what is atherosclerosis?
a progressive build up of plaque within the arteries
what is athersclerotic plaque formed from?
fatty substances choleserol cellular waste calcium fibrin
what are the 2 main consequences of an artherosclerotic plaque?
(what do these both cause?)
- bleeding into the plaque
- rupture causing clot formation
(both can result in artery occlusion)
what is an atherothrombosis?
formation of an acute thrombosis superimposed on atherosclerosis
what are the stages from normal artery to atherothrombosis?
- normal artery
- fatty streak
- fibrous plaque
- atherosclerotic plaque
- plaque rupture + thrombosis
why does the rupture of a atherosclerotic plaque cause clot formation?
platelets adhere to damaged area to try and heal the broken area
(especially since components such as collagen and vWF have been exposed)
why does a fatty streak form on the endothelium of a normal artery?
- endothelial damage
- protective response results in production of cellular adhesion molecules
- monocytes and T-cells attach to the sticky surface of endothelial cells
- migration into the subendothelial space
- macrophages take up oxidised LDL-C
- instead of clearing OXLDL, macrophages become lipid-rich foam cells
- fatty streak forms
what factors can cause damage to the endothlium?
- haemodynamic forces
- vasoactive substances
- cytokines from blood cells
- cigarette smoke
- atherogenic diet
- elevated glucose levels
- oxidied LDL-C
what type of haemodynamic force can cause endothelial damage?
due to sheer stress
what 4 things does OXLDL cause?
- promotes damage of endothelial cells
- promotes inflammatory response
- causes vasodilatory impairment
- induces prothrombic state (by affecting platelets and coagulation factors)
how does OXLDL cause vasodilatory impairment?
by modifying endothelial response to angiotensin II
why does a fibrous lesion form over the fatty streak?
a protective response to the endothelial damage
what are 4 major risk factors for cardiovascular disease
why do CVD risk factors (such as hypertension, dyslipidaemia, diabetes and smoking) cause endothelial cells to decrease production of some compounds and increase production of others? (endothelial dysfunction)
by causing oxidative stress in the vessel wall
what is intermittent claudication a symptom of?
peripheral arterial disease
why are many patients with PAD not diagnosed?
most are asymptomatic
what are the 4 minor risk factors for cardiovascular disease?
what type of cholesterol do statins reduce?
what is the statin with the greatest efficacy?
which is the statin with the least likelihood of side effects? (myopathy)
what are xanthelasma?
xanthomas of the eyelids
why do tendon xanthomas form?
infiltration of tendon by lipid: hypercholesterolaemia
where are the most common places for tendon xanthomas?
extensor tendons of fingers, patella, elbows
why do tuberous xanthomas form?
what are the 3 causes of tuberous xanthomas?
what do eruptive xanthomas suggest?
abrupt increase in serum triglyceride levels
where are eruptive xanthomas more likely to me?
for patients with diabetes, what is their target blood pressure?
what does smoking do to your blood pressure?
increases blood pressure
what does smoking do to your HDL?
what are the 5 features of metabolic syndrome?
abdominal obesity high blood pressure high triglycerides low HDL high fasting glucose (patients must have 3 of these characteristics)
what does an assign score allow you to measure?
risk of developing cardiovascular disease
what is ischaemia?
the result of impaired vascular perfusion which deprives the affected tissue of nutrient
(can be reversible)
what is infarction?
ischaemic necrosis of a tissue secondary to occlusion/reduction of arterial supply or venous drainage
(irreversible, recovery will depend on tissues regenerative ability)
why can reduced venous drainage cause ischaemia/infarction?
venous blood backs up and doesn’t allow oxygenated arterial blood to get to the tissue
what is the difference between a thrombus and a clot?
- thrombus occurs in vasculature, during life
- blood clot is not within vascular space or not in life.
what 2 types of granules to platelets have?
what type of contents do alpha granules contain?
adhesion components eg fibrinogen
what type of contents do dense granules contatin?
aggregation components eg ADP
what affects do stasis and turbulence of blood cause?
- platelets come into contact with endothelium
- activated clotting factors are not diluted by the normal rapid flow of blood
- inflow of anticoagulant factors is slowed allowing thrombi to persit
- activation of endothelial cells is promoted
what type of situations cause turbulence within blood vessels?
- blood flowing round and occluding atherosclerotic plaque
what type of situations cause stasis within blood vessels?
-impaired venous drainage of lower limbs
non-contractile areas of -myocardium following a myocardial infarction
what are the 2 subsections of abnormal blood flow? (1/3 of virchows triad)
list 9 acquired hypercoaguable states?
MI immobilisation tissue damage cancer prosthetic heart valves AF pregnancy smoking oral contraceptive use
what 3 genetic abnormalities can cause hypercoaguable states?
factor V mutations
defects in anticoagulant pathways (eg AT III deficiency)
defects in fibrinolysis
what type of thrombi show lines of Zahn?
why do lines of zahn form in an arterial thrombi?
alternating pale (platelet and fibrin) and dark (RBC and WBC) bands
what is an emboli?
a detached intravascular mass which is carried by the bloodstream to a site distant from point of origin
what are the most common type of emboli?
fragments of a detached thrombus
what are the 7 types of embolism?
thromboembolism fat embolism marrow embolism air embolism septic embolism amniotic fluid embolism tumour embolism
what colour is a lung infarct?
due to leaking of secondary bronchial blood supply onto infarcts
what colour do arterial infarcts tend to be?
no secondary blood supply leaking onto area
why might a venous emboli cause an arterial infarct?
atrial/ventricular septal defect
when do fat embolisms usually occur?
follow major soft tissue trauma or bone fractures
what can gas/air embolisms cause?
when do amniotic fluid embolisms occur? and why?
amniotic fluid and debris enters torn veins after birthing
what is arteriolosclerosis associated with?
diabetes and hypertension
what are the main target vessels for atherosclerosis?
what 3 sections make up an atherosclerotic plaque?
rasied focal lesion of intima
lipid core of cholesterol and lipoproteins
what 2 things occur when an atherosclerotic plaque increases in size?
luminal diameter decreases
blood flow reduces
how can atherosclerotic plaques lead to aneurysm development?
progressively degrade (and therefore weaken) the arterial wall
what are the 3 results of an atherosclerotic plaque?
what does resolution of an atherosclerotic plaque involve?
reabsorbtion of the lipids at fatty streak stage
what does repair of an atherosclerotic plaque involve?
stabilisation by fibrosis scarring
what are the general risk factors for DVTs? (8)
age obesity immobilisation (ie hospital, long journeys) pregnancy major surgery varicose veins OCP smoking
what are the medical conditions which have risk factors for DVTs? (9)
cancer previous DVT cerebrovascular accident acute myocardial infarction congestive heart failure sepis nephrotic syndrome inflammatory bowel disease vasculitis
what part of virchows triad does sepsis affect?
change in blood constituents:
what 4 types of trauma are risk factors to DVTs?
CNS/spinal cord injury
lower extremity fractures
what part of virchows triad do burns affect?
change in blood constituents:
what drugs/drug habits can are risk factors to DVTs?
intravenous drug abuse
oestrogens (OCP, HRT)
what are the symptoms and signs of a DVT?
calf/leg would be: painful swelling redness hot/inflamed localised tenderness over certain deep vein
what blood tests do you use as an investigation for a DVT?
(not specific: infection, MI, surgery, liver disease pregnancy
what does a D-dimers test look for? (in order to see the likelihood of a DVT)
a fibrin breakdown product
how should you use a D-dimer test when looking for a DVT?
rule out test
not a rule in test
(ie low D-dimers- unlikely to be a DVT
high D-dimers- don’t necessarily mean a DVT)
what investigational tests would you use if you suspect a DVT?
how do you treat a DVT?
anticoagulation with LMWH and warfarin
for the treatment of DVT what stockings should you use?
TEDs for 6 weeks
grade 2 compression stockings for up to 5 years to reduce post phlebitic syndrome
what is post-phlebitic syndrome?
chronic venous insufficiency when the valves are destroyed and so the vein becomes large and flaccid causing a persistently swollen leg
what is a phlegmasia dolens?
A medical emergenct where a DVT causes obstruction of arterial inflow
how do you treat a phlegmasia dolens?
IVC filter femoral arterial line tPA intra-arterially surgical review decompression amputation
why do you put in an IVC filter for a patient with phlegmasia dolens?
to prevent bits of the clot embolising and causing a PE
what is the difference between wet gangrene and dry gangrene?
wet gangrene is due to a venous blockage causing a back flow preventing oxygenation of tissues
dry gangrene is due to an arterial blockage preventing oxygenation of tissues
what are the 4 classifications of an acute PE?
major with normal RV function
major with RV dysfunction
massive with shock or syncope
what are the symptoms of a PE?
SOB collapse pleuritic chest pain haemoptysis sudden death
what are the signs of a PE on general examination?
tachypnea, tachycardia hypotenstion, wheeze
what are the signs of a PE on auscultation?
what are the signs of a PE on CXR?
what is oligemia?
segmental loss of pulmonary vaculature
what are the main investiagtions for a PE?
ABGs D-Dimers CXR V/Q scan CTPA echocardiogram
what are the findings of a PE on ECG?
explain what S1Q3T3 mean on an ECG?
large S wave on lead 1
Q wave present on lead 3
inverted T wave present on lead 3
what is the investigation pathway for a PE
- D-dimer if clinical suspicion is not high
- If clinical suspician is high or D-dimers are positive: start fragmin and CXR
- if abnormal start warfarin, if normal V/Q scan
- if V/Q scan probability is low, discount PE, otherwise do CTPA
why can ventilation-perfusion scan sometimes be a poor discriminator of a PE?
if there is background lung disease
when are CT pulmonary angiograms poor in detecting PEs?
what is the con about CTPA?
what does an echocardiography tell you about a PE?
shows right heart strain and pressures
what are the 4 different treatment options in the treatmenf of a PTE?
- thrombolytic therapy
- IVC filter
- surgical removal
what is the treatment of choice for a minor PE?
what is the treatment of choice for a major PE without RV dysfunction?
what is the treatment of choice for a major PE with RV dysfunction
what is the treatment of choice for a massive PE with shock or syncope?
thrombolysis or surgery
what anticoagulant treatment is given for the treatment of a PE?
5 days afterwards: LMWH/heparin
after discharge: warfarin
what are the major pro and major con of an IVC filter?
pro: prevent recurrent PE in short term
con: increase risk of recurrent DVT in long term
why are IVC filters not recommened for long term, and if they are needed in the long term why is anticoagulation also needed?
because in the long term they increase risk of recurrent DVT
what are the 3 indications for a IVE filter?
- recurrent PTE despite adequate anticoagulation
- PTE when anticoagulation is contraindicated
- high risk (eg phlegmasia dolens)
what 4 major reasons might anticoagulants be contraindicated?
severe live disease
what type of surgery is needed for a patient with an acute massive PE with shock/syncope?
what type of elective surgery can be used for patients with chronic thromboembolic pulmonary hypertension?
what are the 4 vitamin K dependent clotting factors?
II, VII, IX, X
these are the factors that warfarin prevents forming
where are the 4 vitamin K dependent clotting factors synthesised?
in the liver
why is bleeding effects of dabigatran much easier to reverse than warfarin?
dabigatran half life is 12-17 hours (compared to warfarins: 40 hours) and so drug cessation is usually sufficient
give a reason why a patient might have angina without coronary disease?
blood supply not supplying enough oxygen for energy
what are the main way for testing for angina?
despite angina being a clinical diagnosis
exercise training testing
what revascularisation techniques can be used for angina patients to releve symptoms?
what are the 4 pros of exercise testing?
shows risk stratification (ie positive test at low workload imples poor prognosis)
what are the 2 cons of exercise testing?
- poor diagnostic accuracy in certain sub groups (eg less mobile patients)
- some patients struggle to get a maximal test- submaximal test
what are the 3 pros of perfusion imaging?
- non invasive
- accuracy in sub groups that dont have accuracy in ETT
- risk strarification
what are the 2 cons of perfusion imaging?
what are the 3 pros of CT angiography?
what are the 3 cons of CT angiography?
can be less precise when calcium is present
what is angiography?
a catheter is inserted into artery in wrist or groin and advanced to coronary ostium
contrast agent injected
video recorded X-ray taken in muliple views
what are the 4 pros of angiography?
can follow on with angioplasty if needed
what are the 3 const of angiography?
- risk of stroke or death
- contrast can cause renal dysfunction, rash. nausea
what drugs can be used to relieve angina symptoms?
nitrates B-blockers calcium antagonists nicorandil statin aspirin ACE inhibitor
what is intermittent claudication?
ischaemic pain which develops in the affected limb after variable periods of exercise, pain is relieved by rest
what are 2 non-invasive investigations of the lower limb?
ABPI (ankle brachial pressure index)
duplex ultrasound scanning
what are 3 invasive investigation of the lower limb?
how do calculate ABPI?
ankle systolic pressure (mmHg)/
brachial systolic pressure (mm Hg)
what is does the ABPI value have to be to suggest claudication
what does an eABPI
(exercise ankle brachial pressure index) show in a normal response?
increased ABPI during exercise
what does an eABPI (exercise ankle brachial pressure index) show in a claudication response?
decreased ABPI during exercise
how does walking (/exercise programs) improve intermittent claudication?
develops collateral circulation
for the management of intermittent claudication what exercise training program should be implemented?
duration: 1 hr/day to 30mins 3x a weel
for a minimum of 6 months
must be supervised
‘beyond pain’ exercise
what drug is used for relivation of intermittent claudication
what is the name of the disease which causes pain in limbs at rest due to insufficient vascular perfusion?
critical limb ischaemia
what is the main difference between intermittent claudication and critical limb ischaemia?
intermittent claudication is only pain during exercise (pain is relieved by resting(
critical limb ischaemia has pain even during rest
why is the pain in critical limb ischaemia worse at night?
no gravity to help the blood flow
what are 2 major risk factors for a patient with critical limb ischaemia to go on to needing a amputation?
what would you expect to find on examination of a acute ischaemic leg?
6Ps Pallor Perishingly cold Pulseless Pain Paresthesia Paralysis
what are the 10 main risk factors for an aortic aneurysm?
male/ female post-menopaus family history age smoking PVD cardiac disease cerebrovasclar disease hypercholesterolaemia diabetes
what types of abdominal aortic aneurysms can be symptomatic?
both ruptured and non-ruptured
what 2 investigations are useful for a suspected asymptomatic abdominal aortic aneurysm?
at what phase must the IV contrast be in during a CT angiography of the abdominal aorta?
what 1 investigation is useful for a suspected symptomatic abdominal aortic aneurysm?
what is the difference between elective aneurysm repair and emergency aneurysm repair?
elective aneurysm repair is a prophylactic operation to reduce risk of rupture
emergency aneurysm repair is a life saving therapeutic procedure
what is endovascular repair of an abdominal aortic aneursym?
inserting a graft within the aorta
(via a peripheral artery)
what 2 type of interventions can be used for an elective aneurysm repair?
endovascular repair open repair (laparotomy)
compare an endovascular repair of an abdominal aorta aneurysm to an open repair?
elective aorta aneurysm only possible in 25% of patients, less mortality risk, faster recovery but needs ongoing follow up and may need further interventions
open repair is possible in almost everyone, greater mortality risk, slower recovery but noesn’t need ongoing follow up and rarely needs further interventions. known to be effective for life
what are the 2 types of venous system?
in the lower limbs what major veins make up the deep system?
in the lower limb what major veins make up the superficial system?
saphenous veins (parallel to the deep system) perforator veins (link to deep system)
what are the 4 major risk factors for varicose veins?
what are primary varicose veins the result of?
incompetent valves (usually in superficial veins)
what are secondary varicose veins the result of?
venous obstruction (causing blood to flow through perforator veins to the superficial veins)
what type of varicose veins to DVTs cause?
secondary varicose veins
how is the appearance of varicose veins effected by standing?
more prominent when standing
what are the 3 major complications of varicose veins?
bleeding and bruising
chronic venous insufficiency
what are 3 signs of chronic venous insufficiency on inspection of the leg?
what is thrombophlebitis?
inflammation of a vein caused by a blood clot
can be due to chronic venous insufficiencu
what are haemosiderin depositis?
red cell breakdown and leakage visible on the skin
can be due to chronic venous insufficiency
what are the investigations used for suspected chronic venous insufficiency?
what is the non-interventional management of chronic venous insufficiency?
graduated compression using bandaging (for ulcers) and class II-IV stockings (ulcer prevention/symptomatic relief)
when is graduated compression for chronic venous insufficiency contraindicated?
low ABPI (intermittent claudication/critical limb ischaemia)
what is the interventional management of chronic venous insufficiency
foam sclerotherapy (duplex guided) endovenous ablation surgical
what are the complications of chronic venous insufficiency interventions?
thrombophlebitis skin staining ulceration wound infection nerve damage recurrence
what are the 2 revascularisation techniques for coronary heart disease?
what is the artery usually used for peripheral access for a PCI?
what is a stroke?
acute onset of focal neurological symptoms and signs due to disruption of blood supply
what is the most common type of stroke?
what 2 factors contribute to a haemorrhagic stroke?
raised blood pressure
weakened blood vessel wall
why might a cerebral artery wall be weakened?
structural abnormalities (aneurysm, arteriovenous malformation) inflammation (vasculitis)
what are the 5 non-modifiable risk factors for a stroke?
age family history gender race prev stroke
what are 10 potentially modifiable risk factors for a stroke?
hypertension hyperlipidaemia smoking diabetes AF congestive heart failure alcohol excess obesity physical inactivity poor socioeconomic status
which blood pressure value (systolic or diastolic?) has the strongest relationship with stroke risk?
what therapy is recommended in all patients who have an ischaemic stroke? (with the intention of controlling hyperlipidaemia)
what is the only way of accurately differentiating between an ischaemic and haemorrhagic stroke?
what type of brain imaging can be used to differentiate/confirm the type of stroke?
CT +/- angiography
MRI with diffusion weighted imaging (DWI) +/- angiography
MRI with gradient echo sequences (GRE)
what does an MRI with GRE (gradient echo sequences) look for?
looks for old haemosiderin deposits
ie an old bleed
how do you differentiate between a cardioembolism (ie cardiac cause for embolism) and an atheroembolism (ie atherosclerosis cause for embolism)?
infarcts present in the same side as teh affected carotid artery
cardioembolism: infarcts present in more than one arterial territory- bilateral
what are transient ischaemic attackes?
focal neurological symptoms that resolve within 24 hours
what is the medical management post ischaemic stroke?
(if in AF- anticoagulation)
what is the medical management for an ischaemic acute stroke?
(if prev aspirin-associated dyspepsia also give PPI)
what is the post-ischaemic stroke surgical management?
what type of atheromatous plaque causes chronic stable angina?
fixed atheromatous plaque
how would you describe the ischaemia that occurs in chronic stable angina?
demand led ischamia
why can eating a large meal cause angina to occur?
because cardiac work load increases
what 3 conditions does the phrase ‘acute coronary syndromes’ cover?
what are acute coronary syndromes caused by?
atherosclerotic plaque rupture/fissure and thrombosis occluding the coronary arteries
how would you describe the ischaemia that occurs in acute coronary syndromes?
supply led ischaemia
how do MI’s lead to cardiac failure?
infarctions causes chunks of myocardium to die, resulting in poorly-contracting scar tissue. heart loses efficiency.
what type of chest pain occurs in MIs?
severe crushing central chest pain
in an MI, where does the pain radiate?
jaws and arms
especially the left
how can an MI be differentiated to angina?
angina only lasts max 15 minutes, MI is prolonged
angina is relieved by GTN, MI is not
angina occurs on exertion, MI occurs at rest
what symptoms are often associated with an MI?
sweating, nausea, vomitting
what are the main changes in an acute STEMI?
T wave inversion
when do signs of ST elevation occur in an acute STEMI?
first few hours
when do Q wave formation and T wave inversion occur in an acute STEMI?
what is the usual evidence of an old STEMI?
Q waves present,
+/- inverted T waves
(ST no longer as elevated)
how much must ST segment be raised by for an STEMI?
1mm+ ST elevation in 2 adjacent limb leads
2mm+ ST elevation in at lesat 2 contingous precordial leads
new onset bundle branch block
what leads have ST elevation in an inferior STEMI?
II, III, aVF
what leads have ST elevation in an anteroseptal STEMI?
what leads have ST elevation in a lateral STEMI?
1, aVL, V5, V6
what leads show ischaemic changes that correlate with a STEMI?
leads which look at the opposite location of the heart to the infarction
what are 2 diagnostic markers of an MI?
TnT (troponin T)
CK (creatinine kinase)
which is more specific for cardiac muscle damage- troponin or creatinine kinase?
creatinine kinase also peaks in skeletal muscle and brain
what is the treatment of an acute MI?
MONA+C morphine (diamorphine) + anti-emetic oxygen (if hypoxic) nitrate (GTN) aspirin (antiplatelet) clopidogrel (antiplatelet)
in the treatment of an acute MI how is the diamorphine and the anti-emetic administered?
what are the doses of aspirin and clopdiogrel in the treatment of an acute MI?
when would you not give GTN in the treatment of an acute MI?
if blood pressure is below 90mmHg
if PCI (angioplasty) is not available within 90 minutes what is the alternative treatment for an acute MI?
in patients who have had an STEMI, what aspirin and clopidogrel therapy should be continued?
clopigorel for up to 4 weeks
what are the 2 indicatations for reperfusion therapy? (PCI or thrombolysis)
- chest pain suggestive of acute MI (>20mins)
- ECT changes (acute ST elevation or new left bundle branch block)
[only if no contraindications]
why does thrombolysis need to be administered early?
as time increases the clot becomes organised and hard and so cannot be broken down by anti-thrombolytics
what percentage of patients does thrombolysis not work in?
how long must the ambulance drive be over for prehospital thrombolytics to be given instead of PCI?
what happens to the 50% of patients where thrombolysis doesnt work? (but is used because the ambulance drive is over 40 minutes)
what are the 4 categories of complications of an acute MI?
what structural complications can occur due to an acute MI?
cardiac rupture (untreatable) ventricular septal defect valve defects mural thrombus +/-sysemic emboli LV aneurysm formation inflammation acute pericarditis dresslers syndrome
what dunctional complications can occur due to an acute MI?
acute ventricular failure
chronic cardiac failure
usually when a valve defect occurs as a structural complication of an MI, what sign is heard on precordial auscultation?
new heart murmur
after the acute MI, what intervention should occur once patient is stable?
what are the 4 phases of cardiac rehabilitation?
phase 1: in patient
phase 2: early post discharge period
phase 3: structured exercise programme (hospital based)
phase 4: long term maintenance of physical activity and lifestyle change (community based)
what is dresslers syndrome?
secondary pericarditis which occur after damage to the heart (eg few weeks post MI) and causes fever and pleuritic pain
what is ischaemic heart disease (a type of congestive cardiac failure) the result of?
what is cor pulmonale?
hypertrophy and failure of the right ventricle due to resistance in the pulmonary circulation (pulmonary hypertension)
what are the 4 main symptoms of left heart failure?
dyspnoea on exertion/rest
paroxysmal nocturnal dyspnoea
pink frothy sputum
what are the 4 clinical signs of LVF?
3rd heart sound
what is gallop rhythm?
third heart sound + tachycardia
what are the 4 signs of LVF on a CXR?
bats wing shadowing
kerbey B lines
what is the main symptoms of right heart failure?
what are the 4 clinical signs of RVF?
what are the sings of RVF on CXR?
what 3 causes of CCF dont use standard CCF treatment, and instead treating the underlying problem is enough?
cor pulmonale: diuretics and oxygen
valvular disease: surgery
fast AF: digoxin or shock
what 6 drugs are standard medical treatment options for congestive cardiac failure?
diuretics ACE inhibitors beta blockers spironolactone (digoxin nitrates)
when is spironolactone used in congestive cardiac failure?
in severe cases only
what 3 interventions can be used for congestive cardiac failure?
implantable cardiac defibrillators
cardiac resynchronisation therapy
what type of diuretic is used in congestive cardiac failure?
thiazide diruretics occasionally used in mild CCF
what is spironolactone?
an aldosterone receptor antagonist
what are the 3 possible side effects of spironolactone?
what is cardiac resynchronisation therapy?
3 pacemakers inserted to force LV and RV to contract together
what type of patients need cardiac resynchronisation therapy?
what is digoxins main use?
can sometimes be used for CCF
what are the 4 steps of management of a patient with acute LVF?
- sit up
- oxygen (caution in COPD)
- IV durosemide
- IV diamorphine (not in COPD)
what cardiovascular drug should be used with caution in patients with COPD?
what CVD are diuretics used in?
what CVD are B blockers used in?
what CVD are ACE inhibitors used in?
what CVD are calcium antagonists used in?
what CVF are nitrates used in?
what are the 2 main markers of deterioration of a patient?
what type of rhythm does the patient in cardiac arrest need to have for a defibrillator to work?
what are shockable rhythms that a patient might have if in cardiac arrest?
what are non-shockable rhythms that a patient might have if in cardiac arrest?
pulseless electrical activity (PEA)
what are the 8 reversible causes of cardiac arrest?
hypoxia hypovolaemia hypothermia hyper/hypo glycaemia toxin thrombus tension pneumothorax tamponade
during the assessment of an unconscious patient how long should you look, listen and feel for breathing?
what is the rate of chest compressions during CPR?
100-120compressions per minute
what is the depth of chest compressions during CPR?
what is marfans syndrome?
a genetic condition that affects the connective tissue in the body
what are the main 3 side effects of beta blockers?
shortness of breath
what is the main side effect of ACE I?
persistent dry cough
what is the side effect caues by both digoxin and spironolactone?
what are the 3 main side effects of amiodarone?
what is the main GI side effect of verapamil?
what are the 3 main side effects of nifedipine? (calcium channel blocker)
what is the main side effect of thiazide diuretics?
what is the main side effect of minoxidil?
vasodilator for hypertension
increased hair growth
what is the main side effect of hydralazine?
vasodilator for hypertension