CVS Flashcards
whats formula for CO?
SV X HR
most common type of avrt?
wolff parkinson white syndrome
symptoms of avrt or avnrt?
both are svt
palpitations
SOB
dizziness/lightheadedness
syncope
RFs for CVD
family history of CVD, smoking, DM, obesity, lack of exercise, hyperlipidaemia, stress, HTN,
give 3 characteristics of typical stable angina. how is this different from atypical angina
- constricting pain/discomfort in front of the chest, neck, shoulders, jaw or arms
- precipitated by exertion (mostly exercise but can also be emotional stress)
- Relieved by rest or GTN in about five minutes
atypical angina will have 2 of the above and if only 1 of the above or none is present then it is non-anginal pain
give 5 differentials for chest pain
cardiac - stable angina, ACS, coronary artery vasospasm, aortic dissection, arrhythmias, pericarditis
breast disease
MSK pain eg costochondritis
pulmomary - pneumothorax, PE, pneumonia, lung cancer
gastro - GORD, PUD, cholecystitis
psychological - anxiety, panic disorder
ix to do in someone with suspected stable angina?
initially -
Physical Examination (heart sounds, signs of heart failure, BMI)
12 lead ECG
FBC (check for anaemia)
U&Es (prior to ACEi and other meds)
LFTs (prior to statins)
Lipid profile
Thyroid function tests (thyrotoxicosis will increase the work of the heart whilst hypothyroidism is associated with raised cholesterol)
HbA1C and fasting blood glucose (to check for diabetes)
CT Coronary Angiography is the Gold Standard diagnostic investigation BUT -
The diagnosis of stable angina is based on clinical assessment alone or clinical assessment with diagnostic testing.
1. estimate likelihood of CAD
-If there are typical features of angina based on clinical assessment and their estimated likelihood of CAD is greater than 90%, further investigation is unnecessary and the patient should be managed as having angina.
-if estimated likelihood of CAD 61-90% - offer invasive coronary angiography. if not appropriate offer non-invasive functional testing (eg Myocardial perfusion scintigraphy (MPS) using single photon emission computed tomography (SPECT), Stress echocardiography, etc.)
- 30-60% - offer non-invasive functional imaging for myocardial ischaemia
- 10-29% - offer CT calcium scoring (coronary artery calcification scanning). if score:
- 0 - consider other causes of chest pain
- 1-400 - offer CT coronary angiography
- >400: offer invasive coronary angiography
- <10% - consider other causes of chest pain/angina
management of stable angina
RAMP -
Refer to cardiology
Advise about diagnosis, lifestyle modification, management and when to call an ambulance
Medical treatment
Procedural or surgical interventions
lifestyle modification -
- smoking cessation (if applicable)
- weight loss (if applicable)
- dietary advice
- advice re physical activity
- limit alcohol consumption
medical management -
1. immediate symptom relief: sublingual GTN spray.The patient should be advised that, when an attack of angina occurs, they should:
Stop what they are doing and rest.
Use GTN spray or tablets as instructed.
Take a second dose of GTN after five minutes if the pain has not eased.
Take a third dose of GTN after a further five minutes if the pain has still not eased.
Call 999/112/911 for an ambulance if the pain has not eased after another five minutes (ie 15 minutes after onset of pain), or earlier if the pain is intensifying or the person is unwell.
2. long term symptomatic relief: betablocker eg bisoprolol or CCB (eg amlodipine)
some other non-1st line options include - ivabradine(a selective inhibitor of sinus node pacemaker activity), isosorbide mononitrate, ranolazine and nicorandil
3. secondary prevention of CVD: Aspirin 75mg OD PO, Atorvastatin 80mg OD PO, consider ACEi in ppl who have comorbid diabetes
procedural interventions -
- Primary percutaneous coronary intervention with coronary angioplasty in pts with proximal or extensive disease
- coronary artery bypasss graft - pts with severe stenosis
what does the right coronary artery supply?
right atrium
right ventricle
inferior surface of left ventricle
posterior septal area
what does the circumflex supply?
left atrium
posterior aspect of left ventricle
what does the left anterior descending artery supply?
anterior septal area
anterior aspect of left ventricle
How is ACS divided?
ACS is a medical emergency. person with ACS symptoms shd have an ECG.
If ECG shows ST elevation or new LBBB - then this is STEMI
If ECG shows no changes or ST segment depression or T-wave inversion or flattening of T waves, then this can be either unstable angina or NSTEMI. we do troponin levels. if troponin lvls are normal then this is unstable angina or other cause of chest pain and if they are not normal then this is NSTEMI.
how can ACS present?
Central, constricting chest pain associated with:
Nausea and vomiting
Sweating and clamminess
Feeling of impending doom
Shortness of breath
Palpitations
Pain radiating to jaw or arms
Symptoms should continue at rest for more than 20 minutes. If they settle with rest consider angina
Some patients, particularly the elderly and patients with diabetes, may not have typical chest pain. This is often referred to as a “silent MI”. Patients from some ethnic groups may also present with atypical pains.
ecg leads changes and associated heart area and artery affected?
anterolateral - V1-V6, I, aVL - left coronary artery
anterior - V1-V4 - LAD
lateral - V5,V6, I, aVL - circumflex
inferior - II, III, aVF- right coronary artery
when shd we test troponin?
The specific type of troponin, the normal range and diagnostic criteria vary based on different laboratories (so check your policy). Diagnosis of ACS typically requires serial troponins. A rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle. They are non-specific, meaning that a raised troponin does not automatically mean ACS.
Troponin I and T become detectable in serum three to six hours after infarction, peak at 12-24 hours, and remain raised for up to 14 days.
Troponins are therefore usually tested six and 12 hours after the onset of pain. BUT refer to local guidelines
alt causes of raised troponins:
PE
aortic dissection
sepsis
myocarditis
chronic renal failure
Ix to carry out after immediate management in someone suspected to have ACS
Physical Examination (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&Es (prior to ACEi and other meds)
LFTs (prior to statins)
Lipid profile
Thyroid function tests (check for hypo / hyper thyroid)
HbA1C and fasting glucose (for diabetes)
Chest xray to investigate for other causes of chest pain and pulmonary oedema
Echocardiogram after the event to assess the functional damage
CT coronary angiogram to assess for coronary artery disease
Offer immediate coronary angiography to patients with unstable angina or NSTEMI if their clinical condition is unstable.
Immediate management of suspected ACS -
- Arrange urgent hospital admission (phone 999/112/911).
- Resuscitation as required.
- Pain relief: GTN and/or an intravenous opioid (use an antiemetic with opioids).
- Single loading dose of 300 mg aspirin unless the person is allergic.
- A resting 12-lead ECG - but don’t delay transfer to hospital.
- Assess oxygen saturation, using pulse oximetry before hospital admission if possible. Give oxygen if oxygen saturation (SpO2) is less than 94% with no risk of hypercapnic respiratory failure; aim for SpO2 of 94-98% (aim for 88-92% for people with chronic obstructive pulmonary disease).
Acute STEMI Treatment
Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either:
Primary PCI (if available within 2 hours of presentation) Thrombolysis (if PCI not available within 2 hours) (eg using alteplase, streptokinase, etc)
acute NSTEMI and unstable angina mx
aspirin 300mg STAT
ticagrelor 180mg STAT or clopidogrel 300mg if higher bleeding risk
morphine titrated to control pain
anti-thrombin therapy (unless high bleeding risk) - fondaparinux unless angiography planned within 24 hours, in which case Unfractionated heparin was recommended
Nitrates - GTN
oxygen if sats below 94%
Then use GRACE score -
the Global Registry of Acute Coronary Events (GRACE) Risk Scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:
<5% Low Risk
5-10% Medium Risk
>10% High Risk
If they are medium or high risk they are considered for early coronary angiography and follow on PCI if indicated (within 72 hrs of admission) to treat underlying coronary artery disease.
other treatments -
- beta blockers
- ACEi
- statins
- cardiac rehab
- lifestyle and comorbidity mx
complications of ACS
acute MI
cardiogenic shock
ischaemic mitral regurg
arrhythmias
AV nodal blockade
complications of MI
D – Death
R – Rupture of the heart septum or papillary muscles
E – “Edema” (Heart Failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
dressler’s syndrome - post MI pericarditis.
types of MI
It is worth avoiding as it could confuse people unless they are a medical registrar or cardiologist.
Type 1: Traditional MI due to an acute coronary event
Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with PCI / coronary stunting / CABG
2ndary prevention post acute MI/unstable angina
lifestyle -
Stop smoking
Reduce alcohol consumption
diet and exercise advice
wt loss if relevant
Cardiac rehabilitation (a specific exercise regime for patients post MI)
Optimise treatment of other medical conditions (e.g. diabetes and hypertension)
medical -
aspirin 75mg OD
clopidogrel or ticagrelor for upto 12 months
atorvastatin 80mg OD
beta blocker
acei
aldosterone antagonist for those with clinical heart failure
what are some factors associated with high bleeding risk?
advancing age
known bleeding complications
renal impairment
low body weight.
what are the values for prolonged QT interval
At 60bpm,
in males - >440
in females - >460
If not 60bpm,
then use QTc and then compare to 440 or 460
QTc = QT (in milliseconds)/ sqaure root of R-R interval in seconds
hypokalaemia?
Hypokalaemia is usually defined as a serum concentration of potassium <3.5 mmol/L.
Severe - <2.5 mmol/L - needs urgent treatment
causes of hypokalaemia
diuretics
loss of GI fluids - diarrhoea, vomiting, laxative abuse
hyperaldosteronism, cushing’s syndrome/steroids/ACTH
alkalosis
burns
insulin and glucose administration
catecholamines and beta-2-sympathomimetics (salbutamol)
malnutrition
anorexia nervosa
presentation of hypokalaemia
can be asymptomatic
Lassitude.
Generalised weakness and muscle pain.
Constipation.
hypotonia
hyporeflexia
cramps
palpitations
light headedness
when severe -
Severe muscle weakness and paralysis (beginning in the lower extremities, progressing to the upper extremities and torso).
Respiratory failure (due to involvement of respiratory muscles).
Ileus (due to involvement of GI muscles).
Paraesthesia.
Tetany.
ix to carry out in hypokalaemia
U&Es
serum bicarbonate
Serum magnesium
ECG
typical ecg findings in someone with hypokalaemia
Flat T waves
ST depression
Prominent U waves
**the QT interval may appear prolonged but this is usually a pseudo-prolongation as the flattened T waves merge into the U waves.
Ventricular arrhythmias such as premature ventricular contractions, torsades de pointes, ventricular tachycardia and ventricular fibrillation can also occur
management of hypokalaemia
check and correct Mg2+ as hypokalaemia hard to correct unless magnesium is normalised
mild - low risk moderate:
- treat underlying cause
- dietary supplementation
- potassium supplementation if required
high risk moderate - severe:
- managed in hospital setting
- manage underlying condition
- oral supplements can still be used if they can be taken, absorbed and are likely to correct lvls rapidly enough
- where oral supplementation not possible, IV KCl can be given. NEVER bolus IV KCl as it can cause fatal arrhythmias.
IV KCl -
- given in a normal saline infusion
- rate via peripheral line should not exceed 10mmol/hour and no more concentrated than 40mmol/L
- careful monitoring of clinical condition and bloods (1-3 hrly) req
- once ECG abnormalities, muscle weakness or paralysis are resolving, slow rate of replacement or switch to oral replacement
complications of hypokalaemia
cardiac arrhythmias and sudden cardiac death
Muscle weakness, flaccid paralysis, rhabdomyolysis.
Abnormal renal function including nephrogenic diabetes insipidus, metabolic alkalosis (due to enhanced bicarbonate absorption) and enhanced renal chloride excretion.
Iatrogenic hyperkalaemia.
Contributes to digoxin toxicity.
Contributes to the development of hepatic encephalopathy in cirrhosis.
4 possible rhythms that can be seen in an unresponsive patient in cardiac arrest
Shockable rhythms -
1.VT
2.VF
Non-shockable rhythms -
3.PEA (pulseless electrical activity - all electrical activity except VF/VT, including sinus rhythm without a pulse)
4. Asystole (no significant electrical activity)
what are supraventricular tachyarrhythmias?
tachyarrhythmias originating above the ventricles, ie, in the SAN or atria or AVN/junctional tissue are called supraventricular tachyarrhythmias.
pathophysiology behind physiological sinus arrhythmia
SAN is under vagal influence. vagus is inhibited during inspiration and activated during expiration leading to faster HR during inspiration and slower HR during expiration
causes of sinus tachycardia
exercise, fever, hyperthyroidism
causes of sinus bradycardia
atheltes, hypothyroidism, hypothermia, obstructive jaundice
