoperfusion with Fluid resuscitation with rapid IV infusion of large volumes

Fluid of choice- isotonic crystalloid
(normal saline)

Front 16

other than maintenance of fluid of pt in hypovolemic shock what other important factors must be carefully monitored since this is the reason most pt die

Back 16

adequate oxygenation
PaO2 > 60 mmHg;

SaO2 > 90% adequate ventilation

normalization of ABG’s

Front 17

name the type of shock

Myocardial loss/dysfunction

Decreased CO:

Decreased contractility- Fast/slow heart rate

Mortality = 50% - 80%

7% of AMI’s

Back 17

cardiogenic shock

Front 18

what is defined as acute cardiogenic shock

Back 18

> 40% loss of LV myocardium

Front 19

what are the 4 big causes of cardiogenic shock

Back 19

1. AMI

2. RVI

3. Acute mitral regurgitation

4. Ventricular septal rupture

Front 20

how can we differential hypovolemic shock from cardiogenic shock since both pt have cool, clamy skin with hypovolemia

Back 20

cardiogenic Characteristic features:

JVD
S3/S4
rales

Front 21

what Hemodynamic parameters are increased or decreased in cardiogenic shock

Back 21

Decreased:
BP, CI, SVI

Increased:
HR, SVR, CVP, PAWP

Front 22

what 4 components determine cardiac output

Back 22

Heart rate

Contractility

Preload

Afterload

Front 23

in cardiogenic shock, the main problem is contractility. what is done to hopefully improve contractility.

Back 23

Poor contractility
inotropic agent

dobutamine, dopamine, digoxin

Front 24

in cardiogenic shock, a major problem is increased preload, what is done to decrease the preload

Back 24

loop diuretics- furosemide

vasodilator agent- nitroglycerin

Front 25

for the high afterload in cardiogenic shock. what is done to hopefully reverse this effect

Back 25

vasodilator agent (if sBP > 100)- nitroglycerin, sodium nitroprusside

vasoconstrictor agent (if sBP < 90)

Front 26

t/f thrombolytic agents or
PTCA should be considered in pts with hypovolemic shock

Back 26

false- should be considered in pt with cardiogenic shock

Front 27

what are 4 causes of distributive shock and how does it present

Back 27

Septic shock
Anaphylactic
Spinal
Drug/toxin ingestion

Most common site of infection- pneumonia

Warm type - most common
hypotension, fever, warm/pink skin, confusion

Front 28

most common causes of septic shock are due to which class of organism

Back 28

60% Gram (-) rods

Gram Negative Rods

1. Anaerobes-Bacteroidaceae (e.g. Bacteroides fragilis)

2. Facultative Anaerobes
Enterobacteriaceae (e.g. Escherichia coli)
Vibrionaceae (e.g. Vibrio Cholerae)
Pasteurellae (e.g. Haemophilus Influenzae)

3. Aerobes
Pseudomonadaceae (e.g. Pseudomonas aeruginosa)

Gram Negative Cocci
Aerobes
Neisseriaceae (e.g. Neisseria Meningitidis)

Gram Negative Obligate Intracellular Parasites- Rickettsiae (e.g. Rickettsia)

Front 29

Describe the pathophysiology of septic shock-

Back 29

Infectious material released from organisms like endotoxin, exotoxin

Cytokines released from macrophages like TNF, interleukins -1, -2

Neutrophils, platelets, endothelial cells release-
nitric oxide, free O2 radicals

Activation of humoral defenses- coagulation, compliment, kinins

Secondary mediator release
prostaglandins, leukotrienes, endorphins,

Front 30

in septic shock, what is the effect of the inflammatory response to an organism

Back 30

Vasodilatation (redistribution of blood flow) to Decreased afterload and Decreased preload

Myocardial depression which Decreased contractility

Increased endothelial permeability leading to Decreased preload

Altered cellular metabolism

Front 31

list 4 causes for obstructive shock

Back 31

Cardiac tamponade

Tension pneumothorax

Massive pulmonary embolus

Thoracic aortic dissection

Front 32

Chapter 26 Heart Failure

what is the definition of heart failure

Back 32

the heart is unable to pump an adequate supply of blood at normal filling pressures to meet the metabolic needs of the body.

Front 33

what does the term congestive heart failure more clearly suggest

Back 33

the subset of HF patients who have biventricular failure, with elevated filling pressures of both ventricles, causing pulmonary and systemic venous hypertension.

Clinically, the term CHF best describes those HF patients with decreased effort tolerance, dyspnea, jugular venous distention (JVD), hepatic engorgement, and peripheral edema

Front 34

in the prognosis of heart failure, which factors will worsened survival is predicted by: (4)

Back 34

1. Increasing severity of LV dysfunction (typically assessed by LV ejection fraction)

2. Reduced cardiac output / index

3. Elevated ventricular filling pressures

4. Reduced exercise capacity

Front 35

New York Heart Association Functional Class describes class 1 as __

Back 35

Patients with cardiac disease but without symptoms during routine activity

Front 36

New York Heart Association Functional Class describes class 2 as __

Back 36

Class II: Asymptomatic at rest.

Become symptomatic with routine activity, resulting in slight limitation of activity

Front 37

New York Heart Association Functional Class describes class 3 as __

Back 37

Class III: Comfortable at rest, but symptomatic with less-than-routine activity, resulting in marked limitation of activity

Front 38

New York Heart Association Functional Class describes class 4 as __

Back 38

Class IV: Unable to carry on any activity without symptoms. Often symptomatic at rest

Front 39

what is the difference in a pt with acute HF vs chronic heart failure

Back 39

Acute HF: Occurs with an abrupt onset, as after acute myocardial infarction (MI) or severe valvular dysfunction after chorda tendinae rupture

Chronic HF: Clinical features of HF often begin insidiously and progress to a chronic state

Front 40

what is the most common presenting symptom of LV failure and why

Back 40

Dyspnea (difficulty breathing) is the most common presenting symptom of LV failure. Dyspnea is a direct consequence of elevated LV filling pressure and pulmonary congestion.

Front 41

what is the most common presenting symptom of RV failure

Back 41

Systemic venous congestion and peripheral edema are the predominant clinical findings

Front 42

what is the most common cause of RV heart failure and what causes this

Back 42

left sided heart failure due to

1. Pulmonary hypertension

2.Failure of shared myocytes in the ventricular septum

Front 43

describe the clinical findings of biventricular heart failure

Back 43

biventricualr is both left and right HF, which cause pulmonary and systemic HTN (CHF)

Clinical findings of CHF:
- Decreased exercise tolerance
- Dyspnea; shortness of breath (SOB)
- JVD
- Hepatic congestion
- Peripheral edema

Front 44

describe high output cardiac failure

Back 44

HF in which the circulation remains brisk and the skin and extremities remain warm, despite increased venous pressures and a decreased cardiac output (CO) that existed prior to the onset of HF

Front 45

list 5 caused of high output failure

Back 45

- Anemia
- Hyperthyroidism (thyrotoxicosis)
- Beriberi (thiamine deficiency)
- A-V fistula
- Paget’s disease of bone (hypercalcemia)

Front 46

list 5 causes of low output failure

Back 46

1. Hypertension; hypertensive heart disease

2. Myocardial ischemia or infarct (i.e. Coronary atherosclerosis)

3. Valvular heart disease

4. Pericardial disease 

5. cardiomyopathy

Front 47

which type of heart failure (systolic or diastolic)

decreased contractility, causing a reduction in stroke volume (SV), leading to a decreased CO

Back 47

systolic

Front 48

how is ejection fraction calculated

Back 48

the volume of blood ejected from the ventricle (SV) divided by the LV end diastolic volume (LV EDV)

Front 49

which type of heart failure (systolic or diastolic)

Pulmonary and/or systemic venous congestion with resulting clinical findings in the presence of normal or near-normal systolic function

Back 49

diastolic

Front 50

what can cause diastolic heart failure

Back 50

Increased chamber stiffness

Chamber dilation

Impaired ventricular relaxation

Chamber hypertrophy

Front 51

pts with diastolic HF has 1 or more of which conditions

Back 51

LVH : due to HTN, aortic stenosis , hypertrophic cardiomyopathy (increase chamber stiffness)

or Ischemic Heart Disease (IHD): (impairs ventricular relaxation )-

or Infiltrative disease: amyloidosis, sarcoidosis, hemachromatosis (Chamber hypertrophy)

Front 52

pt with which condition in his past med hx is 4 times more likely to have a systolic dysfunction than a diastolic dysfunction

Back 52

valvular heart disease

Front 53

on EKG, a pt with low voltage is more likely to suggest which type of dysfunction (systolic or diastolic)

Back 53

systolic

Front 54

on echocardiogram, a pt with which 2 conditions will indicate a systolic dysfunction rather than a diastolic dysfunction

Back 54

left ventricular dilation and reduced ejection fraction

Front 55

although HTN can indicate both systolic and diastolic dysfunction, which one is it more likely suggestive of

Back 55

diastolic dysfunction

Front 56

left ventricular hypertrophy indicates more of which type of dysfunction (systolic or diastolic)

Back 56

diastolic dysfunction

Front 57

an S3 gallop on auscultation indicates more of which type of dysfunction (systolic or diastolic)

Back 57

systolic

Front 58

an S4 gallop on auscultation indicates more of which type of dysfunction (systolic or diastolic)

Back 58

diastolic

Front 59

on chest roentfenogram indicating cardiomegaly, is suggestive of which type of dysfunction (systolic or diastolic)

Back 59

systolic

Front 60

cardiac causes of HF include :
1. Hypertensive heart disease, Myocardial ischemia or infarction accompanied by LV dysfunction, Valvular heart disease, Cardiac dysrhythmias and Cardiomyopathies:

List 3 different types of cardiomyopathies that cause HF and which one is more likely due to infection, or alcohol related causes

Back 60

1. dilated (congestive) - more likely due to infection (parasite or viral), alcohol or connective tissue disease

2. hypertrophic- concentric LVH

3. Restrictive- from amyloidosis, hemachormoatosis, or sarcoid

Front 61

t/f alcohol can precipitate heart failure

Back 61

ture

Front 62

how can fever precipitate Heart failure

Back 62

for every 1 degree increase in core body temp,there is an increase of 10% of metabolic demand placed on the body

Front 63

why can hypoxemia precipitate HF

Back 63

o2 is a vasodilator...

Front 64

what is the effect of Na+ and H2O retention on ventricular function and ventricle size

Back 64

increase in Na and H20, increase preload which will increase ventricular function leading to volume overload causing metabolic stress and hypertrophy

Front 65

what is the effect of Na+ and H2O retention on ventricular function and ventricle size

Back 65

increase in Na and H20, increase preload which will increase ventricular function leading to volume overload causing metabolic stress and hypertrophy

Front 66

describe the effect of increase sympathetic activity on the vasculature, RAAS and afterload

Back 66

increase in sympathetic activity activates the RAAS to hold on to Na which will hold on to H2O, increasing preload and increasing ventricular function

increase sympathetic activity also increases vascular resistance and increase ventricular preload

Front 67

Frank-Starling mechanism during HF increases preload to compensate for what

Back 67

a decreased contractility and therefore decreased cardiac output,

FS helps to sustain cardiac performance

As preload is increased, heart’s contractility is increases.

Stretching the muscle fiber to an optimal length produces a more forceful contraction

Front 68

which type of hypertrophy (eccentric or concentric)

thickened ventricular walls with the potential for reduced chamber volume. Increases ventricular stiffness, necessitating higher-than-normal diastolic pressures to fill the ventricle, leading to diastolic dysfunction and diastolic HF.

Back 68

concentric

Front 69

which type of hypertrophy (eccentric or concentric)

ventricular walls are not thickened, but the chamber is dilated. hypertrophy impairs ventricular relaxation, leading to diastolic HF.

Back 69

eccentric

Front 70

which type of heart failure ( eccentric of concentric HF)

LVH (caused by IHD, MI and other conditions resulting in dilated LV) impairs relaxation of the ventricle, causing diastolic dysfunction

Back 70

eccentric

Front 71

which type of heart failure ( eccentric of concentric HF)

LVH ( as occurs in HTN, aortic stenosis, and hypertrophic cardiomyopathy) results in increased ventricular stiffness, necessitating higher-than-normal diastolic pressures to fill the hypertrophied ventricle.

Back 71

concentric LVH

Front 72

Name the symptom in LV failure

breathlessness predominant symptom, usually associated with tachypnea, due to increase blood volume and alveolar congestion

Back 72

dyspnea

Front 73

Name the symptom in LV failure

dyspnea that occurs soon after lying flat and is relieved by sitting up.

what causes this

Back 73

orthopnea- caused by increases venous return to the right heart and lungs in recumbent position

Front 74

Name the symptom in LV failure

severe dyspnea may awaken a pt from sleep, relief urgently sough by sitting up or finding an open window

Back 74

paroxysmal nocturnal dyspnea

Front 75

Name the symptom in LV failure

decreased renal flow with upright activity this gives way to more normal renal perfusion and diuresis while in supine at night

Back 75

nocturia

Front 76

Name the symptom in LV failure

pulmonary venous and capillary pressure can increase abruptly, resulting in rapid accumulation of fluid in the alveoli and interstitial space of the lungs.

what symptoms are seen

Back 76

acute pulmonary edema

symptoms: nonproductive cough, wheezing, severe dyspnea

Front 77

Name the symptom in LV failure

rust colored sputum containing alveolar macrophages

Back 77

hemoptysis

Front 78

Name the symptom in LV failure

in advanced HF, may be accompanied by periodic breathing with alternating apnea and hyperventilation

Back 78

cheynes- stokes respiration

Front 79

describe the general appearance and Signs of LV Failure in a pt

Back 79

Anxious; sitting up if acute pulmonary edema
- Respiratory distress
- Pale
- Dusky
- Sweaty
- Cool skin / extremities

Front 80

describe the vital in a pt with LV failure

Back 80

Tachypnea

Tachycardia

Narrowed pulse pressure- Diastolic BP may be increased - Systolic BP often low, but may be normal

Front 81

describe the heart sounds and location in a pt with LV failure

Back 81

Cardiomegaly
Muffled heart sounds
Accentuated pulmonic component of S2
Muffled heart sounds
S3 gallop
S4 gallop
Murmurs
Pulsus alternans-

Front 82

what is Pulsus alternans in a pt with LV failure

Back 82

alternating strong and weak pulse in an underlying regular rhythm usually indicating a progressed HF

Front 83

Isolated RV failure is uncommon in adults, and is usually caused by (other than LV heart failure):

Back 83

1. - Cor pulmonale secondary to intrinsic lung disease

2. Congenital intracardiac left-to-right shunt (e.g. Atrial septal defect) with chronic volume overload

Front 84

what causes the SYMPTOMS described by pt (sign: by examiner) in RV failure

Back 84

Caused by the elevation of systemic venous pressure

Front 85

Describe the 2 big symptoms of RV failure

Back 85

1. Hepatic and G.I.congestion and edema
- Anorexia
- Nausea
- Vomiting
- Abdominal discomfort / pain
- Ascites

2. Symptoms due to systemic venous congestion
Peripheral edema
Weight gain
Venous stasis

Front 86

what are the SIGNS of RV failure

Back 86

Cyanosis (usually absent in LV failure unless pulmonary edema)
JVD
Hepatic engorgement with hepatomegaly and tenderness.
Hepatojugular reflux- push on liver and increases distention in neck

Peripheral Edema

Oliguria

Front 87

why is prevention of HF preferred over treatment of HF

Back 87

since high rates of mortality and mobidity persist in pt with HF, despite advance in treatment

Front 88

to prevent HF, pt should reduce which risk factors for coronary heart disease

Back 88

HTN, diabetes mellitus, dyslipidemia, obesity, smoking, increase exercise

Front 89

Acute HF is A medical emergency, what are the ABCs

Back 89

ABC’s: Airway, Breathing, Circulation

Front 90

how does O2 help in a pt with RV failure

Back 90

a) Increases arterial oxygenation in hypoxemic patient

b) O2 is a potent vasodilator of pulmonary arterial circulation (improves RV failure)

Front 91

what is used to measure the Saturation of O2 (arterial oxygen saturation)

Back 91

pulse oximeter

Front 92

what 6 pharmacological agent classes are used in HF and why

Back 92

1. I.V. Diuretics- to decrease preload

2. Nitroglycerin (sublingual, intravenous, topical)

3. Morphine sulfate- decrease pain and anxitety

3. Intropic agents (dobutamine, amrinone, digoxin): to improve cardiac contractility

4. Pressors (e.g. Dopamine): to raise SBP and to improve renal/gut perfusion

5. Vasodilators (ACE inhibitors, hydralazine)- to decrease afterload

Front 93

which cardiac glycoside is used in heart failure

Back 93

digoxin

Front 94

which 3 types of diuretics are used in heat failure and give examples of each type

Back 94

1. loop diuretics- bumetanide, furosemide

2. thiazides- hydrocholothiazide, metolazone

3. K+ sparring diuretics- spironolactone, amiloride, triamterene

Front 95

list the 6 types of vasodilators used in heart failure

Back 95

1. hydralazine-interferes with the action of the second messenger IP3, limiting calcium release from the sarcoplasmic reticulum of smooth muscle. This results in an arterial and arteriolar relaxation.

2. angiotensin converting enzyme inhibitor

3. angiotensin II receptor antagonists

4. nitrovasodilators- isosobide, nitroglycerin, nitroprusside

5. nesiritide

6. phosphodiesterase 3 inhibitor- inamrinone, milrinone

Front 96

which 2 sympathetic amines can be used in heart failure

Back 96

dopamine or dobutamine

Front 97

which 3 beta blockers are used in heart failure

Back 97

carvedilol, metoprolol, bisprolol

Front 98

what type of diuretic is the following: mannitol

a. potassium sparring
b. thiazide
c. loop diuretic
d. carbonic annhydrase inhibitor
e. osmotic

Back 98

osmotic along with urea

Front 99

what type of diuretic is the following: acetazolamide

a. potassium sparring
b. thiazide
c. loop diuretic
d. carbonic annhydrase inhibitor
e. osmotic

Back 99

carbonic anhydrase inhibitor

Front 100

what type of diuretic is the following: furosemide

a. potassium sparring
b. thiazide
c. loop diuretic
d. carbonic annhydrase inhibitor
e. osmotic

Back 100

trade name is Lasix- loop diuretic

Front 101

what type of diuretic is the following: bumetanide

a. potassium sparring
b. thiazide
c. loop diuretic
d. carbonic annhydrase inhibitor
e. osmotic

Back 101

loop diuertic

Front 102

what type of diuretic is the following: hydrocholothiazide

a. potassium sparring
b. thiazide
c. loop diuretic
d. carbonic annhydrase inhibitor
e. osmotic

Back 102

thiazide-

Front 103

what type of diuretic is the following: spironolactone

a. potassium sparring
b. thiazide
c. loop diuretic
d. carbonic annhydrase inhibitor
e. osmotic

Back 103

K+ sparring

Front 104

what type of diuretic is the following: triamterene

a. potassium sparring
b. thiazide
c. loop diuretic
d. carbonic annhydrase inhibitor
e. osmotic

Back 104

K+ sparring

Front 105

what type of diuretic is the following: amiloride

a. potassium sparring
b. thiazide
c. loop diuretic
d. carbonic annhydrase inhibitor
e. osmotic

Back 105

K+ sparring

Front 106

what type of diuretic is the following: urea

a. potassium sparring
b. thiazide
c. loop diuretic
d. carbonic annhydrase inhibitor
e. osmotic

Back 106

osmotic

Front 107

which diuretics are used to reduce the vascular volume in pt

Back 107

hydrocholorothiazide and chlorthalidone

Front 108

which centrally acting sympatholytics alpha adreneric agonist were used to reduce sympathetic tone but the side effects of postural HTN and sexual dysfunction lead to its discontinuation for use as antihypertensives

Back 108

methldopa or clonidine

Front 109

which centrally acting sympatholytics alpha adreneric ANTAGONISTS were used to reduce sympathetic tone but the side effects of postural HTN and sexual dysfunction lead to its discontinuation for use as antihypertensives

Back 109

prazosin, doxazosin, terazosin

Front 110

name 6 beta adrenergic blockers that are used as antianginal, antihypertensives and adjuncts to MI therapy by non selectively blocking beta 1 adrenergic receptors and thus decreasing the O2 requirement.

What are the clinical effects of blocking the beta receptors

Back 110

carteolol, carvedilol, labetalol, propanolol, sotalol, timolol

clinical effects: decrease in sinus node HR, decrease cardiac output and decrease in BP

Front 111

name 4 beta adrenergic blockers that are used as antianginal, antihypertensives and adjuncts to MI therapy by selectively blocking beta 1 adrenergic receptors and thus decreasing the O2 requirement.

What are the clinical effects of blocking the beta receptors

Back 111

acebutolol, atenolol, betaxolol, metoprolol

clinical effects: decrease in sinus node HR, decrease cardiac output and decrease in BP

Front 112

which drug is a combined alpha and beta blocker

Back 112

labetalol

Front 113

name 2 vasodilators

Back 113

hydralzine and minoxidil

Front 114

what are the 3 modes of action for angiotensin-converting enzyme inhibitors and the results of their 3 actions

Back 114

1. block the conversion of angiotensin 1 to angiotensin 2 ( Agio2 is a major vasoconstrictor)

2. ACEI inactivate the pulmonary bradykinin- a major vasodilator but causes cough

3. increase plasma renin level and reduce aldosterone levels

so their systemic effect is to vasodilate resulting in lower BP, decrease afterload in CHF, and decrease development of CHF, increased survival of MI pt and decrease progression of diabetic nephotoxicity

Front 115

name 3 angiotensin-converting enzyme inhibitor

Back 115

captopril, lisonopril, benazepril

Front 116

angiotensin II antagonists share many of the same features as angiotensin-converting enzyme inhibitor. how are ARBs different than ACEI

Back 116

ARBs- block the binding of angiotensin II to the recptor but do not prevent the degradation of bradykinin so there is less cough

Front 117

list 2 angiontenin II receptor blockers (ARB)

Back 117

losartan, valsartan

Front 118

what is the mechanism of action for calcium channel blocker in the heart and what are they used for

Back 118

MOA: inhibit influx of intracellular Ca+2 through L-type channels so

1. decrease TPR

2. reduce contractility of smooth cardiac muscle

3.

Front 119

list 2 dihrydropyridine calcium channel blockers

Back 119

amlodipine, ifedipine

Front 120

list 2 non-dihrydropyridine calcium channel blockers

Back 120

diltiazem, verapamil

Front 121

in a hypertensive emergency, what 3 drugs could be given

Back 121

1. nitroprusside- NO analougue

2. diazoxide- causes local relaxation in smooth muscle by increasing membrane permeability to potassium ions. This switches off voltage-gated calcium ion channels

3. trimethaphan- counteracts cholinergic transmission at the ganglion type of nicotinic receptors of the autonomic ganglia and therefore blocks both the sympathetic nervous system and the parasympathetic nervous system

Front 122

which cardiac glycoside can be given to a pt in heart failure. and how does it work

Back 122

digoxin, - inotropic

Front 123

which drug can be given in case of a digitalis overdoes as an antidote

Back 123

digoxin

Front 124

t/f amrinone or milrinone are 2 positive inotropic agents can be given to pt in heart failure

Back 124

true

Front 125

t/f dopamine, dobutamine are 2 beta-blockers that can be given to a pt in heart failure

Back 125

false- dopamine, dobutamine are sympathomimetics

Front 126

t/f captopril, enalapril are 2 angiotensin converting enzyme receptor blockers that can be given to a pt in heart failure

Back 126

false- captopril, enalapril are ACE INHIBITORS not receptor blockrers

Front 127

which type of anti-arrhythmics are the following:

quinidine, procainamide, disopyramide, lidocaine, phenytoin, mexiletine

a. calcium channel blockers
b. drugs to prolong repolarization
c. beta blockers
d. sodium channel blockers
e. vasodilators

Back 127

d. sodium channel blockers

Front 128

which type of anti-arrhythmics are the following:

propranolol, pindolol,bisoprolol and HCTZ combo

a. calcium channel blockers
b. drugs to prolong repolarization
c. beta blockers
d. sodium channel blockers
e. vasodilators

Back 128

c. beta blockers

Front 129

which type of anti-arrhythmics are the following:

bretylium, amiodarone

a. calcium channel blockers
b. drugs to prolong repolarization
c. beta blockers
d. sodium channel blockers
e. vasodilators

Back 129

b. drugs to prolong repolarization

Front 130

which type of anti-arrhythmics are the following:

verapamil, diltiazem

a. calcium channel blockers
b. drugs to prolong repolarization
c. beta blockers
d. sodium channel blockers
e. vasodilators

Back 130

a. calcium channel blockers

Front 131

which type of anti-anginal drugs are the following:

nitroglycerin, isosorbide dinitrate

a. calcium channel blockers
b. drugs to prolong repolarization
c. beta blockers
d. sodium channel blockers
e. vasodilators

Back 131

e. vasodilators

Front 132

which beta blocker is used as an anti-anginal drug

Back 132

propranolol

Front 133

what are the 6 top selling calcium channel blocking drugs sold in the us for anti-angina

Back 133

verapamil, diltazem, nifedipine, amlodipine, lisinopril+HCTZ, benazepril+HCTZ

Front 134

what are the 3 main goal in the management of CHF

Back 134

1. normalize bp

2. promote regression of LVH

3. prevent tachycardia

Front 135

what is the standard therapy for a systolic CHF pt

Back 135

ACEI + Loop + Digoxin

Front 136

which drugs are beneficial for reducing preload (choose up to 2)

a. diuretics
b. sympathomimetics
c. beta blockers
d vasodilators
e. ACEI
f. ARBs
g calcium channel blocker
h. phosphodiesterase inhibitor

Back 136

1. diuretics- to reduce pulmonary congestion in order to reduce preload and SV can also use K+ sparring diuretics like spironolactone

2. vasodilators like nitrates or hydralize or minoxidil

Front 137

which drugs are beneficial for reducing afterload (choose up to 2)

a. diuretics
b. sympathomimetics
c. beta blockers
d vasodilators
e. ACEI
f. ARBs
g calcium channel blocker
h. phosphodiesterase inhibitor

Back 137

1. ACEI- cause regression of LVH, lower bp, prevent cardiac remodeling

2. beta blockers- to decrease HR, increase diastolic filling time, decrease O2 consumption, lower BP and cause regression of LVH

Front 138

which drugs are beneficial for reducing preload AND afterload (choose up to 2)

a. diuretics
b. sympathomimetics
c. beta blockers
d vasodilators
e. ACEI
f. ARBs
g calcium channel blocker
h. phosphodiesterase inhibito

Back 138

1. sympathomimetic amines like dobutamine or dopamine

2. phosphodiesterase inhibitors like amrinone or milrinone

Front 139

how is the heart muscle affected by digoxin

Back 139

cardiac glycoside like digoxin, inhibit the Na/K ATPase pump on cardiac cell membranes which results in an increase in intracelluar Na+. This increase in Na+ is exchanged for Ca+2 by the Na/Ca exchanges so then there is more Ca+2 intracellularly. this increase in Ca+2 increases the contractility of the heart

Front 140

which 4 Factors affecting cardiac output:

Back 140

1. Chronotropy- Heart rate

2. Inotropy- Contractility

3. Preload - Intravascular volume

4. Afterload-Systemic vascular resistance

Front 141

what is the formula for cardiac output

Back 141

Cardiac output (CO) = stroke volume (SV) x heart rate

Front 142

Pressure = ___ x Resistance

Back 142

Pressure = Flow x Resistance

Front 143

MAP = CO x __

Back 143

MAP = CO x systemic vascular resistance

Front 144

Describe which type of heart failure (systolic or diastolic)

↓ Contractility leads to ↓ CO and ↓ SV

Compensatory result: ↑ Afterload, ↑ Preload, ↑ Heart rate

Back 144

systolic dysfunction

Front 145

Describe which type of heart failure (systolic or diastolic)

CO maintained @ resting heart rate

Contractility and heart rate maintained

↓ Ventricular relaxation (remains stiff)

decrease in Preload, +/- ↑ Afterload

Back 145

diastolic

Front 146

what are the clinical effects of digoxin in HF pt

Back 146

↑Contractility (inotropy)
↑ Stroke volume/Cardiac Output

Weak inotrope

There is mild systemic, coronary arterial, and venous vasoconstriction ( especially when given by intravenously)

There is some diuretic effect as it inhibits reabsorption of Na+ at the kidneys.

Front 147

t/f the use of digoxin in HF has positive effects on long-term survival

Back 147

false- use of digoxin has little to no effect on long-term survival

Front 148

what is digoxin indicated for (2)

Back 148

Congestive Heart Failure

Antidysrhythmic agent
Used to slow the ventricular rate (< 100 bpm) in atrial flutter/fibrillation.

Front 149

Digoxin is know to cause- GI ,most common, AEs such as Nausea, vomiting, diarrhea, anorexia

What other AE is associated with Digoxin

Back 149

CNS
Confusion, visual disturbances (yellow halos around lights)

Front 150

list 5 drug interactions of digoxin

Back 150

Sulfa, anatacids, diuretics, licorice, fiber, phenytoin, phenobarital

Front 151

why is digoxin toxicity so common

Back 151

Excretion is proportional to glomerular filtration rate (GFR)

Narrow therapeutic index: need to avoid toxicity

T ½ = 1.5 days –2 days ( easy to build up blood levels)

Front 152

what are diuretics

Back 152

drugs which increase the excretion of NaCl and NaHCO3 and thus increase the volume of urine,

in the absence of diuretics less than 1% filtered Na+ is excreted

Front 153

t/f thiazides are used in severe HTN with GFR < 30 cc/min

Back 153

false- thiazides can be used in with mild to moderate HRN with normal renal and cardiac function

Front 154

how do diuretics work

Back 154

kidneys control the extracellular volume by altering NaCl and H2O

BP maintained at the expenes of extracellular fluid

Na resorption is driven primarly by Na/K ATPase pump wihin the tubular epithelium

primary goal of diuretics is to reduce edema by reducing extracelluarl volume

diuretics prevent reabsorption of Na in the nephron

Front 155

what is the first line agent of diuretic for HTN and how does it work

Back 155

1st line is thiazide

work by inhibiting NaCl transporters in loop of Henle and distal tubule thus increasing Na excretion causing diuresis.

the reduction in plasma volume decrease cardiac output which decreases BP

Front 156

where does spironolactone work in kidney and give two other examples of drugs that work by this same mechanism

. in what pt population are they given to

Back 156

inhibits the Na reabsoption in the distal tubules and decreased K+ excretion

triamterene and amiloride work in same way

Spironolactone used in pt with CHF, hepatic cirrhosis, ascites

Front 157

which class of diuretics inhibit the ability of the adrenal hormone, aldosterone, to stimulate Na+ reabsorption

Back 157

potassium sparing diuretics like spinonolacton, amiloride, tramterene. blocking aldosterone's ability promotes K+ retention rather than loss into the luminal fluid

Front 158

Definition
Chapter 31

any structural or functional abnormality of the ventricular myocardium

Back 158

cardiomyopathy

Front 159

what are the 3 major types of cardiomyopathies

Back 159

1. dilated

2. hypertrophic

3. restrictive/obliterative

Front 160

what are the 4 primary features of dilated cardiomyopathy

Back 160

1. cardiomegaly

2. dilated ventricles

3. impaired systolic function

4. increased myocardial mass

Front 161

List 4 etiologies of dilated cardiomyopathies

Back 161

1. Alcohol, arterial HTN

2. Beriberi, Babies( pregnancy)

3. Catecholamines (Pheo), Coxasackie, Cocaine, Chagas

4. Danorubicin,

Front 162

Describe the pathology of cardiomyopathy

Back 162

1. cardiomegaly- hemodynamic changes due to failure as a pump since after time, heart will become stiff, leading to decreased cardiac output with decreased renal perfusion, which leads to increase sympathetic activity and activation of RAAS and increase peripheral resistance, leading to CHF

2. dilated ventricles-biventricularly

3. impaired systolic function- and high end systolic volume and impaired emptying leading to intraventricular thrombi

4. increased myocardial mass- leading to huge heart on CXR

Front 163

what are the clinical manifestations of dilated cardiomyopathy

Back 163

dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pedal edema, decreased exercise tolerance

Front 164

On physical exam list 4 findings of cardiomyopathy

Back 164

1. tachycardia at rest

2. lateral displacement of cardiac impulses

3. JVD with hepatomegaly

4. S3 gallop

Front 165

which exam technique is used to differentiate between dilated cardiomyopathy and myocarditis

Back 165

biopsy- not recommended as routine

Front 166

atherosclerortic coronary heart disease leads to CHF and present similar to dilated cardiomyopathy, what can be used to "clinch the diagnosis" of atherosclerortic coronary heart disease

Back 166

nuclear treadmilling and cardiac catherization

atherosclerortic coronary heart disease also presents with angina or preceding hx of MI

Front 167

hypertensive heart disease leads to CHF and present similar to dilated cardiomyopathy, what can be used to "clinch the diagnosis" of hypertensive heart disease

Back 167

marked LVH on EKG and on Echo

CXR of LVH

signs of target end organ damage

elevated BP during episode of CHF

Front 168

t/f left ventricular dysfunction can be systolic or diastolic dysfunction

Back 168

true

systolic dysfunction =impaired contractility

diastolic dysfunction =impaired filling

Front 169

what are the treatments for dilated cardiomyopathy

Back 169

1. Na and H20 restriction to avoid volume overload

2. diuretics to decrease preload

3. ACEI or ARBS to decrease afterload

4. Digoxin for refractory symptoms

Front 170

what is the abnormal physiology in hypertrophic cardiomyopathy (4)

Back 170

1. decreased ventricular compliance leading to diastolic dysfunction

2. mitral regurg

3. systolic pressure gradient below the aortic valve in LV which creates obstruction outflow

4. systolic anterior motion of mitral valve may be due to Venturi effect

Front 171

what are 3 physical exam findings for hypertrophic cardiomyopathy

Back 171

1. systolic murmur increased by standing up valsalva maneuver, murmur reduced by squatting an handgrip

2. arterial pulse abrupt, jerky and ill sustained

3. S3 and S4

Front 172

t/f an echo is very specific for hypertrophic cardiomyopathy

Back 172

false- very sensitive

Front 173

t/f cardiac catherterization is very specific for hypertrophic cardiomyopathy

Back 173

true

Front 174

what is the sudden death in people with HOCM from

Back 174

ventricular arrhythmias or a fib

Front 175

what is the treatment for pt with HOCM

Back 175

1. negative inotropes to reduce the gradient- beta blockers or Ca+2 blockers

2. treat dsyrrthmia- amiodarone

Front 176

t/f restrictive cardiomyopathy has diastolic dysfunction without systolic dysfunction

Back 176

true- most common endomyocardial fibrosis and causes of death is CHF

Front 177

what is endomyocardial fibrosis

Back 177

travels's disease ( no ETEC like :-)

related to tropical environment

fibrosis of ventricles and eosinophilia

diastolic dysfunction and eventual obliteration of left ventricle- lead to death by CHF

Front 178

restrictive cardiomyopathy caused by amyloid would have which features on physical exam

Back 178

1. kussmal's sign- JVD on inspiration!! supposed to have JVD on expiration

2. orthostatic hypotension reflecting autonomic nerve infiltration

Front 179

restrictive cardiomyopathy caused by amyloid would have which features on Echo, doppler, cxr, biopsy

Back 179

"graunular sparkling"

doppler shows diastolic dysfunction

cxr- cardiomegaly

biopsy- definitive

Front 180

what causes the cardiac manifestation in pt with hemochromatosis and what is the classic tetrad of hemochromatosis

Back 180

cardiac manifestation caused by Fe deposits in heart leading to arrhythmias, conduction problems and CHF bc ventricles dilate too much, leading to both diastolic and systolic dysfunction

tetrad- liver disease, heart disease, diabetes mellitus, and bronze skin pigmentation

Front 181

what is the effect of the following drugs on the heart

a. cyclophosphamide
b. daunorubicin,doxorubicin
c. amphetamine
d. ETOH

Back 181

a. cyclophosphamide- myocarditis and myocardial necrosis

b. daunorubicin,doxorubicin- myocarditis and pericarditis

c. amphetamine- cardiomyopathy

d. ETOH- cardiomyopathy

Front 182

Chapter 31

what isthe most common virus implicated in myocarditis

Back 182

Coxsackie B

Echo could also be contributing

Front 183

Name 5 other infectious etiologies of myocarditis other than Coxsackie B virus and the vectors when appropriate

Back 183

1. trapanasoma cruzi- Chagas' Reduuvi- lays indolent for 10-20 yrs!!

2. Trichinella spiralis- pig

3. Echinococcosis- sheep

4. acute rheumatic fever- Step

5. Cory. diptheria-

6. clostridium perfingenes- gas gangrene

Front 184

chapter 33

definition:

transient disturbance of mechanical, biochemical and electrical function of the myocardium due to inadequate oxygenation induced by coronary atherosclerosis

Back 184

ischemic heart disease

Front 185

Defintion:

inadequate blood supply to the heart muscle usually caused by coronary atherosclerosis resulting in a relative deficiency of oxygen

Back 185

myocardial ischemia

Front 186

Definition:

recurrent,prolonged episodes of severe ischemia caused by focal spasms of the epicardial coronary artery, usually occurs at rest may awaken pt from sleep

Back 186

prinzmetal angina

Front 187

The pathophysiology of ischemic heart disease centers around myocardial O2 demand exceeding O2 supply. One such cause is reduced coronary blood flow.

List 5 causes of reduced coronary blood flow to the heart

Back 187

1. atherosclerosis- most common

2. coronary vasospasm

3. bradyarrhythmias

4. hypotension

5. arterial thrombi

Front 188

The pathophysiology of ischemic heart disease centers around myocardial O2 demand exceeding O2 supply. One such cause is decreased arterial oxygenation.

List 2 causes of decreased arterial oxygenation to the heart

Back 188

COPD

Cor pulmonale- RV hypertrophy and failure bc there is a disorder of the lung, pulmonary vessel and chest wall

Front 189

The pathophysiology of ischemic heart disease centers around myocardial O2 demand exceeding O2 supply. One such cause isreduced O2 carrying capacity of the blood.

List 2 causes of reduced O2 carrying capacity of the blood

Back 189

anemia

carboxyhemoglobin- from tobacco smoking

Front 190

The pathophysiology of ischemic heart disease centers around myocardial O2 demand exceeding O2 supply. One such cause is reduced perfusion pressure (aortic pressure).

List 3 causes of reduced perfusion pressure (aortic pressure)

Back 190

hypotension

shock

coronary steal syndrome

Front 191

What EKG finding suggest ischemia

Back 191

T wave inversion

ST depression

Front 192

What EKG finding suggest myocardial infarction

Back 192

hyperacute t wave

ST elevation

Q waves

Front 193

Name 3 drugs used in the nuclear treadmilling test

Back 193

dipyridamole, adenosine, dobutamine

Front 194

which 2 management options are available for pt who need to have coronary revascularization

Back 194

percutaneous transluminal coronary angioplasty PTCA, stents

aortocoronary bypass grafting

Front 195

what factors determine myocardial oxygen demand

Back 195

1. Heart rate

2. contractility

3. preload- ventricular volume

4. afterload- LV pressure

Front 196

describe the pathogenesis of atherosclerosis

Back 196

1. fatty streak from precursor lesions

2. intima thickening

3. fibrous plaque- can either be stable or unstable plaque

if stable- can lead to coronary artery stenosis, reduced coronary artery blood flow or ischemia all of which could lead to silent ischemia or stable angina

if unstable, plaque can rupture and cause a thrombus leading to a non-occlusive or occlusive thombus

if non-occlusive can produce unstable angina, NSTEMI or sudden cardiac death

if occlusive- Actue STEMI

Front 197

typical angina has which 3 clinical presentation

Back 197

1. chest discomfort retrosternal

2. chest discomfort provoked by exertion or emotional stress

3. chest discomfort relieved by rest or nitroglycerin

Front 198

if the general appearance of pt is a follows, what do we think is wrong

respiratory distress, JVD, pink frothy sputum, rales, S3 gallop, hepatojugular reflex

Back 198

heart failure and pulmonary edema

Front 199

Chapter 36

what is the drug therapy choice for stable angina

Back 199

single drug therapy

nitrates, or beta-blockers or Ca+2 blockers

Front 200

what is the drug therapy choice for prinzmetal angina

Back 200

nitrates + Ca+2 blockers

Front 201

what is the drug therapy choice for unstable angina

Back 201

CCB, beta-blocker, nitrates, aspirin, IV heparin, antiplatelet drugs

Front 202

t/f normally, coronary vasodilation due to release of NO by vascular endothelium predominates over vascular constriction by sympathetic

Back 202

true

Front 203

what time of day does a myocardial ischemic attack intensify

Back 203

during the morning surge of catecholamines and later afternoon peak

Front 204

what is the major limiting factor of using nitrates or organic nitrates for pt with initial stable or unstable angina

Back 204

rapid tolerance develops

Front 205

t/f arteriolar dilation predominates over the venous dilation at the therapeutic doses of organic nitrates

Back 205

false- venous dilates predominates over arteriolar

Front 206

in which pt population are nitrates contraindicated

Back 206

in pt taking viagra bc sildenafil is a phosphodiesterase inhibitor so pathway geared to cGMP which will dephosphorlyate the myosin light chain to myosin-LC and relax

that's toooo much vasodilation in one organ especially if add organic nitrates

Front 207

how does the therapeutic doses of nitrates work

Back 207

reduce preload by dilating capacitance vessels-veins

Front 208

t/f higher doses of nitrates reduce afterload on heart by dilating arterioles and reducing left ventricular volume

Back 208

true

Front 209

which drug causes coronary steal phenomenon

Back 209

dypyridamole- or any drug that dilated coronary resistance vessels and will increase angina

Front 210

t/f nitrates cause non-specific smooth muscle relaxation of bronchi, GI tract, but have no effect on cardiac or skeletal muscles

Back 210

true

Front 211

which has better bioavailability- isosobide mononitrate or isosobide dinitrate

Back 211

isosobide mononitrate- no 1st pass metabolism and a longer duration of action, renal excretion after glucuronidation

Front 212

what are the AE of nitrates

Back 212

1. HA

2. postural hypotension

3. rash

Front 213

which drug can be given to produce methemglobin in treating cyanide poisoning

Back 213

bitrates

Front 214

what is the DOC for chronic stable angina

Back 214

beta blocker or CCB (verapamil)

Front 215

T/F CCB dilate coronary arteries and peripheral arterioles but not veins

Back 215

true- increase vasodilation, and decrease afterload and myocardial O2 demand

Front 216

why do CCB have little effect on skeletal muscle

Back 216

bc skeletal muscle depends on intracellular Ca rather than on Ca+2 influx through membrane channels

Front 217

what is the DOC for pt with chronic angina and HTN

Back 217

beta blocker- nadolol

or if contraindicated use CCBs

Front 218

where are L-type Ca2 channels located

Back 218

in sarcolemma of cardiac and smooth muscles

Front 219

where are T-type Ca2 channels located

Back 219

SA node and have role in automaticity

Front 220

of the following Ca+2 channel blocking drugs ( Nifedipine, nimodipine, diltiazem and verapamil) which one has the most vasodilatation effect

Back 220

nifedipine

Front 221

of the following Ca+2 channel blocking drugs ( Nifedipine, nimodipine, diltiazem and verapamil) which one has the most depression on the cardiac contractility

Back 221

verapamil

Front 222

of the following Ca+2 channel blocking drugs ( Nifedipine, nimodipine, diltiazem and verapamil) which one has the most effect on the depression of the automaticity of the SA node

Back 222

verapamil

Front 223

of the following Ca+2 channel blocking drugs ( Nifedipine, nimodipinediltiazem and verapamil) which one has the most depression of the automaticity of the AV node

Back 223

verapamil

Front 224

of the following Ca+2 channel blocking drugs ( Nifedipine, nimodipine, diltiazem and verapamil) which does not cause bronchiolar constriction

Back 224

nifedipine

Front 225

of the following Ca+2 channel blocking drugs ( Nifedipine, diltiazem, nimodipine, verapamil) which one reduces morbidity following a subarachnoid hemorrhage

Back 225

nimodipine

Front 226

describe fetal circulation

Back 226

Front 227

what is the normal pressure in the right atrium of a child

Back 227

about 0- 5 mm Hg

Front 228

what is the normal pressure in the right ventricle of a child ( systolic and diastolic)

Back 228

25/5 mmHg

Front 229

what is the normal pressure in the pulmonary artery of a child ( systolic and diastolic)

Back 229

25/10 mmHg

Front 230

what is the normal pressure in the left atrium of a child ( systolic and diastolic)

Back 230

10 mm Hg

Front 231

what is the normal pressure in the left ventricle of a child ( systolic and diastolic)

Back 231

100/5

Front 232

what is the normal pressure in the aorta of a child ( systolic and diastolic)

Back 232

120/80 mmHg

Front 233

describe the blood flow in a child

Back 233

Front 234

Name 3 types of ASD and in which gender they are more common

Back 234

starting from the top of the atrium
1. sinus venosus
2. ostium secundum
3. ostium primum

more common in girls

Front 235

1. in pts with ASD, what type of shunting is there (R to L or L to R) and why

2-4. what are the symptoms and signs of pts with ASD

5. how do we treat pts

Back 235

1. left to right shunting bc RV more compliant with volume changes than LV so no pulmonary edema

2. so pt have minimal cardiac symptoms the RV pressure is actually normal in pt with ASD

3. fixed split of S2

4. pulmonary ejection murmur

5. surgical closure or transcatheter closure

Front 236

what is the most common location for a VSD

Back 236

perimembranous

others include: muscular and supracristal

Front 237

what are symptoms of a VSD

Back 237

1. tachypnea

2. poor feeding

3. slow growth

4. irritability

Front 238

1. what type of shunting happens in VSD

2. does pulmonary venous congestion occur

Back 238

1. left to right shunting bc LV is poorly compliant and intolerant of volume overload but it can respond to pressure changes well

2. since LV poorly compliant there is pulmonary venous congestion leading to pulmonary edema, pulmonary HTN and LVH

Front 239

1. what type of shunting happens in VSD

2. does pulmonary venous congestion occur

Back 239

1. left to right shunting bc LV is poorly compliant and intolerant of volume overload but it can respond to pressure changes well

2. since LV poorly compliant there is pulmonary venous congestion leading to pulmonary edema, pulmonary HTN and LVH

Front 240

which type of overciruculatory lesion will pts have bounding pulses, continuous murmurs, and tachypnea, tachycardia, and growth failure

Back 240

patent ductus arteriosus

Front 241

name 3 cyanotic heart lesions

Back 241

1. transposition of great vessels

2. tetrology of fallot

3. tricuspid atresia

Front 242

1. what is the hallmark of cyanotic heat lesions

2. what is the response to O2 in cyanotic lesions

Back 242

1. hallmark is cyanosis without tachypnea

2. little response to O2

Front 243

Name 5 cyanotic lesion of children

Back 243

1transposition of great vessels

2. tetrology of fallot

3. truncus arteriosus

4. tricuspid/ pulmonary atresia

5. total anomalous pulmonary venous

Front 244

Transposition of the great vessel

1. why is this considered a ductal dependent lesion

2. what is the management of this pt

Back 244

1. mixing at the level of the atrial septum and the ductus, while the RV is the systemic ventricle

2. mgt. is O2, prostglandin E1 to maintain patency of ductus, then need sugery

Front 245

what are the components of Tetrology

Back 245

1. Pulmonary stensosis

2. RVH

3. Overriding aorta

4. VSD

Front 246

what is an obligate characteristic in this condition

and what medication is needed

Back 246

Tricuspid Atresia

1 ASD

2. VSD

3. PGE1 to keep ductus arteriosus opened

Front 247

list 6 congenital heart diseases that present with cardiogenic shock

Back 247

1. hypoplastic left heart syndrome

2. severe coartation of the aorta

3. critical aortic stenosis

4. ebstein anomaly of tricuspid

5. large PDA

6. systemic AV malformation

Front 248

what is the clinical presentation of this pt and then the treatment

Back 248

ashen, tachypnea, tachycardia, pulseless, hepatomegaly,

treatment: give PGE1 to keep ductus open, mechanically

Front 249

Define this condition

Back 249

narrowing of the aorta resulting from localized thickening of the media protruding posteriorly into the lumen of the vessel causing obstruction

Front 250

what type of murmur is heard and where on this pt

Back 250

loud harsh systolic murmur at lower left sternal boarder

Front 251

what type of hypertrophy (RVH or LVH)

Back 251

right VH

Front 252

what type of hypertrophy (RVH or LVH)

Back 252

right VH

Front 253

what type of hypertrophy is seen this pt

Back 253

LVH possibly both

Front 254

t/f this is the most commonly reported congenital heart disease

Back 254

VSD is the most common

Front 255

what is the clinical mgt

Back 255

digoxin, diuretics- preload reduction and afterload reduction with hyralzaine or captopril

Front 256

In which type of septal defect is pulmonary edema and pulmonary HTN noted

Back 256

VSD

Front 257

which congenital heart disease presents in more females and is associated with congenital rubella

Back 257

PDA

Front 258

t/f indomethacin must quickly be given to this pt

Back 258

transpositon of great vessels, False- must give PGE1

Front 259

how long does it take for the patent ductus to close

Back 259

primary- 10-15 hrs

secondary 14-21 days

Front 260

what medication must be given within few hours and what are the AE of this medication

Back 260

PGE1 to keep ductus open, causes apnea

Front 261

what is a technique kids use to decrease hypercyanotic spells. what meds are given

Back 261

TOF,

kids used knee chest to decrease blood back to heart

given phenylephrine to raise Bp or ketamine

Front 262

what are the surgery options for this condition

Back 262

1. Blalock taussig

2. gore-tex

3. potts

4. waterston

5. glenn

Front 263

this condition is most commonly associated with what else

Back 263

bicuspid aortic valve

Front 264

describe the pulses and BP

Back 264

absent femoral pulses with BP differences

Front 265

Chapter 38

what is the normal direction of depolarization of the myocardium

Back 265

endocardium ---> epicardium

Front 266

what is the normal direction of repolarization of the myocardium

Back 266

epicardium ----> endocardium

upright T wave

Front 267

what is the effect of myocardial ischemia reducing regional ATP

Back 267

1. altered Na/K ATPase pump

2. decrease intracellular K

3. prolonging phase 3

4. epicardial repolarization delayed

Front 268

what is the direction of replorization of ischemia area

Back 268

in epicardial region ischemia
endocardium---> epicardium, inverted T wave

endocardial region of ischemia
epicardium---> endocardium but hyperacute T waves

Front 269

what are the finding on EKG for myocardial injury

Back 269

Altered ion transport across myocardial cell membrane

Reduced regional ATP produces

Altered Na+-K+ ATPase pump
↓ Intracellular K+
Altered Phase 2 & Phase 3 of APD
Results in ↑ ST segment

Front 270

what are the EKG finding of myocardial infarction

Back 270

1. abnormal Q-wave- Duration > 0.04 sec

2. ST elevation

3. inverted T waves

Front 271

what is the difference between ischemia and infarction EKG

Back 271

Ischemia
ST segment depression
Inverted T-waves

Infarction
ST segment elevation
T-wave inversion
Q-waves

Front 272

how can you tell how old an infarct is on EKG

Back 272

acute- ST segment elevation

subacute- inverted t waves

old- q waves

Front 273

describe the changes that take place on EKG from a normal EKG to ischemic EKG

Back 273

Front 274

which lead repesent which part of the LV

Back 274

Anterioseptal- V1-2

Anterior wall- V3-4

Lateral wall- V5-6 an I and AVL

Inferior wall II, III, aVF

Posterior wall- V1-2 but ST depression, upright T waves and R waver > S wave (so everything opposit)

Front 275

describe the EKG

Back 275

AMI

Front 276

describe the EKG

Back 276

septal Ami

Front 277

describe the ekg

Back 277

inferior ekg

Front 278

describe the EKG

Back 278

Front 279

what type of cardiac abnormality is this and in what population.

Back 279

Ebstein's

Ebstein's anomaly is the downward displacement of a portion of the tricuspid valve with atrialization of a large part of the RV (see Figure 12). There is often an associated ostium secundum ASD. The atrialized portion of the ventricle hinders rather than helps the forward flow of blood and there is tricuspid regurgitation. Occasionally Ebstein's anomaly is asymptomatic, but it generally presents in childhood or early adulthood with dyspnea, fatigue, signs of tricuspid regurgitation, and right-sided cardiac failure. Patients with Ebstein's anomaly require prophylaxis for endocarditis.

In pt of mothers who took lithium during preganancy

Front 280

name the condition:

name given to reversal in the direction of a cardiac shunt caused by the development of pulmonary hypertension. It applies regardless of whether the shunt is atrial or ventricular. Initial flow is always from high pressure (left) to low pressure (right), but pulmonary pressure can rise above systemic pressure and cause a reversal of flow.

Back 280

Eisenmenger's syndrome