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Medicine MBBS year 2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

heart failure impairs which part of the cardiac cycle

A

Isovolumetric relaxation phase

Same phase where coronary arteries supply the myocardium

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2
Q

2 determinants of cardiac stroke volume?

A

preload and afterload

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3
Q

preload is determined by which two things?

A
  1. starlings law of the heart

2. cardiac contractibility

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4
Q

high blood pressure increases____of heart

A

afterload

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5
Q

what is Laplaces law?

A

As radius of heart increases for example with dilated cardiomyopathies, decrease in pressure generated and therefore the contractility of the heart falls
P= 2T/R P= 2SW/r

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6
Q

describe:
1 finding in aortic stenosis
1 possible side effect

A

finding = systolic murmur

side effect = left ventricular hypertrophy (increased afterload in LV)

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7
Q

describe:
1 finding in mitral stenosis
1 possible side effect

A

finding = diastolic murmur

side effect = atrial fibrillation (increased pressure in LA)

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8
Q

describe:
1 finding in mitral regurgitation
1 possible side effect

A

systolic murmur

decreased cardiac output -> congestive heart failure

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9
Q

describe:
1 finding in aortic regurgitation
1 possible side effect

A

diastolic murmur

left ventricular dilation, heart failure

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10
Q

describe the pathophysiology of dilated cardiomyopathy

A

Dilated and thin-walled heart chambers with reduced contractility

  • VOLUME overload - eccentric hypertrophy
  • reduced contractility
  • reduced systolic function
  • reduced ejection fraction
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11
Q

most common causes of dilated cardiomyopathy?

A

alcohol, chemotherapy, pregnancy, genetic, idiopathic, viral infections, tachycardia-related cardiomyopathy
also thyroid disease, muscular dystrophy

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12
Q

What genes have been implicated in the diagnosis of dilated cardiomyopathy

A

Mutations in genes encoding cardiac cytoskeleton proteins. E.g. titin, lamin

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13
Q

treatments for dilated cardiomyopathy?

A 
ACE inhibitors
beta-blockers
anticoagulants for atrial fibrillation 
mineralocorticoid receptor antagonists
 diuretics for fluid overload
ICD
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14
Q

signs of dilated cardiomyopathy

A
  • GLOBAL HYPOKENESIS on echocardiogram
  • edema
  • chest pain
  • reduced exercise capacity
  • fatigue
  • ascites
  • complications like abnormal heart rhythms
  • heart murmurs
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15
Q

risks of dilated cardiomyopathy?

A
  • heart failure
  • cardiac arrhythmias
  • sudden cardiac death due to ventricular arrhythmia
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16
Q

causes of hypertrophic cardiomyopathy?

A

chronic PRESSURE overload - e.g due to aortic stenosis or Hypertension

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17
Q

describe the pathophysiology of Arrhythmogenic right ventricular cardiomyopathy.
what are the possible side effects?

A
  • heart muscle of RV replaced by fatty and or fibrous tissue
  • right ventricle dilated
  • ventricular tachycardia and sudden death
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18
Q

treatment for structural heart diseases?

A

aortic valve replacement

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19
Q

what is cardiogenic shock?

A

Impairment in cardiac systolic function, resulting in reduced cardiac output causing end organ dysfunction -

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20
Q

findings in cardiogenic shock?

A

echocardiogram shows ventricles not pumping

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21
Q

cause of cardiogenic shock?

A
  • mostly MI - STEMI mostly
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22
Q

how do you treat cardiogenic shock?

A

PCI/CABG and inotropes to increase stroke volume

persistent shock -> Impella, VA-ECMO.

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23
Q

Angiosarcoma is …..?

A

malignancy of vascular endothelial cells

of skin, heart, liver etc

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24
Q

Myxoma is …..?

A

tumour of connective tissue of heart

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25
Q

state 3 reasons why cardiac cancers are rare

A

Low exposure to carcinogens
High turnover rate of myocytes
Strong selective advantage against things that can compromise function

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26
Q

stroke volume equation?

A

SV = EDV - ESV

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27
Q

cardiac output equation?

A

CO = SV x HR

convert SV from ml to L

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28
Q

ejection fraction equation?

A

ejection fraction = (SV/EDV) x 100

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29
Q

Mean arterial pressure equation?

A 
MAP = DBP + 1/3PP
PP = SBP - DBP
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30
Q

what is infective endocarditis?

A

infection caused by bacteria that enters blood stream and affects heart lining, a heart valve or a blood vessel

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31
Q

what are the dukes criteria for infective endocarditis?

A

major criteria:

  • May be a new regurgitation murmur
  • Blood cultures may isolate a microorganism
  • Echocardiogram can show vegetation, abscess, valve perforation and/or new dehiscence of prosthetic valve.
  • Blood tests show anemia and raised markers of infection
  • coxiella burnetti infection

minor criteria:

  • FEVER >38
  • predisposing heart condition or IV drug use
  • emboli to organs, brain
  • immunologic - glomerulonephritis, oslers nodes, roth spots
  • must have a certain combination to ascertain IE
  • blood tests may also show aneamia or raised markers of infection, night sweats
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32
Q

what features of decompensation would you look for in infective endocarditis?

A

Cardiac decompensation - swelling of legs and abdomen, fatigue, frequent coughing, shortness of breath
Clinical signs like raised JVP, lung crackles, oedema
Vascular and embolic phenomena - stroke, janeway lesions, splinter/conjunctival haemorrhages
Immunological phenomena - osler nodes, roth spots

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33
Q

which part of the heart does infective endocarditis affect?

A

Endocardium, especially the valves of the heart

Aortic valve is most frequently affected (aortic > mitral > right sided valves)

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34
Q

describe the mechanism of ACE inhibitors

A

Inhibit the angiotensin converting enzyme. Prevent the conversion of angiotensin I to angiotensin II by ACE.
preventing arteriolar vasoconstriction, pituitary ADH secretion, sympathetic activity, adrenal adolsterone secretion and resulting salt and water retention.

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35
Q

Which drug classes are used to treat hypertension?

A
  1. ACE inhibitors
  2. Calcium Channel Blockers
  3. Thiazide or Thiazide like diuretics
  4. ARBs
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36
Q

Name ACE inhibitors.

A

“PRIL” drugs

Ramipril, lisinopril, Perindopril

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37
Q

what are some side effects of ACE inhibitors?

A

cough, hyperkalemia, foetal injury, renal failure (in patients with renal artery stenosis), Angioedema

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38
Q

why are ACE inhibitors associated with cough whereas ARBS are not?

A

Increase of bradykinin as ACE enzyme can not break it down

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39
Q

Why might ACE inhibitors and ARBs have a negative effect on eGFR?

A

Angiotensin II is the major determinant of efferent vasoconstriction.
Ang II effect helps maintain GFR when renal perfusion is low e.g. bilateral renal artery stenosis, volume depletion, and elderly patients with CHF
Blocking the effect of Ang II with ACE and ARBS can cause acute renal failure (GFR decreases because glomerular capillary pressure falls as a result of efferent arteriole vasodilation)

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40
Q

Ramipril like most ace inhibitors is a pro drug where lisinopril is not. what does this mean?

A

Pro-drug - inactive before metabolism

Active drug - takes the effect directly

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41
Q

what is the mechanism of ARBs?

A

non-competitive antagonists at AT1 receptor on kidneys and vasculature

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42
Q

some side effects of ARBs

A

hyperkalemia, foetal injury, renal failure (in patients with renal artery stenosis)

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43
Q

Name ARBs

A

“Sartan” drugs

Losartan, Irbesartan, Candesartan

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44
Q

what is the mechanism of calcium channel blockers?

A

Block L-type calcium channels – predominantly on vascular smooth muscle. This results in a decrease in calcium influx, with downstream inhibition of myosin light chain kinase and prevention of cross-bridge formation.

vasodilation - > decreased peripheral resistance

Some block the channels on cardiac muscle and decrease contractility -> decreased CO

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45
Q

Name some calcium channel blockers

A

“PINE” drugs
amlodipine
felodipine

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46
Q

side effects of CCBs?

A

peripheral eodema, flushing headaches, palpitations

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47
Q

What is the key difference in treating patients with amlodipine vs felodipine?

A

Felodipine has a higher plasma clearance rate, a shorter elimination half life, and a shorter time to peak in plasma levels than amlodipine

  • thus felodipine is faster acting
  • but amlodipine will still be effective in morning after sleep
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48
Q

which CCB causes reflex tachycardia ( vasodilation and drop in bp causes increase in SNS activity)?

A

Felodipine

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49
Q

when might you avoid ACE inhibitors and ARBs?

A

before surgery as hyperkalemia may cause problems

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50
Q

what is the mechanism of thiazide like diuretics?

A

They block the Na+, Cl- co-transporter in the early DCT.

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51
Q

name some thiazide like diuretics.

A

thiaziade, indapamide (thaizide-like)

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52
Q

what are some side effects of thiazide like diuretics?

A

Hypokalemia, Hyponatremia,Metabolic alkalosis (increased hydrogen ion excretion), Hypercalcemia, Hyperglycemia (hyperpolarised pancreatic beta cells), Hyperuricemia.

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53
Q

describe the electrode placement for Leads 1-3

A

Lead 1 = right arm to L eft arm
Lead 2 = right arm to L eft L eg
Lead 3 = L eft arm to L eft L eg

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54
Q

describe the electrode placement for V1-6

A 
V1 = right sternal border-4th intercostal space 
V2 = left sternal border 4th intercostal space 
V4 =  left midclavicular line 5th space
V5 =  at level of V4, anterior axillary line 
V6 = at level of V4, mid-axillary line
V3 = halfway between V2 and 4
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55
Q

label an ECG trace with the leads, their corresponding views of the heart and corresponding arteries (arteries occluded during ST elevation of each lead)

A

refer to notes

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56
Q

label an ECG trace with the leads, their corresponding views of the heart and corresponding arteries (arteries occluded during MI shown through ST elevation of lead)

A

refer to notes

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57
Q

1 small vertical square on an ecg represents?

A

1 small vertical square in ECG = 0.1 mV. 1mV (2 large squares) = 10mm. So 1 small square = 1mm

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58
Q

1 small horizontal square on an ecg represents?

A

0.04 seconds

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59
Q

a normal cardiac axis range is between?

A

-30 to + 90

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60
Q

to calculate the cardiac axis what do you need?

A

two leads that are perpendicular/90 degrees apart

e.g. lead II and AVL

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61
Q

what happens in sinus arhhythmia?

A

R-R interval varies with breathing cycle

62
Q

what happens in sinus bradycardia

A

even R-R but slow

- can be healthy, caused by medicaition or vagal stimulation

63
Q

what happens in sinus bradycardia

A

even R-R/ regular rate but slow

- can be healthy, caused by medication or vagal stimulation

64
Q

what happens in sinus tachycardia

A

even R-R/ rate regular but fast

65
Q

what happens in atrial flutter?

A

regular saw tooth pattern in baseline in leads II, III, aVF

66
Q

what happens in 1st degree heart block?

A

prolonged PR interval. normal is 0.12-0.2s
1:1 ratio of p waves to QRS complex
a progressive disease of ageing

67
Q

what happens in second degree heart block type 1?

A

gradual prolongation of PR interval until a beat is skipped (QRS missed out)
caused by diseased AV node

68
Q

what happens in second degree heart block type 2?

A

no PR elongation, however missing QRS complex. can be in a ratio e.g. 2:1 or random

69
Q

what happens in 3rd degree/ complete heart block?

A

p waves are not spaced at the same rhythm as R-R intervals. Constant P-P and R-R intervals
P waves can also be hidden within bigger vectors and not show up on ECG
Atria and ventricles beat asynchronously. Atrial is faster. Can be missing QRS.

70
Q

what happens in ventricular tachycardia?

A
  • rate is fast and regular - 100-200bpm
  • risk of deteriorating into fibrillation
  • hidden p waves
  • shockable rhythm
71
Q

what happens in ventricular fibrillation?

A
  • rate is fast and irregular- 250 bpm and above
  • shockable rhythm
  • VF = CARDIAC ARREST
72
Q

what causes ST elevation?

A

infarction - ST segment is elevated >2mm

73
Q

what causes ST depression?

A

myocardial ischeamia.

ST segment depressed > 2mm

74
Q

what is a normal PR interval?

A

0.12 - 0.20 seconds

75
Q

left and right bundle branch blocks result in?

A

wide QRS complex

76
Q

treatment for a myocardial infarction?

A

stent insertion, bypass

77
Q

how do you calculate heart rate from ECG strip

A

1/R-R = Beats per second

x 60 = per minute

78
Q

how do you calculate pH

A

-log10[H+]

79
Q

what is Fi02?

A

Inspired oxygen - 0.21= 21% oxygen = room air

80
Q

Percentage of respiratory acid to metabolic acid in body?

A

99% respiratory

81
Q

how does your body compensate for changes in pH?

A

Changes in ventilation rate

Kidneys change in HCO3- and H+ secretion and excretion

82
Q

how do you interpret an arterial blood gas? give tips

A

high pH= alkalosis and vice versa
base excess is neutral =uncompensated respiratory
PaCo2 is neutral = uncompensated metabolic
mixed issue= base excess and PaCO2 are going in opposite directions.
Partially compensated issue - PaCO2 and base excess are going in the same direction. Ph has not normalised
Fully compensated - pH is normal, can’t determine exact issue

83
Q

hyperventilation causes____?

A

respiratory alkalosis

84
Q

hypoventilation causes___?

A

respiratory acidosis

85
Q

diarrhoea causes ___?

A

metabolic acidosis

86
Q

vomiting causes____?

A

metabolic alkalosis. (loss of gastric acid secretions/H+)

87
Q

What is the basic structure of blood vessels?

A 
Tunica intima (endothelium) - inner layer
Tunica media (smooth muscle cells)
Tunica adventitia (vasa vasorum, nerves) - outer layer
88
Q

Describe how capillary and venule structure differ from arteries

A

They only have an endothelium supported by mural cells and a basement membrane

89
Q

State 3 functions of the vascular endothelium

A 
Promotes tissue homeostasis and regeneration (it is a source of angiocrine factors) 
Permeability
Inflammation 
Haemostasis and thrombosis
Angiogenesis
Vascular tone
90
Q

What evidence is there that vascular endothelium promotes tissue homeostasis?

A

damage of endothelium can cause end-organ dysfunction

91
Q

State 4 diseases in which the vascular endothelium is dysfunctional

A

Cancer, diabetes, chronic inflammatory diseases, ischemia, atherosclerosis

92
Q

Endothelial cells form a flat monolayer and have cell-cell junctions. Tell each other to stop proliferating. This is called ____ _____

A

contact inhibition

93
Q

In which type of blood vessel do the majority of endothelial cells reside?

A

capillary

94
Q

What responses do you see in an activated epithelium?

A

Pro-inflammatory, pro-thrombotic, pro-angiogenic

In the resting state you get anti-inflammatory etc

95
Q

State 4 risk factors for atherosclerosis

A

Hypertension, Diabetes, Hypercholesterolaemia, Sex hormone imbalance, Ageing
Infectious agents, Proinflammatory cytokines, Oxidative stress
Environmental toxins, Heamodynamic forces

96
Q

State the 4 Mechanisms contributing to atherosclerosis

A
  1. Leukocyte recruitment
  2. Permeability
  3. Shear stress
  4. Angiogenesis
97
Q

Describe how Leukocyte recruitment contributes to atherosclerosis

A
  • Leukocyte adhere to endothelium of large arteries and get stuck in sub-endothelial space. They differentiate into macrophages and foam cells
  • In a normal person leukocytes would adhere to endothelium of post-capillary venules and transmigrate into tissues
98
Q

Describe how Permeability contributes to atherosclerosis

A
  • Increased permeability causes leakage of plasma proteins into sub-endothelial space
  • LDLs sticks to proteoglycans and is oxidised by free radicals
  • Macrophage engulf oxidised LDLs and form foam cells (fatty streak formation)
99
Q

Describe how shear stress contributes to atherosclerosis

A
  • Atherosclerotic plaques occur preferentially at bifurcations and curvatures of vasculature
  • This is because blood flow is disturbed. Irregular distribution of low wall sher stress
  • Disturbed blood flow promotes thrombosis, inflammation, endothelial apoptosis, SMC proliferation, loss of NO production!!!!
100
Q

Describe how angiogenesis contributes to atherosclerosis

A

It is triggered by hypoxia
Endothelial cell migration, proliferation and formation of new vessel sprouting out from old
It promotes plaque growth

101
Q

state 1 reason why NO is essential for cardiovascular health?

A

Dilates blood vessels, reduces platelet activation, reduces proliferation of SMC, reduces release of superoxide radicals, reduces oxidation of LDL cholesterol

102
Q

what mechanism is involved in the LATE stage of atherosclerotic plaques development?

A

angiogenesis

103
Q

State ways in which the vascular endothelium plays a role in covid 19

A
  • Increased circulating endothelial cells

- Cytokine storm -> activates the endothelium -> thrombi formation

104
Q

Which risk factor for atherosclerosis hasnt been reduced over the last decade through medication?

A

diabetes

105
Q

State 2 complications of an advanced atherosclerotic plaque

A

plaque rupture, stenosis

106
Q

What is the main function of T lymphocytes in atherosclerosis

A

macrophage activation

107
Q

State a function of vascular smooth muscle in atherosclerosis?

A

Migration and proliferation - formation of fibrous cap

108
Q

state 5 functions of macrophages in atherosclerosis

A
  1. Foam cell formation
  2. Cytokine release (IL-1) and chemokine release (MCP-1)
  3. Source of free radicals - oxidative enzymes like NADPH oxidase and Myeloperoxidase needed for free radical generation - radicals further oxidise LDL
  4. Growth factor release - PDGF + TGF-b - causes VSMC proliferation and extracellular matrix deposition (fibrous cap formation)
  5. Express Metalloproteinases - lead to plaque erosion/rupture -> occlusive thrombus
109
Q

State 2 functions of vascular endothelial cells in atherosclerosis

A

Barrier function - to lipoproteins

Leukocyte recruitment

110
Q

Macrophage specific protein CD68 stains___ colour?

A

brown

111
Q

What role does OXIDISED LDL play in atherosclerosis?

A

Chronic Inflammation - damages epithelium and smooth muscle. Also phagocytosed by macrophages which triggers inflammation

112
Q

In Familial hyperlipidemia, there is a deficiency of LDL ___. LDL levels climb. __ receptors on macrophages cause them to accumulate OXIDISED LDL. Xanthomas form and contain _ cells. An associated disease is _.

A

Receptors
Scavenger
Foam
Atherosclerosis

113
Q

Compare and contrast macrophage scavenger receptor A and B

A

A= CD204 B = CD36
A binds to gram+ bacteria, B binds to malaria parasites
Both bind to oxidised LDL and dead cells

114
Q

What are the findings in a vulnerable atherosclerotic plaque?

A

Thin fibrous cap, reduced VSMC and collagen, infiltrate of activated macrophages expressing MMPs, large eccentric lipid rich necrotic core

115
Q

What causes macrophage apoptosis in atherosclerosis and what happens after?

A

Toxic oxidised LDL derivatives

Lipids are released into lipid necrotic core

116
Q

What transcription factor is the “master” regulation of inflammation?

A

NFkB

117
Q

What are the signs and symptoms of ischemic heart disease?

A

angina chest pain - can radiate to arms, back, jaw, neck, shoulder
High or low bp, syncope
Heart rhythm problems
General important signs - leg swelling, reduced exercise capacity, diaphoresis, nausea, fatigue, SOB, dizziness

118
Q

What are the risk factors of ischemic heart disease

A

non - modifiable - age, gender (more in male), ethnicity(more in eastern european), genetic evidence, family history, previous history of CVD

Modifiable - high blood pressure, cholesterol, smoking, alcohol, diabetes, bmi, diet, low socio-economic background, stress

119
Q

What is the greatest risk factor for IHD?

A

diet

120
Q

An atherosclerotic plaque is mainly made of?

A

fibrous tissue

121
Q

State 3 things that cause obstruction of coronary blood flow

A
  1. Atheroma
  2. Thrombosis
  3. Spasm
  4. Embolus
  5. Coronary ostial stenosis
  6. Coronary arteritis
122
Q

Describe the different ways in which a patient with IHD can present

A 
Asymptomatic
Chronic stable angina
Acute Coronary Syndromes - Unstable angina, NSTEMI, STEMI
Heart Failure 
Sudden Death
123
Q

When atherosclerotic plaque breaks and becomes in contact with blood. State 3 ways in which thrombus could form

A

Fibrin deposition
RBCs entrapped
Blood platelets adhere to it

124
Q

During hypoxia. ___ in the heart dilate. It is more effective in __ atherosclerosis than chronic.

A

collaterals

acute

125
Q

In the late staves of MI, Vessels walls ___ increases, fluid leak and local tissue oedematous. Cardiac muscle cells swell and due to no blood supply die within few hours

A

permeability

126
Q

State 2 causes of death after a MI

A
  1. Decreased cardiac output-systolic stretch and cardiac shock
  2. Damming of blood in body’s venous system
  3. Ventricular fibrillation
  4. Rupture of infarcted area
127
Q

Differentiate between the effect on muscle of small vs large area ischemia

A

Small area - centre of lesion is temporarily non functional

Large area - centre is dead, surrounding non-functional tissue

128
Q

State a risk assessment tool used for IHD

A

JBS3, QRISK*3

129
Q

how do you diagnose IHD?

A

Clinical history and symptoms - e.g. chest pain
Serum markers of cardiac event - troponin, LDH, CK, AST
lipid profile
Clinical examinations - heart auscultation, BP, BMI, GPE
Biomarkers for predicting death - BNP, CRP, Renin, ACR
ECG
Echocardiography (transesophageal can be used to assess for aortic dissection)
Coronary angiography
US and doppler velocity probes - ultrasonography of common and internal carotid arteries.

130
Q

ECG findings in stable angina?

A

Normal - ST depression only during stress test

131
Q

ECG findings in unstable angina and NSTEMI?

A

Both have ST depression and T wave inversion

Only NSTEMI has elevated Troponins

132
Q

ECGG in acute MI/STEMI

A

ST segment elevation with T wave inversion.

Q waves

133
Q

state 3 pharmacological treatments for IHD

A 
HMG-Coa reductase inhibitors
Bile acid sequestrants 
CCBS, ACE inhibitors
Beta blockers
Anti-anginal agents
Platelet aggregation inhibitors
Nitrates
134
Q

State 2 surgical treatments for IHD

A

PCI and CABG

135
Q

Which 3 features must be present in typical angina?

A

Precipitated by physical exertion
Constricting discomfort in the front of the chest, neck, shoulders, jaw or arms
Relieved by rest or GTN within 5 minutes

136
Q

What 3 features must be present in atypical angina?

A

2 features in typical angina

Plus GI discomfort and/or breathlessness and or nausea

137
Q

Pain associated with dizziness, palpitations, tingling, difficulty swallowing or brought on by breathing is ___ to be stable angina

A

unlikely

138
Q

A 64 year old man presents with increasing breathlessness and chest pain on exertion. what are the differentials?

A
  1. Pulmonary - Asthma, copd, pulmonary embolism
  2. Cardiovascular - Stable angina, unstable angina, pericarditis
  3. GI -Heartburn
  4. MSK
139
Q

__ angina occurs when resting, lasts longer than stable, rest and medicine don’t relive it, can get worse over time/lead to MI

A

unstable

140
Q

__ angina is caused by a spasm in coronary artery due to cold, stress, smoking

A

Prinzmetal/Variant/Vasospastic

141
Q

why is it important to check troponin levels when a patient presents with increasing breathlessness and chest pain on exercise for instance? how do you interpret the troponin results?

A

Troponin rises after 4 hours of MI and is elevated for up to two weeks

If troponin levels are normal - less likely symptoms due to heart muscle damage. Stable angina more likely.

Rise and or fall in series of troponin indicates heart attack

142
Q

what is the first line treatment for stable angina?

A
  1. short acting nitrate (e..g sublingual nitrogen) + B blocker OR CCB

Low heart rate (<60) - consider DHP CCB

symptoms remain uncontrolled - consider B-blocker + DHP CCB

143
Q

what is the second line treatment for stable angina if first line fails?

A 
long acting nitrate 
ivabradine
nicorandil
ranolazine 
trimetazidine

if these fail - consider revascularisation

144
Q

ST elevation in leads 1, aVL and V6
Reciprocal changes - ST depression in inferior leads (III and aVF)

what is your diagnosis?

A

Lateral STEMI

145
Q

Table ST segment elevation, reciprocal changes, coronary artery involved and type of MI

A

refer to notes

146
Q

ST depression leads 2,3. T wave inversions.

what is your diagnosis?

A

NSTEMI or Unstable Angina

147
Q

What is the 1st line management for a STEMI?

A
  1. antiplatelet and anticoagulant therapy
  2. reperfusion - PCI first line
  3. long term management (antiplatelets, B-blocker, statin, ACE inhibitor)
148
Q

How would you treat NSTEMI and Unstable angina?

A
  1. If patient is unstable, has positive troponin or ST changes = high risk - PCI, CABG
  2. If patient is low risk. perform stress ECG. Positive stress ECG - coronary angiography, PCI, CABG
149
Q

why does sublingual glycerol trinitrate alleviate stable angina?

A

vasodilation increases blood supply

150
Q

describe the mechanism of digoxin. what is it used to treat?

A

Digoxin inhibits the Na+/K+ exchange ATPase on cardiac myocytes and nodal tissue.
Competes for K+ binding site. Increases heart contractility. Decreases heart rate.

atrial fibrillation, Heart failure

151
Q

why are potassium blood levels important when a patient is on digoxin?

A

Hypokalemia means more digoxin binding (less competition by K+) . Enhanced therapeutic and adverse effects of digoxin (heart block)

Hyperkalemia (e.g. in kidney disease) -> reduced clearance -> more digoxin

Medicine MBBS year 2 (11 decks)

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