Cardiology 🫀 Flashcards

1
Q

Abdominal aortic aneurysm screening. When, how, who

A

Abdominal ultrasound is used to screen for abdominal aortic aneurysm (AAA) in men age 65-
75 with a smoking history.

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2
Q

, patients age <45 with AUB who have failed medical management require what

A

an endometrial biopsy.

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3
Q

Why is a hystersalpkngogram and ablation CI in AUB, when not identified cause

A

Could be CA, and therefore CA can be spread

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4
Q

Why do patients with AUB refractory to COCP need biopsy

A

In such patients, the endometrial lining is likely too thick for the progestin to completely shed the endometrium during menstruation; as a result, the unshed endometrium continues to undergo dysregulated proliferation, which leads to an increased risk of endometrial hyperplasia/cancer.

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5
Q

Three main indications to biopsy endometrium in AUB <45 yo

A

indications for endometrial biopsy in women age <45 include persistent (>6 months) AUB, obesity, or
tamoxifen therapy, all of which increase the amount of unopposed endometrial estrogen exposure. Also if there is failed medical therapy

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6
Q

Main risks of vecicular vaginal fistula

A

due to young maternal age (ie, small pelvis) and limited or no prenatal care, which results in delayed diagnosis and labor intervention. Obstructed labor is the most common cause.

continuous vaginal discharge with an abnormally elevated pH (ie, >4.5) due to urine,
which may be malodorous due to surrounding necrotic tissue. Pelvic examination typically shows vaginal
pooling of urine, a visible defect, or an area of raised, red granulation tissue on the anterior vaginal wall.
Bladder dye testing is performed to confirm the diagnosis,

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7
Q

Echo finding for MS

A

Increased transmittal flow velocity

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8
Q

Run through Dukes criteria for endocarditis

A

BE FIVOR
Bacteraemia, endocardial signs (mama), fever, immune phenomena, vascular phenomena, organism culture, risk factors.

B and E are the major criteria. The rest are minor. Diagnose i.e. if two major, or one major and three minor, or five minor

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9
Q

If CHADVAS says so… how do we prevent thromboemb in AF

A

NOACs are best. Not anti PLT for sure

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10
Q

HTN and Low dose diuretic causing significantly low K+…. Cause?

A

Primary hyperaldo

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11
Q

An early peaking systolic murmur is seen in mild or severe AS

A

Mild AS

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12
Q

A loud S1 is seen in which murmur

A

M.S.

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13
Q

Some differences between athletes heart and hypertrophic cardiomyopathy

A

Hypertrophic cardiomyopathy will have focal areas of enlargement (IV septum).

Cavity of the left ventricle will be decreased in HCM (it is usually increased in athletes). The thickness is usually above 15 mm in HCM. Diastolic function is compromised in HCM. The left atria can be enlarged in HCN.

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14
Q

What is masked hypertension

A

Hypertension fluctuates throughout the day, making it hard to establish a diagnosis.

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15
Q

Which cardiovascular issues are a contraindication for pregnancy

A

Symptomatic mitral stenosis, aortic stenosis. Heart failure with a ejection fraction of less than 30. Pulmonary artery hypertension. Should try and address these things and then do pregnancy

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16
Q

Why is pregnancy a contraindication for patients with severe symptomatic M.S.and A.S.

A

In pregnancy we have an increase total volume, which will exacerbate the stretching of the heart, which could predisposed to emboli, AF, pulmonary oedema

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17
Q

Mitral valve replacement surgery

A

Balloon mitral Valvulotomy. If you can’t do that you can do open mitral repair or replacement

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18
Q

What medication can be given to help mitral stenosis in pregnancy

A

If a symptomatic, can give a beta blocker. This will decrease the heart rate, increase the left ventricle filling time, lowering the pressure in the left atrium. If symptomatic must do surgery before pregnancy

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19
Q

What is the cornerstone for medical management 4NSTEMI

A

Dual antiplatelet therapy. P2Y 12 inhibitor and aspirin

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20
Q

Do we give NOAC in acute coronary syndrome

A

No. Increases the risk of bleeding. So we do dual antiplatelet, and a bit of low molecular weight heparin

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21
Q

Murmur of both papillary muscle rupture, and interventricular wall rupture

A

Papillary muscle rupture will cause a soft mitral regurgitation. Interventricular will rupture will cause a half pan systolic murmur had left sternal border plus a thrill.

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22
Q

In a cute mitral regurgitation, do we see enlargement of the atria and ventricles

A

No, there is not enough time for eccentric hypertrophy. Therefore we don’t get accommodation of high-volume, so we get acute pulmonary oedema

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23
Q

Indications for aortic valve replacement. Otherwise do what?

A

Severe AS & >=1 of the following:
• Onset of symptoms (eg, angina, syncope)
• Left ventricular ejection fraction <50%
• Undergoing other cardiac surgery (eg, CABG)

Severe AS see on another FC

Otherwise do serial monitoring with echo

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24
Q

Criteria for severe AS

Jet velocity of….
Mean Transvaal u,at pressure gradient of….
Valve area of……

A

Aortic jet velocity 24.0 m/sec, or
• Mean transvalvular pressure gradient 240 mm Hg
• Valve area usually $1.0 cm? but not required

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25
Q

What is secondary mitral regurgitation

A

Mitral regurgitation, but nothing wrong with the valve itself. Usually due to ventricular movement issues, or ventricular dilation

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26
Q

Which is the only shock type that has elevated SVO2 and cardiac output

A

Distributive shock

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27
Q

Describe the potential radiation of pericarditis

A

Pleuritic chest pain that can radiate posteriorly To the bilateral trapezius ridges

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28
Q

Describe the potential radiation of pericarditis

A

Pleuritic chest pain that can radiate posteriorly To the bilateral trapezius ridges

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29
Q

We all know pericarditis can cause diffuse ST elevation. Eventually what else can we see on the ECG

A

T-wave inversion

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30
Q

Patient contraindicated for NSAID in pericarditis. What can be given

A

Corticosteroid

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31
Q

Two ways to definitively diagnose aortic dissection. One of them is for stable, the other is for unstable patient

A

Unstable, do transoesophageal echocardiogram. Stable patients can have a CTA

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32
Q

Medical management of acute aortic dissection

A

Pain control, Ivy beta blockers, nitroprusside if the systolic blood pressure is above 120.

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33
Q

Why might a Peri operative MI be painless

A

Because the patient is probably on morphine for pain control

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34
Q

What kind of shock does adrenal crisis cause

A

Both distributive and hypovolaemic shock

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35
Q

When does infective endocarditis cases require surgical intervention

A

If there is heart failure from valve dysfunction, if there is localised extension of infection (abscess, fistula, heart block). Difficult to treat pathogens like fungi or multidrug resistant. Vegetation is more than 1 cm which are high risk of embolisation

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36
Q

What is a pericardial window, and when is it used

A

It’s a removal of part of the pericardium, to allow pericardial fluid drain into either the flora or peritoneum. Used when there is continuous tamponade after days, or is recurrent.

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37
Q

How to manage malignant pericardial effusion

A

Acute drainage to relieve symptoms and do psychology. To prevent accumulation either do pericardial window or catheter drainage

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38
Q

A couple of things to manage a tit spell

A

Knee chest positioning, and inhale oxygen

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39
Q

what size aortic stenosis can usually cause a final symptoms

A

<1cm and increased pulse pressure. Otherwise the cause is likely CAD

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40
Q

Signs of purulent pericardial effusion

A

Acute, fever and illness. Chest pain and chills. Fatal. Usually pericarditis ECG and maybe low QRS amp. Need to do centesis

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41
Q

Risk factors for purulent pericardial effusion

A

Immunosupressed, dialysis, recent thoracic surgery

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42
Q

Patient with Taki arrhythmia who is haemodynamically unstable. Patient has a pulse. What do we do

A

Direct current cardioversion (i.e. synchronised cardioversion). This could be in a fib or a flutter or other arrhythmia which is unstable. If the patient has pulseless VT or VF, THEN of course we do defib

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43
Q

What is transcutaneous pacing used for

A

Heart block. Usually complete heart block, or symptomatic bradycardia

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44
Q

Are plural effusions common after coronary artery bypass surgery

A

Yes

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45
Q

Name me three elements to a Plural effusion, post coronary artery bypass graft surgery, That would make you want to investigate it further

A

If it’s large in size, it’s enlarging, it’s late onset (many days after surgery), is associated with significant respiratory symptoms. If none of these exist can just observe

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46
Q

Name some complications for acute aortic dissection

A

Stroke, aortic regurgitation, Horners syndrome, myo infarction, Tamponade, haemothorax, renal injury, abdominal injury, paraplegia

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47
Q

How can an aortic dissection cause MI

A

Dissection can affect the coronary Ostei

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48
Q

Which different symptoms can you see in aortic regurgitation

A

Water hammer pulse, pistol shot femoral pulse, crescendo diastolic murmur, widened pulse pressure, Palpitations, head bobbing, quincke pulse

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49
Q

Persistent pulmonary HTN of newborn.
Pathogenesis?
RF?
Exam?
Tx?

A

High pulmonary BP, usually due to low O2 states (potters, meconium aspiration, neonatal pneumonia, CDH). Get high PVR and this PDA remain open with Right to left shunt. This causes low o2 in the legs but normal in upper body. Give O2 and NO

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50
Q

Pulses bisferiens can be seen in which diseases

A

Aortic regurgitation and HCM and large PDA. It’s essentially a biphasic pulse

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51
Q

What are the lifestyle interventions to decrease hypertension. And roughly rank them in order

A

Dash diet. Weight loss (SBP decrease by six per 10 kg weight loss). Aerobic exercise. Reduce dietary sodium. Alcohol limitation

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52
Q

What is the single biggest risk factor for hypertension

A

Visceral/central obesity

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53
Q

Talk about cholesterol embolise syndrome

A

Usually after fracture or stent/Angio. Can cause Davido reticularis, hypocomplementaemia, eosinophilia, renal damage, GI issues

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54
Q

Causes of high output heart failure

A

Obesity, AV fistula, hypothyroidism, anaemia, cirrhosis, Paget disease, thiamine deficiency beriberi

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55
Q

 Strongest risk factor for aortic dissection

A

Hypertension history

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56
Q

List as many complications as you can from aortic dissection

A

Stroke, Acute aortic regurgitation, Horner syndrome, MI, Tamponade, haemothorax, renal injury, abdominal pain, paraplegia of lower limbs

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57
Q

Symptoms of sudden aortic regurgitation

A

Chest pain, low blood pressure, pulmonary oedema

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58
Q

Does Tamponade
Affect the left or right side of the heart

A

The right side. Therefore there should not be pulmonary oedema, but rather peripheral oedema

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59
Q

A risk carotid pulse is indicative of aortic stenosis or hypertrophic cardiomyopathy

A

Hypertrophic cardiomyopathy

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60
Q

Left atria Increase size, is a sign of chronic or acute mitral regurgitation

A

Chronic only

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61
Q

Why is the Chad Vaz score done, what does it indicate

A

Patients with low Chad virus unlikely to have recurrent AF. So younger patients, non-comob patients, generally have one episode of AF. Therefore do not need anticoagulant

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62
Q

Causes of constrictive pericarditis

A

Radiation therapy, previous cardiac surgery, recurrent viral pericarditis, Tb in endemic areas

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63
Q

ECG and venous tracing findings of constrictive pericarditis

A

 Low voltage QRS. Venus tracing shows prominent X and Y descent

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64
Q

Recap on the A CV an XY descent On Venus tracing

A

 A wave is for atrial contraction, Seawave is for ventricular contraction closing the tricuspid, the wave is for right atrial filling.

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65
Q

Canon a wave on Venus tracing is seen in which pathology

A

Atrioventricular dissociation

66
Q

What pathology causes prominent V wave on Venus tracing

A

Tricuspid regurgitation

67
Q

Which arrhythmia causes an absent a wave on Venus tracing

A

Atrial fibrillation

68
Q

Which pathology causes flattened Y decent

A

Cardiac tamponade

69
Q

Pregnant woman has high blood pressure, urine has 0/1+ protein. Management to do

A

24 hour urine collection. Needed since protein in urine dipstick has high false negative

70
Q

The mum heard in a cute interventricular wall septum perforation

A

Harsh holo systolic murmur, with palpable thrill

71
Q

t Contrast the murmur between papillary muscle rupture and interventricular wall rupture.

A

Acute mitral regurgitation is soft, and there is no palpable thrill.

72
Q

 If patient who has M I is not revascularised in until up to 24 hours, what does this mean clinically for the future

A

Highlights of complications, like IV septum rupture, freewheel rupture et cetera

73
Q

A cute limb ischaemia management

A

Anticoagulation at 1st (heparin). Then thrombolyses or surgery

74
Q

Ventricular aneurysm and three wall rupture, both show what ECG finding which is interesting

A

Persistent ST elevation is in correspondence to the MI preceding 

75
Q

Three times you hear S4

A

 Concentric hypertrophy, restrictive cardiomyopathy, myocardial infarcti

76
Q

Thyro toxicosis can cause what heart sound

A

S3

77
Q

Where is S3 and S4 heard best

A

Apex, with the bell stethoscope

78
Q

 Why do patients who have acute on chronic limb ischaemia, have slower onset

A

Because chronic plaques in the legs will cause collaterals to form

79
Q

AAA screening

A

Ultrasound in 65 to 70-year-old man who have any history of smoking

80
Q

Went to do surgical repair for AAA

A

If above 5.5 cm, if symptomatic, or on

81
Q

SAD of aortic stenosis

A

Syncope, angina, dyspnoea

82
Q

What is an Austin Flint Mumma

A

Apical diastolic rumbling, seen in aortic regurgitation

83
Q

Thrill/Mama over femoral arteries is a sign of which valvular disease

A

Aortic regurgitation

84
Q

Associated conditions with Mitral valve prolapse

A

Polycystic kidney disease, ehrlos Danlos syndrome, Marfan syndrome, fragile X

85
Q

Aside from mitral regurg/prolapse what are the pathology can cause a systolic click

A

Myxoma

86
Q

Greatest risk factor for aortic dissection, and aneurysm respectively

A

Hypertension and smoking respectively

87
Q

Leriche syndrome
Area occluded

A

Aortoiliac obstruction

88
Q

If a woman who is on oestrogen for her hot flushes, and end up getting a DVT. What medication change you to make

A

Swap to SSRI Or SNRI

89
Q

Distended veins above and below the ankle. Significance?

A

Hello the ankle is normal. Above the ankle is a sign of venous insufficiency

90
Q

If thrombosed vein is palpable in superficial. Is it more DVT or superficial thrombophlebitis

A

Superficial thrombophlebitis

91
Q

What is lemierre disease 

A

A complication of pharyngitis/tonsillitis/peritonsillar abscess. Where we get septic thrombophlebitis of internal jugular vein

92
Q

Went to give statins in primary prevention and secondary prevention

A

Primary prevention, after ACS angina CABG/TIA PAD

Secondary prevention, LDL above 190, about 40 years old and diabetes

93
Q

Can prostaglandin be given after the ductus arteriosus is closed

A

Yes, it can reopen

94
Q

What kind of check should turner syndrome patients have the cardiac problems

A

They need screening with for extremity blood pressure measurements, an echocardiogram. This can diagnose coartcion or bicuspid aortic valve

95
Q

 How to differentiate between pleural friction rub and pericardial friction rub

A

Ask the patient to hold their breath, if the rub remains it’s pericardial

96
Q

 Syncope with exertion, what are your thoughts

A

Either ventricular arrhythmia secondary to ischaemia, or an outflow obstruction like aortic stenosis

97
Q

And when diagnosing coronary artery disease (angina), when is an exercise ECG test done

A

With intermediate pretest probability. In patients who can do exercising, and reach a target heart rate. ECG at baseline is normal. Not allowed if the patient has left bundle branch block, a pacemaker, patient unable to reach target heart rate

98
Q

And when diagnosing coronary artery disease (angina), when is an exercise Donumatime stress test done

A

Of course when there is an intermediate pretest probability. I done when a patient is unable to meet the target heart rate, or has reactive airway disease. This is not allowed if somebody has a tachyarrhythmia

99
Q

And when diagnosing coronary artery disease (angina), when is a Coronary steel stress test done

A

Of course done when there is intermediate pretest probability. Good if the patient has left bundle branch block, a pacemaker, unable to reach target heart rate. Not allowed if the patient has reactive Airway disease, or is on dipyridamole or theophylline

100
Q

How does COPD, or severe asthma cause pulsus paradoxus

A

It creates negative pressure in the thorax, which when breathing in causes big drop in intrathoracic pressure. The pressure causes blood to pool in the pulmonary vasculature, leading to less ventricular preload

101
Q

How can an aortic regurgitation even prevent pulses paradoxus in patients with Tamponade

A

Severe regurgitation will cause higher left ventricle and diastolic pressure, that would preclude the IV septum from shifting into the left ventricular cavity

102
Q

Mamma heard in co-arched aorta

A

Systolic heard at the left infraclavicular area anteriorly and left interscapular area posteriorly

103
Q

Clues for syncope being cardiac origin

A

Sudden onset, no prodromal, heart structural issues, occurs at rest or excretion, ECG clues

104
Q

Discuss the murmur heard in atrial myxoma

A

Because the mass is typically mobile, obstructive symptoms may be transient and influenced by position (ie, mitral obstruction is exacerbated by upright posture but is alleviated by lying down); tumor movement occasionally causes a characteristic “tumor plop” sound at the end of diastole on auscultation.

105
Q

Discuss the murmur heard in atrial myxoma

A

Because the mass is typically mobile, obstructive symptoms may be transient and influenced by position (ie, mitral obstruction is exacerbated by upright posture but is alleviated by lying down); tumor movement occasionally causes a characteristic “tumor plop” sound at the end of diastole on auscultation.

106
Q

Regular wide-complex tachycardia with 2 fusion beats, Dx?

A

Sustained monomorphic ventricular tachycardia (SMVT).

107
Q

In hypertensive emergencies… how much can we lower BP by in 1st hour, then in next 23 hours.

A

mean arterial pressure should be lowered by 10%-20% in the 1st hour and by
another 5%-15% over the next 23 hours.

108
Q

Pacemaker insertion causes risk for which valve disease

A

TC regurg

109
Q

QT prolongation stuff

A

Hypocalcemia
Hypokalemia
.
Hypomagnesemia
Antibiotics (eg, macrolides,
fluoroquinolones)
• Psychotropics (eg, antipsychotics, TCAs,
SSRIs)
Opioids (eg, methadone, oxycodone)
Antiemetics (eg, ondansetron, granisetron)
Antiarrhythmics (eg, quinidine,
procainamide, flecainide, amiodarone,
sotalol)

And our channelipathies (K channels)

110
Q

Can cor pulmonale be secondary to left side HF

A

No

111
Q

Someone with subacute symptoms of fever, aortic regurgitate, heart block

A

Peri valvular abcess

112
Q

Perivalvular abcess sus, invx?

A

TEE echo

113
Q

Eccentric hypetrophy. Compensation to decomp story

A

Increase LV VOL. increase stretch and thus SV (frank starling). More vol means eccentric hypertrophic over time. Keeps SV, but wall stress increases. Eventuallly stress is too much and we decompensate.

114
Q

What is the passive and active cause for pulmonary artery BP to increase in MS/left HF

A

The passive (or postcapillary) component of pulmonary hypertension is most prominent and results from transmission of elevated pressure backward from the left atrium to the pulmonary veins, pulmonary capillaries, and pulmonary arteries. Clinically, this process is typically evidenced by pulmonary edema and its associated symptoms (eg, orthopnea,
paroxysmal nocturnal dyspnea, hemoptysis), as well as peripheral edema.

• The reactive (or precapillary) component of pulmonary hypertension is only sometimes present and occurs independent of left atrial pressure. In this process, MS triggers endothelin-mediated pulmonary arteriolar vasoconstriction and pathologic vascular remodeling through a poorly understood mechanism.

115
Q

PAH vs other pulmonary HTN Mx approach

A

PAH, use endothelium antag, prostenoids, PDE inhib etc.

Other pulmonary HTN, focus on cause

116
Q

Flags to suggest psychigeninc psuedosyncope….. aka conversion disorder

A

Prolonged LOC (eg, 20 min): PPS episodes typically last many minutes to hours versus approximately 1-2 minutes in
syncope.
• Absence of objective findings during the episode: As in this patient, typical objective findings accompanying syncope
(eg, abnormal vital signs, pallor, sweating) are usually absent on examination.
• Patient’s reports of symptoms/events that occurred during the episode (eg, “I felt my head throbbing after it hit the
floor”): This awareness rules out true LOC. Symptoms are often reported in a detached or disassociated manner (la
belle indifférence).

117
Q

Discuss the retroperitoneal hematoma from cardiac catheterisation

A

If the arterial puncture site is
above the inguinal ligament, the hematoma can extend into the retroperitoneal space, even with minimal visible localized
hematoma, and present with sudden hemodynamic instability and ipsilateral flank or back pain.

118
Q

 Seizure versus syncope

Consider preceding symptoms, patient position, tongue biting, convulsive movement, urine incontinence, post episode recovery

A

Seizures have auras, syncopating may have a prodrome (vasovagal). Seizure can happen in any position, syncope can happen when standing in vasovagal only. Tongue biting is very indicative of seizure. Convulsive movements can be seen in both (is usually before or with the consciousness loss in seizure, and after the LOC in syncope). Your incontinence is seen more in seizure. Post-episode recovery is usually longer in seizure

119
Q

Which symptom in seizures has the highest specificity against Syncope

A

Tongue biting

120
Q

A patient newly diagnosed with hypertension. What other investigations do we need to do in a normal primary hypertension patient

A

Consider renal function test, lipids, glucose/haemoglobin A1 C, ECG, full blood count

121
Q

 Patient with recurrent palpitations, potential arrhythmia. Do ECG a normal. Might we have to do to identify this problem

A

24 hour ambulatory monitoring

122
Q

What is the most common cause for foci in atrial fibrillation

A

Usually left atrial enlargement. Most of the time it’s hypertension, causing left ventricle hypertrophy, decreasing diastolic volume, transferring the pressure back to the left atria, causing it to enlarge. This can create an atrial substrate for a fib

123
Q

Changes in right ventricular preload, left on curricular preload, SVr in right-sided is STEMI

A

Right ventricular preload increase, left entrepreneur decrease, SVR increase

124
Q

ALS guidelines for treatment of:

A fib or a flutter

Superventricular tachycardia

A fib with aberrant conduction

Monomorphic VT

A

Rate control

Vago manoeuvre, Than adenosine

Rhythm control

Pharmacological cardioversion (amiodarone, procainamide, lidocaine, sotalol

125
Q

Amiodarone is a good rhythm control drug. How does it also have some rate control elements

A

It’s a potassium channel blocker, but also blocks some calcium channels in the AV node, thus having rate control properties

126
Q

Does decrease aortic compliance increase systolic or diastolic blood pressure

A

It increases the systolic blood pressure, and thus the pulse pressure

127
Q

How does a mild aortic regurgitation sound compared to a severe

A

Mild AR is heard only at early diastole, where as severe AR is heard throughout diastole

128
Q

How does restrictive cardiomyopathy appear on an echo

A

Usually concentric hypertrophy, and atria enlargement.

129
Q

Recall the presentation of restrictive cardiomyopathy

A

Predominantly right sided heart issue. JVD, ascites, hepato-megaly, pitting oedema. Concentric ventricular hypertrophy, with dilated atria. Diastolic dysfunction

130
Q

Patient has aortic dissection, vitals are okay. History of kidney problems. Investigation of choice

A

Transoesophageal echocardiogram UF***Retard. Anyone with contrast allergy or renal problems must have for TEE instead of CTA

131
Q

How might elevated systemic venous pressure is caused a protein losing enteropathy

A

Patients can get intestinal lymphangiectasia secondary to protein loss in the GI system.

132
Q

What is the pericardial knock

A

A mid diastolic sound, that is indicative

133
Q
A
134
Q

Multifocal atrial, tachycardia management

A

 usually don’t have to treat. But definitely treat any underlying cause (pulmonary, septic, metabolic et cetera). If patient has ischaemia or heart failure signs due to this, we can give rate control therapy

135
Q

Anterolateral MI can cause which deviation in axis

A

Right

136
Q

Inferior MI can cause which deviation in axis

A

Left

137
Q

PR interval

QRS interval

A

<5 small square

< 3 small squares

138
Q

Comprehensive list of causes of drugs causing long QT

A

Class 1A, Class III, ondensetron, macrolides, quinolones, opioids,

139
Q

General electrolytes causing long QT

A

Low Mg, low Ca, low K

140
Q

After days of an MI what ECG signs remain

A

T inversion (go within months) and patho Q waves

141
Q

Do my NSTEMI have Q waves

A

No

142
Q

Lft and Rt atrial enlargement mneumonic

A

Pulmonale causes peaked P wave

Mitrale causes M shaped P wave

143
Q

More than ?cm is increased JVP

A

3cm

144
Q

Increase preload with increase most murmurs except ??

A

HOCM and MVP

145
Q

Other causes of collapsing pulse

A

Aortic incompetence of course, then also, AV malf, thyrotox, severe anemia, (like high output HF)

146
Q

Other than tamponade and severe asthma/COPD. What else can cause pulses paradox

A

Tension pneumothorax, foreign airway obs

147
Q

Pulsus alternans and causes

A

Alternating string and weak pulse. Cardiomyopathy’s (like a poor LV stroke vol). Poor Px

148
Q

Jerky pulse seen where

A

HCOM

149
Q

Bifid pulse

A

Twice beating in systole. Aortic regurg. Or AR AND AS together. HOCM

150
Q

Third-degree block. What is the RR and pee pee intervals

A

The R&R intervals will be regular. The PP intervals will also be regular. But they are just not in Synkro

151
Q

Most common indication for pacemaker placement

A

Sick sinus syndrome (because of increased risk of AF or other superventricular tachyarrhythmias)

152
Q

Why do patients with sick sinus syndrome get junctional escape

A

Because the P-wave has dropped, there is a long paws, so the ventricle generates its own rhythm.

153
Q

List me the contraindications to do carotid sinus massage

A

Three months past history of MI, TIA, stroke, carotid stenosis, carotid atheroma, ventricle fibrillation, ventricular tachycardia

154
Q

What is a retrograde P-wave

A

Essentially where the P-wave comes before the T-wave. And is often seen in AVNRT or AVRT

155
Q

If an AVRT is secondary to wolf Parkinson white, how do we treat

A

Observation if no symptoms. Procainamide or amiodarone. The whole vagal maneuvres or adenosine is for AVRT not due to WPW. Can put on procainamide if has Hx of syncope/palpitations

156
Q

Main cause of multifocal atrial tachycardia

A

Anything that causes cardiac remodelling. For example COPD, heart failure et cetera

157
Q

 General management for multifocal atrial tachycardia

A

IV beta blocker or CCB (normal rate control

158
Q

What is an atrial tachycardia, and what do I give to try and uncover the underlying ectopia

A

It is an ectopic foci but within the atria. Give adenosine Musk underlying activity

159
Q

Monomorphic VT recap of management

A

If stable can just give rhythm control (amiodarone, lidocaine, procainamide). If haemodynamically unstable do synchronised cardioversion. If pulseless VT do defib

160
Q

Review of torsade de pointes management

A

If stable give magnesium. If unstable to synchronised cardioversion. If pulseless do defibrillation. And correct electrolytes or remove offending medication

161
Q

Should hyperthyroidism always be considered in A fibrillation work up

A

Yes

162
Q

If a wolf Parkinson white patient develops recurrent AF. What should I give

A

Procainamide. Remember never give adenosine, beta blocker, non-dihydropyridine CCB in wolf Parkinson white. Even if AVRT or AF occurs