Cardio Flashcards 2

Question 1

What is shock?

Answer 1

Clinical syndrome resulting from inadequate tissue perfusion and oxygen delivery to meet metabolic demands.

Results in global tissue hypoperfusion and metabolic acidosis

Question 2

What occurs in cells in response to decreased systemic oxygen delivery?

Answer 2

Switch to anaerobic metabolism, causing systematic acidosis

ATP depletion causes ion pump dysfunction

Cellular edema and hydrolysis of cellular membranes occurs, resulting in cell death

Question 3

What is the goal of the body in shock?

Answer 3

Maintain cerebral and cardiac perfusion

Vasoconstriction of splanchnic, musculoskeletal and renal blood flow

Can cause mulit-organ failure and death if the underlying abnormalities are not corrected

Question 4

What is the ultimate outcome of shock, if underlying abnormalities are not corrected?

Answer 4

Multiorgan failure and death - caused by systemic metabolic lacti acidosis that overcomes the body’s compensatory mechanisms

Question 5

What are useful hemodynamic parameters in shock?

Answer 5

Systemic vascular resistance

Cardiac output

Mixed venous oxygen saturation

Pulmonary capillary wedge pressure

central venous pressure

Question 6

What is SVR?

Answer 6

Systemic vascular resistance

reflects degree of vasoconstriction/vasodilation in peripheral vasculature

Question 7

What is CO?

Answer 7

Cardiac output

HR*Stroke volume

Question 8

What is SvO2?

Answer 8

Mixed venous oxygen saturation

Saturation of systemic venous blood after delivering oxygen to peripheral tissues

Question 9

What is PCWP?

Answer 9

Pulmonary capillary wedge pressure

surrogate for left arterial pressure

Question 10

What is CVP?

Answer 10

Central venous pressure

surrogate for right atrial pressure

Question 11

What hemodynamic measurement is a surrogate for left atrial pressure?

Answer 11

pulmonary capillary wedge pressure

Question 12

Which hemodynamic measurement is a surrogate for right atrial pressure?

Answer 12

Central venous pressure

Question 13

What is the normal value of right atrial pressure/central venous pressure?

Answer 13

0-6 mmHg

Question 14

What is the normal value for systolic pulmonary artery pressure?

Answer 14

15-30 mmHg

Question 15

What is the normal value for End-diastolic pulmonary artery pressure?

Answer 15

4-12 mmHg

Question 16

What is the normal value for mean pulmonary artery pressure?

Answer 16

9-19 mmHg

Question 17

What is the normal value for mean pulmonary capillary wedge pressure (PCWP)

Answer 17

i.e. left atrial pressure

4-12 mmHg

Question 18

What is the normal value for cardiac output?

Answer 18

4-8 L/min

Question 19

What is the normal value for mixed venous oxygen saturation (SvO2)?

Answer 19

>70%

Question 20

What is the normal value for systemic vascular resistance?

Answer 20

800-1200 dynes*sec/cm^5

Question 21

How is mean arterial pressure calculated?

Answer 21

MAP = CO x SVR

Recall, CO = HR * SV

Question 22

What defines hypovolemic shock?

Answer 22

Heart pumps well, but not enough blood volume to pump

Question 23

What causes hypovolemic shock?

Answer 23

decreased intravascular volume (preload) - causes decreased stroke volume

Hemorrhagic (trauma, GI bleed, AAA rupture)

Hypovolemic - burns, GI losses, dehydration, third spacing, diabetic ketoacidosis

Question 24

What is another name for distributive shock?

Answer 24

Vasodilatory shock

Question 25

What is distributive (or vasodilatory) shock?

Answer 25

Heart pumps well, but there is peripheral vasodilation due to loss of vessel tone  

Question 26

What caues distributive (vasodilatory) shock?

Answer 26

Loss of vessel tone Can be caused by overwhelming **inflammation** (sepsis, toxic shock syndrome, anaphylaxis) Can be caused by C-spine or thoracic cord injuries - **decreased sympathetic tone** **Toxins** - cellular poisons (Carbon monoxide, methemoglobinema, cyanide)

Question 27

What is cardiogenic shock?

Answer 27

Heart fails to pump blood out  

Question 28

What are causes of cardiogenic shock?

Answer 28

Decreased contractility (MI, myocarditis, cardiomyopathy) Mechanical dysfunction (papillary muscle rupture post MI, severe aortic stenosis, rupture of ventricular aneurysms) Arrhythmia (heart block, ventricular achycardia, supraventricular tachycardia, atrial fibrillation, etc.) Caridotoxicity (β-blocker or CCB overdose)

Question 29

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Question 35

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Question 36

What are the stages of shock?

Answer 36

Insult Preshock Shock End organ dysfunction

Question 37

What occurs during the insult stage of shock?

Answer 37

Splenic rupture, blood loss, MI, anaphylaxis, etc.

Question 38

What occurs during the preshock stage of shock?

Answer 38

Hemostatic compensation to maintain MAP within normal ranges (After insult)

Question 39

What occurs during the shock stage of shock?

Answer 39

After preshock stage Compensatory mechanisms fail and MAP declines

Question 40

What occurs during the end-organ dysfunction stage of shock?

Answer 40

Occurs after shock stage Cell death and organ failure

Question 41

What is the definition of cardiogenic shock?

Answer 41

Systemic hypoperfusion secondary to **severe depression of cardiac output** and **sustained systolic arterial hypotension** despite **elevating filling pressures**

Question 42

What are the three main keys to categorize someone as having cardiogenic shock?

Answer 42

Severe depression of cardiac output Sustained arterial hypotension Elevated filling pressures

Question 43

How do patients with cardiogenic shock present?

Answer 43

Hypotension Tachycardia/tachypnea Elevated neck veins Rales, gallop rhythm (S3) New murmur Cool extremities

Question 44

Will patients in cardiogenic shock present with cool or warm extremities?

Answer 44

Cool extremities - physiological response to maintain perfusion to vital organs

Question 45

What is the goal of medical treatment of shock?

Answer 45

Try to maintain mean arterial pressure

Question 46

What agents are useful in the treatment of shock?

Answer 46

Dopamine - α1, β1, β2 and DA agonist Dobutamine- α1, β1, β2 agonist Norepinephrine - α1, β1, β2 agonist Epinephrine - α1, β1, β2 agonist

Question 47

How does dopamine help patients in shock?

Answer 47

Stimulates D1 receptors (coronary, renal, mesenteric and cerebral beds) Promotes vasodilation and increased flow Also direct precursor to norepinephrine

Question 48

How does dobutamine help patients in shock?

Answer 48

Vascular smooth muscle binding results in β1 adrenergic agonism/antagonism and β2 stimulation with net vasodilation (low doses) Tolerance can develop though (not the best agent)

Question 49

How does norepinephrine help patients in shock?

Answer 49

increases systolic, diastolic, and pulse pressure wtih minimal impact on cardiac output Coronary flow is increased owing to elevated diastolic blood pressure and indirect stimulation of cardiomyocytes - release vasodilators

Question 50

What are downfalls of adrenergic inotropes in shock patients?

Answer 50

Can further increase heart rate, afterload, and wall tension Further exacerbating the problem

Question 51

What non-pharmacologic treatmetns are available to treat shock?

Answer 51

Left ventricular assist devices (LVAD), which unload the heart, boost coronary and systemic flow, and promotes myocardial and end-organ recovery 

Question 52

What is an intra-aortic balloon pump (IABP)?

Answer 52

Inflates in diastole, deflates in systole Displaces blood that is upstream towards the heart, increasing diastolic pressure When deflated - draws blood volume downstream, reducing end-diastolic pressure and left ventricular afterload (creates suction) Can also decrease LV volume, systolic work and **myocardial oxygen consumption** Reduces end-diastolic and peak diastolic aortic pressure 

Question 53

What are the hemodynamic effects of IABP (intraaortic balloon pump)?

Answer 53

Reduce systolic pressure Increase diastolic pressure Reduces heart rate Decreases pulmonary wedge pressure (LA pressure Elevate cardiac output Decrease LV wall stress

Question 54

What is the most common cause of cardiogenic shock?

Answer 54

Acute MI

Question 55

What two broad categories of pharmacologic treatment is available for the treatment of shock?

Answer 55

Vasopressors and inotropic agents

Question 56

What are the two aortic valve diseases?

Answer 56

Stenois Insufficiency

Question 57

What is the normal aortic valve area?

Answer 57

3-4 cm^2

Question 58

When do aortic valve stenosis symptoms start presenting?

Answer 58

Shen stenosis makes valve area 1/4 of normal area

Question 59

What defines aortic stenosis and severe aortic stenosis?

Answer 59

When area becomes less than 2 cm^2 ( less than 1 cm^2 for severe) Normal is 3-4 cm^2

Question 60

What are three types of aortic stenosis?

Answer 60

Supravalvular - in ascending aorta Subvalvular - from hypertrophic caridiomyopathy, for instance Valvular

Question 61

What are etiologies of aortic stenosis?

Answer 61

Congenital - leaflet cusps are deformed - can be unicuspid or bicuspid valve; or a fused tricuspid valve Acquired - degenerative, rehumatic, or other Congenital will present earlier than acquired or degenerative

Question 62

What type of aortic stenosis do patients under 70 usually present with?

Answer 62

Congenital

Question 63

What type of aortic stenosis do patients over 70 yo usually present with?

Answer 63

Acquired

Question 64

What is the most common etiology of aortic stenosis that will be seen in the next 10-20 years?

Answer 64

Degenerative calcification - seen in patients in their 70s-80s, comorbid with risk factors for CAD (because of aging population)

Question 65

What is the effect of aortic stenosis on the left ventricle?

Answer 65

Imposes increased afterload Causes concentric hypertrophy

Question 66

What type of hypertrophy is seen in aortic stenosis?

Answer 66

Concentric left ventricular hypertrophy

Question 67

What symptoms do you see in aortic stenosis?

Answer 67

Decreased outflow - dizziness, etc Left heart failure symptoms - elevated left atrium pressures - backup to lungs - shortness of breath Angina - increased work load of left ventricle

Question 68

What type of murmur is heard in aortic stenosis?

Answer 68

Systolic crescendo/decrescendo - diamond shape Ejection systolic murmur 

Question 69

What can happen to the second heart sound in aortic stenosis?

Answer 69

Can run into pulmonic valve sound - can even run past it and become paradoxical split

Question 70

What occurs during paradoxical S2 splitting?

Answer 70

Occurs in Aortic Stenosis Upon inspiration - split decreases. Upon exhalation, split increases Normally - aortic first, pulmonary second; split on inspiration

Question 71

What changes in the heart sounds do you see with aortic stenosis?

Answer 71

Systolic ejection murmur (crescendo decrescendo) S2 sound changes - A2 delays - may even occur after P2 (reversal of splitting/timing) More noticable upon expiration

Question 72

What is the difference between the systolic murmur seen in aortic stenosis and in obstructive hypertrophic cardiomyopathy?

Answer 72

Aortic stenosis - there is a delay between S1 and murmur - also crescendo, decrescendo HCM - starts at S1 and is relatively constant throughout AS:  HCM: 

Question 73

How do you reduce the hypertrophic cardiomyopathy murmur sounds?

Answer 73

Squat Opens up LV outflow

Question 74

How do you increase the murmur from a hypertrophic cardiomyopathy?

Answer 74

Stand up from squating position Valsalva maneuver to reduce size of LV

Question 75

How do you exacerbate murmur seen in aortic stenosis?

Answer 75

Make patient run around and then you can hear it better - but does not help to differentiate from HCM

Question 76

How do patients with aortic stenosis usually present?

Answer 76

Asymptomatic - onset of symptoms is a poor prognostic indicator

Question 77

How good of a prognostic indicator is symptom onset in aortic stenosis?

Answer 77

Poor

Question 78

What are the classical symptoms of severe aortic stenosis?

Answer 78

Dyspnea on exertion Syncope - low forward cardiac output Angina Sudden death

Question 79

What is DOE?

Answer 79

Dypsnea on exertion

Question 80

What are physical findings of aortic stenosis?

Answer 80

Slow rising carotid pulse (pulsus tardus) and decreased pulse amplitude (pulsus parvus) Soft and split second heart sound, S4 gallop Systolic ejection murmur (crescendo-decrescendo Other manifestations - bleeding, embolic events, CAD)

Question 81

What are pulse findings in aortic stenosis?

Answer 81

Slow rising carotid pulse (pulsus tardus) Decreased pulse amplitude (pulsus parvus)

Question 82

What are heart sound findings in aortic stenosis?

Answer 82

Soft and split second heart sound and reverse split S4 gallop due to left ventricular hypertrophy Systolic ejection murmur - diamond shaped crescendo-decrescendo (peaks later as severity of stenosis increases)

Question 83

What is pulsus tardus?

Answer 83

Slwo rising carotid pulse

Question 84

What is pulsus parvus?

Answer 84

Decreased pulse amplitud

Question 85

What is characteristic of the natural history of aortic stenosis after developing symptoms?

Answer 85

Sudden deaths soon after devleopment of symptoms if no valve replacement 

Question 86

What EKG findings do you see on AS?

Answer 86

Left axis deviation from hypertrophy Conduction blocks from calcification

Question 87

What can you see on chest x-ray in aortic stenosis?

Answer 87

Calcification Other non-specific findings (hypertrophy)

Question 88

What is the most specific diagnostic tool for diagnosing valvular heart disease?

Answer 88

Echocardiogram

Question 89

Why must you perform cardiac catheterization on aortic stenosis patients?

Answer 89

Must ensure there is no coronary artery disease before undergoing surgery for valvular repair

Question 90

What defines mild aortic stenosis?

Answer 90

Valve area \> 1.5 cm^2

Question 91

What defines moderate aortic stenosis?

Answer 91

Valve area 1-1.5 cm^2

Question 92

What defines severe aortic stenosis?

Answer 92

Valve area \< 1 cm^2

Question 93

How do you manage patients with aortic stenosis?

Answer 93

Antibiotic prophylaxis in dental procedures or with prostetic valves or with patients with history of endocarditis Few mediations - don't want to give vasodilators because you'll increase chances of syncope **Aortic valve replacement is definitive treatment** Aortic balloon valvotomy as a bridge to surgery

Question 94

Why does aortic balloon valvotomy not work for aortic stenosis?

Answer 94

Too much calcium - can reclose or spread to brain

Question 95

What are indications for surgery in aortic stenosis?

Answer 95

Any symptomatic patient with severe aortic stenosis Any patient with decreasing ejection fraction Any patient already undergoing CABG with moderate or severe stenosis

Question 96

What is the only situation in which patients with moderate aortic stenosis are indicated for replacement surgery?

Answer 96

When they are already undergoing CABG

Question 97

What is aortic regurgitation?

Answer 97

Leakage of blood back into the LV during diastole

Question 98

What causes aortic regurgitation?

Answer 98

Ineffective coaptation of the aortic cusps

Question 99

What is the pathophysiological result of aortic regurgitation?

Answer 99

Combined pressure and volume overload Causes compensatory LV dilatation and hypertrophy Progressive dilation leads to heart failure

Question 100

What can cause acute aortic regurgitation?

Answer 100

Endocarditis - leaflet perforation or rupture from infection Aortic dissection - can split aortic wall and continue through to the valve

Question 101

What are avenues for treatment for patients with acute aortic regurgitation?

Answer 101

True surgical emergency Medicines as a bridge to surgery: Give positive ionotrope (dopamine, dobutamine) Give vasodilators (nitroprusside) Avoid beta blockers **NO balloon pumps**

Question 102

How do vasodilators help in the short-term treatment of aortic regurgitation?

Answer 102

Keeps blood in periphery and reduces amount of blood that flows back into heart

Question 103

What are balloon pumps contraindicated in aortic regurgitation/aortic insufficiency?

Answer 103

Will only make it worse - make more blood flow backwards

Question 104

What can cause chronic aortic regurgitation?

Answer 104

Bicuspid aortic valve (normally tricuspid) Rheumatic Infective endocarditis Marfans

Question 105

What type of murmur will you see in aortic regurgitation?

Answer 105

Early, low pitched diastolic murmur 

Question 106

What is the most common diastolic murmur?

Answer 106

Aortic regurgitation murmur

Question 107

What changes in heart sounds will you see in aortic regurgitation?

Answer 107

Functional stenosis of aortic valve too - small crescendo-decrescendo systolic murmur More importantly, low-pitched early diastolic murmur 

Question 108

What are differences in heart sounds between acute and chronic aortic regurgitation murmurs?

Answer 108

In acute - the diastolic murmur is very quick and faint - difficult to pick up 

Question 109

What are cliical features of aortic regurgitation?

Answer 109

Asymptomatic until 30s-40s Progressive symptoms: Dyspnea - exertional, orthopnea, PND Angina **Palpitations** - increased contractile force **No syncope**

Question 110

What clinical features of aortic stenosis are absent in aortic regurgitation?

Answer 110

Syncope - instead feel palpitations Issue is increased volume!

Question 111

What physical findings do oyu see in patients with aortic regurgitaiton?

Answer 111

Wide pulse pressure -very sensitive Hyperdynamic and displaced apical impulse - can see chest wall excursion and feel it Diastolic blowing murmur Austin flint murmur - at apex - regurgitant jet impinges on anterior mitral valve leaflet causing vibration (resembles mitral valve murmur) Systolic ejection murmur - increased flow across aortic valve

Question 112

What is an Austin flint murmur?

Answer 112

Regurgitant jet impinges on anterior mitral valve leaflet causing vibration (resembles mitral valve murmur) Heard best at apex

Question 113

What pulse changes do you see in patients with aortic regurgitation?

Answer 113

Wide pulse pressure - very sensitive finding

Question 114

When do you see Austin flint murmurs?

Answer 114

In aortic regurgitation Regurgitant jet impinges on anterior mitral valve leaflet causing vibration (resembles mitral valve murmur)

Question 115

What is Corrigan's sign?

Answer 115

In aortic regurgitation - dancing carotids

Question 116

What is Quincke's pulse?

Answer 116

Exaggerated redennign and blanching of nail beds -pulsatile seen in Aortic regurgitation

Question 117

What is the main feature of aortic regurgitation that you can see signs of in almost all organs?

Answer 117

Hyperdynamism of the cardiac system - nail beds, chest excursion, etc

Question 118

What do you see on chest x-ray in patients wtih aortic regurgitation?

Answer 118

Enlarged cardiac silhouette Aortic root enlargement

Question 119

What do you see on echocardiogram in patients with aortic regurgitation?

Answer 119

AV and aortic root measurements LV dimensions and funciton Can see flow-back via doppler

Question 120

What do you do to manage aortic regurgitation in patients?

Answer 120

Prophylaxis for infectious endocarditis in dental procedures Vasodilators (ACE inhibitors), Nifedipine improve stroke volume and reduce regurgitation **(only if patient is symptomatic or hypertensive)** Surgical treatment is definitive

Question 121

When do you perform surgery on patients with aortic regurgitation?

Answer 121

When there are any symptoms at rest or with exercise Or in patients who are asymptomatic and whose ejection fraction drops below 50% or LV becomes dilated

Question 122

What pharmacologic treatments are given to patients with aortic regurgitation?

Answer 122

Vasodilators (ACE inhbitors), Nifedipine to improve stroke volume Only if patient is symptomatic or hypertensive

Question 123

What is infectious endocarditis?

Answer 123

Infection of endocardial surface

Question 124

What are the four classification groups of infective endocarditis?

Answer 124

Native valve endocarditis Prosthetic valve endocarditis IV druge abuse endocarditis Nosocomial endocarditis

Question 125

What are charactaristics of acute infectious endocarditis?

Answer 125

Fulminant - rapidly destructive Affects normal heart valves Metastatic foci Commonly Staph Usually fatal within 6 weeks if untreated

Question 126

What are characteristics of subacute infectious endocarditis?

Answer 126

Often affects damaged heart valves Indolent in nature - slower Fatal if untreated, usually by one year

Question 127

What is the common cause of acute infectious endocarditis?

Answer 127

Staph - staph aureus or coagulase negative

Question 128

What type of endocarditis is caused by staphylococci?

Answer 128

Acute

Question 129

What organisms are commonly implicated in subacute infectious endocarditis?

Answer 129

Streptococci species

Question 130

What kind of endocarditis is seen with stretpococcal infections?

Answer 130

Subacute (viridans, enterococci, bovis, others)

Question 131

What is IE?

Answer 131

Infectious endocarditis

Question 132

What is the pathogenesis of IE?

Answer 132

Turbulent blood flow leads to the development of thrombus at site of injury Bacteria that enters the circulation can adhere and colonize the injured surface

Question 133

What is the most common non-bacterial thrombotic endocarditis seen?

Answer 133

In SLE - generalized state of inflammation Libman-Sacks Endocarditis

Question 134

What are cardiac lesions that predispose to endocarditis?

Answer 134

Rheumatic valvular disease Acquired valvular lesions (left sided more common - higher shear stress) Hypertrophic obstructive cardiomyopathy Congenital heart disease Surgically implantable intravascular hardware

Question 135

Which side of the heart are lesions that predispose to endocarditis more commonly seen? Why? What is the exception?

Answer 135

On the left side - higher flow rates - more shear stress On the right side in IV drug use

Question 136

What are symptoms of acute IE?

Answer 136

High grade fever, chills Shortness of breath Arthralgias/myalgias Abdominal pain (emboli) Pleuritic chest pain (emboli) Back pain (emboli)

Question 137

What are symptoms of subacute IE?

Answer 137

Low-grade fever (indolent course) Anorexia Weight loss Fatigue Arthralgias/myalgias Abdominal pain N/V (many non-specific symptoms) Can be over days to weeks to months

Question 138

What are signs of IE?

Answer 138

Fever Clubbing - not specific Splenomegaly Neurological manifestations Heart murmur - NEW Peripheral manifestations - Osler's nodes, Subungal hemorrhage, Janeway lesions, Roth Spots, petechiae

Question 139

Why do you see splenomegaly in IE?

Answer 139

Attempting to clear the infection

Question 140

What types of murmurs are seen in IE?

Answer 140

NEW murmurs

Question 141

What are cardiac manifestations of IE?

Answer 141

New murmurs - regurgitations CHF - valvular damage, myocarditis, intracardiac fistulas Perivalvular abscesses Fistula Pericarditis Heart block **essentially, all sorts of things**

Question 142

What are non-cardiac signs of IE?

Answer 142

Septic embolization - petechial hemorrhage, Janeway lesions, Oslers nodes Infarcts in skin, spleen, kidney, meninges, skeletal system Embolic strokes Mycotic aneurysms - infetion of vasa vasorium of the blood vessel Brain microabscesses Glomerulonephritis

Question 143

WHereaWhere can you see petechia from IE?

Answer 143

Skin, conjuntiva, palate Mucous membranes and extremities

Question 144

What are splinter hemorrhages?

Answer 144

Non-specific, nonblanching, linear reddish-brown lesions found under nail bed 

Question 145

What are Osler's Nodes?

Answer 145

Extremely painful nodes in fingers More specific for IE and more common in subacute Erythematous 

Question 146

What are Janeway lesions?

Answer 146

Specific, erythematous, blanching macules that are **not painful** On palms and soles Seen in IE 

Question 147

What are Roth spots?

Answer 147

Seen on fundoscopic examination Indicative of IE 

Question 148

What labs are helpful in identifying IE?

Answer 148

CBC showing anemia, leukocytosis Blood cultures - from 3 different sites at least 1 hour apart Evidence of brucella, bartonella, legionella, c. burnetti Signs of inflammation: Elevated ESR, CRP Reduction of serum complement Elevated Rheumatoid factor

Question 149

What do you see in chest x-ray in IE?

Answer 149

Try to find clear lung fields to rule out pulmonary infections May see multiple focal infiltrates and calcification

Question 150

What can you see on EKG in IE?

Answer 150

May see ischemia or arrhythmias, or heart blocks

Question 151

What can you see on echocardiography in IE?

Answer 151

Can see vegetations

Question 152

What are major criteria for diagnosis of endocarditis?

Answer 152

Persistently positive blood culture for typical organisms Vegetations, dehiscence, abscesses on echocardiogram New valvular regurgitation murmur Coxiella burnetii infection

Question 153

What are indications of definite endocarditis?

Answer 153

2 major clinical criteria 1 major and any 3 minor 5 minor critera Histology findings + Gram stain or cultures from surgery or autopsy

Question 154

What are minor critera for the diagnosis of endocarditis?

Answer 154

Predisposing heart condition or IV drug use Fever Emboli to organs/brain, hemorrhages Glomerulonephritis, Osler's nodes, Roth spots, Rheumatoid factor Positive blood cultures that don't meet specific criteria

Question 155

When do you treat a patient for infectious endocarditis?

Answer 155

Wait until blood samples come back from microbiology before treating with antibiotics - don't want to conflate results You can wait 24 hours

Question 156

How do you treat IE?

Answer 156

4-6 weeks of IV parenteral antibiotics

Question 157

When might surgery benefit a patient with IE?

Answer 157

If they are in congestive heart failure If there is a prosthetic valve endocarditis If it is caused by fungal or other highly-resistant organisms If there are perivalvular infections with abscesses or fistula formations

Question 158

When is prophylaxis indicated for IE?

Answer 158

Patients have: Prosthetic heart valves Prior history of IE Unrepaired cyanotic congenital heart disease (shunts and gradients and non-laminar flow)

Question 159

When do you give prophylaxis for IE?

Answer 159

To protect in the time frame during which bacteremia will happen - i.e. right before, through, and after a dental procedure

Question 160

What procedures warrant prophylaxis for endocarditis?

Answer 160

Dental procedures If there is evidence of infection during: Upper respiratory tract procedures GU or GI procedures Procedures of skin, or MSK

Question 161

If there is a gradient between the left atrium and left ventricle during diastole, which valve is affected?

Answer 161

Mitral

Question 162

What type of murmur will be present in mitral valve issues?

Answer 162

Diastolic

Question 163

What happens to S1 in mitral stenosis?

Answer 163

Fast mitral valve closure - S1 is loud

Question 164

What happens to S2 in mitral stenosis?

Answer 164

Loud becuase of pulmonary hypertension

Question 165

During which cardiac phase will you see a murmur in mitral regurgitation?

Answer 165

Systole - it is holosystolic (pansystolic)

Question 166

What type of murmur do you see during mitral regurgitation?

Answer 166

Holosystolic (pansystolic)

Question 167

Do you see a diastolic murmur in mitral regurgitation?

Answer 167

Yes - lots of blood that entered the atrium is trying to now enter the ventricle Flow murmur (relative mitral stenosis, for the amount of blood that is flowing through)

Question 168

Durign what stage of the cardiac cycle do we see murmurs during mitral valve prolapse?

Answer 168

Systole

Question 169

What maneuvers can you perform to help diagnose mitral valve prolapse?

Answer 169

Delay the click - make the patient squat - this makes the venous return increase. SVR increases. LV dilates a bit and tightens. Valve has lesser tendency to prolapse and it takes longer in systole for it to prolapse Accelerate the click - standing will bring it back

Question 170

How do the murmurs of aortic stenosis and hypertrophic cardiomyopathy differ with valsalva/squatting?

Answer 170


Question 171

Do dihydropyridines have more of a vasodilating or cardiac depressan effect?

Answer 171

Vasodilating Decrease myocardial oxygen demand (venodilation and arterial dilation) These are CCBs

Question 172

How do dihydropyridines work?

Answer 172

Vasodilate more than cardiac depressant Decreased myocardial O2 demand by venodilating and dilating arteries

Question 173

how do nondihydropyridines work?

Answer 173

Cardiac depressants more than vasodilating Reduce HR, contractility to lower O2 demand Careful with β-blockers

Question 174

Do nondihydropyridines have more of a vasodilating or cardiac depressant effect?

Answer 174

Cardiac depressant Reduce HR, contractility (Calcium channel blocker)

Question 175

What is the effect of ranolazine on stable CAD?

Answer 175

Decreases anginal frequency Improves exercise tolerane Unclear how

Question 176

What drug can be given to CAD patients to decrease anginal frequency and improve exercise tolerance?

Answer 176

Ranolazine

Question 177

What is a benefit of a drug-eluting stent?

Answer 177

Reduces risk for restenosis and subsequent revascularization May result in higher thrombotic risk

Question 178

What is a potential risk in drug-eluting stents?

Answer 178

Higher thrombotic risk

Question 179

What are indications for percutaneous coronary intervention?

Answer 179

Refractory symptoms despite optimizing medical therapy Intolerance to medical hterapy Always attempt medical therapy first!!

Question 180

What is a benefit from arterial vs venous grafts for coronary revascularization?

Answer 180

Higher patency at 10 years, but used for most critical epicardial stenoses typically use saphenous veins from leg

Question 181

What is PCI?

Answer 181

Percutaneous coronary intervention (i.e. stent)

Question 182

What is CABG?

Answer 182

Coronary artery bypass graft

Question 183

What are advantages of PCI vs CABG?

Answer 183

Lower procedural risk Minimal recuperation (more and more done on outpatient basis)

Question 184

What are advantages of CABG vs PCI?

Answer 184

Complete revascularization No need for long term dual antiplatelet therapy (causing bleeding risk) Has a proven mortality benefit

Question 185

What is antithrombin?

Answer 185

Plasma protein that inactivates thrombin (Factor IIa) Heparan increases its efficacy 1000 fold 

Question 186

What is the effect of heparan on antithrombin?

Answer 186

Increases efficacy 1000 fold antithrombin inactivates thrombin (factor IIa) 

Question 187

What is thrombomodulin/proteinC/protein S?

Answer 187

Trombin receptor present on endothelial cells Bound thrombin is unable to convert fibrinogen to fibrin The thrombin/thrombomodulin complex activates protein C which degrades Factors Va and VIIa 

Question 188

What is tissue factor pathway inhibitor (TFPI?

Answer 188

Factor VIIa + TFPI initiate the extrinsic pathway of coagulation This is inhibited by factor Xa (negative feedback) 

Question 189

What is tissue plasminogen activator (TPA)?

Answer 189

Cleaves plasminogen to plasmin, which degrades fibrin clots Is secreted by endothelial cells in response to clot formation Important in clot lysis 

Question 190

What are the components of a clot?

Answer 190

Platelets + fibrin 

Question 191

What are clotting factors important in preventing thrombosis?

Answer 191

Antithrombin Protein C/Protein S/Thrombomodulin Tissue Factor Pathway Inhibitor (TFPI)

Question 192

What are endothelial anti-thrombotic mechanisms?

Answer 192

Platelet inhibition - prostacyclin and NO; ADP-\>adenosine conversion Vasodilation

Question 193

What is the effect of prostacycin on thrombosis?

Answer 193

Prostacyclin released by endothelial cells inhibits platelet activation Prostacyclin is also vasodilatory (minimizes contact between procoagulant factors (reducing propensity of thrombus formation)

Question 194

What is the effect of NO on thrombus formation?

Answer 194

NO inhibits platelet activation NO is a vasodilator - minimizes contact between procoagulant factors, reducing propensity to form thrombus

Question 195

What is the major cause of coronary thrombosis?

Answer 195

Plaque rupture

Question 196

What can cause plaque rupture that leads to coronary thrombosis?

Answer 196

Chemical factors that destabilize fibrous cap (cytokines inhibit collagen synthesis, a key component; MMPs within plaques degrade matrix) Physical stresses (shoulder region prone to rupture due to high stress; high BP; torsion from myocardial contraction) Triggers (strenuous activity or emotional upset; early morning with high BP, viscosity, sympathetic tone)

Question 197

What are chemical factors that can estabilize a fibrous cap and cause plaque rupture?

Answer 197

T lymphocytes secrete cytokines that inhibit collagen synthesis Enzymes in plaques degrade matrix - matrix metalloproteinases

Question 198

What are physical stresses that can cause plaque rupture and cause coronary thrombosis?

Answer 198

High stress on the shoulder region of the cap (most prone) Intraluminal blood pressure Torsion from myocardial contraction

Question 199

What are triggers of plaque rupture that can cause coronary thrombosis?

Answer 199

Strenuous physical activity or emotional upset MIs usually occur in the early morning hours when physiologic stress is highest (BP, blood viscosity, sympathetic tone)

Question 200

What time of day is more likely for an MI to occur? Why?

Answer 200

Early mornin hours Physiologic stress is highest - BP, blood viscosity, sympathetic tone

Question 201

What role does endothelium dysfunction play in the pathogenesis of coronary thrombosis?

Answer 201

Reduced secretion of NO and prostacyclin by endothelial cells results in a state where vasoconstriction is favored over vasodilation Platelet products (thromboxane, 5-HT) and thrombin promote vasoconstriciton while ADP (vasodilatory) is attenuated in endothelial cell dysfunction This increases hemodynamic stress on plaque and reduces coronary flow and normal clearance of procoagulant factors

Question 202

What are some triggers of acute plaque rupture?

Answer 202

Exertion Sexual activity Anger, mental stress Cocaine use Tobacco, marijuana use Exposure to air pollution Fever, specific infections (e.g. influenza)

Question 203

What are functional sequellae of MIs?

Answer 203

Impaired contractility (systolic dysfunction) - due to necrosis of functional myocytes (hypo-,a-, or dys-kinesis) Impaired relaxation (diastolic dysfunction) - this is an energy-dependent process, thus impaired duringMI; Reduces compliance and increases filling pressures Stunned myocardium - prolonged, but reversible period of contractile dysfunction; restored days-weeks later; adjacent to MI Ischemic preconditioning - episodes of ischemia render tissue resistant to subsequent; seen in stable angina - increases ischemic threshold

Question 204

What is hypokinesis of the myocardium?

Answer 204

reduced contraction

Question 205

What is akinesis of the myocardium?

Answer 205

Loss of contraction

Question 206

What is dyskinesis of the myocardium?

Answer 206

Outward bulging during contraction

Question 207

Why is diastole dysfunctional after MI?

Answer 207

Diastole is energy dependent - thus MI causes problems (Oxygen, ATP, etc) If compliance is reduced, filling pressures increase

Question 208

What is stunned myocardium?

Answer 208

Prolonged, but reversible period of contractile dysfunction seen after MI Function is restored days to weeks after episode Commonly seen in areas adjacent to region of MI

Question 209

What is ischemic preconditioning?

Answer 209

Episodes of ischemia render tissue resistant to subsequent episodes (sometimes) Observed in the setting of stable angina, which causes an increase in the ischemic threshold with continued exercise

Question 210

What is ventricular remodeling?

Answer 210

Changes in cardiac size, shape, structure and physiology May be physiological and adaptive during normal growth Or pathological in the setting of MI, cardiomyopathy, HTN, or valvular heart disease

Question 211

What cardiac remodeling occurs initially, post-MI?

Answer 211

Fibrotic repair of necrotic area and scar formation and elongation Thinning of the infarcted zone LV volumes increase in the adaptive response - associated with increased stroke volume to maintain normal cardiac output 

Question 212

What is the significance of infarct expansion in the context of MI?

Answer 212

Associated with higher mortality, incidence of non-fatal complications such as heart failure or ventricular aneurysm Seen on echo Can be severe and lead to systolic function deterioration, new/louder gallops, or new/worsening pulmonary congestion

Question 213

What remodeling occurs late, post-MI?

Answer 213

Hypertrophy Myocytes hypertrophy due to neurohormonal activation, myocardial stretch, activation of local tissue RAS, an para-/autocrine factors Ang II production locally, likely stimulates hypertrophy in non-infacted myocardium 

Question 214

What is acute coronary syndrome?

Answer 214

Acute MI, unstable angina or sudden cardiac death

Question 215

What are non-atherosclerotic causes of acute coronary syndroem?

Answer 215

In young patients or in pts with no coronary risk factors: - Mechanical valves or infectious endocarditis (emboli resultin gin coronary occlusion) - Inflammatory disorders (vasculitis) - peripartum female (spontaneous coronary dissection) **Cocaine** abuse - causes vasospasm (decreasing O2 supply), increases HR (increased O2 demand), and associated with increased atherosclerosis

Question 216

What is type 1 MI?

Answer 216

Classic case of plaque rupture with thrombus 

Question 217

What is type 2 MI?

Answer 217

Supply/demand imbalance without a plaque rupture 

Question 218

What is type 3 MI?

Answer 218

Sudden cardiac death - fixed atherosclerosis and supply/demand imbalance

Question 219

What is type 4/5 MI?

Answer 219

MI in the setting of revascularization procedures

Question 220

What is a transmural infarction?

Answer 220

(Q wave MI) Necrosis spans the entire thickness of the myocardium Caused by a total, prolonged occlusion of a coronary artery

Question 221

What is a subendocardial infarction?

Answer 221

(non-Q wave MI) Subendocardium susceptible to ischemia, exposed to the highest pressures from the ventricles with few collaterals. Vessels that supply O2 must pass through the contracting myocardium

Question 222

What is the most common cause of ACS (acute coronary syndrome)?

Answer 222

Rupture of an atherosclerotic plaque leading to superimposed thrombus Plaque erosion may lead to thrombus More common in younger women, smokers

Question 223

What demographics are more likely to have plaque erosion leading to thrombus as a cause of ACS?

Answer 223

Younger women Smokers

Question 224

What is the result of a non-occlusive thrombus in the coronary vasculature?

Answer 224

Unstable angina NSTEMI (non-ST-elevation MI) Transient occlusion or distal imbolization may cause necrosis

Question 225

What is the result of an occlusive thrombus in the coronary vasculature?

Answer 225

ST-elevation MI (STEMI)

Question 226

What is the least severe on the spectrum of ACS?

Answer 226

unstable angina

Question 227

What is the most severe on the spectrum of ACS?

Answer 227

STEMI

Question 228

What is the spectrum of ACS?

Answer 228

Unstable angina -\> NSTEMI -\> STEMI

Question 229

What are the three classifications of unstable angina?

Answer 229

Rest angina - at rest and prolonged (\>20 mins) New-onset angina - \<2 months Increasing (crescendo) angina - previously diagnosed angina has become more frequent, longer, or worse in severity

Question 230

What is the effect of nitroglycerin on MI?

Answer 230

No improvement and minimal releif

Question 231

What are clinical symptoms in myocardial infarction?

Answer 231

More severe, longer, and more radiating chest pain, compared to stable angina No improvement with rest and minimal releif with nitroglycerin Sympathetic response (diaphoresis, nausea, tachycardia, cool skin) 25% may have no symptoms (diabetes) Shortness of breath

Question 232

In what population of patients might you not see symptoms of MI?

Answer 232

Diabetics

Question 233

What are physical findings of MI?

Answer 233

S4 - atrial contraction into non-compliant LV (atrial kick) S3 - volume overload (blood sloshing in) Systolic murmur due to papillary muscle dysfunction causing MR or ventricular septal defect from rupture Fever (low grade), as inflammatory response

Question 234

How is ACS (acute coronary syndrome) diagnosed?

Answer 234

Clinical symptoms, ECG findings, biomarkers of necrosis Unstable angina/NSTEMI = T wave inversion; ST depression or normal :: elevated biomarkers in NSTEMI; normal in USA STEMI = ST elevation, elevated biomarkers

Question 235

What ECG findings do you find in NSTEMI or unstable angina?

Answer 235

T wave inversion ST depression or normal

Question 236

What ECG findings do you see in STEMI?

Answer 236

ST elevation

Question 237

What EKG findings do you find within minutes to hours after STEMI?

Answer 237

ST elevation and perhaps hyperacute T 

Question 238

What EKG findings do you see hours-1 day after STEMI?

Answer 238

T wave inversion, elevated ST, depressed Q wave 

Question 239

What EKG findings do you see ~1 week after STEMI?

Answer 239

Pronounced Q, ST elevation, T wave inversion 

Question 240

What findings do you see months after STEMI?

Answer 240

Pronounced Q, ST elevation, marked T wave 

Question 241

How is STEMI defined?

Answer 241

Angina unreleived by nitroglycerin with ST elevation on EKG and rise in biomarkers

Question 242

How is NSTEMi defined?

Answer 242

Angina at rest \>20 minutes without ST elevation but with rise in cardiac biomarkers

Question 243

What is the pathophysiology of STEMI?

Answer 243

Total or near-total thrombotic occlusion of coronary artery

Question 244

What is the pathophysiology of NSTEMI?

Answer 244

Abrupt decrease in myocardial oxygen supply Thrombus formation on an atherosclerotic plaque

Question 245

What are biomarkers of myocardial necrosis?

Answer 245

Troponin core complex (TnT, TnI, TnC) Creatinine kinase myocardial band (CK-MB)

Question 246

What is the value of using troponin as a biomarker for MI?

Answer 246

They are generally not detected in blood of healthy individuals Levels rise within 3-4 hours, peak between 18-36 hours and decline slowly (~2 weeks) 

Question 247

What is the time course of troponin as a biomarker for MI?

Answer 247

Rises within 3-4 hours, peaks between 18-36, and declines slowly (up to 2 weeks) 

Question 248

What is the value of creatinine kinase myocardial band (CK-MB) as a biomarker for MI?

Answer 248

Has sharper kinetics than troponin (peaks faster and returns to normal faster) Good for identifying subsequent MIs after initial event 

Question 249

What are the kinetics of CK-MB as a biomarker for MI?

Answer 249

Peak wtihin 24 hours and decline quickly (couple of days) 

Question 250

What are the narrow complex tachycardias?

Answer 250

Sinus tachycardia AVNRT/AVRT Atrial fibrillation Atrial flutter Atrial tachycardia Multi-focal atrial tachycardia

Question 251

How do you approach an EKG with narrow complex supraventricular tachycardia?

Answer 251

Regular or irregular R-R intervals? P waves or no P waves Long RP or Short RP? - transect R-R segment (P on left or right side?) Response to adenosine -AV nodal blocker

Question 252

What is the classic irregular narrow complex tachycardia?

Answer 252

Atrial fibrillation

Question 253

What does an irregular narrow complex tachycardia tell you?

Answer 253

atrial fibrillation

Question 254

What does a regular narrow complex tachycardia tell you?

Answer 254

It's NOT atrial fibrillation - check for long or short RP segments

Question 255

What does a short RP, regular narrow complex tachycardia tell oyu?

Answer 255

AVNRT/AVRT

Question 256

What does a long RP, regular, narrow complex tachycardia tell you?

Answer 256

Sinus tachycardia or atrial tachycardia - check nodal block effects

Question 257

What does a regular, narrow complex tachycardia with multiple p waves tell you?

Answer 257

atrial flutter

Question 258

What is AVNRT?

Answer 258

Narrow complex tachycardia seen in all ages Manifests as palpitations "racing heart" **Re-entrant arrhythmia** dependent on having **dual AV nodal physiology** Psuedo R' in V1 Pseudo S in II, III, aVF no P wave (short RP) - P and QRS often on top of each other

Question 259

In AVNRT, the [...] pathway has slower conduction and faster recovery

Answer 259

In AVNRT, the slow pathway has slower conduction and faster recovery Fast pathway has faster conduction, slower recovery If you walk a mile, you only need short rest If you run a mile, you have to rest for a long time 

Question 260

In AVNRT the [...] pathway has faster conduction and slower recovery

Answer 260

In AVNRT the fast pathway has faster conduction and slower recovery Slow pathway has slower conduction and faster recovery If you walk a mile, you only need short rest If you run a mile, you have to rest for a long time 

Question 261

How do you treat AVNRT acutely?

Answer 261

Adenosine, Vagal maneuvers, AVN blocking agent

Question 262

How do you treat AVNRT chronically?

Answer 262

AVN blockers Single dose during episodes, daily dosing Class I and Class III anti-arrhythmics are effective ABLATION of slow pathway is most efficacious (low risk)

Question 263

Which pathway (slow or fast) do you attempt to ablate to resolve an AVNRT?

Answer 263

slow!

Question 264

What is AVRT?

Answer 264

AV reciprocal tachycardia Re-entrant arrhythmia Dependent upon **accessory pathway** Can be manifest on EKG = Wolff-parkinson-white (WPW) Risk for sudden death

Question 265

What is WPW?

Answer 265

Wolff-Parkinson-White Type of AVRT - re-entrant arrhythmia with accessory pathway Characteristic Δ-wave on EKG and short PR interval 

Question 266

What is atrial flutter?

Answer 266

Common arrhythmia in patients with heart disease Can present with palpitations, dyspnea, heart failure, stroke Re-entrant arrhythmia involving atria Atria beating at 250-300 bpm, with ventricles at 2:1, or 3:1 or slower rate **Saw-tooth pattern P waves** ****

Question 267

What is atrial fibrillation?

Answer 267

Highly prevalent arrhythmia Risk factors are numerous (age, HTN, DM, etc) Can be paroxysmal (in and out) or persistent Variable symptomaticity EKG is Irregularly irregular Atria at \>300bpm but uncoordinated **Originate from impulses from the pulmonary veins** **Tx with AV nodal blockade, anti-arrhythmics, catheter ablation** ****

Question 268

What are you thinking? 

Answer 268

Atrial fibrillation Irregularly irregular Atria at \>300 bpm

Question 269

What do you see here? 

Answer 269

Atrial Flutter Saw-tooth appearance

Question 270

What are clinical manifestations of lower extremity atherosclerosis?

Answer 270

Intermittent claudication Critical limb ischemia

Question 271

What is intermittent claudication?

Answer 271

Pain, ache, or fatigue in the calf, thigh, hip, buttock, or low back that **occurs on walking** and is releived with rest Location of symptoms correlates with level of obstruction

Question 272

What is critical limb ischemia?

Answer 272

Pain or paresthesia in the toes, foot, or leg **at rest** Exacerbated by leg elevation or when supine Releived with dependency Persistent pain +/- ulceration with severe ischemia

Question 273

What is the Leriche triad?

Answer 273

Bilateral high claudication Impotence Global Atrophy

Question 274

What is aorto-iliac disease?

Answer 274

Peripheral artery disease characterized by the Leriche triad (bilateral high claudication, impotence, global atrophy) Collaterals are typically well develope There are multiple revascularization options with high patency

Question 275

What is Femoropopliteal disease?

Answer 275

Most frequent peripheral artery disease Collaterals determine course of disease Intermediate graft patency

Question 276

What is tibeal-peroneal disease?

Answer 276

Peripheral artery disease commonly seen in diabetes Low graft patency without in-situ vein techniques

Question 277

What are trophic signs of acute limb ischemia on examination?

Answer 277

Ulceration Petichae Calf tenderness Dependent edema

Question 278

What are trophic signs of chronic arterial obstructive disease?

Answer 278

Hair loss Subcutaneous atrophy Thickened nails Dependent rubor

Question 279

How do you treat limb obstructive arterial disease pharmacologically?

Answer 279

Platelet inhibitors (aspirin, clopidogrel) Lipid-lowering agents (statins) ACE inhibitors **NO role for vasodilators**

Question 280

What are etiologies of acute arterial occlusion?

Answer 280

In-situ thrombosis (ruptured atherosclerotic plaque) Embolism from a proximal source Arterial trauma Vasculitis Hypercoagulable state Severe venous thrombosis

Question 281

What are sources of arterial emboli?

Answer 281

Atrial fibrillation Valvular heart disease (rheumatic mitral stenosis, prosthetic valves, endocarditis) Thrombus in cardiac chambers (left atrial appendage, LV mural thrombus) Proximal arterial disease (AAA, atherosclerosis)

Question 282

What is a true aneurysm?

Answer 282

Intima, media and adventitia are in tact, but balloon out 

Question 283

What is a false aneurysm?

Answer 283

Hole in intima and media that allows for hematoma to balloon the adventitia out and give the appearance of an aneurysm 

Question 284

What are etiologies of aortic aneurysmal diseases?

Answer 284

Atherosclerosis Cystic medial necrosis (primary, Marfan, Ehlers-Danlos) Vasculitis Dissection Post-stenotic Infections Trauma Congenital

Question 285

What are risk factors for abdominal aortic aneurysms?

Answer 285

Age HTN Tobacco smoking Family history (males) Hyperlipidemia Atherosclerosis

Question 286

What is the natural history of an abdominal aortic aneurysm (AAA)?

Answer 286

Expand at 1-4 mm/ year Predictors of expansion include initial size, active smoking, HTN)

Question 287

What are risk factors for aortic dissection?

Answer 287

HTN Tobacco smoking Cocaine use or stimulant use Connective tissue disease (Marfans, Ehlers-Danlos) Congenital structural abnormalities (bicuspid aortic valve, coarctation of aorta) Inflammatory disease of aorta Pregnancy Weight lifting Trauma

Question 288

What is Raynaud's Phenomenon??

Answer 288

"asphyxiation of digits" 

Question 289

What is primary raynaud's disease?

Answer 289

most cutaneous vasospasm Females more than males 15-40 year old onset Symmetrical involvement of digits, earlobes, tip of nose, elbows, knees Spontaneous improvement in 15%; progression in 30% Ulceration is rare

Question 290

What is Buerger's Disease??

Answer 290

Medium vessel vasculitis associated wtih tobacco smoking Cessation of smoking is theapy

Question 291

What is Virchow's Triad?

Answer 291

Stasis of blood flow Endothelial injury Hypercoagulable state Describes factors that contribute to thrombosis

Question 292

Where are DVTs more common?

Answer 292

Calf \> popliteal \> femoral \> iliac (more distal = more common)

Question 293

What sites of DVTs are more dangerous?

Answer 293

Proximal Iliac \> femoral \> popliteal \> calf Deep \> superficial veins

Question 294

What symptoms are seen in massive pulmonary embolism?

Answer 294

Syncope, profound dyspnea, cardiogenic shock, cardiac arrest sub-massive = chest pain, dyspnea

Question 295

What symptoms are seen in sub-massive pulmonary embolism?

Answer 295

chest pain, dyspnea massive = Syncope, profound dyspnea, cardiogenic shock, cardiac arrest

Question 296

What symptoms are seen in pulmonary infarction?

Answer 296

Hemoptysis (coughing blood), chest pain, dyspnea

Question 297

What are signs of chronic venous insufficiency?

Answer 297

Edema and induration Hemosiderin pigmentation Ulceration

Question 298

What are clinical syndromes associated with chronic venous insufficiency?

Answer 298

Superficial varicose veins Deep venous incompetence Postphlebitic syndrome

Question 299

What are symptoms of lymphedema?

Answer 299

limb swelling heaviness recurrent lymphanigitis or erysipelas Skin changes fungal infestation

Question 300

What are physical findings of lymphedema?

Answer 300

Non-pitting edema Dorsal pedal hump Elephantine distribution Chronic induration without pigmentation Lichenification

Question 301

What are causes of primary lymphedema?

Answer 301

Aplasia, hypoplasia or hyperplasia of lymphatic channels Obstruction Incompetence of lymphatic valves 

Question 302

What can cause secondary lymphedema?

Answer 302

Malignancy Radiation Infection - pyogenic lymphangitis, filariasis Surgery trauma

Question 303

Where is the most common location for atherosclerotic aneurysms in the aorta?

Answer 303

Below renal arteries and above bifurcation of iliac artery 

Question 304

How do β-blockers help in treating MIs?

Answer 304

Releive ischemic pain Reduce infarct size and life-threatening arrhythmias Presumed to decrease cardiac work and myocardial oxygen demand

Question 305

How do nitrates help treat MI?

Answer 305

They enhance coronary blood flow by coronary vasodilation Decrease ventricular preload by increasing venous capacitance (reduce wall stress) Contraindicated in pts with hypotension

Question 306

How do calcium channel blockers help MIs?

Answer 306

Symptom improvement Nondihydropyridines reduce heart rate and contractility Useful in pts with contraindications to β-blockers or ischemia refractory to β-blockade or nitrates

Question 307

What is the risk with antithrombotic therapies?

Answer 307

Can go too far, and thin blood, causing a bleeding risk

Question 308

What is the effect of Aspirin on MI?

Answer 308

Effective across all ACS categories Give as soon as possible Produces rapid antiplatelet effect Reduces oronary occlusion and recurrent ischemic events after fibrinolytic therapy

Question 309

What is a drawback/issue with using clopidogrel?

Answer 309

There is substantial interindividual variability in the response

Question 310

How do glycoprotein IIb/IIIa receptor antagonists work/help in MIs?

Answer 310

Potent inhibitors of the **final common pathway** of platelet aggregation Use has declined with advent of more potent antiplatelet drugs Beneficial in highest risk patients undergoing PCI

Question 311

What is the goal of STEMI treatment?

Answer 311

To achieve reperfusion. Restores flow in the infarct-related artery, limits infarct size and translates into early mortality benefit.

Question 312

What are treatment avenues for STEMI patients?

Answer 312

Fibrinolysis and invasive strategies are essentially equal in efficacy unless there are reasons not to do one (occupied cath lab, no access, delay to invasive, etc)

Question 313

What are complications of MIs?

Answer 313

Arrhythmias - signiicantly V. fib = sudden cardiac death;also supraventricular arrhythmias and conduction blocks Pump failure Free wall rupture/pseudoaneurysm Papillary muscle rupture Pericarditis

Question 314

What are left sided heart failure signs/symptoms?

Answer 314

Dyspnea, pulmonary rales, third heart sound Diuretics can relieve volume overload Standard heart failure meds indicated

Question 315

What are right sided heart failure signs/symptoms?

Answer 315

Elevations in JVD and hypotension (LV is underfilled) Treat with volume expansion Usually due to MI of RCA

Question 316

During what time scale does a free wall rupture typically occur after MI?

Answer 316

Within first 2 weeks This is a surgical emergency, and usually fatal

Question 317

What is a psuedoaneurysm?

Answer 317

Caused by a contained myocardial rupture, still at risk for rupture 

Question 318

What is a LV aneurysm?

Answer 318

Discrete dyskinetic area of LV wall with broad neck Develops weeks to months after MI No communication between LV cavity and pericardium Complications include thrombus, arrhythmias, heart failure Tissue bulges with cardiac contractions LV aneurysm can be associated with ST elevation

Question 319

What are some issues with a papillary muscle rupture?

Answer 319

Complete rupture may result in severe mitral regurgitation -\> heart failure or death Partial rupture may cause moderate MR and symptoms of heart failure

Question 320

Which aspect of the papillary muscle is more susceptible to rupture?

Answer 320

Posteromedial papillary more susceptible than anterolateral 

Question 321

What is acute pericarditis?

Answer 321

Inflammation that occurs early in the post-MI period taht extends from myocardium to pericardium

Question 322

What is Dressler syndrome?

Answer 322

Pericarditis that occurs several weeks after MI autoimmune process may be contributory

Question 323

What is ischemic injury?

Answer 323

Injury resulting from reduced blood flow

Question 324

What are the effects of impaired blood inflow?

Answer 324

Inadequate oxygen supply Insufficient availability of nutrients

Question 325

What are the effects of impaired blood outflow?

Answer 325

Insufficient removal of metabolites

Question 326

What is the etiology of most myocardial ischemia cases?

Answer 326

Obstructive coronary artery disease (CAD)

Question 327

What is myocardial infarction?

Answer 327

The irreversible myocardial muscle damage caused by prolonged ischemia resulting from a sustained imbalance of perfusion and demand Discrete focus of ischemic muscle necrosis

Question 328

What cardiac areas does the right coronary arery supply?

Answer 328

Right atrium Right ventricle Bottom portion of left ventricle Back of septum

Question 329

What cardiac areas does the left anterior descending artery supply?

Answer 329

Front and bottom of left ventricle Front of the septum

Question 330

What cardiac areas does the circumflex artery supply?

Answer 330

Left atrium Side and back of the left ventricle

Question 331

You find ischemia on the anterior wall of the LV and down to the apex of the heart. Where do you suspect a coronary artery occlusion?

Answer 331

Left anterior descending (LAD) branch of the left coronary artery

Question 332

You find necrosis on the posterior wall of the LV. Where do you suspect an occlusion of the coronary arteries?

Answer 332

Right coronary artery

Question 333

You find necrosis on the lateral wall of the left ventricle. Where do you suspect a coronary artery occlusion?

Answer 333

Circumflex artery - a branch of the left coronary artery

Question 334

Whhat is a transmural infarct?

Answer 334

ischemic necrosis that involves full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery

Question 335

What is a subendocardial infarct?

Answer 335

Ischemic necrosis limited to inner 1/3 or 1/2 of the ventricular wall Zone is least perfused and most vulnerable to any reduction in flow Regional: transient obstructoin which is releived before necrosis extends across thickness Circumferential: Prolonged, severe hypotension even without coronary stenosis

Question 336

What type of infarct can lead to pericarditis or ventricular rupture?

Answer 336

Transmural infarcts Subendocardial infarts do not

Question 337

What do you see on pathology of an MI within 4 hours?

Answer 337

Nothing!

Question 338

What do you see on pathology of an MI after 1-3 days?

Answer 338

Mottling with yellow-tan infarct center Seen maximally at 7-10 days

Question 339

When do you see yellow-tan areas in the myocardium following an MI?

Answer 339

After about 3-10 days

Question 340

What do you see on pathology of an MI after over 2 months?

Answer 340

Complete scarring

Question 341

How old is this MI? 

Answer 341

~ 7 days Note the yellow-tan zone of necrosis with the surrounding red granulation tissue.

Question 342

What are clinical findings in Giant Cell Arteritis?

Answer 342

Diminished temporal pulses/headache Facial pain/jaw claudication Impaired vision Elevated inflammatory markers Treat with high dose steroids before confirming diagnosis to save vision

Question 343

What is thrombangiitis obliterans?

Answer 343

Buerger disease Smoking-related vasculitis that presents with triad of symptoms: Distal arterial occlusion (corkscrew collaterals) Raynaud's phenomenon Superficial vein thrombophlebitis Smoking cessation is critical treatment 

Question 344

You see corkscrew collaterals in a patient's angiogram. What are you thinking? 

Answer 344

Thrombangiitis obliterans (Buerger disease) Stop smoking!

Question 345

What sex is affected more commonly by giant cell/Takayasu arteritis?

Answer 345

Females Males are affected more by thrombangiitis obliterans (Buerger's)

Question 346

What is the diagnosis? 

Answer 346

A fibrillation

Question 347

What is the diagnosis? 

Answer 347

Atrial flutter

Question 348

Which arrhythmia is dependent on having dual AV nodal physiology?

Answer 348

AVNRT

Question 349

What is the most likely diagnosis? 

Answer 349

3rd degree heart block (complete heart block)

Question 350

What is the most likely diagnosis? 

Answer 350

2nd Degree AVB - Mobitz I

Question 351

What do you see in this EKG? 

Answer 351

Atrial fibrillation Right Bundle Branch Block (RBBB) 3rd Degree AV Block (complete heart block) - no correlation b/w p waves and qrs complexes

Question 352

What are characteristics of WPW on EKG?

Answer 352

Short PR (less than 120ms) Slurred QRS upstroke (delta wave) Broad QRS Secondary ST and T wave changes 

Question 353

What is the diagnosis? 

Answer 353

WPW

Question 354

What is an orthodromic AVRT?

Answer 354

Electrical activity occurs in a circle but proceeds down septum and around free walls and up to atria 

Question 355

What is an antidromic AVRT?

Answer 355

Re-entrant arrhythmia where the electrical impulse passes from atria down free wall of ventricle and up through septum (backwards) 

Question 356

What is the effect of hyperkalemia on the membrane resting potential of a myocyte?

Answer 356

Decreases it from -90 to -80 mV 

Question 357

What changes are present on EKG in hyperkalemia?

Answer 357

Slowed conduction - fewer cells recruited Everything delayed until it stops 

Question 358

What is a clear EKG finding of hyperkalemia?

Answer 358

Pointy T waves Prolonged QRS Prolonged PR 

Question 359

What is the diagnosis? 

Answer 359

Hyperkalemia! pointy T waves, prolonged QRS, PR Give IV Ca

Question 360

What are the congenital long QT syndromes?

Answer 360

LQTS1 - Triggered by exercise, swimming LQTS2 - triggered by auditory ques (doorbell) LQTS3 - triggered by sleep 

Question 361

What is the finding? 

Answer 361

Long QT Syndrome LQTS3 - found while sleeping

Question 362

What is this? 

Answer 362

Torsades de Pointes Causes sudden deaths in Long QT Syndromes when sustained Can be OK if occurs briefly

Question 363

What is Brugada Syndrome?

Answer 363

Inherited syndrome that is most common cause of sudden death in southeast asian countries EKG shows RBBB with downslowing ST segment elevation in the right precordial leads Pts die from Torsades de Pointes 

Question 364

What are you thinking? 

Answer 364

Brugada Syndrome - downsloping ST segment elevation in right precordial leads

Question 365

What is the shared defining feature of all categories of vasculitis?

Answer 365

Inflammation of blood vessel walls at least at some time during the course of the disease

Question 366

What are the two broad etiologic categories of vasculitis?

Answer 366

Infectious (direct invasion and proliferation in vessel walls by pathogens) Non-infectious (not known to be caused by pathogenic invasion)

Question 367

What are the vessels most frequently involved in polyarteritis nodosa (PAN)?

Answer 367

Renal vessels Leads to arterial hypertension and ischemic nephropathy with renal failure No glomerulonephritis

Question 368

What is Mucocutaneous Lymph Node Syndrome?

Answer 368

Sequellae associated with Kawasaki disease (medium vessel vasculitis) Seen in infants and young children 

Question 369

What is levocardia?

Answer 369

Heart to the left 

Question 370

What is dextrocardia?

Answer 370

Heart to the right 

Question 371

What is mesocardia?

Answer 371

Heart not left nor right 

Question 372

What defines the right atrium?

Answer 372

The atrium with the broad triangular-shaped appendage (right atrium appendage) Usually recieves connection from hepatic segment of IVC Coronary sinus always opens into the morphologically right atrium

Question 373

What defines the left atrium?

Answer 373

The atrium that is not the right atrium Flap valve of the foramen ovale is attached to its septal surface Has a smaller finger-like appendage

Question 374

What defines the tricuspid valve?

Answer 374

Valve that serves the morphologically right ventricle, regardless of its leaflet morphology Typically tri-leaflet valve with attachments of septal leaflet to septum via chordae

Question 375

What defines a mitral valve?

Answer 375

Defined as the valve that serves the morphologically left ventricle, regardless of its leaflet morphology (can be cleft and appear tricuspid) Typically has two leaflets, connected by chordae to two free wall papillary muscle groups

Question 376

What defines a right ventricle?

Answer 376

Heavy trabeculations Septal band Prominent septal attachments of the tricuspid valve Pyramidal shape Moderator band

Question 377

What defines a left ventricle?

Answer 377

Fine trabeculation Smooth septal surface Absent septal connections to mitral valve (generally) Prolate ellipsoidal shape

Question 378

What defines the pulmonary artery?

Answer 378

Great vessel that usually gives rise to branch pulmonary arteries (if present)

Question 379

What defines the aorta?

Answer 379

Great vessel which gives rise to at least one coronary artery and the aortic arch and its brachiocephalic vessels (though this may be interrupted)

Question 380

What is atrial situs solitus?

Answer 380

RA on the right and receives the hepatic IVC connection LA on the left, as are attachments of septum primum - flap valve of foramen ovale

Question 381

What is atrial situs inversus?

Answer 381

RA on the left and receives the left-sided hepatic IVC connection LA on the right, as well as attachments of septum primum

Question 382

What is atrial situs ambiguus?

Answer 382

Unclear - typically includes common atrium with multiple venous connection anomalies

Question 383

What is a d-looped ventricular loop?

Answer 383

Normal (Dextro-looping), but only for solitus atrial position in which the RV has developed to the right of the LV 

Question 384

What is a L-looped ventricular loop?

Answer 384

Inverted ventricular loop, wherein the morphologically right ventrile is to the left of the morphologically left ventricle. Normal only for situs inversus of the atria (left handed) 

Question 385

What is x-looped ventricular looping?

Answer 385

For cases where there is a single ventricle, it is impossible to figure out the ventricular situs or loop (catch-all)

Question 386

What are the characteristics of normally related great arteries?

Answer 386

Aorta arises in fibrous continuity with the anterior mitral leaflet (no conus separating aortic valve from mitral) Pulmonary valve is separated from tricuspid by subpulmonary muslce (conus) LV with aorta; RV with pulmonic Solitus: aortic valve to right and posterior of pulmonary valve Inversus: aorta is leftward and posterior to pulmonary

Question 387

What does D mean with respect to the position of the great arteries?

Answer 387

Aortic valve is rightward of the pulmonary valve

Question 388

What does A mean with regards to the malpositions of the great arteries?

Answer 388

Aortic valve is anterior to the pulmonary valve

Question 389

What does L mean with regards to the malpositions of the great arteries?

Answer 389

Aortic valve is leftward and anterior to the pulmonary

Question 390

What does P mean with respect to the malpositions of the great arteries?

Answer 390

Aortic valve is posterior to the pulmonary valve, irrespective of right-left position

Question 391

What is AV discordance?

Answer 391

Morphologically right atrium connects abnormally with the morphologically left ventricle Can be caused by solitus atria and L-looped ventricles or by inversus atria and d-looped ventricles

Question 392

What is V-A discordance?

Answer 392

When the morphologically left ventricle is aligned with the pulmonary valve Refers to the great arterial malpositions (Transposition of great arteries, TGA; double outlet right ventricle, DORV; double outlet left ventricle, DOLV, anatomically corrected malposition of the great arteries, ACM, aortic atresia   

Question 393

What does atresia mean?

Answer 393

"without an opening" Refers to valves that do not form well - have no opening

Question 394

What is the conotruncus?

Answer 394

Segment which joins the ventricle to the great artery

Question 395

Why are ventral septal defects not diagnosed until a few days after birth?

Answer 395

Pulmonary resistance takes a while to decrease to "adult" levels. Once this happens, though, blood will flow to least resistance (pulmonary)

Question 396

What is the tetralogy of Fallot?

Answer 396

Pulmonary stenosis Right Ventricular Hypertrophy Overriding Aorta Ventricular Septal Defect PROVe Cyanotic heart disease - Right to left shunting

Question 397

What is Rheumatic Fever?

Answer 397

Immunologic response to acute streptococcal pharyngitis (Group A strept) Cross-reactivity b/w antigen and structural glycoprotein found in heart, joints, connective tissues) Leads to chronic rheumatic valvular heart disease

Question 398

What are the Jones Critera useful for?

Answer 398

Diagnosis of Rheumatic Fever 2 major or 1 major and 2 minor; PLUS evidence of infection 

Question 399

How do you treat Rheumatic Fever??

Answer 399

Penicillin Anti-inflammatories (ASA, corticosteroids) Treat complications

Question 400

What is Mitral Stenosis?

Answer 400

Obstruction of LV **inflow** that prevents proper filling during **diastole** Normal MV area is 4-6 cm^2 Severe disease is \<2cm^2

Question 401

What is the normal mitral valve area?

Answer 401

4-6 cm^2

Question 402

What is severe mitral stenosis valve area?

Answer 402

\<2 cm^2

Question 403

What are etiologies of mitral stenosis?

Answer 403

Rheumatic heart disease - most common Infective endocarditis Mitral annular calcification Congenital

Question 404

What would you hear on auscultation of mitral stenosis?

Answer 404

Loud S1 Opening snap after S2, with diastolic murmur with pre-systolic accentuation 

Question 405

What are clinical manifestations of mitral stenosis?

Answer 405

Can be asymptomatic, but depends on degree of reduction of valve area Dyspnea, reduced exercise tolerance, fatigue Pulmonary congestion (orthopnea, paroxysmal nocturnal dyspnea) RV failure

Question 406

What does a shorter S2 to opening snap time indicate about mitral stenosis?

Answer 406

More severe disease Snap represents reachign maximally open aperture

Question 407

What are complications of mitral stenosis?

Answer 407

Pulmonary edema Pulmonary HTN Right heart failure A fibrillation Infective endocarditis Systemic thromboembolism

Question 408

What can you see on EKG in a patient with mitral stenosis?

Answer 408

Maybe A. Fibrillation Maybe LA enlargement and RV hypertrophy

Question 409

What do you see on chest x-ray in patients with mitral stenosis?

Answer 409

LA enlargement Signs of pulmonary congestion

Question 410

What do you see on echo in a patient with mitral stenosis?

Answer 410

Can assess mitral valve mobility, and area Can identify gradients and severity of disease

Question 411

How do you treat mitral stenosis?

Answer 411

Medicines do not prevent progression - useful for symptoms β-blockers, CCBs, digoxin control HR and prolong diastole Diuretics for fluid overload **Surgery** is definitive treatment for patients with symptoms or pulmonary HTN

Question 412

What are causes of mitral regurgitation?

Answer 412

Abnormalities of valve leaflets (Rheumatic heart disease, infective endocarditis, myxomatous degeneration) Abnormalities of mitral annulus (dilatation, calcification) Abnormalities of chordae tendinae (congenital, infective, trauma) Involvement of papillary muscles (CAD)

Question 413

What happens to LV/LA pressures in mitral regurgitation?

Answer 413


Question 414

How does the murmur in mitral regurgitation differ in acute vs chronic cases?

Answer 414

Acute - may not be holosystolic; is shorter and softer Chronic - holosystolic

Question 415

What are differences between acute mitral regurgitation and chronic mitral regurgitation?

Answer 415

Acute - normal LA size and compliance, increased LA pressure causes backup into pulmonary system (edema) Chronic - dilated LA, increased compliance; normal LA and pulmonary pressures with decreased CO 

Question 416

What are symptoms of mitral regurgitation?

Answer 416

Can be asymptomatic Palpitations Fatigue Dyspnea Paroxysmal Nocturnal Dyspnea Signs of RV failure

Question 417

What are clinical signs of mitral regurgitation?

Answer 417

Low, collapsing pulse Heaving apex Soft S1, loud P2 (pulmonary HTN) S3 sound Holosystolic murmur at apex that radiates to left axilla Increased murmor on expiration, handgrip, squatting (increase resistance)

Question 418

How do you treat actue mitral regurgitatioN?

Answer 418

Diuretics, nitroprusside (reduce afterload to increase cardiac output that goes forward) Balloon pump Surgery (this is an emergency)

Question 419

How do you treat chronic mitral regurgitation?

Answer 419

Vasodilators for HTN, LV systolic dysfunction MItral valve repair

Question 420

What can you see on EKG for a patient with mitral regurgitation?

Answer 420

LA enlargement, LV hypertrophy, A. Fib

Question 421

What can you see on chest x-ray of mitral regurgitation?

Answer 421

Chronic - cardiomegaly (LV, LA) Acute - interstitial edema

Question 422

What can you see on echocardiogram for a patient with mitral regurgitation?

Answer 422

Estimate LA, LV size and function Assess valve structure - Definitive for diagnosis

Question 423

What is mitral valve prolapse?

Answer 423

Autosomal dominant inherited disease that is associated with Marfan Syndrome, Ehler-Danlos syndrome Pathophysiology includes enlarged valvular leaflets that prolapse into left atrium during systole Can be asymptomatic, have chest pain or palpitations Midsystolic click, late systolic murmur Decreased murmur by squatting, increased by valsalva, standing, handgrip

Question 424

What are clinical signs of mitral valve prolapse?

Answer 424

Midsystolic click, late murmur Heard best at apex Decreased murmur with squatting. Increased murmur with valsalva, standing, handgrip

Question 425

What can you see on echo for mitral valve prolapse?

Answer 425

Confirm the diagnosis

Question 426

How do you treat mitral valve prolapse?

Answer 426

Usually benign Monitor to ensure no development of mitral regurgitation

Question 427

What are complications associated with mitral valve prolapse?

Answer 427

Rupture of choardae can cause mitral regurgitaiton, pulmonary edema Infective endocarditis Thromboembolism Arrhythmias