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Phase 2a > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

what infective endocarditis infections cannot be cultures

A

coxiella burnetti

chlamydia psittaci

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2
Q

what are the 3 groups of people who suffer infective endocarditis

A
  1. those with native valve disease
  2. IV drug users
  3. those with prosthetic valves
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3
Q

what is atherosclerosis

A

a plaque blockage of an artery

can form thrombus when ruptures

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4
Q

what is atherogenesis

A

the process of plaque forming in arteries

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5
Q

where are atherosclerotic plaques located

A

peripheral and coronary arteries usually

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6
Q

what factors affect where plaques are found

A

changes in flow
altered gene expression
wall thickness changes

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7
Q

what is the structure of an astherosclerotic plaque

A

lipid
necrotic core
connective tissue
fibrous cap

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8
Q

what is the cause of atheroscelrotic plaque formation

A

endothelial cells respond to injury but this is innapropriate as there is not injury - endothelial dysfunction - signals sent to leukocytes = inflammation

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9
Q

what inflammatory markers are found in plaque

A 
IL2,6,8
IFN gamma
TGF beta
MCP1
C reactive protein = non-specific inflamm marker, can be elevated in STEMI
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10
Q

what are the complications of plaque

A 
haemorrhage
plaque rupture/fissure
overlying thrombosis
progression of plaque
artery dissection
aneurysm
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11
Q

describe artery dissection as a result of plaque

A

blood enters between intima and media = pushes the plaque into lumen of vessel
= can cause dissection of adventitia and media

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12
Q

describe an aneurysm as a result of plaque

A

blood enters between intima and media and causes the vessel to expand

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13
Q

name some treatments of coronary artery disease

A 
percutaneous coronary intervention (PCI)
drug elution stent
aspirin
clopidogrel
statins
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14
Q

what is an interval on ECG

A

from start of one bit to end f another bit

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15
Q

what is a segment on ECG

A

from end of one bit to start of another bit

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16
Q

how long is a small box on ECG

A

0.04s

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17
Q

how long is large box on ECG

A

0.2s

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18
Q

what is angina

A

symptom which occurs as a consequence of restricted coronary artery which causes ischaemia

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19
Q

what is prinzmetal’s angina

A

unstable angina caused by coronary artery spasm not related to exertion

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20
Q

what is unstable angina

A

plaque ruptures and thrombus forms = partial or full occlusion of coronary artery = increased risk of MI
pain at rest
also called acute coronary syndrome

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21
Q

what are the 3 features that confirm stable angina

A
  1. heavy tight radiating to arm cardiac chest pain
  2. chest pain especially on exertion
  3. pain relieved by GTN spray
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22
Q

what 2 features suggest unstable angina

A
  1. pain at rest

2. partially relieved by GTN

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23
Q

what age and gender are at higher risk of angina

A

males, old

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24
Q

name 6 differential diagnoses for angina (5Ps)

A 
pericarditis
pleural effusion
pulmonary embolism
pneumonia
pneumothorax
GORD
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25
Q

what will an ECG of angina look like

A

normal, may show ST depression and flat T wave

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26
Q

what investigations should be carried out for suspected angina

A 
ECG
CT angiogram (gold standard)
stress echo, cardiac MRI, echo = differential diagnoses
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27
Q

what is a SCORE quiz

A

systematic coronary risk estimation quiz

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28
Q

describe primary prevention of coronary artery disease

A
  1. lifestyle changes

2. pharmacological = antihypertensives, statins, diabetes treatment for T2

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29
Q

describe the pharmacological secondary prevention of coronary artery disease

A
  1. nitrates = GTN spray = venodilator = decrease pre-load and dilate coronary arteries
  2. beta blockers = inotropic heart effects = propranolol
  3. calcium channel blockers = prevent smooth muscle contraction/coronary spasm = arterodilator
  4. antiplatelets = prevent clots
  5. statins = reduce LDL
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30
Q

what are the significant side effects of beta blockers

A

bronchospasm

cold fingers

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31
Q

name 2 beta blockers

A

atenolol

bisoprolol

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32
Q

name 2 calcium channel blockers

A

amlodipine

verapamil

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33
Q

name 3 anti-platelet drugs

A

aspirin
clopidogrel = P2Y12 inhibitor
ticagrelor = P2Y12 inhibitor

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34
Q

name 2 statins

A

atorvastatin

simvastatin

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35
Q

what type of acute coronary syndrome is it not suitable to use beta blockers as treatment

A

prinzmetals angina

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36
Q

describe the surgical methods to manage acute coronary syndromes

A
  1. percutaneous coronary intervention PCI = stenting increases vessel diameter
  2. coronary artery bypass graft CABG = saphenous vein and internal mammary artery graft to bypass blocked coronary artery
  3. in MI = urgent coronary angioplasty if ST elevation in more than 2 leads/LBBB present
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37
Q

what is acute coronary syndrome

A

encompasses unstable angina, NSTEMI, STEMI = coronary artery blockage via thrombus or embolism

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38
Q

what are the general symptoms for acute coronary syndrome

A 
acute central chest pain longer than 20 mins radiating to arm neck and jaw
nausea
sweating
SOB
palpitation
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39
Q

what is the initial management for all acute coronary syndromes (NSTEMI, MI)

A 
MOAN
morphine
oxygen
aspirin/clopidogrel
nitrates
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40
Q

what are the signs of acute coronary syndrome

A

distress, pallor, anxiety
bradycardic or tachycardic
high or low BP
4th heart sound

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41
Q

name a chronic coronary syndrome

A

stable angina

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42
Q

what is an acute myocardial infarction

A

complete blockage of a coronary artery

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43
Q

what investigations would you do for an MI

A

ECG
CXR
FBC, U&E, glucose, lipids
cardiac enzymes - troponin T and I

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44
Q

what is significant on an ECG during an MI

A

STEMI = ST elevation

NSTEMI/unstable angina = ST depression or T wave inversion, new Q waves

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45
Q

what can an ECG indicate about a patients history

A

can show whether have suffered an MI in the past

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46
Q

how are acute coronary syndromes treated lifelong

A

P2Y12 inhibitor e.g. clopidogrel = at least 1 year
aspirin = lifelong
statins = lifelong
ACE inhibitors = long term at highest dose poss
Beta blockers = long term if LV function reduced, stop BB if LV function good
anticoagulant e.g. heparin ?

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47
Q

what are the main causes of acute coronary syndromes

A 
plaque rupture causing thrombosis
coronary vasospasm
drug abuse
dissection of coronary artery bc of connective tissue defects
thoracic aorta dissection
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48
Q

what is troponin

A

protein complex that regulates actin/myosin interaction

highly sensitive marker for cardiac muscle injury

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49
Q

what conditions cause raised troponin

A

MI
arrhythmias
heart failure

myocarditis
gram negative sepsis
PE

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50
Q

describe the layers of the pericardium

A

dual layer:
thin visceral layer attached to epicardium
thick fibrous parietal layer anchored to diaphragm

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51
Q

what is the role of the pericardium

A

acts to restrain filling volume of heart so it doesnt overfill
is able to stretch but will become stiff at high tension

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52
Q

describe the pathophysiology of chronic pericardial effusion

A

fluid builds up slowly = pericardium stretches instead of becoming stiff
changes compliance and reduced effect on diastolic filling of chambers

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53
Q

describe the pathophysiology of a cardiac tamponade

A

occurs acutely
pericardium fills quickly and therefore becomes stiff
pericardium continues to fill = compress the heart

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54
Q

what is becks triad

A

= 3 signs of cardiac tamponade

  1. muffled heart sounds
  2. jugular vein distension
  3. hypotension with narrowed pulse pressure
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55
Q

what is pericarditis

A

inflammation of the pericardium with or without effusion

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56
Q

name the infectious causes of pericarditis

A

enterovirus
adenovirus
parvovirus B19
herpes

mycobacterium TB
rheumatic fever
staph/strep

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57
Q

name the autoimmune causes of pericarditis

A

sjogren syndrome
rheumatoid arthritis
scleroderma

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58
Q

what is the main non infectious cause of pericarditis

A

neoplasm = mets

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59
Q

what is pulses paradoxus

A

fall of systolic blood pressure on inspiration

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60
Q

what is Kussmaul’s sign

A

increase of or failure for systolic blood pressure to fall during inspiration (jugular venous pressure)

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61
Q

what is particular about an ECG in pericarditis

A

saddle shaped ST segment across lots of territories

widespread ST elevation

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62
Q

what are the major predictors of complications of pericarditis

A

fever above 38
subacute onset
large pericardial effusion
lack of response to aspirin/NSAID

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63
Q

what are the minor predictors of complications of pericarditis

A

myopericarditis
immunosuppression
trauma
oral anticoagulation therapy

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64
Q

what are the differential diagnoses of pericarditis

A 
pneumonia
pleurisy
GORD
MI
pancreatitis
herpes zoster
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65
Q

what is cardiac myopathy

A

primary heart muscle disease

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66
Q

name the 3 main types of cardiac myopathy

A

hypertrophic
dilated
arrhythmogenic

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67
Q

what is signifcant about the chest pain associated with pericarditis

A

worse when lying down

relieved by sitting forward

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68
Q

what are the signs of cardiac tamponade

A

high HR
low BP
pulses paradoxus
high JVP

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69
Q

what may a CXR of pericarditis show

A

cardiomegaly

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70
Q

what is hypertrophic cardiomyopathy HCM

A

heart muscles become thicker (larger than 12mm) = ventricles become smaller
increases systolic function
causes dystolic dysfunction
caused by sarcomeric protein gene mutation

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71
Q

describe the pathophysiology of hypertrophic cardiomyopathy causing arrhythmias

A

fibrosis and scarring of heart
myofibrils in disarray microscopically
vessels supplying myocardium decrease in size
= changes in electrical conduction/ CAN CAUSE ARRHYTHMIAS

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72
Q

what is dilated cardiomyopathy DCM

A

ventricles and atria are dilated
in 1V, 2V or all chambers of heart
walls of heart normal thickness or too thin

73
Q

what would someone with dilated cardiomyopathy DCM usually present with

A

heart failure due to decreased contractability

74
Q

what is arrythmogenic cardiomyopathy

A

ventricular myocardium is eaten away and replaced by fibrous tissue which leads to conduction abnormalities and therefore ventricular arrhythmias
caused by desmosome gene mutation

75
Q

what else is affected in arrythmogenic cardiomyopathy

A

desmosomes

= difficulty transferring action potentials through heart

76
Q

what is naxos disease and what is its significance

A

characteristic wooly hair
palmar planter keratoderma
people with naxos = predisposition to arrythmogenic cardiomyopathy

77
Q

what is long QT syndrome

A

issue with repolarisation of the heart = increased risk of arrhythmias
exercise/certain drugs can cause sudden death

78
Q

what is Brugada syndrome

A

a genetic predisposition to arrhythmias

79
Q

what is CPVT

A

catecholaminergic polymorphic ventricular tachycardia
= ventricular tachycardia triggered by adrenaline
increase in adrenaline can cause cardiac arrest and sudden death
tendency for arrhythmias to occur all day

80
Q

what is Marfans disease

A

genetic lack of fibrillin
can cause aortic aneurisms (typically at aortic root due to high fibrillin levels)
individuals = long legs, chest wall abnormalities, long arms, short sighted

81
Q

what is familiar hypercholesteraemia FH

A

genetically high cholesterol levels (above 12)
fatty deposits on corneas and tendons often present
coronary artery blockage often present

82
Q

describe the pathophysiology of familiar hypercholesteraemia FH

A

abnormal LDL receptors present = LDL not absorbed by liver = high blood LDL
treated with statins

83
Q

what is the prevalence of HCM

A

1 in 500

84
Q

name 4 inherited channelopathies

A

long QT syndrome
short QT syndrome
Brugada syndrome
CPVT

85
Q

what is congenital heart disease

A

changes in heart structure present at birth

lesions may be minor or incompatible with life ex utero

86
Q

what defects cause a severe risk in pregnancy

A

pulmonary hypertension
left heart obstruction
reduced ejection fraction (below 30%)
marfans

87
Q

what defects cause a moderate risk in pregnancy

A 
unrepaired coarctations (narrowing)
aortic stenosis
mechanical heart valves
88
Q

what is tetrology of Fallot (blue babies)

A

= combination of 4 congenital anomalies due to abnormal separation of truncus arteriosus into aorta and PA

  1. ventricular septal defect VSD
  2. pulmonary valve stenosis
  3. misplaced/overriding aorta
  4. RV hypertrophy
89
Q

describe the pathophysiology of tetrology of Fallot

A

failure of fusion of IV septum = stenosis of pulmonary artery
results in blood flowing from right to left due to increase in RV pressure due to PA stenosis = deoxygenated blood passes from RV to LV = causes cyanosis
RV often becomes dilated

90
Q

what is eisenmenger’s syndrome

A

long standing left to right shunt = oxygenated blood entering pulmonary arteries and going to lungs = high pulmonary blood flow and therefore damage to vasculature
= increased resistance to blood flow through lungs = increased RV pressure
= shunt direction reverses and blood travels from right to left = cyanosis occurs
over time this can develop into pulmonary hypertension

91
Q

name the 3 main types of atrial septal defect

A

primum
secondum
sinus venosus

92
Q

what is sinus venosus atrial septal defect

A

defect occurs at superior vena cava and right atrium junction where R pulmonary artery enters heart

93
Q

what is an atrio-ventricular septal defect AVSD

A

hole in centre of heart which involves ventricular and atrial septum
can also involve mitral and tricuspid valve
can be complete or partial defect

94
Q

what genetic condition is related to AVSD

A

down syndrome trisomy 21

95
Q

describe complete AVSD

A

involvement of both AV valves = large malformed one
breathless as neonate
poor weight and feeding
torrential pulmonary blood flow = need repairing to prevent eisenmengers syndrome

96
Q

describe partial AVSD

A

can present late into adulthood - small VSD or ASD

97
Q

what is the difference between large and small ductus arteriosus

A 
large = can cause eisenmengers, needs to be surgically closed
small = usually asymptomatic , slight increased risk of IE
98
Q

what is pulmonary stenosis

A

narrowing of outflow of right ventricle

can be valvar, sub-valvar, supra-valvar, branch

99
Q

what is the treatment for pulmonary stenosis

A

shunt
balloon valvuloplasty
open valvotomy
trans-annualr patch

100
Q

what occurs in severe pulmonary stenosis

A 
RV failure in neonates
RV hypertrophy
poor pulmonary blood flow
tricuspid regurgitation
collapse
101
Q

what occurs in mild pulmonary stenosis

A

well tolerated for many years

RV hypertrophy occurs

102
Q

what is heart failure

A

inability of heart to deliver blood and oxygen at a rate commensurate with the requirements of the metabolising tissues despite normal or increased cardiac filling pressures

103
Q

describe the pathophysiology of heart failure

A

reduced ability of myocardium = reduced contractile forces
= when ventricles fill the heart cannot increase contractile forces to respond
= failure of frank starling mechanism
= increased end diastolic volume

104
Q

describe the compensatory mechanism for heart failure

A
  1. activation of RAAS = increase peripheral vasoconstriction/Na and H2O retention = increase preload
  2. activation of sympathetic NS = increase HR and cause peripheral vasoconstriction = increase after load
    chronic activation of these = worsens HF and increases cardiac damage
105
Q

name the 4 ways HF can be classified

A
  1. right or left sided
  2. reduced ejection fraction or preserved ejection fraction
  3. arrhythmias
  4. valvular dysfunction
106
Q

what is BNP

A

B-type natriuretic peptide
secreted from ventricles in response to increased pressure and stretch
biomarker for HF
= if above 100 = best diagnosis of HF

107
Q

describe the New York Heart Association classification of heart failure

A 
class I = no limitations/symptoms
class II = slight limitation
class III = marked limitation 
class IV = inability to carry out any phys activities without discomfort
108
Q

inotropic definition

A

modifying speed or force of CONTRACTION on heart muscles

109
Q

chronotropic definition

A

modifying heart rate or rhythm by affecting electrical conduction and nerves that influence conduction

110
Q

describe systolic HF

A 
ventricles cant contract properly = ejection fraction below 40% + reduced CO
caused by
IHD 
MI
cardiomyopathy
111
Q

describe diastolic HF

A

ventricles cant relax properly = ejection fraction above 50%

caused by ventricular hypertrophy, constricted pericarditis, restricted cardiomyopathy

112
Q

describe class 1 antiarrhythmics

A 
= sodium channel blockers
e.g.
disopyramide
lidocaine
flecainide
113
Q

describe the classes of antiarrhythmia drugs

A 
class I = sodium channel blockers
class II = beta blockers
class III = prolong action potential AMIODARONE
class IV = calcium channel blockers
114
Q

describe the mechanism of aspirin

A

permanently binds to COX-1 which inhibits thromboxane formation = therefore decreases platelet activation and aggregation
acts for lifetime of platelets

115
Q

what is the life cycle of platelets

A

7-10 days

116
Q

name 4 ways aspirin is used for treatment

A
  1. anticoagulation
  2. MI risk reduction
  3. analgesic
  4. arterial thrombus
117
Q

what are the side effects of aspirin

A

GI bleeding
hives
allergic reaction

118
Q

describe the mechanism of P2Y12 inhibitors

A

inhibit P2Y12 pathway = reduce platelet aggregation
usually dual therapy with aspirin
inhibited by morphine = give more if morphine also being used

119
Q

what are the side effects of P2Y12 inhibitors

A

bleeding
dyspnoea
neutropenia (low neutrophils)
diarrhoea

120
Q

describe the mechanism of GPIIb/IIa antagonists

A

act to inhibit glycoprotein IIb/IIa = prevent platelet aggregation and thrombus formation
has MAJOR risk of bleeding
risk of thrombocytopenia

121
Q

name 2 GPIIb/IIa antagonists

A

roxifiban

abciximab

122
Q

describe the mechanism of statins

A

inhibit HMG-CoA reductase = decrease cholesterol synthesis in the liver and increase expression of LDL receptor on cell membranes = more LDL cleared from bloodstream

123
Q

describe the side effects of statins

A 
haemorrhagic stroke
liver dysfunction
sexual dysfunction
neuropathy
muscle pain
rhabdomyolysis = muscle breakdown
124
Q

what is fondaparinux

A

binds to antithrombin 3
inhibits factor X = decrease platelet aggregation
used to treat pre-angiogram in MI, DVT prevention/treatment

125
Q

describe the mechanism of heparin

A

acts as anticoagulant by indirectly inhibiting thrombin

126
Q

what is bivalirudin

A

anticoagulant which directly inhibits thrombin
used to treat PCI for STEMI, thrombotic events
can cause headache, nausea, vomiting, pelvic/back pain

127
Q

what is colchicine

A

used to treat pericarditis

side effects = regularly cause nausea and diarrhoea

128
Q

describe the mechanism of warfarin

A

prevents synthesis of clotting factors 1972 (1 is 10) by acting as Vitamin K antagonist = prolong PT time

129
Q

describe the side effects of warfarin

A

haemorrhage
warfarin necrosis (gross limb necrosis_ caused by protein C deficiency
osteoporosis

130
Q

describe the mechanism of direct oral anticoagulant

A 
directly acts on factors II and X (2 and 10)
used to treat 
AF
DVT
PE
for prophylaxis
131
Q

name 2 DOAC’s

A

rivaroxaban

apixaban

132
Q

what are the side effects of DOACs

A

cross across placenta in pregnancy

haemorrhage

133
Q

name the 3 signs of IE that have funky names

A

Roth’s spots = haemorrhage in retina
Osler’s nodes = red lesions on fingers and toes
Janeway lesions = on palms and plantar

134
Q

what are the major criteria for IE

A
  1. positive blood culture
  2. vegetations on echo
  3. new valvular regurgitation
135
Q

what are the minor criteria for IE

A
  1. predisposing factor
  2. fever more than 38
  3. vascular signs e.g. emboli, janeway lesions
  4. immmunological phenomenon e.g. oslers nodes, roths spots
  5. microbiological evidence = positive blood culture but does not meet other criteria
136
Q

what are ectopic beats

A

extra heart beats/skipped heartbeat

137
Q

describe Virchow’s triad

A

3 categories that contribute to thrombus formation:

  1. hypercoagubility
  2. haemodynamic changes
  3. endothelial injury or dysfunction
138
Q

how does sedentary behaviour physiologically increase the risk of thrombus formation

A

= haemodynamic change

greater contact between platelets and coagulation factors with vascular endothelium

139
Q

how does hypertension physiologically increase the risk of thrombus formation

A

higher blood pressure = greater shearing forces = cause greater platelet aggregation and activation

140
Q

how does smoking physiologically increase the risk of thrombus formation

A

nicotine, free radicals, NO = increase endothelial damage = increase thrombosis

141
Q

describe a WELLS score

A

2+ = likely DVT

under 1 = do D-dimer to rule out DVT

142
Q

name 3 differentials of DVT

A

infection
oedema
lymphoedema

143
Q

what is a D dimer test

A

fibrin degradation product present when coagulation system has been activated and clot is being broken down

144
Q

what is the action of heparin on the coagulation cascade

A

heparin binds to antithrombin 3 = activates antithrombin = inactivates thrombin and factor Xa = prevents clot forming FAST

145
Q

what is the action of warfarin on the coagulation cascade

A

inhibits vitamin K reductase = inhibits synthesis of clotting factors 10,9,7,2 (1972) and protein C

146
Q

name 4 complications of DVT

A

PE
atrial septal defect
oesophageal varices
GI varices

147
Q

name 5 differentials for a PE

A 
pneumothorax
pneumonia
MI
MSK pain
COPD
148
Q

describe the features of HF on CXR

A 
ABCDEF
Alveolar bat wing shadowing (oedema)
B kerly B lines
Cardiomegaly
D upper lobe diversion
Effusions
Fluid in fissures
149
Q

describe the treatment of chronic HF

A 
1st line:
ACEi or BB
2nd line:
- aldosterone antagonist = sprionolactone (watch K+ levels)
- ? SGLT2 inhibitor (-flozin)
3rd line/if have arrhythmias = DIGOXIN/specialist
150
Q

what drugs should never be used in HF

A

calcium channel blockers = verapamil/diltiazem
lithium
NSAIDS/COX2inhibitors

151
Q

what BP value = hypertension

A

over 140/90

ambulatory over 135/85

152
Q

what is the treatment for hypertension

A 
1st line:
under 55 = ACEi/ARBs
over 55/black = CCB
2nd line:
ACEi/ARB AND CCB
3rd line:
ACEi/ARB + CCB + thiazide diuretic
153
Q

what is the treatment for resistant HTN (4th line)

A 
ACEi/ARB
CCB
thiazide like diuretic
BB
spironolactone
154
Q

what is the main finding on ECG for heart block

A

long PR interval
progressively longer = 2nd degree, Mobitz I
constant PR interval = 2nd degree, Mobitz II
dissociated P wave from QRS = 3rd degree

155
Q

what would an ECG show in atrial fibrillation

A

irregularly irregular QRS

absent P

156
Q

what drug can be given in heart block

A

atropine

157
Q

what is wolf parkinson white disease

A

congenital
extra atrial pathways = when atria contract = increased AVN stimulation = tachycardia
ECG = broad QRS

158
Q

how does ventricular tachycardia appear on ECG

A

crescendo to decrescendo amplitude = tourades de pointes

irregular QRS

159
Q

describe the presentation of aortic stenosis

A 
symptoms = SAD
syncope
angina
dyspnoea
signs =
slow rising pulse
narrow pulse pressure
ejection systolic murmur
absent 2nd heart sound
160
Q

describe the presentation of aortic regurgitation

A 
SOBOE + angina + syncope
signs =
wide pulse pressure
collapsing pulse
early diastolic and austin flint murmur
displaced apex beat
161
Q

how does mitral stenosis and regurgitation show differently on ECG

A 
stenosis = AF and LA enlargement on ECG
regurgitation = AF and LV hypertrophy on ECG
162
Q

which way does blood shunt in atrial or ventricular septal defects

A

left to right due to high pressure in left side of heart

163
Q

what is patent ductus arteriosus

A

failure of ductus arteriosus to close = aorta and PA still connected
left to right shunt

164
Q

what is patent foramun ovale

A

failure of foramen ovale to close = atria still connected with a flap thats usually closed
during high pressure blood moves from right to left

165
Q

what is coarctation of the aorta

A

narrowing of aorta

treat with balloon aneurysm = dilates lumen

166
Q

what is bicuspid aortic valve

A

aortic valve only has 2 flaps instead of 3 = degradation of aortic valve over time
can cause aortic regurgitation

167
Q

describe the dukes criteria for IE diagnosis

A

2 major criteria
1 major + 3 minor criteria
5 minor criteria

168
Q

how is IE diagnosed

A

blood cultures from 3 sites!!
urinalysis = microscopic haematuria
transthoraccic echoCG = vegetation/regurgitation but images are POOR

169
Q

what are the most common causes of IE

A

staph Aureus
coagulase negative staph
viridans strep

170
Q

what is digoxin used to treat

A

HF

AF

171
Q

what drug commonly causes a bradykinin cough

A

ACEi

172
Q

what is a damaging SE of amiodarone

A

QT prolongation

can cause arrhythmias - ventricular tachycardia

173
Q

what is the equation for CO

A

HR x SV

174
Q

what is the equation for BP

A

CO x total peripheral resistance TPR

175
Q

what is the equation for ejection fraction

A

SV/end diastolic volume

176
Q

what are the features of cardiogenic shock

A 
heart cannot pump enough blood around body
hypotension 
tachycardia
oliguria
cold extremities
177
Q

what is hypovolaemic shock

A 
loss of >20% blood volume/fluid = heart cant pump sufficient blood
cold/pale/clammy/grey skin
drowsy/confused
weak pulse
bradycardia
178
Q

what is septic shock

A 
sepsis = systemic inflammatory response syndrome
high or low temp
high or low WCC
tachycardia >90 BPM
nausea/vomiting
vasodilation and warm peripheries
179
Q

what is hemorrhagic shock

A

great loss of blood volume causing hypovolaemic shock
= trauma
= fractures
= ruptured AA

Phase 2a (15 decks)

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