Cardiovascular Flashcards
what is the main reason for loss of consciousness in a young person
vasovagal syncope
what is the main cause for loss of consciousness in a middle aged person
vasovagal syncope and also cardiac arrhythmia
In elderly patients what is the common cause of loss of consciousness?
orthostatic hypo tension secondary to meds
look at duiretics, ARB, B blockers, calcium channel blockers.
B blockers
decrease the heart rate and are negative ionotropes.
differentiate between epilepsy, vasovagal, and arrythmias in their presentation.
Epilepsy: there can be a warning aura before (partial) or no warning (general)
During the can have tongue biting, defectation or urination, tonic clonic movements.
after post ictal phase of confusion for 5-30min
vasovagal: before: vagal symptoms (sweating palp, nausea)
lasts only seconds and have rapid recovery afterward.
arrthymias there are no warning it may lasts seconds and maybe incontinant.
but have rapid spontaneous recovery.
Aortic stenosis cause
young- congenital bicuspid valve
elderly- calcification pf the valve leads to stenosis
Rheumatic fever (rare)
aortic stenosis on examination
slow rising carotid pulse
loud ejection systolic murmer
what is a stokes adams attack
sudden loos of consciousness induced by a slow or absent pulse and subsequent loss of cardiac output. caused by complete heart block or a sinoatrial disease.
attacks are not associated with change in posture or trigger. afterwards the patient appears flushed.
Heart block
first degree
second degree: mobitz type 1 and mobitz type 2
third degree or complete heart block
first degree heart block
every atrial contraction is transmitted to the ventricles
but conduction is slower than normal. it can be caused by damage to the AV node (IHD, fibrosis, and inflammation). On the electrocardiogram, there is a prolongation of the gap between the p wave and the QRS complex, making the PR interval greater than 200 ms. Normally is asymptomatic.
second degree heart block: Mobitz type I
each heart beat shows a progressively increased PR interval until a QRS (ventricular contraction) is missed entirely. This can be normal in ultrafit athletes.
second degree heart block: Mobitz type 2
QRs complexes are found to be missing after the P waves without a prolonged PR intervbal prior to the proceeding QRS complex. There is often a pattern with QRS complexes missed every third or second P wave. hig risk of progressing to 3rd heart block.
complete heart block
no conduction between the SA node and the AV node. On the ECG there are broad QRS complexes that are out of sync with the P waves or atrial contraction.
table tilt test is contraindicated in
those with orthostatic hypotension
what must you do before attempting a carotid artery message?
doppler on both carotid esp. if history of stroke, TIA, or carotid bruit on auscultation. Need to be done with resus trolley at hand.
wells score
clinical signs of a DVT 3 PE is the most likely diagnosis 3 HR greater than 100 (1.5) immobilisation greater than 3 days or surgery in the last 4 weeks (1.5) DVT or PE in past 1.5 heamoptysis 1 malignancy in the last 6 months 1 greater than 4 CTPA less than 4 D dimer to exclude DVT
characteristics of aortic dissection
sudden onset tearing pain radiating to the back
absent pulses in one arm
hypertension or hypotension
a difference in blood pressure greater than 20 mmHg (1/3 of AD)
new onset aortic regurgitation
pleural effusion
RF other than normal CVD is aortic valve replacement
troponin when it is elevated? how is it excreted? what is it specific to?
elevated 3-12 hours after the onset of chest pain
excreted renally
it is specific for cardiac damage but not ACS
therefore think about coronary artery spasm, aortic dissection, myopericarditis
HOCM, heart failure cardiac contusion from trauma, and PE
what is the management for a myocardial infarct
Morphine
Oxygen 100%
Nitrates (triglycerol)
Antiplatelets (dual antiplatelet therapy aspirin and cloplidogrel)
beta blockers C.I if the patietn is in heart block, has asthma, or signs of acute heart failure
ACE inh preventing cardiac remodelling improve cardiac blood flow and also the after load
statins reduce stain levels and help with endothelial function reduce CRP and mainstina plaque stability
Heparin LMWH
STEMI patient specific considerations for management
primary angioplasty or thrombolysis within 12 hours of onset of pain
angioplasty is superior but should not be the reason for withholding tx if not able to preform intervention within one hour
NSTEMI receive angioplasty when
if heamodynamtically unstable, severe LV dysfunction, ongoing chest pain despite medical mgx, new mitral regurg, VSD, sustained ventricular arrhythmias.
choice of blood control medications after MI
less than 55 and white ACE inh
if greater than 55 or black ca channel blocker
how to reduce thromboembolic risk after MI
low dose aspirin for life and ADR receptor inhibitor for 1 year
what is the GRACE score?
This is for patients who have an NSTEMI on ECG with chest pain. It is a risk stratification tool in order to assess the benefit of angioplasty.
variables are based on age, heart rate, systolic bp, creatinine, congestive heart failure, cardiac arrest on admission, st segment deviation, elevated cardiac enzymes
complications fo a MI
death arrhythmia rupture tamponade heart failure valve disease aneurysm dressers syndrome embolism reinfarction
dressler’s syndrome
2-10 weeks after the MI positional - worse lying down better leaning forward worse on inspiration radiantes to the left shoulder tx high dose NSAIDS
aortic dissection involving the ascending aorta
stanford A class and is a surgical emergency
aortic dissection involving the descending aorta
type B and are managed medically
patients with diabetes target blood pressure
130/80
patients with diabetes and protienuria target blood pressure
less than 125/75
approach to the management of heart failure
- symptomatic relief *too much fluid in lungs and limbs
- pathological mechanism of heart failure
- the underlying cause of the problem (atherosclerosis)
symptomatic relief in heart failure
- acute positional- sit upright give oxygen and reduce cardiac preload with vasodilator (nitrates and frusemide)
CPAP (optional) - chronic loop diuretic furosemide which may be combined with a potassium sparing diuretic
fixing the pathophysiological mechanism of heart failure
reduced CO activates
1. sympathetic system: increases heart rate and contractility via beta adrenergic receptors *increases metabolic demand and also increases HR leads to decreased CO
can use B blockers but never in acute LV failure. (start low and titrate slow)
2. renin-angiotensin system: increased water retention
ACE inhibitors, ARB spirolactone (aldosterone antagonist can be used in moderate to severe heart failure)
fixing the underlying cause of the heart failure
atherosclerosis: angiography (revascularisation if the myocardium is still viable cardiac MRI, thallium scans debutamine stess echo)
stinks to reduce cholesterol levels
asprin to reduce the risk of thrombolysis
medications for diabetes mellitus
advanced heart failure digoxin, cardiac resynchonization, implantable cardioversion device, (biventricular) heart transplantation
pyroderma gangrenosum
ibd or heam malignancies has a characteristic purple halo around it
In an arterial ulcer what is the pattern of pain?
painful to wake up at night. better when hang foot out of the bed and when the put the blanket off feet. May have claudication.
in a venous ulcer what is the pattern of pain?
less painful when elevated and drained of blood.
arterial ulcers most often appear after what?
minor trauma
a long history of an ulcer should make you suspicious of what?
marjolin ulcer.
what should you always ask in a patient where you suspect an arterial ulcer?
other atherosclerotic disease CVD, angina
claudication, and night pain
What might you notice when examining a neuropathic ulcer?
secondary infection caused by anaerobes causing smell.
What are the risk factors of venous ulcers?
previous DVT, oral contraceptive pill, HRT, varicose veins, immobile, pelvic mass, arteriovenous malformation, joint replacement.,
what are the risk factors for arterial vascular disease?
risk factors for atherosclerosis
AAA, CVD, stroke,and peripheral vascular disease
Associated symptoms for venous ulceration?
varicose veins, stasis, eczema, heavy legs, swelling around the ulcer.
What are the treatment options for AS
open aortic valve replacement
trans catheter valve replacement
tissue valves last 15 years
metal need lifelong anti-coagulation
commonest cause of endocarditis
staph aureus
what would you choose for dual anti platelet therapy?
aspirin and ticagrelor
