Cardiovascular System Flashcards

1
Q

The most common ECG finding of hypercalcemia is a ___ __ _________

A

short QT interval

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2
Q

Long QT syndrome (LQTS) is an inherited condition associated with _________________________________________

A

delayed repolarization of the ventricles.

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3
Q

LQTS can lead to ______________________

A

ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death.

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4
Q

What are the most common variants of LQTS and what are they caused by?

A

LQT1 and LQT2
caused by defects in the alpha subunit of the slow delayed rectifier potassium channel

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5
Q

A normal corrected QT interval is less than ____ ms in males and ___ ms in females.

A

430 ; 450

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6
Q

Congenital causes of LQTS

A

Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)

Romano-Ward syndrome (no deafness)

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7
Q

Drugs that can cause LQTS

A

amiodarone, sotalol, class 1a antiarrhythmic drugs

tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)

methadone

chloroquine

terfenadine (a non-sedating antihistamine and classic cause of prolonged QT in a patient, especially if also taking P450 enzyme inhibitor, e.g. Patient with a cold takes terfenadine and erythromycin at the same time)

erythromycin

haloperidol

ondanestron

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8
Q

Diseases/conditions that cause LQTS

A

electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage

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9
Q

Long QT1

A

usually associated with exertional syncope, often swimming

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10
Q

Long QT2

A

often associated with syncope occurring following emotional stress, exercise or auditory stimuli

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11
Q

Long QT3

A

events often occur at night or at rest
sudden cardiac death

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12
Q

Management of LQTS

A

avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)

beta-blockers (note sotalol may exacerbate long QT syndrome)

implantable cardioverter defibrillators in high risk cases

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13
Q

What are the 4 factors affecting stroke volume?

A

Cardiac size, contractility, preload and afterload are the 4 factors affecting stroke volume

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14
Q

Stroke volume (SV)

A

SV is the amount of blood pumped by the left ventricle in one contraction.

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15
Q

Cardiac output

A

This is the total volume of blood the heart pumps per minute and is calculated as cardiac output = SV x heart rate.

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16
Q

Ejection fraction

A

This is the percentage of blood ejected from the left ventricle during systole, calculated as ejection fraction = SV / end-diastolic volume x 100.

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17
Q

End-systolic volume (ESV)

A

ESV refers to the volume of blood remaining in the ventricle after systole. It is related to stroke volume through the formula SV = end-diastolic volume − end-systolic volume.

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18
Q

Total peripheral resistance (TPR)

A

TPR is the resistance to blood flow in the systemic circulation and is calculated as TPR = mean arterial pressure / cardiac output

19
Q

B-type natriuretic peptide is released in response to _________

A

ventricular strain

[Ventricular strain occurs when there is increased pressure or volume load on the ventricles, often seen in conditions like heart failure. This strain leads to the stretching of the ventricular walls, triggering the release of BNP.]

20
Q

Endothelin is a peptide that is released locally by endothelial cells and contributes to arteriolar ___________

A

constriction.

22
Q

Vasoconstrictor mediators

A

Endothelin

noradrenaline from the sympathetic nervous system

circulating catecholamines

angiotensin-2

23
Q

Endothelin acts on ____receptors in order to cause constriction but can also cause dilation of arterioles by acting on ____ receptors.

A

ET(A) ; ET(B)

24
Mediators of arteriolar dilation
The parasympathetic nervous system, nitric oxide and prostacyclin
25
Possible ECG signs in patients with pulmonary embolism are:
Sinus tachycardia (the most common) Signs of right heart strain T wave inversion in the anterior leads S1Q3T3 the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - 'S1Q3T3'. However, this change is seen in no more than 20% of patients right bundle branch block and right axis deviation are also associated with PE sinus tachycardia may also be seen
26
PE common triad of Sx
few patients (around 10%) present with the textbook triad of pleuritic chest pain, dyspnoea and haemoptysis. The relative frequency of common clinical signs is shown below: Tachypnea (respiratory rate >20/min) - 96% Crackles - 58% Tachycardia (heart rate >100/min) - 44% Fever (temperature >37.8°C) - 43%
27
Atheroma formation:
initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large 'foam cells'. As these macrophages die the result can further propagate the inflammatory process. smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.
28
There are many causes of infective endocarditis, ________ is now the commonest cause in the developed world and is particularly likely if the patient is an intravenous drug user
S. aureus
29
______________ is the commonest cause of IE in patients from developing countries with an absence of other specific risk factors.
Streptococcus viridans
30
____________ is a more likely causative organism of infective endocarditis if the patient has prosthetic valves
S. epidermidis
31
_________ is a causative organism for IE that can be found in patients who have colorectal cancer
S. bovis
32
_______ is an unusual cause of infective endocarditis and is typically only found in immunocompromised patients.
Candida albicans
33
ECG features of hypokalaemia
U waves small or absent T waves (occasionally inversion) prolong PR interval ST depression long QT
34
The fastest conduction velocities in the heart are in the ________
Purkinje fibres
35
S4 is caused by______________
the atria contracting forcefully in an effort to overcome an abnormally stiff ventricle
36
S3 occurs __________and is caused by ____________________
earlier in diastole ; rapid movement of blood into the ventricle.
37
S1
closure of mitral and tricuspid valves soft if long PR or mitral regurgitation loud in mitral stenosis
38
S2
closure of aortic and pulmonary valves soft in aortic stenosis splitting during inspiration is normal
39
S3
caused by diastolic filling of the ventricle considered normal if < 30 years old (may persist in women up to 50 years old) heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation
40
S4
may be heard in aortic stenosis, HOCM, hypertension caused by atrial contraction against a stiff ventricle therefore coincides with the P wave on ECG in HOCM a double apical impulse may be felt as a result of a palpable S4
41
_______kalaemia can lead to long QT syndrome
Hypo
42
Patients with heart failure with reduced LVEF should be given a _________ and an___________ as first-line treatment
beta blocker ; ACE inhibitor
43