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Extra ESA2 > CVS MMF S7-12 > Flashcards

CVS MMF S7-12 Flashcards

1
Q

causes of tachycardic arrhythmias

A

ectopic pacemaker activity

  • damaged myocardium
  • pacemaker region activated from ischaemia (damaged myocardium doesn’t conduct well so spontaneously generates own AP)

Afterdepolarisations

Atrial flutter

Re-entry loops

  • conduction delay
  • accessory pathway (WPW)
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2
Q

causes of bradycardia arrhythmias

A

sinus Brady

  • intrinsic SAN dysfunction
  • extrinsic factors e.g. drugs

conduction block

  • problem at AVN/ bundle of His (R/LBBB)
  • slowed conduction at AVN due to drugs
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3
Q

which is worse VF or AF

A

AF

treat AF so it doesn’t turn to VF > harder to treat VF

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4
Q

example of re-entry loop condition and its presentations

A

wolf parkinson white
- congenital accessory pathway

  • atrioventricular re-entrant tachycardia
    > pre excitation of vessels
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5
Q

give an example of when re-entry loop can occur

A

post MI due to damaged tissue
instead of excitation spreading in a loop in opposite directions then cancelling out, one will be blocked and then the other will re-circulate causing arrhythmia

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6
Q

what are class 1 anti-arrythmics

A

1B
Na+ channel blockers
- slows conduction in phase 0
- slows Na entry, slows upstroke > stops new impulse arising as channels blocked

dec ARP. and dec AP duration.

e.g. lidocaine. fast acting!!

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7
Q

what are class 2 anti-arrythmics

A

Beta blockers
inhibit sympathetic action on. heart
decreases adrenaline action on B1 adrenoreceptors, less Ca entry into cell, reduced contraction. lowers HR

at pacemaker cells: slows upstroke of funny current (phase4)

no pacemaker cells: low Ca entry, longer plateau in phase 3> longer ARP >dec re entry of arrhythmia

e.g. attenalol

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8
Q

problem with beta blockers in asthmatics?

A

some aren’t cardio selective and can work on B1 too causing bronchospasms

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9
Q

what are class 3 anti-arrythmics

A

K+ channel blockers
> prolong ARP and AP duration
prevents another AP from occurring

e.g. amiodarone multi class effects> dec conduction across all cardiac tissue

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10
Q

problem with K+ channel blockers?

A

can easily devolve and produce early after depolarisations > develop into VT

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11
Q

which drugs can also have a pro-arrhythmic effect?

A

any drug that prolongs cardiac AP> prolongs QT interval

class 3!!

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12
Q

why do early after depolarisations occur

A

reactivation of Ca channels

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13
Q

why do delayed after depolarisations occur

A

abnormally increased intracellular Ca

hypercalcemia or hypokalaemia

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14
Q

what is digoxin toxicity

A

class 5 drug

lead to an overload. of Ca into SR
spontaneous Ca release
net depolarisation effect
> delayed afterdepolarisations occur

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15
Q

what are class 4 anti-arrythmics

A

Ca channel blockers
pacemaker cells:slower Ca entry, shallow upstroke, slow HR
inc ARP

non: slow Ca entry, dip in plateau phase> dec contractility

dec HR and inotropy!!

e.g. verapamil

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16
Q

what are class 5 anti-arrythmics

A

positive inotropes

Digoxin - cardiac glycoside
Dobutamine- Beta agonist

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17
Q

How does digoxin work?

A

enhances vagal activity
lower HR and slows conduction through AVN > inc diastolic filling time

Blocks Na/K ATPase, inc intracellular Na, dec activity of NCX> more Ca stored in SR
> contractility increases

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18
Q

how does dobutamine work

A

stimulates B1 adrenoreceptors at SAN and AVN
steeper funny current > HR inc
contractility inc

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19
Q

in what locations do you take pulses from in the lower limb

A

femoral area
popliteal area
tibialis posterior area
dorsalis pedis area

20
Q

what is intermittent claudication

A

peripheral vascular disease> causes arterial insufficiency due to atherosclerosis in vessels

  • cramping pain
  • relieved by rest
  • pain that’s reproducible
21
Q

what are the signs associated with acute limb ischaemia?

A

6Ps

  • pallor
  • pain
  • perishing with cold
  • paraesthesia
  • paralysis /reduced power
  • pulselessness
22
Q

stages of atherosclerosis formation?

A

repeated injury to endothelium
tunica intima becomes permeable to LDL/ lipoproteins
macrophage migration. to endothelial wall
macrophages absorb LDL> form foam cells
further inflammatory mediators enter
platelets aggregate and adhere to foam cells
smooth muscle cells migrate to surface of plaque > fibrous plaque formation

23
Q

difference between stable and unstable angina?

A

stable- ischaemia that happens when metabolic demand increases e.g.during exercise >symptoms don’t last long. relieved with rest

unstable-pain doesn’t resolve
usually more painful.

24
Q

treatment for angina how does it work?

A

beta blockers
ca blockers

GTN spray>venodilator > decpreload on heart > dec isotropy. > muscle doesn’t. have to contract as hard so doesn’t require as much oxygen

25
Q

diff between NSTEMI and STEMI

A

NSTEMI

  • ST depression
  • partial occlusion, reduced perfusion

STEMI

  • ST elevation
  • full thickness, complete occlusion
26
Q

how to differentiate between NSTEMI and unstable angina

A

troponin test
I and T
> indicates myocyte damage in NSTEMI

27
Q

what is the ECG progression of a stemi

A

hyper acute T waves (wide and tall)
ST elevation
inverted T waves
pathological Q waves

28
Q

causes of peripheral oedema?

A

3Ps

physiological- heat> leaky vessels or pregnancy vasodilation

pharmacological-calcium channel blockers or IV fluids

physiological- cardiovascular , liver, renal

29
Q

causes of left sided HF

A

caused by pressure overload from long term hypertension or valve dysfunction (aortic stenosis)

volume overload >valve regard

myocardium dysfunction >ishcaemic HD

30
Q

causes of right sided HF

A

LHF

backup of blood through the pulmonary system > RV pushing against higher pressure > ventricular hypertrophy > eventually RHF

31
Q

what is Cor pulmonale

A

RHF from pulmonary hypertension

32
Q

what is diastolic dysfunction in HF?

A

ventricles still can relax normally > cant fill as much >blood backs up to lungs > ventricular muscle hypertrophies > wall thickens

33
Q

what is systolic dysfunction in HF?

A

IHD/HTN > chambers of heart enlarge >walls thin > overstretches sarcomeres in muscle>prevent efficient contractions > less blood pumped out

34
Q

what is ejection fraction

A

amount of blood pumped out the ventricles over the total amount of blood in ventricles

normal= 50%ish

35
Q

reduced ejection fraction?

A

<40%

seen in systolic dysfunction (increased volume in but less pushed out)

36
Q

diastolic dysfunction ejection fraction?

A

preserved>smaller volume in but ventricular contraction not compromised

37
Q

describe the RAAS in relation to heart failure

A

HF> reduced CO > reduced blood flow to kidneys > renin released > angiotensinogen converted into Ang-1> ACE converts Ang 1 to Ang 2

> causes vasoconstriction> inc afterload

> causes inc Na and water reabsorption > inc intravascular volume >inc pre load !!

38
Q

what is preload

A

volume of blood entering right side of heart

39
Q

afterload?

A

resistance that the LV must overcome to push blood out

40
Q

what is cariogenic shock?

A

when heart cannot maintain CO (pump failure) > tissues poorly perfused >ishcaemia > organ failure

e.g. MI/ dilated cardiomyopathy/ heart failure

41
Q

types of shock

A

distributive
hypovolaemic
cariogenic
mechanical

> > all produce reduction in BP>tissue ishcaemia > multi organ failure

do this by dec TPR or CO

42
Q

effect of ACE inhibitors

A

reduced ADH and aldosterone release. These both reduce blood pressure.

43
Q

mechanism of action of diuretics

A

act to lower the preload and afterload to decrease the load on the heart, and also to increase fluid loss to lower blood pressure.

44
Q

initial pharmacological therapy for heart failure patient

A 
ACE inhibitor
ARBs (angiotensin receptor blockers)
diuretics
beta blockers
aldosterone receptor antagonist (spironolactone)
45
Q

RAAS system activation causes

A
  • Increased sodium retention leading to increased water retention
  • Increased ADH release
  • Vasoconstriction
  • Enhances Sympathetic activity

> all inc BP!!

46
Q

mitral stenosis effect on pulmonary capillary pressure ?

A
  • inc pulmonary capillary pressure

bc the left atrial pressure increase, which will increase the capillary pressure in the lungs.

Extra ESA2 (32 decks)

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