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first year med > cardio > Flashcards

cardio Flashcards

1
Q

what is a normal resting heart rate?

A

60 - 100 BPM

< 60 = bradycardia
> 100 = tachycardia

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2
Q

what does the AV node delay allow to occur?

A

allows atrial systole (contraction) to precede ventricular systole

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3
Q

describe the parasympathetic supply to the heart

A

vagal tone dominates under normal resting conditions - continuously slows from 100bpm to produce normal (70bpm)
vagus nerve supplies SA node and AV mode
vagal stimulation slows rate of firing from SA node and increases AV nodal delay
== negative chronotropic effect

neurotransmitter = acetyl choline via muscarinic M2 receptors

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4
Q

what do cardiac sympathetic nerves supply? what is the neurotransmitter?

A

SA node, AV node and MYOCARDIUM (increases firing and contraction, decreases delay)

neurotransmitter = noradrenaline via beta1 adrenoceptors

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5
Q

what are the different waves seen in an ECG and what do they represent?

A

P wave = atrial depolarisation

QRS complex = ventricular depolarisation (masks atrial repolarisation)

T wave = ventricular repolarisation

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6
Q

what are the main intervals/segments seen on an ECG and what happens there?

A

PR interval = largely AV node delay

ST segment = ventricular systole occurs here

TP interval = diastole occurs here

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7
Q

where is the only point of electrical contact between atria and ventricles?

A

AV node

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8
Q

what is the refractory period?

A

a period following an AP in which it is not possible to produce another action potential

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9
Q

how is muscle tension produced?

A

sliding of actin filaments on myocin filaments - requires ATP

desmosomes provide mechanical adhesion between adjacent cardiac cells and ensure the tension is transmitted from one to the next

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10
Q

what is stroke volume? how is it calculated? what is it affected by?

A

the volume of blood ejected by each ventricle per HEART BEAT

SV = end diastolic volume (EDV) - end systolic volume (ESV)

affected by:

  • cardiac preload
  • myocardial contractility
  • cardiac afterload
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11
Q

what effect does sympathetic nerve stimulation have on ventricular contraction + frank starling curve?

A

peak ventricular pressure rises - contractility of heart at given EDV rises

= frank-starling curve shifts to left

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12
Q

what effect does an increased afterload have on the heart?

A

unable to eject fully = decreased SV
–> leads to increase EDV –> increase force of contraction

eventually, ventricular hypertrophy to overcome resistance

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13
Q

what is a normal arterial blood pressure?

A

120/80 - 90/60
pulse pressure = 30 - 50 mmHg

hypertension = 140/90 mmHg (daytime average 135/85 or higher

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14
Q

what determines the cardiac preload?

A

cardiac preload = diastolic length/diastolic stretch of myocardial fibres

determined by EDV -> EDV determined by venous return

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15
Q

what is MAP? how is it estimated?

A

mean arterial blood pressure = average arterial blood pressure during a single cardiac cycle

MAP = ((2xdiastolic) + systolic) / 3
–> ((2x80) + 120) / 3 = 93.3 mmHg

normal = 70 - 105mmHg
at least 60 needed to perfuse vital organs

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16
Q

how do you calculate MAP? how can MAP be regulated?

A

MAP = cardiac output (CO) x systemic vascular resistance (SVR)

heart rate, stroke volume, systemic vascular resistance

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17
Q

what is cardiac output? how is it calculated?

A

the volume of blood pumped by each ventricle of the heart PER MINUTE

CO = SV x HR

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18
Q

how do baroreceptors respond to an increase in BP?

A

increase baroreceptor discharge –> CV integrating centre (medulla)

  • increase vagal activity - decrease HR hence decrease CO
  • decrease cardiac sympathetic activity - decrease SV + HR, hence CO
  • decrease sympathetic constrictor tone - venodilation+vasodilation, reduced SVR+SV
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19
Q

what hormones regulate extracellular fluid volume?

A
  1. the Renin-Angiotensin-Aldosterone System (RAAS)
  2. Natriuretic Peptides (NPs)
  3. Antidiuretic Hormone (ADH)
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20
Q

What is shock?

A

an abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation

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21
Q

what are the 4 types of shock and how are they caused?

A
  1. hypovolaemic shock - caused by loss of blood volume
  2. cardiogenic shock - caused by sudden severe impairment of cardiac function
  3. obstructive shock - caused by physical obstruction to circulation in/out of heart
  4. distributive shock - caused by excessive vasodilation and abnormal distribution of blood flow
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22
Q

what is meant by cardiac tamponade?

A

increased pressure in pericardial cavity which prevents cardiac contraction

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23
Q

what is mean by pericardiocentesis?

A

drainage of fluid from pericardial cavity

needle inserted via infrasternal angle and directed superoposteriorly, aspirating continuously

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24
Q

where would you palpate the apex (beat of the heart)?

A

5th left intercostal space in the midclavicular line

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25
Q

where is the coronary sinus? what does it do?

A

atrioventricular groove posteriorly - separates base from diaphragmatic surface

receives deoxygenated blood from most cardiac veins and drains into right atrium
- main venous drainage for myocardium

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26
Q

name the branches of the right coronary artery

A

1 - right marginal artery - long bottom one along margin

2 - posterior interventricular artery - in interventricular groove

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27
Q

name the branches of the left coronary artery

A

(main stem is short)

1 - left anterior descending (LAD)
2 - lateral (diagonal) branch - branches from LAD
3 - left marginal artery
4 - circumflex artery - anastomoses with branches of right coronary artery

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28
Q

how many openings are there into the right atrium? what are they?

A

3 - SVC, coronary sinus, IVC

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29
Q

which of the heart valves are leaflet valves?

A

tricuspid (RA-RV) + mitral (LA-LV)

consist of:

  • valve leaflets
  • tendinous cords - close + prevent prolapse of leaflets (+ regurgitation of blood)
  • papillary muscles - cardiac muscle attached to chamber wall

pulmonary + aortic = semilunar

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30
Q

where do you auscultate the aortic valve?

A

2nd right ICS sternal angle

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31
Q

what valve can be auscultated at the 5th left ICS in midclavicular line?

A

mitral valve

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32
Q

where do you auscultate the tricuspid valve?

A

4th left ICS sternal edge

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33
Q

where do you auscultate the pulmonary valve?

A

2nd left ICS sternal edge

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34
Q

what is the first branch of the aorta?

A

coronary arteries from coronary sinuses just above aortic valve

coronary arteries = blood supply to epicardium + myocardium

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35
Q

what are the 5 dilations of the initial heart tube and what is their fate?

A

most caudal
1. sinus venosus (inflow area, 2 horns) contributes to smooth part of RA (right horn) + coronary sinus (left horn)

  1. atrium - forms trabeculated (muscular part) of both atria
  2. ventricle - forms trabeculated part of LEFT ventricle
  3. bulbus cordis - forms trabeculated part of right ventricle + outflow part of both ventricle
  4. truncus arterious - forms aorta and pulmonary trunk (most proximal part)
    most cranial
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36
Q

when does looping and folding of the heart begin?

A

approx. day 21-23

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37
Q

how do the different dilations of the heart fold?

A

atrium = dorsal and cranially
ventricle = displaced left
bulbus cordis = inferiorly, ventrally to the right

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38
Q

what are the 2 atrial septums?

A

septum primum - flexible, forms valve for foramen ovale

septum secundum - more rigid, right of septum primum and grows over it but never divides atria

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39
Q

what is the foramen ovale?

A

opening that continues until birth that allows communication between right and left atria (avoids lungs as not in use)

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40
Q

describe the process of ventricular septation

A

muscular portion (growing upwards from wall of expanding ventricle) and membranous protein (growth of tissue from endocardial tissue - cranial) fuse to form ventricular septum

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41
Q

what is the fate of the 6 pairs of the aortic arches

A

never all present at one time, develop cranial-caudal sequence

1 + 2 - mostly obliterated, contribute to maxilllary and stapedial aa.

3 - common carotid + first part of internal carotid

4 - right subclavian a. + part of aortic arch

5 - absent / rudimentary

6 - sprout branches that form pulmonary aa. + ductus arteriosus on left

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42
Q

why do the 2 atrial septums fuse at birth?

A

at birth, pressure becomes greater in left side, causes septum primum to push against septum secundum and eventually fuse

leaves “thumb print” in right atrium = fossa ovalis

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43
Q

what is the recommended weekly exercise duration for adults?

A

150 mins of moderate

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44
Q

what are some clinical signs of hypertension?

A
  • loud aortic second sound
  • fourth heat sound
  • prominent left ventricular impulse
  • hypertensive retinopathy
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45
Q

what are secondary causes of hypertension?

A
  • renal disease
    • renal stenosis
  • endocrine disease
    • Conn’s syndrome = excess aldosterone
    • Cushing’s syndrome = excess corticosteriod
    • Phaeochromocytoma = excess noradrenaline
  • aortic disease
    • coarctation of aorta (congenital narrowing of
      segments of the aorta
  • drug therapy
46
Q

what are the stages of hypertension?

A

Stage 1: >=140/90 AND daytime >=135/85

stage 2: >= 160/100 AND daytime 150/95

severe: systolic >= 180 OR diastolic >= 110

47
Q

how does a atheromatous plaque progress?

A
  • fatty streak (flat)
  • fibrofatty plaque (raised)
  • complicated plaque (overlying thrombus)
  • superadded thrombus
48
Q

what are complications of atheroma?

A
  1. stenosis
  2. thrombosis
  3. aneurysm - persistent dilation
  4. dissection - flowing blood splitting media
  5. embolism
49
Q

name a potent vasoconstrictor/dilator

A

constrictor = angiotensin II

dilator = nitric oxide

50
Q

list the 3 types of syncope

A
  1. reflex syncope - vasovagal, situational, carotid sinus
  2. orthostatic (postural) hypotension
  3. cardiac syncope
51
Q

what is a positive result for orthostatic hypotension indicated by?

A

a drop within 3 minutes of standing from lying position of at least 20 mmHg in systolic bp (with or without symptoms)

or

drop in diastolic by 10mmHg WITH symptoms

(symptoms = lightheaded, dizziness)

52
Q

name side effects of ACE inhibitors

A

dry cough

angioneuretic oedema

53
Q

name side effects of diuretics

A

hypokalaemia (low potassium)

hyperglycaemia (high blood glucose)

54
Q

name a side effect of CCBs

A

ankle oedema

55
Q

what is a sign of hyperlipidaemia?

A

xanthelasma - plasma/lipids round eyes, weird backs of ankles and ringed eyes

56
Q

what are the 4 main causes of oedema?

A
  1. raised capillary hydrostatic pressure - arteriolar dilatation, raised venous pressure (ankle swelling)
  2. reduced plasma osmotic pressure - <30g/l, malnutrition, hepatic failure
  3. lymphatic insufficiency - lymph node damage, filariasis
  4. changes in capillary permeability - inflammation, histamine increases leakage of protein
57
Q

what is oedema?

A

accumulation of fluid in interstitial space

58
Q

what regulates blood flow to the capillary bed? how fast is this blood flow?

A

terminal arterioles (mostly), precapillary sphincters in a few

blood flow throw capillary bed is slow - allows time for exchanges

59
Q

where do hydrophilic and lipophilic molecules cross the capillary wall?

A

hydrophilic - go through water-filled pores

lipophilic - go through endothelial cells

60
Q

what are the major forces involved in systemic transcapillary flow?

A
  • capillary hydrostatic pressure -> favouring filtration
  • capillary osmotic (oncotic) pressure -> opposing filtration

capillary hydrostatic pressure falls from 35mmHg at arteriole end to 17mmHg at venule end

capillary osmotic (oncotic) pressure remains constant at 25mmHG due to plasma proteins staying in capillaries (too big to diffuse)

61
Q

what do starling forces favour in transcapillary flow?

what happens to the excess fluid?

A

favour filtrations at arteriolar end + reabsorption at venule end

filtration exceeds absorption so excess fluid is returned to circulation via lymphatics as lymph
-> able to reabsorb due to osmotic pressure

62
Q

what is ERBs point and where is it?

A

best area for listening to S1 + S2

3rd intercostal space on sternal edge

63
Q

where does an aortic stenosis murmur radiate to?

A

carotid arteries

64
Q

where does a mitral regurgitation murmur radiate to?

A

axilla

65
Q

what manoeuvre could you do to a patient to better hear mitral stenosis?

A

turn patient on left hand side

66
Q

what manoeuvre could you do to a patient to better hear aortic regurgitation?

A

sit patient up and leaning forward, exhale and hold

67
Q

which valves are heard loudest on inspiration?

A

tricuspid + pulmonary

68
Q

which valves are heard loudest on expiration?

A

Mitral + aortic

69
Q

what murmurs are heard during systole?

A
  • aortic + pulmonary stenosis
  • mitral + tricuspid regurgitation
  • mitral valve prolapse causes systolic murmur with opening click
70
Q

what are the inferior leads of an ECG?

A

II, III, aVF

71
Q

what are the lateral leads of an ECG?

A

aVL, I, V5, V6

72
Q

what causes a 4th heart sound?

A

atrial contraction causing rapid blood flow into a less compliant (STIFF) VENTRICLE

common causes of decreased LV compliance -

  • myocardial ischaemia
  • hypertension
  • aortic stenosis

** always pathological + should be referred for echocardiography

73
Q

what causes an innocent murmur?

A

turbulence of blood in the right ventricular outflow tract

  • normal in child/young adult
  • soft mid systolic (diastolic always pathological)
  • usually heard in pulmonary area
  • localised
  • no other cardiac abnormalities
74
Q

what happens in each of the phases of ventricular muscle excitation?

A

phase 0 = depolarisation due to Na influx

phase 1 = closure of Na channels and transient K efflux

phase 2 = Ca2+ influx through L-type Ca2+ channels

phase 3 = closure of Ca channels and K efflux

phase 4 = resting potential due to K efflux

75
Q

what is a tall, tented T wave on an ECG a sign of?

A

hyperkalaemia

76
Q

what is T wave inversion a sign of?

A

myocardial ischaemia

PE

77
Q

what are features of first degree heart block?

A

PR interval longer than 0.12s-0.2s

no treatment, monitor for progression

78
Q

what are the different types of second degree heart block?

A

mobitz type 1 = PR interval progressively gets longer and eventually drops a beat

mobitz type 2 = P:QRS ratio

requires ventricular pacemaker

79
Q

what are features of 3rd degree heart block?

A

complete heart block - no electrical current getting through AV node

no correlation between P waves and QRS

requires ventricular pacemaker

80
Q

what should pregnant woman be given instead of ACE or ARB?

A

ACE + ARB effect feotus

give beta blocker instead - atenolol

81
Q

give an example of an ACE inhibitor and describe it’s mechanism of action

A

lisinopril

Block angiotensin converting enzyme, i.e. prevent conversion of angiotensin I to angiotensin II; aldosterone is not stimulated, so vasodilation occurs.

first line hypertension
heart failure - lengthens prognosis

82
Q

give an example of an ARB and describe it’s mechanism of action

A

losartan

Angiotensin II receptor blocker; angiotensin II is a vasoconstrictor. Antagonising its action leads to vasodilation.

hypertension
heart failure

83
Q

give an example of a thiazide diuretic and describe it’s mechanism of action

A

bendrofluazide

Inhibit NaCl reabsorption in distal tubules by blocking NaCl co-transporter

hypertension

84
Q

give an example of a loop diuretic and describe it’s mechanism of action

A

furosemide

Inhibit NaCl reabsorption in the thick ascending loop of Henle

heart failure

85
Q

describe amiodarone’s mechanism of action

A

block K+ channels

slows repolarisation and prolong AP + refractory period in cardiac tissue

86
Q

give an example of a statin and describe it’s mechanism of action

A

simvastatin, atorvastatin

Block HGM-CoA reductase (competitive inhibition)
Reduction of LDL production in liver
Increased clearance of LDL in liver

87
Q

describe the mechanism of action of glyceryl trinitrate?

A

arginine is converted into a neurotransmitter that activates guanylate cyclase

88
Q

what is the primary drug target of atorvastatin?

A

hepatocytes

atorvastatin = HMG-CoA reductase inhibitor that reduces plasma cholesterol

89
Q

Main way an increase sympathetic outflow results in increase preload

A

increases renin secretion

90
Q

what is the mechanism of action of natriuretic peptides?

A

promotes excretion of sodium
lowers bp
antagonises actions of angiotensin II, aldosterone

91
Q

what would an ECG of someone with hypOkalaemia look like?

A

U waves - deflections immediately after T wave

92
Q

what criteria is used in infective endocarditis?

A

Duke criteria

93
Q

which nerve supplies the pericardium?

A

phrenic nerve

94
Q

what are the only 2 shockable rhythms? how would you differentiated between them?

A

VF
sustained VT

most patients with VT remain conscious
In VF the patient is pulseless and cardioversion is always required. In sustained VT the patient can be cardioverted with amiodarone if they are stable

95
Q

Dressler syndrome

A

autoimmune mediated pericarditis 2-6 weeks post MI

96
Q

Fever and new onset murmur

A

bacterial endocarditis until proven otherwise

97
Q

myocardial necrosis

A

coagulative necrosis due to ischaemia and hypoxia in first 3 days post MI

98
Q

torsades de pointes treatment

A

magnesium sulphate

99
Q

what would be seen in V1 + V6 in LBBB?

A

V1 - W shape

V6 - M shape

100
Q

what is the pacemaker potential due to?

A

decreased K+ efflux

101
Q

how do cardiac muscles relax + contract?

A

both require ATP

relax - troponin-tropomyosin complex prevents myosin bridge binding by covering site on actin

contract - calcium displaces troponin-tropomyosin complex, myosin cross bridge binds to binding sites - calcium comes from sarcoplasmic reticulum

–> binding triggers power stroke that pulls filament inward during contraction

102
Q

rate limiting step of RAAS

A

renin secretion

103
Q

how is renin secretion reduced

A

natriuretic peptides

104
Q

what effect does adrenaline have on alpha and beta receptors respectively?

A

alpha1 = vasoconstriction

beta2 = vasodilation

105
Q

intrinsic chemicals that cause vasoconstriction

A

serotonin
thromboxane A2
leukotrienes

106
Q

factors that influence venous return

A

skeletal muscle pump
venomotor tone
blood volume
respiratory pump

–> increase in any of these increases venous return - increase arterial pressure, EDV + SV

107
Q

what do cardiac muscle fibrils contain?

A

myofibrils which contain actin + myocin

actin = thin
myocin = thick

these are arranged into sacromeres

108
Q

what effect does exercise have on the frank starling curve?

A

shifts to left

exercise causes peal ventricular pressure to rise –> increasing contractility of heart at a given EDV

109
Q

frank-starling law

A

stroke volume of LV will increase as the LV volume increases

–> due to myocyte stretch causing more forceful systolic contraction

changes in contractility shifts curve -
increase = left
decrease = right - increase afterload (increase SVR)

110
Q

phases of pacemaker potential

A

phase 0 - depolarisation, Ca influx via L-type channels

phase 3 - repolarisation, Ca channels close + K open = K efflux

phase 4(pacemaker potential) = slow depolarisation (funny current) - mixed Na/K –> important to determine HR

** pacemaker potential due to decrease K+ efflux **

111
Q

give examples of drugs that increase + decrease pacemaker potential respectively

A

decrease = adenosine

increase = catecholamines

first year med (15 decks)

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