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cardio amboss Flashcards

1
Q

what happens to the hemodynamic parameters in septic shock

A

pathologic vasodilation caused by inflammation results in reduced systemic vascular resistance, as well as decreased CVP and PCWP. The decrease in the preload and the afterload will cause an increase in heart rate and thus an increase in the cardiac output
warm and flushed skin

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2
Q

what happens to the hemodynamic parameters in neurogenic shock.

A

there is a decrease in all of the parameters

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3
Q

what happens to the hemodynamic parameters in hypovolemic shock

A

There is an increase in SVR. a decrease in CVP and PCWP as the blood volume is reduced. There is also a decrease in the CO as there is less blood return to the heart due to reduced stroke volume
Cold and clammy skin

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4
Q

what happens to the hemodynamic parameters in cardiogenic shock

A

There is a decrease in the CO. There is an increase in SVR due to sympathetic response of poor output. Furthermore PCWP and CVP both increased due to the lack of forward flow from the heart

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5
Q

what is the diagnosis in an ECG showing no P waves but tachycardia

A

this is AV node reentrant tachycardia

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6
Q

what is the best first treatment for paroxysmal supreventricular tachycardia

A

vagal maneuvers

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7
Q

what is second line treatment for PSVT

A

adenosine

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8
Q

can you use procainamide for pSVT

A

yes, as second line therapy

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9
Q

premature ventricular contractions are what

A

brief episodes of V tach caused by lack of sleep, alcohol, caffeine, nicotine

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10
Q

what is the treatment for PVC in a young person that has been staying up late studying in college with no drug use

A

observation and rest

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11
Q

what are PVC usually described as by the patient

A

feels like my heart is skipping a beat

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12
Q

what is the treatment for ventricular tachycardia

A

synchronized cardioversion NOT defibrillation

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13
Q

what are beck’s triad and what does it indicate

A

muffled heart sounds, hypotension and JVD

cardiac tamponade

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14
Q

what is a physiological cause of cardiac tamponade

A

diabetes can cause renal insufficiency and then accumulation of urea. urea can cause a pericardial effusion

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15
Q

what is the treatment for pericardial tamponade

A

pericardial centesis

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16
Q

if a patient is found to be septic with strep. gallolyticus what should be a follow up test

A

a colonoscopy to assess for colorectal cancer as this is a common GI bug. there is a well known link between strep gallolyticus/GI cancer and bacterial endocarditis

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17
Q

what is the initial treatment and the follow up treatment for rheumatic heart disease with carditis but no valvular damage

A

initially treat with aspirin and penicillin then follow up Intramuscular benzathine penicillin every 4 weeks for 10 years (or until 21 years of age, whichever is longer) is recommended for secondary prophylaxis of recurrent acute rheumatic fever in patients with manifestations of carditis but no permanent valvular damage.

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18
Q

what are the jones criteria

A

Major criteria
Arthritis (migratory polyarthritis involving primarily the large joints)
Carditis (pancarditis, including valvulitis)
Sydenham chorea (CNS involvement)
Subcutaneous nodules
Erythema marginatum

Minor criteria
Arthralgia
Fever
↑ Acute phase reactants (ESR, CRP)
Prolonged PR interval on electrocardiogram
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19
Q

what is the most common cause of viral myocarditis in children

A

coxsackie B virus

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20
Q

what are the echo findings for viral myocarditis

A

Left ventricular dilation and (usually global) hypokinesis

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21
Q

what is the presentation of viral myocarditis

A

Subacute onset of dyspnea, chest pain, jugular distention, and inspiratory crackles on lung auscultation is consistent with heart failure, most likely secondary to myocarditis.

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22
Q

what are the lab findings for myocardiitis

A 
↑ Cardiac enzymes (CK, CK-MB, troponin T)
↑ ESR (and CRP)
Leukocytosis
↑ BNP
Virus serology
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23
Q

what type of myopathy is viral cardiomyopahty

A

dilated

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24
Q

what does pericarditis put you at risk for

A

cardiac tamponade due to effusion

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25
Q

Antimicrobial prophylaxis for endocarditis is recommended for

A

high-risk patients (e.g., patients with prosthetic heart valves, a history of infectious endocarditis, or an unrepaired cyanotic congenital heart defect) undergoing procedures that often result in bacteremia with common pathogens of infective endocarditis.

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26
Q

what is the most commonly used antibiotic for prophylaxis

A

amoxicillin

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27
Q

do patients have to stop their anticoagulants for dental procedures

A

no

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28
Q

what is the most common cause of prosthetic valve endocarditis, when is it of particular concern

A

Staphylococcus epidermidis

and is of particular concern in the first year after valve placement surgery.

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29
Q

what is the treatment for staph epidermidis endocarditis

A

IV combination therapy with nafcillin and rifampin can be used for at least 6 weeks in combination with gentamicin for 2 weeks to treat S. epidermidis prosthetic valve endocarditis, which requires a longer duration of therapy than native valve endocarditis. Surgical valve replacement may be required.

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30
Q

what is the most likely sequalae of drug-use infective endocarditis

A

pulmonary embolus

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31
Q

are splinter hemorrhages found in drug-use induced infective endocarditis

A

no. they are found in left0-sided endocarditis

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32
Q

Patients with left-sided (aortic valve or mitral valve) endocarditis more commonly present with

A

emboli to the retina (Roth spots), extremities (Janeway lesions, Osler nodes, splinter hemorrhages), kidney, brain, and spleen.

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33
Q

what is the most common cause of bacterial endocarditis in all groups

A

staph aureus

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34
Q

what is the most common cause of bacterial endocarditis in people with damaged heart valves, such as bicuspid aortic valve

A

strep sanguinis

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35
Q

what at the HACEK organisms are why are they important

A

A group of fastidious organisms that are normally part of the oral and pharyngeal flora. Members of this group include species of the Haemophilus genus, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae. HACEK organisms can cause infective endocarditis.

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36
Q

what is the treatment for HACEK endfocarditis

A

IV ceftriaxone

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37
Q

what are the duke criteria

A

two major criteria, one major and three minor criteria, or five minor criteria.

Major criteria include: (1) two separate blood cultures positive for typical pathogens and (2) evidence of endocardial involvement in echocardiography.

Minor criteria include: (1) underlying heart disease or IV drug abuse, (2) fever, (3) signs of embolism, (4) immunologic findings (e.g., Osler nodes), (5) Roth spots, and (6) positive blood culture for an atypical pathogen.

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38
Q

what is coagulase negative staph

and where does it usually come from to cause disease

A

staph epidermidis

infected peripheral venous catheter

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39
Q

pulsus paradoxus

A

A drop in systolic blood pressure > 10 mm Hg during inspiration is a sign observed in pathologies such as severe asthma, tension pneumothorax, constrictive pericarditis, and moderate and severe cardiac tamponade. I

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40
Q

what does an S3 indicate

A

An S3 gallop is due to a sudden deceleration of blood flow from the left atrium into the left ventricle

Can be normal variant in young, healthy individuals, but can be also associated with congestive heart failure, dilated cardiomyopathy, and/or volume overload.

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41
Q

aortic regurgitation

A

A valvular disease characterized by incomplete closure of the aortic valve, causing reflux of blood from the aorta into the left ventricle during diastole. On auscultation, characterized by S3 and a high-pitched, decrescendo, early diastolic murmur.

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42
Q

what is the treatment for acute mesenteric ischemia

A

balloon angioplasty and stenting

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43
Q

Mitral valve regurgitation presents as a

A

high-frequency, holosystolic blowing murmur that may radiate to the axilla and is best heard at the apex.

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44
Q

Mitral valve prolapse (MVP) is how common and presents how

A

the most common valvular abnormality in the US and is usually asymptomatic, as in this patient. It typically presents as a high-frequency, mid-systolic click combined with a high-frequency, mid-to-late systolic murmur heard best at the apex

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45
Q

what is the next step if claudication/PAD is assumed

A

ankle brachial index

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46
Q

Reduced ABI values between what values indicate mild to moderate PAD with claudication and below those values indicates what

A

0.4–0.9 whereas values below 0.4 correlate to severe PAD with resting pain and/or gangrene.

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47
Q

what causes a plopping heart murmur

A

cardiac myxoma

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48
Q

does tamsulosin cause orthostatic hypotensino

A

rarely. it has the most specificity for the prostate

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49
Q

what causes a systolic murmur at the apex

A

mitral regurgitation

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50
Q

what can cause a new onset mitral regurg

A

MI subsequent rupture of the papillary muscles.

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51
Q

what can cause a new onset LBBB

A

MI

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52
Q

cardiogenic shock

A

hemodynamically unstable patient with a history of atherosclerotic disease has a combination of pulmonary edema, jugular venous distention, and cold, clammy skin,

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53
Q

what is the alternative to CT angio for diagnosing aortic dissection

A

trans esophageal echo

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54
Q

what is a contraindication to CT angio for diagnosing aortic dissection

A

renal insufficiency

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55
Q

cardiac contusion can cause what

A

cardiogenic shock

arrhythmias

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56
Q

if the well’s score is above 4 what is the next step

A

begin heparin. then CT angio

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57
Q

what is correct management for a pseudoaneurysm

A

ultrasound guided thrombin injection

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58
Q

what is the strongest risk factor for development and rupture of AAA

A

smoking

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59
Q

what is the best test for diagnosing acute limb ischemia

A

digital subtraction angiography

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60
Q

what is Digital subtraction angiography

A

An imaging method that involves taking a series of x-rays at timed intervals while injecting IV contrast. The pre-contrast images are then digitally subtracted from the images taken with IV contrast to visualize the artery of interest. This test has the highest diagnostic accuracy in testing for peripheral arterial disease and allows real-time visualization of the patient’s arteries.

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61
Q

what is the presentation of mitral valve stenosis

A

elevated left atrial pressure, causing both left atrial dilatation (resulting in atrial fibrillation) and an increase in pulmonary arterial pressure to overcome the increased left heart pressure (pulmonary hypertension). Over time, this will lead to pulmonary vascular remodeling, increased pulmonary vascular resistance, an S2 split, and right ventricular hypertrophy (as indicated by the right axis deviation) to compensate. RV failure eventually leads to characteristic signs of right heart failure (jugular venous distention and pitting edema).

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62
Q

features of mitral stenosis murmur and consequence s

A

(opening snap and diastolic murmur along with atrial fibrillation

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63
Q

constrictive pericarditis,

A

dyspnea, ascites (distended abdomen, shifting dullness), and peripheral edema has a positive Kussmaul’s sign (increase in jugular venous pressure during inspiration) and a pericardial knock (early diastolic sound over the left sternal border). calcifications on chest x-ray and an exaggerated variation of blood flow with respiration on echocardiography indicate which may be confirmed by a positive square root sign on cardiac catheterization (dip-and-plateau waveform).

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64
Q

the fixed (no change with respiration), widely split S2 being the most specific.

A

atrial septal defect (ASD)

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65
Q

ASD presents how

A

systolic ejection murmur left upper sternal border and mid-diastolic murmur along the lower left eternal border

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66
Q

when does rib notching show up on X ray and what is the diagnosis

A

coarctation and not until 5

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67
Q

what is the diagnosis if someone has syncope while tightening a tie

A

carotid sinus hypersensitivity

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68
Q

what is the cause of VSD intracardiac shunting as the child gets older

A

As the child gets older they will start to have sweating and cyanosis while feeding. this is due to decreased pulmonary vascular resistance causing the left to right shunt as the child gets older.

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69
Q

what is the presentation of DiGeorge syndrome

A

micrognathia, cleft palate, a broad nasal bridge, a short philtrum, and low-set ears
truncus arteriosus defect (single overriding vessel seen on echocardiography). Conotruncal abnormalities (e.g., tetralogy of Fallot or persistent truncus arteriosus)
Ventricular septal defect (VSD)
Atrial septal defect (ASD)
impaired development of the parathyroid glands, leading to hypoparathyroidism and hypocalcemia,
thymus aplasia

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70
Q

ebsteins anomaly.

A

This anomaly typically leads to right atrial enlargement, elongation of the tricuspid valve leaflets, and tricuspid regurgitation, Displaced valve reduces the ventricular volume → regurgitation into the right atrium (tricuspid regurgitation) → atrial dilatation; poorly functioning, small RV (atrialization of the right ventricle); functional pulmonary valve atresia ; obstruction of the RV outflow by the large, sail-like anterior leaflet → blood flows through the patent foramen ovale (right-to-left shunt) → cyanosis

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71
Q

what is the most common heart defect in down syndrome

A

atrioventricular septal defect

endocardial cushion defects.

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72
Q

treatment for endocardial cushion defects in downs

A

Diuretics, inotropic agents, and ACE inhibitors are usually given to improve cardiac function. Definitive treatment consists of complete surgical repair.

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73
Q

what are the associated causes of endocardial defects

A

down sydnrome, maternal diabetes and obesity

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74
Q

what is a endocardial cushion defect

A

Defect of atrioventricular valves (i.e., mitral and tricuspid valves) as well as the atrial septum and/or ventricular septum
Complete form: ASD and VSD, common AV valve
Partial form: only ASD and minor atrioventricular valve abnormalities
where there is literally only one atrio-ventricular valve and a VSD and ASD; so no tricuspid and mitral, just one valve

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75
Q

what is the management for a small VSD in newborn

A

outpatient followup. they usually close spontaneously

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76
Q

what do you NOT give to a baby with VSD

A

prostaglandin; this would increase the left to right shunting and exacerbate the symptoms of the VSD

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77
Q

what is the management of an ASD/PFO

A

no intervention

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78
Q

what is a venous hum

A

common benign finding in childhood caused by turbulence in the jugular vein. characteristically disappears when the child flexes the neck or increases the pressure in the jugular.

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79
Q

what is tetralogy of fallot

A

(a) Pulmonary stenosis
(b) Right ventricular hypertrophy
(c) Ventricular septal defect (VSD)
(d) An overriding aorta (above the VSD)

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80
Q

what determines the degree of cyanosis in TOF

A

The degree of right ventricular outflow tract obstruction
THE FUCKING DEGREE OF RIGHT-SIDED. RIGHT-SIDED RIGHT-SIDED OUTFLOW TRACT OBSTRUCTION
The more obstructed the right side, the more deoxygenated blood will flow out the left side

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81
Q

what is tricuspid valve atresia

A

cyanotic neonate, an imperforate atrioventricular septum in the right side. blood is unable to pass from the right atrium (RA) to the right ventricle (RV). Consequently, the RV is almost always hypoplastic. Venous blood, therefore, passes from the RA via the atrial septal defect (ASD) to the left atrium (LA), where it mixes with oxygenated blood from the lungs. The mixed blood is pumped from the left ventricle (LV) into the systemic circulation (resulting in cyanosis) and pulmonary circulation (via a patent ductus arteriosus). LV hypertrophy occurs because the LV is single-handedly pumping blood through both the pulmonary and systemic circulation.

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82
Q

What is the cause of cyanosis with crying and playing and failure to thrive

A

tet spell.

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83
Q

what is likely to be found with TOF

A

right axis deviation.

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84
Q

what’s a common heart defect of marfans and how does it present

A

aortic regurgitation.
diastolic murmur, water hammer pulse

also find mitral valve prolapse

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85
Q

what is the treatment for WPW with tachycardia

A

procainamide

86
Q

do you give beta blockers in WPW

A

no. it can cause reinforcement of the alternate path

87
Q

Hypertrophic cardiomyopathy (HCM) typically presents with a

A

systolic ejection murmur caused by left ventricular outflow tract obstruction (LVOT). Rapid squatting increases left ventricular preload, decreasing the LVOT and softening the intensity of the murmur, whereas the Valsalva maneuver decreases preload, which exacerbates obstruction and makes the murmur louder.

88
Q

Bidirectional blood flow in the great saphenous vein on duplex ultrasonography, rather than the normal unilateral blood flow from the superficial to the deep system, is diagnostic of

A

chronic venous insufficiency.

89
Q

what is the most common cause of sudden death in athletes under the age 30

A

HOCM

90
Q

what is an important diagnostic feature of HOCM

A

A systolic ejection murmur that increases with valsalva maneuver and standing and decreases with hand grip, squatting, or lying down can be an important clue toward the diagnosis.

91
Q

what drugs are contraindicated in HOCM

A

Positive inotropic and afterload-reducing or preload-reducing drugs (e.g., digitalis, glyceryl trinitrate, calcium channel blockers of the dihydropyridine class, ACE inhibitors) are contraindicated in cases of obstructive hypertrophic cardiomyopathy!

92
Q

what is the most common type of cardiomyopathy

A

dilated

93
Q

what is the presentation of hereditary angioedema

A

A deficiency or dysfunction of C1 inhibitor results in elevated levels of bradykinin, which is as a strong vasodilator. Hereditary angioedema is characterized by recurrent episodes of swelling without urticaria or pruritus that primarily affects the skin and mucosa of the gastrointestinal and upper respiratory tracts.

94
Q

The treatment of hereditary angioedema involves

A

rapid administration of purified C1-INH concentrate or bradykinin B2 receptor antagonists (icatibant) and close monitoring for laryngeal involvement (signs of dyspnea, respiratory stridor) with immediate airway management if such signs occur.

95
Q

what treatments are ineffective against hereditary angioedema

A

Glucocorticoids and antihistamines are ineffective in treating this type of angioedema.

96
Q

where is central venous hum found

A

more commonly on the right side

97
Q

what are the cardiac specific beta blockers

A

atenolol, betaxolol, bisoprolol, esmolol, acebutolol, metoprolol, and nebivolol

98
Q

what drugs are contraindicated in cocaine induced coronary syndrome

A

propanolol

99
Q

what is the presentation of cocaine induced coronary sydnrome

A

inverted t waves in several or all leads, cocaine intox, angina.

100
Q

Can labetalol be used for cocaine induced coronary syndrome

A

yes. has both alpha- and beta-antagonist effects and has been shown in studies to be safe and effective in the management of cocaine use.

101
Q

what is the presentation of dilated cardiomyopathy

A

palpitations, exertional dyspnea, hypoxia, increased jugular venous pressure, bibasilar crackles, an S3 gallop, displaced point of maximum impulse, and lower extremity edema. These findings suggest dilated cardiomyopathy.

102
Q

what is the diagnosis in someone with hypertension ischemic heart disease and heart failure (systolic or diastolic dysfunction)

A

systolic dysfunction

103
Q

what antibiotic class can cause torsades

A

macrolide

104
Q

what is the treatment for torsades if the mag level is normal

A

mag sulfate. doesnt matter what the level is

105
Q

whaat is the treatment for A fib in hemodynamically unstable person

A

cardioversion

106
Q

what is the treatment of a fib is hemodynamically stable

A

diltiazem or esmolol

107
Q

when considering treatment for a fib what is the first question

A

is this person hemodynamically stable or not

108
Q

what I the treatment of a fib in someone with hyperthyroidism

A

antithyroid drugs usually spontaneously converts the person to normal rate and rhythm

109
Q

Patients with a CHA2DS2-VASc score ≥ 2

A

increased risk for ischemic events and should be anticoagulated

110
Q

treatment for pulseless VTACH

A

chest compressions and defibrillation

111
Q

one of the early complications of myocardial infarction (MI). It can occur in up to 30% of patients after MI within the first 48 hours.

A

Ventricular tachycardia

112
Q

The ECG shows tachycardia with no clear P waves (the P waves are actually hidden within the QRS complexes).

A

This suggests atrioventricular nodal reentrant tachycardia (AVNRT), a supraventricular tachycardia caused by a reentry circuit in the AV node.

113
Q

If vagal maneuvers are ineffective in terminating AVNRT, intravenous administration of is the next step in management.

A

adenosine

114
Q

second line therapy for AVNRT

A

diltizem and beta blockers

115
Q

can trigger episodes of AVNRT.

A

Stress, alcohol, and caffeine

116
Q

if you want to start warfarin what screeen needs to be performed

A

CHADVASC

117
Q

what is the management to atrial premature beats

A

you can get an echo or holter monitor reading.

beta blockers and antiarrhythmics can be used, but the mainstay is trigger avoidance (caffeine, stress, smoking alcohol)

118
Q

whaat is the presentation of thromboangitis obliterans and what is the treatment

A

younger person that smokes with ulcers, reduced blood flow and moderate ABIs. stop smoking idiot

119
Q

what is the treatment for V fib

A

epi and compressions. 2 rounds.

then give either lidocaine or amiodarone

120
Q

what is the first step in managing V fib

A

defibrillation or unsynchronized cardioversion.

121
Q

what is the test of choice for someone with typical angina

A

nuclear stress test either exercising or pharmacological

122
Q

post surgery what is the test of choice for stress test

A

pharmacological unless the person can undertake 85% of their normal activity level

123
Q

if someone just had an infarct and now is suspected of a new infarct, what is the lab that will be most specific for diagnosing and why

A

CKMB.
specific for myocardial injury, peak 12–24 hours after an infarction, and take only 2–3 days to normalize.

trops would not be useful at this point because they would not have normalized from the original MI

124
Q

first degreee heart block

A

prolonged PR >200

125
Q

mobitz i

A

progressively elongating PR

126
Q

Mobits II

A

nonconducting P wave without warning
an unstable bradyarrhythmia that can progress to third-degree heart block and death, and therefore requires immediate treatment
usually it will be patterned, for example, every third beat has a dropped QRS, but there is no warning as PR prolongation

127
Q

stage 3 heart block

A

disconnected P and QRS

128
Q

treatment Mobits II

A

pacing

129
Q

coronary steal syndrome is what

A

A phenomenon in which long-standing coronary artery disease requires maximal coronary arterial dilation distal to the stenosis to maintain normal function. Administration of vasodilators (e.g., dipyridamole) causes dilation of normal vessels, thereby resulting in shunting of blood to well-perfused myocardium. Subsequent myocardial ischemia downstream of the pathologically dilated vessels manifests as angina.

130
Q

what is the treatment for PAD and when do we give it

A

cilostazol
It is indicated in patients with lifestyle-limiting intermittent claudication only after 3 months of supervised graded exercise therapy.

131
Q

what are the most common SE of statins

A

elevated transaminases

upwards of 3%

132
Q

if a patient has myopathy from simvastatin what is the management

A

discontinue and then start another statin 3 weeks later

usually resolves 2-4 weeks

133
Q

what other anti cholesterol drugs are associated with myopathy

A

fibrates

134
Q

what can be given if niacin causes redness and itchiness

A

Niacin upregulates prostaglandin synthesis in the skin by activating a G-protein coupled receptor in keratinocytes and dermal Langerhans cells. These prostaglandins cause cutaneous flushing, which is sometimes accompanied by paresthesias such as tingling or itching. The flushing typically begins within an hour of niacin intake. NSAIDs (e.g., aspirin, ibuprofen) taken 30–60 minutes before niacin can prevent flushing by inhibiting prostaglandin synthesis.

135
Q

what is the next step for pulseless electrical activity

(even if on the rhythm strip there is rhythm

A

epinephrine (given as 1 mg IV, and repeated every 3–5 minutes) and CPR.

136
Q

what is the normal QTc

A

should be less than 440

137
Q

what is the treatment for long QT syndrome

A

Beta-blockers such as propranolol are the mainstay of therapy for congenital long QT syndrome.

138
Q

what is the second line therapy for long QT

A

stellectomy or implantable defibrillator

139
Q

what is long QT and what are the complications

A

A congenital or acquired heart condition in which the QT interval (i.e. ventricular depolarization and repolarization) is prolonged. Most patients remain asymptomatic until they present with syncope, seizures, or life-threatening arrhythmias including torsades de pointes and ventricular fibrillation.

140
Q

what does mitral valve regurgitation do to the left ventricle

A

left ventricular hypertrophy

141
Q

what does long standing mitral valve regurgitation look like on ECG

A

t wave inversions

142
Q

what do the hemodynamic parameters look like for Mitra regurgitation

A

causes decreased stroke volume (↓ cardiac output), increased left ventricular end-diastolic pressure (due to ↑ end-systolic and end-diastolic volume), and increased pulmonary artery pressure (blood backs up into lungs, causing pulmonary edema).

143
Q

what are the ausculatory findings for aortic stenosis

A

crescendo-decrescendo systolic murmur. A delayed pulse supports this diagnosis.

144
Q

what are the symptoms of aortic stenosis

A

If stenosis at the aortic valve is severe enough, it obstructs blood flow, thereby preventing an increase in cardiac output to maintain blood pressure during exertion, which leads to hypotension, decreased cerebral blood flow, syncope, dizziness, dyspnea, and angina pectoris.

145
Q

what is S2

A

closure of the aortic and pulmonic valves

146
Q

This patient has an early diastolic decrescendo murmur that is heard best on the left sternal border and, therefore, suggests

A

aortic regurgitation.

147
Q

what is S1

A

closure of the mitral and tricuspid valves

148
Q

if a murmur occurs after S2 is it diastolic or systolic

A

by definition it is diastolic because at that point the aortic and pulmonic valves have clsoed

149
Q

Carotid endarterectomy (CEA) is indicated for

A

asymptomatic carotid artery stenosis that is ≥ 80% in patients with a periprocedural risk of stroke ≤ 3% who have a life expectancy ≥ 5 years. CEA may also be considered in highly selected asymptomatic patients with 60–79% stenosis,

150
Q

In developed countries, it is the most common cause of mitral valve degeneration and subsequent mitral valve prolapse.

A

Myxomatous degeneration is caused by the accumulation of dermatan sulfate within the connective tissue of the mitral valve

151
Q

This patient’s diastolic murmur at the fifth intercostal space and opening snap indicate

A

mitral stenosis,

152
Q

mitral stenosis,which causes an

A

increase in left atrial pressure (and ↑ PCWP) and a backup of blood into lungs. The volume overload eventually causes symptoms of cardiogenic pulmonary edema, which explain this patient’s orthopnea, hemoptysis, and crackles.

153
Q

is the first-line treatments for Dressler syndrome.

A

High-dose aspirin

154
Q

what are the tests for diagnosis and source of acute limb ischemia

A

diagnosis: digital subtraction angiography
source: echo

155
Q

when you see cholesterol emboli ischemia in the lower legs what should you be thinking

A

watch out for kidney injury

156
Q

what therapy should people with PAD be on

A

Clopidogrel reduces the risk of ischemic stroke, myocardial infarction, and vascular death in patients with symptomatic PAD. Other antiplatelet agents, including aspirin and ticagrelor, also decrease morbidity and mortality

157
Q

Digoxin is a
that acts on what
and does what
what SE

A

cardiac glycoside with inotropic and antiarrhythmic properties used in patients with heart failure and specific supraventricular tachyarrhythmias (e.g., atrial fibrillation). It primarily acts by blocking the Na+/K+ ATPase channel, resulting in decreased Na+/Ca2+ antiporter activity and increased inotropy. Digoxin also increases vagus nerve activity, which has a negative chronotropic effect and leads to PR prolongation with possible AV block.

158
Q

what drug can predispose to digoxin toxicity

A

spironolactone

159
Q

Digoxin has a narrow therapeutic index, and its concentration can be affected by many factors (e.g., impaired renal function). Digitalis toxicity typically presents with

A

nausea, vomiting, diarrhea, abdominal pain, weakness, and blurry vision.

160
Q

what is an esophageal complication of mitral stenosis

A

esophageal compression if the atria becomes enlarged enough

161
Q

what’s the presentation of beta blocker OD

A

Bradycardia, hypotension, wheezing, confusion, hypoglycemia, and prolonged PR intervals strongly suggest severe beta blocker intoxication.

162
Q

what is the antidote for beta blocker oD

A

First line therapy is atropine and IVF, then glucagon

163
Q

Dietary Approaches to Stop Hypertension

A

A dietary pattern promoted by the United States Department of Health and Human Services to prevent and control hypertension. The plan focuses on a diet rich in fruits, vegetables, whole grains, low-fat dairy foods, but also includes meat, fish, poultry, nuts and beans. The intake of sugar-sweetened foods and beverages, red meat, and added fats (especially saturated fat and cholesterol) should be limited.

164
Q

Since hypertension is an asymptomatic and insidious disease with several complications, an evaluation should be performed to assess the extent of end-organ damage once the diagnosis has been established.
what tests should be performed on people with newly diagnosed HTN

A

Electrocardiogram (ECG) should be done in all newly diagnosed hypertensive patients to look for early electrical changes associated with hypertensive heart disease (e.g., left ventricular hypertrophy, left atrial enlargement) or concomitant heart disease (e.g., coronary artery disease, arrhythmias).
serum electrolytes, creatinine, lipids, TSH, and fasting glucose

165
Q

what test should be performed when pericardial effusion/tamponade is suspected

A

treansthroacic echocardiogramp

166
Q

Preceded by an episode of flu-like symptoms, this patient’s history of chest pain that increases with respiration and decreases while sitting up is suggestive of

A

acute pericarditis. This patient most likely has cardiac tamponade as a complication of acute pericarditis. Cardiac tamponade can occur if increased amounts of inflammatory fluid are secreted into the pericardial space, compressing the cardiac chambers. This leads to decreased ventricular diastolic filling and decreased cardiac output. Other common causes of cardiac tamponade include aortic dissection and chest trauma.

167
Q

what should patients discontinue 12-24 hours before a stress test

A

coffee/methylxanthines

168
Q

what should patients do 24-48 before stress test

A

discontinue Beta blockers (e.g., metoprolol), calcium channel blockers (e.g., amlodipine), and nitrates can reduce the sensitivity of cardiac exercise stress testing as a result of their antianginal activity.

169
Q

This patient presents with dyspnea, evidence of right-sided heart failure (peripheral edema, JVD, split S2), and pronounced central pulmonary arteries, all of which are strongly suggestive of

A

pulmonary hypertension, likely related to her history of drug abuse. Correct diagnosis is imperative, as treatment options vary between types of pulmonary hypertension.

170
Q

what is associated with pulmonary hypertension

A

cocaine and methamphetamine usage

171
Q

mitral valve regurg

A

fatigue, exertional dyspnea, paroxysmal nocturnal awakening, dry cough, palpitations, and bibasilar rales, suggesting left-sided heart failure. The auscultation findings reveal a high-frequency, holosystolic blowing murmur that radiates into the axilla and is heard best at the apex, here the midclavicular 5th left intercostal space (ICS)

172
Q

what’s the cause of infective endocarditis in a person with colon cancer

A

enterococcus

gallolyticus

173
Q

obstructive sleep apnea (OSA). Typical features of this disease include
and secondary what

A

nocturnal snoring, morning headaches, and poor concentration, as seen in this patient. Nocturnal apneic episodes in individuals with OSA result in hypercapnia, which, in turn, causes an increased sympathetic response that leads to secondary hypertension.

174
Q

Verapamil inhibits

A

cardiac calcium channels and can lead to PR interval prolongation and first-degree AV block

175
Q

PR interval

A

120 – 200 ms (0.12-0.20s)

176
Q

typically involved in the pathogenesis of atrial fibrillation.

A

Automatic depolarizing foci near the pulmonary vein are

177
Q

Acquired prolongation of the QT interval can be caused by certain medications or electrolyte imbalances

A

(e.g., amiodarone, methadone, ondansetron) or (e.g., hypokalemia, hypomagnesemia, and hypocalcemia).

178
Q

what can cause bouts of polymorphic V tach

A

QTc prolongation

179
Q

diastolic decrescendo murmur heard best along the left sternal border, widened pulse pressure (> 30–40 mm Hg), and head nodding in synchrony with a heart beat (de Musset sign) indicate

A

aortic regurgitation (AR).

180
Q

what is myxomatous valve degeneration

A

MVP

181
Q

what can amoldipine cause

A

peripheral edema, which is not dangerous but can be bothersome

182
Q

Can furosemide be used for CCB-induced edema

A

no

183
Q

what is used to treat CCB-induced peripheral edema

A

ACE or ARB

184
Q

is the most effective method to reduce blood pressure in obese patients

A

Weight loss. Studies have shown a reduction of systolic blood pressure of up to 20 mm Hg for every 10 kg of weight loss.

185
Q

Patients with a suspected asymptomatic abdominal aortic aneurysm (AAA) should undergo

A

abdominal ultrasonography to confirm the diagnosis and evaluate the extent of disease, including size of the aneurysm, presence of a blood clot, and presence of comorbid iliac artery aneurysms.

186
Q

Elective surgical repair of an abdominal aortic aneurysm (AAA) is indicated

A

in asymptomatic AAA ≥ 5.5 cm in diameter, rapid expansion (defined as > 1 cm per year), a symptomatic AAA of any size (as these are most likely to rupture), and saccular aneurysm of any size.

187
Q

what is the treatment for HCM

A

beta blockers such as metoprolol and septectomy if refractory

188
Q

what reduces the murmur of HCM

A

grabbing something with the hand

189
Q

USPSTF recommendations for AAA monitoring

A

The USPSTF recommends that men 65–75 years of age who are current or former smokers should receive a one-time screening with ultrasonography for an abdominal aortic aneurysm. Ultrasonography can determine the presence and size of an aneurysm, as well as the presence of a blood clot in an aneurysm.

190
Q

what is the main reason that nitro relieves angina

A

Decreased end-diastolic pressure (i.e., preload) reduces myocardial wall tension and therefore improves myocardial perfusion.

191
Q

Life-threatening hypotension may occur if nitroglycerin is taken within 24 hours of a

A

PDE-5 inhibitor such as sildenafil.

192
Q

when does radiation induced cardiac toxicity occur

A

within the first year

193
Q

dilated cardiomyopathy often occurs concomittantly with what

A

tachycardia
Supraventricular tachyarrhythmia can both lead to and result from dilated cardiomyopathy, and determining which condition came first can be difficult.

194
Q

what inreases survival in CHF patients

A

Eplerenone is an aldosterone receptor antagonist associated with improved survival in patients with CHF NYHA class II to IV, EF <35%, and/or post-MI (

195
Q

what is the cause of radiation pericarditis

A

neutrophilic infiltration of the pericardium

196
Q

is the standard of care for all patients after reperfusion therapy

A

Long-term dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 receptor inhibitor (e.g., clopidogrel, prasugrel, ticagrelor)

197
Q

what drug can reduce the frequency of angina symptoms

A

Metoprolol is a β1-selective adrenergic receptor blocker used as first-line therapy to reduce the frequency of anginal episodes and improve exercise tolerance in patients with stable ischemic heart disease.

198
Q

what are the SE of daunorubicin

A

significant left ventricular dysfunction

199
Q

what are first line therapies for controlling stable a fib

A

beta blockers and CCB. CANNOT USE BETA BLOCKERS WITH COPD or ASTHMA. this can cause bronchoconstriion

200
Q

PE is usually preceded by deep vein thrombosis (DVT), which in the vast majority of cases (≥ 90%) occurs in the

A

iliac vein and other proximal deep veins of the lower extremities (e.g., femoral and popliteal vein).

201
Q

patient with ST segment elevation on ECG and elevated troponin T was correctly started on unfractionated heparin, dual antiplatelet therapy (aspirin and ticagrelor), and sublingual nitroglycerin for his STEMI.

A

He would also benefit from early initiation of a high-dose statin such as atorvastatin.

202
Q

when is nitroglycerin contraindicated

A

when right sided heart is involved hypotension, bradycardia, or recent use of phosphodiesterase inhibitors.

203
Q

when and why is morphine contraindicated in MI

A

it reduces preload by inducing venous dilation; therefore, it is contraindicated in right ventricular infarction, which is preload-dependent.

204
Q

what does ventricular infarct sound like on auscultation

A

An atrial gallop (S4) results from atrial contraction against a stiff ventricle. It is frequently heard in the acute phase of an MI because of impaired relaxation of the ischemic left ventricle.

205
Q

Interventricular septum rupture typically occurs and presents how

A

3–5 days after myocardial infarction. It manifests with sudden onset hemodynamic instability (hypotension, tachycardia, tachypnea) and signs of right ventricular failure (jugular venous distention, parasternal heave, pedal edema, and characteristically clear lungs) due to the development of a left-to-right shunt.

206
Q

what is typical angina

A

retrosternal pain on exertion, goes away with rest lasting only 20 min.

207
Q

HCM manifests how

A

an area of increased left ventricular wall thickness that is typically asymmetrical and involves the septum or anterolateral LV wall.

208
Q

A VSD sounds like what

A

A ventricular septal defect, which causes a left-to-right shunt, leads to a harsh holosystolic murmur because of turbulent blood flow across the defect. The murmur is heard best at the left lower sternal border (tricuspid area) and becomes louder with maneuvers that increase left ventricular afterload (e.g., handgrip) because of increased left-to-right shunting.

209
Q

Hemochromatosis causes iron deposition in the cardiac

A

conduction system, which can lead to a variety of conduction abnormalities. These include sinus node dysfunction, complete AV block, atrial and ventricular tachyarrythmias, and rarely, sudden cardiac death.

210
Q

most common arrhythmia in hemochromatosis

A

is paroxysmal atrial fibrillation.

211
Q

what is the first sign of hypovolemic shock

A

An increase in heart rate is the first compensatory mechanism for hypovolemic shock and may be seen as early as class I hemorrhagic shock. In this patient, blood loss has resulted in hypovolemia and decreased stroke volume.

step II (22 decks)

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