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
what will an ECG of angina look like
normal, may show ST depression and flat T wave
26
what investigations should be carried out for suspected angina
``` ECG CT angiogram (gold standard) stress echo, cardiac MRI, echo = differential diagnoses ```
27
what is a SCORE quiz
systematic coronary risk estimation quiz
28
describe primary prevention of coronary artery disease
1. lifestyle changes | 2. pharmacological = antihypertensives, statins, diabetes treatment for T2
29
describe the pharmacological secondary prevention of coronary artery disease
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
30
what are the significant side effects of beta blockers
bronchospasm | cold fingers
31
name 2 beta blockers
atenolol | bisoprolol
32
name 2 calcium channel blockers
amlodipine | verapamil
33
name 3 anti-platelet drugs
aspirin clopidogrel = P2Y12 inhibitor ticagrelor = P2Y12 inhibitor
34
name 2 statins
atorvastatin | simvastatin
35
what type of acute coronary syndrome is it not suitable to use beta blockers as treatment
prinzmetals angina
36
describe the surgical methods to manage acute coronary syndromes
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
37
what is acute coronary syndrome
encompasses unstable angina, NSTEMI, STEMI = coronary artery blockage via thrombus or embolism
38
what are the general symptoms for acute coronary syndrome
``` acute central chest pain longer than 20 mins radiating to arm neck and jaw nausea sweating SOB palpitation ```
39
what is the initial management for all acute coronary syndromes (NSTEMI, MI)
``` MOAN morphine oxygen aspirin/clopidogrel nitrates ```
40
what are the signs of acute coronary syndrome
distress, pallor, anxiety bradycardic or tachycardic high or low BP 4th heart sound
41
name a chronic coronary syndrome
stable angina
42
what is an acute myocardial infarction
complete blockage of a coronary artery
43
what investigations would you do for an MI
ECG CXR FBC, U&E, glucose, lipids cardiac enzymes - troponin T and I
44
what is significant on an ECG during an MI
STEMI = ST elevation | NSTEMI/unstable angina = ST depression or T wave inversion, new Q waves
45
what can an ECG indicate about a patients history
can show whether have suffered an MI in the past
46
how are acute coronary syndromes treated lifelong
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 ?
47
what are the main causes of acute coronary syndromes
``` plaque rupture causing thrombosis coronary vasospasm drug abuse dissection of coronary artery bc of connective tissue defects thoracic aorta dissection ```
48
what is troponin
protein complex that regulates actin/myosin interaction | highly sensitive marker for cardiac muscle injury
49
what conditions cause raised troponin
MI arrhythmias heart failure myocarditis gram negative sepsis PE
50
describe the layers of the pericardium
dual layer: thin visceral layer attached to epicardium thick fibrous parietal layer anchored to diaphragm
51
what is the role of the pericardium
acts to restrain filling volume of heart so it doesnt overfill is able to stretch but will become stiff at high tension
52
describe the pathophysiology of chronic pericardial effusion
fluid builds up slowly = pericardium stretches instead of becoming stiff changes compliance and reduced effect on diastolic filling of chambers
53
describe the pathophysiology of a cardiac tamponade
occurs acutely pericardium fills quickly and therefore becomes stiff pericardium continues to fill = compress the heart
54
what is becks triad
= 3 signs of cardiac tamponade 1. muffled heart sounds 2. jugular vein distension 3. hypotension with narrowed pulse pressure
55
what is pericarditis
inflammation of the pericardium with or without effusion
56
name the infectious causes of pericarditis
enterovirus adenovirus parvovirus B19 herpes mycobacterium TB rheumatic fever staph/strep
57
name the autoimmune causes of pericarditis
sjogren syndrome rheumatoid arthritis scleroderma
58
what is the main non infectious cause of pericarditis
neoplasm = mets
59
what is pulses paradoxus
fall of systolic blood pressure on inspiration
60
what is Kussmaul's sign
increase of or failure for systolic blood pressure to fall during inspiration (jugular venous pressure)
61
what is particular about an ECG in pericarditis
saddle shaped ST segment across lots of territories | widespread ST elevation
62
what are the major predictors of complications of pericarditis
fever above 38 subacute onset large pericardial effusion lack of response to aspirin/NSAID
63
what are the minor predictors of complications of pericarditis
myopericarditis immunosuppression trauma oral anticoagulation therapy
64
what are the differential diagnoses of pericarditis
``` pneumonia pleurisy GORD MI pancreatitis herpes zoster ```
65
what is cardiac myopathy
primary heart muscle disease
66
name the 3 main types of cardiac myopathy
hypertrophic dilated arrhythmogenic
67
what is signifcant about the chest pain associated with pericarditis
worse when lying down | relieved by sitting forward
68
what are the signs of cardiac tamponade
high HR low BP pulses paradoxus high JVP
69
what may a CXR of pericarditis show
cardiomegaly
70
what is hypertrophic cardiomyopathy HCM
heart muscles become thicker (larger than 12mm) = ventricles become smaller increases systolic function causes dystolic dysfunction caused by sarcomeric protein gene mutation
71
describe the pathophysiology of hypertrophic cardiomyopathy causing arrhythmias
fibrosis and scarring of heart myofibrils in disarray microscopically vessels supplying myocardium decrease in size = changes in electrical conduction/ CAN CAUSE ARRHYTHMIAS
72
what is dilated cardiomyopathy DCM
ventricles and atria are dilated in 1V, 2V or all chambers of heart walls of heart normal thickness or too thin
73
what would someone with dilated cardiomyopathy DCM usually present with
heart failure due to decreased contractability
74
what is arrythmogenic cardiomyopathy
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
what else is affected in arrythmogenic cardiomyopathy
desmosomes | = difficulty transferring action potentials through heart
76
what is naxos disease and what is its significance
characteristic wooly hair palmar planter keratoderma people with naxos = predisposition to arrythmogenic cardiomyopathy
77
what is long QT syndrome
issue with repolarisation of the heart = increased risk of arrhythmias exercise/certain drugs can cause sudden death
78
what is Brugada syndrome
a genetic predisposition to arrhythmias
79
what is CPVT
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
what is Marfans disease
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
what is familiar hypercholesteraemia FH
genetically high cholesterol levels (above 12) fatty deposits on corneas and tendons often present coronary artery blockage often present
82
describe the pathophysiology of familiar hypercholesteraemia FH
abnormal LDL receptors present = LDL not absorbed by liver = high blood LDL treated with statins
83
what is the prevalence of HCM
1 in 500
84
name 4 inherited channelopathies
long QT syndrome short QT syndrome Brugada syndrome CPVT
85
what is congenital heart disease
changes in heart structure present at birth | lesions may be minor or incompatible with life ex utero
86
what defects cause a severe risk in pregnancy
pulmonary hypertension left heart obstruction reduced ejection fraction (below 30%) marfans
87
what defects cause a moderate risk in pregnancy
``` unrepaired coarctations (narrowing) aortic stenosis mechanical heart valves ```
88
what is tetrology of Fallot (blue babies)
= 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
describe the pathophysiology of tetrology of Fallot
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
what is eisenmenger's syndrome
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
name the 3 main types of atrial septal defect
primum secondum sinus venosus
92
what is sinus venosus atrial septal defect
defect occurs at superior vena cava and right atrium junction where R pulmonary artery enters heart
93
what is an atrio-ventricular septal defect AVSD
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
what genetic condition is related to AVSD
down syndrome trisomy 21
95
describe complete AVSD
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
describe partial AVSD
can present late into adulthood - small VSD or ASD
97
what is the difference between large and small ductus arteriosus
``` large = can cause eisenmengers, needs to be surgically closed small = usually asymptomatic , slight increased risk of IE ```
98
what is pulmonary stenosis
narrowing of outflow of right ventricle | can be valvar, sub-valvar, supra-valvar, branch
99
what is the treatment for pulmonary stenosis
shunt balloon valvuloplasty open valvotomy trans-annualr patch
100
what occurs in severe pulmonary stenosis
``` RV failure in neonates RV hypertrophy poor pulmonary blood flow tricuspid regurgitation collapse ```
101
what occurs in mild pulmonary stenosis
well tolerated for many years | RV hypertrophy occurs
102
what is heart failure
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
describe the pathophysiology of heart failure
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
describe the compensatory mechanism for heart failure
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
name the 4 ways HF can be classified
1. right or left sided 2. reduced ejection fraction or preserved ejection fraction 3. arrhythmias 4. valvular dysfunction
106
what is BNP
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
describe the New York Heart Association classification of heart failure
``` 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
inotropic definition
modifying speed or force of CONTRACTION on heart muscles
109
chronotropic definition
modifying heart rate or rhythm by affecting electrical conduction and nerves that influence conduction
110
describe systolic HF
``` ventricles cant contract properly = ejection fraction below 40% + reduced CO caused by IHD MI cardiomyopathy ```
111
describe diastolic HF
ventricles cant relax properly = ejection fraction above 50% | caused by ventricular hypertrophy, constricted pericarditis, restricted cardiomyopathy
112
describe class 1 antiarrhythmics
``` = sodium channel blockers e.g. disopyramide lidocaine flecainide ```
113
describe the classes of antiarrhythmia drugs
``` class I = sodium channel blockers class II = beta blockers class III = prolong action potential AMIODARONE class IV = calcium channel blockers ```
114
describe the mechanism of aspirin
permanently binds to COX-1 which inhibits thromboxane formation = therefore decreases platelet activation and aggregation acts for lifetime of platelets
115
what is the life cycle of platelets
7-10 days
116
name 4 ways aspirin is used for treatment
1. anticoagulation 2. MI risk reduction 3. analgesic 4. arterial thrombus
117
what are the side effects of aspirin
GI bleeding hives allergic reaction
118
describe the mechanism of P2Y12 inhibitors
inhibit P2Y12 pathway = reduce platelet aggregation usually dual therapy with aspirin inhibited by morphine = give more if morphine also being used
119
what are the side effects of P2Y12 inhibitors
bleeding dyspnoea neutropenia (low neutrophils) diarrhoea
120
describe the mechanism of GPIIb/IIa antagonists
act to inhibit glycoprotein IIb/IIa = prevent platelet aggregation and thrombus formation has MAJOR risk of bleeding risk of thrombocytopenia
121
name 2 GPIIb/IIa antagonists
roxifiban | abciximab
122
describe the mechanism of statins
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
describe the side effects of statins
``` haemorrhagic stroke liver dysfunction sexual dysfunction neuropathy muscle pain rhabdomyolysis = muscle breakdown ```
124
what is fondaparinux
binds to antithrombin 3 inhibits factor X = decrease platelet aggregation used to treat pre-angiogram in MI, DVT prevention/treatment
125
describe the mechanism of heparin
acts as anticoagulant by indirectly inhibiting thrombin
126
what is bivalirudin
anticoagulant which directly inhibits thrombin used to treat PCI for STEMI, thrombotic events can cause headache, nausea, vomiting, pelvic/back pain
127
what is colchicine
used to treat pericarditis | side effects = regularly cause nausea and diarrhoea
128
describe the mechanism of warfarin
prevents synthesis of clotting factors 1972 (1 is 10) by acting as Vitamin K antagonist = prolong PT time
129
describe the side effects of warfarin
haemorrhage warfarin necrosis (gross limb necrosis_ caused by protein C deficiency osteoporosis
130
describe the mechanism of direct oral anticoagulant
``` directly acts on factors II and X (2 and 10) used to treat AF DVT PE for prophylaxis ```
131
name 2 DOAC's
rivaroxaban | apixaban
132
what are the side effects of DOACs
cross across placenta in pregnancy | haemorrhage
133
name the 3 signs of IE that have funky names
Roth's spots = haemorrhage in retina Osler's nodes = red lesions on fingers and toes Janeway lesions = on palms and plantar
134
what are the major criteria for IE
1. positive blood culture 2. vegetations on echo 3. new valvular regurgitation
135
what are the minor criteria for IE
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
what are ectopic beats
extra heart beats/skipped heartbeat
137
describe Virchow's triad
3 categories that contribute to thrombus formation: 1. hypercoagubility 2. haemodynamic changes 3. endothelial injury or dysfunction
138
how does sedentary behaviour physiologically increase the risk of thrombus formation
= haemodynamic change | greater contact between platelets and coagulation factors with vascular endothelium
139
how does hypertension physiologically increase the risk of thrombus formation
higher blood pressure = greater shearing forces = cause greater platelet aggregation and activation
140
how does smoking physiologically increase the risk of thrombus formation
nicotine, free radicals, NO = increase endothelial damage = increase thrombosis
141
describe a WELLS score
2+ = likely DVT | under 1 = do D-dimer to rule out DVT
142
name 3 differentials of DVT
infection oedema lymphoedema
143
what is a D dimer test
fibrin degradation product present when coagulation system has been activated and clot is being broken down
144
what is the action of heparin on the coagulation cascade
heparin binds to antithrombin 3 = activates antithrombin = inactivates thrombin and factor Xa = prevents clot forming FAST
145
what is the action of warfarin on the coagulation cascade
inhibits vitamin K reductase = inhibits synthesis of clotting factors 10,9,7,2 (1972) and protein C
146
name 4 complications of DVT
PE atrial septal defect oesophageal varices GI varices
147
name 5 differentials for a PE
``` pneumothorax pneumonia MI MSK pain COPD ```
148
describe the features of HF on CXR
``` ABCDEF Alveolar bat wing shadowing (oedema) B kerly B lines Cardiomegaly D upper lobe diversion Effusions Fluid in fissures ```
149
describe the treatment of chronic HF
``` 1st line: ACEi or BB 2nd line: - aldosterone antagonist = sprionolactone (watch K+ levels) - ? SGLT2 inhibitor (-flozin) 3rd line/if have arrhythmias = DIGOXIN/specialist ```
150
what drugs should never be used in HF
calcium channel blockers = verapamil/diltiazem lithium NSAIDS/COX2inhibitors
151
what BP value = hypertension
over 140/90 | ambulatory over 135/85
152
what is the treatment for hypertension
``` 1st line: under 55 = ACEi/ARBs over 55/black = CCB 2nd line: ACEi/ARB AND CCB 3rd line: ACEi/ARB + CCB + thiazide diuretic ```
153
what is the treatment for resistant HTN (4th line)
``` ACEi/ARB CCB thiazide like diuretic BB spironolactone ```
154
what is the main finding on ECG for heart block
long PR interval progressively longer = 2nd degree, Mobitz I constant PR interval = 2nd degree, Mobitz II dissociated P wave from QRS = 3rd degree
155
what would an ECG show in atrial fibrillation
irregularly irregular QRS | absent P
156
what drug can be given in heart block
atropine
157
what is wolf parkinson white disease
congenital extra atrial pathways = when atria contract = increased AVN stimulation = tachycardia ECG = broad QRS
158
how does ventricular tachycardia appear on ECG
crescendo to decrescendo amplitude = tourades de pointes | irregular QRS
159
describe the presentation of aortic stenosis
``` symptoms = SAD syncope angina dyspnoea signs = slow rising pulse narrow pulse pressure ejection systolic murmur absent 2nd heart sound ```
160
describe the presentation of aortic regurgitation
``` SOBOE + angina + syncope signs = wide pulse pressure collapsing pulse early diastolic and austin flint murmur displaced apex beat ```
161
how does mitral stenosis and regurgitation show differently on ECG
``` stenosis = AF and LA enlargement on ECG regurgitation = AF and LV hypertrophy on ECG ```
162
which way does blood shunt in atrial or ventricular septal defects
left to right due to high pressure in left side of heart
163
what is patent ductus arteriosus
failure of ductus arteriosus to close = aorta and PA still connected left to right shunt
164
what is patent foramun ovale
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
what is coarctation of the aorta
narrowing of aorta | treat with balloon aneurysm = dilates lumen
166
what is bicuspid aortic valve
aortic valve only has 2 flaps instead of 3 = degradation of aortic valve over time can cause aortic regurgitation
167
describe the dukes criteria for IE diagnosis
2 major criteria 1 major + 3 minor criteria 5 minor criteria
168
how is IE diagnosed
blood cultures from 3 sites!! urinalysis = microscopic haematuria transthoraccic echoCG = vegetation/regurgitation but images are POOR
169
what are the most common causes of IE
staph Aureus coagulase negative staph viridans strep
170
what is digoxin used to treat
HF | AF
171
what drug commonly causes a bradykinin cough
ACEi
172
what is a damaging SE of amiodarone
QT prolongation | can cause arrhythmias - ventricular tachycardia
173
what is the equation for CO
HR x SV
174
what is the equation for BP
CO x total peripheral resistance TPR
175
what is the equation for ejection fraction
SV/end diastolic volume
176
what are the features of cardiogenic shock
``` heart cannot pump enough blood around body hypotension tachycardia oliguria cold extremities ```
177
what is hypovolaemic shock
``` loss of >20% blood volume/fluid = heart cant pump sufficient blood cold/pale/clammy/grey skin drowsy/confused weak pulse bradycardia ```
178
what is septic shock
``` sepsis = systemic inflammatory response syndrome high or low temp high or low WCC tachycardia >90 BPM nausea/vomiting vasodilation and warm peripheries ```
179
what is hemorrhagic shock
great loss of blood volume causing hypovolaemic shock = trauma = fractures = ruptured AA