Cardiolology 2 Flashcards
What is Aortic dissection?
Tear in inner layer of Aorta (Aortic wall intima) allows blood to flow between layer , causing seperation——————> can cause aortic rupture , ischemia.
Acute - if happened in less than 14 days
SIGNS/SYMPTOMS
- Acute severe chest pain (central) - (ripping/tearing sensation)
anterior suggest ascending aorta affected. - Interscapular pain (btw scapulars) and lower pain (suggest dissection of des ending aorta)
- Hypertension
- Diastolic murmur
- pulse deficit (absence or reduction of pulse)
RISK FACTOR
0 Connective tissue disease.
- Marfan syndrome
- Ehlers - Danlos sydrome
(if have typical pain of AD + features of these 2 disease be suspcious)
0 Bicuspid aortic valve (supposed to be 3 - predisposes to aneurysm & dissections)
0 Atheroslerotic aneurysmal disease.
0 Annuloaortic ectasia - dilation or enlargement of ascending aorta.- predisposes to aneurysms/dissections.
0 Coarctation - heart birth defect which part of the aorta is narrowed. - (predisposes to Dissection)
0 smoking
0 Hx of aortic aneuyrsm or dissection.
Diagnosis of Investigation?
0 Blood pressure measurement in both arms - difference btw the 2 - indicative of AD.
ECG - may see ST depression
(1ST LINE - to rule out myocardial ischaemia)
0 CT angiography (includes chest, abdomen, pelvis to look at extent of dissection) - IMPORTANT
CXR - may show widened mediastinum
(rule out other pulmonary causes of pain)
0 Cardiac enzymes (usually negative - to exclude MI)
(MI , infarction can occur with dissection if it extends to coronary ostium )
0 Renal , hepatic test to test if perfusion to liver , kidney.
0 Lactate - elevated (indicates malperfusion (loss of blood supply to vital organ by branch aterial obstruction secondary to dissection)
- can be normal.
0 FBC - anaemia may be present - Haemorrhage.
0 Type and cross - (preperation for surgery)
CAN CONSIDER :
0 Trans - esophageal echocardiogram - if CT angiograph not available to confirm diagnosis
Treatment of AD?
Haemodynamically unstable - suspected AD
1ST LINE
0 Advanced life support + haemodynamic support (fluid , inotropes (noradrenaline +/or Dobutamine)
e.g in hypovolaemic shock , renal failure.
CONFIRMED AD
1ST LINE
IV Beta Blocker - labetalol , esmolol , metopropol (any - used to reduce pulsatile force on thinned walls)- avoid rupture & propagation of dissection.
+ Opiod analgesia (morphine)
if not working (HR still above 60 & systolic P above 120)
ADD - Vasodilators - Nitroprusside - 1st or diltiazem - 2nd)
TYPE A , Type 2 with complications
1ST LINE ( 1st line treatment for CAD + Open surgery or endovascular stent graft)
TYPE B uncomplicated
(1ST line - (1ST LINE for treatment of CAD + Endovascular stent- graft repair)
Type B chronic - (ESGR)
AFTER HOSPITAL DISCHARGE
1ST LINE - antihypertensives
(metoprolol and/or enalapril) or First 2 + Hydrochlorothiazide and/or nifedipine.
- no patient is considered cured after discharge - Beta blocker , ACE are needed.
Type A vs Type B dissection
Type A - involves ascending aorta - most dangerous form.
Type B - involves decending aorta.
What is Angina ?
TYPES?
Chest pain caused by reduced blood flow to the heart.
TYPES
0 Stable Angina - pain has trigger (stress / excercise etc) & stops within minutes of resting. - symptom of stable ischeamic heart disease.
0 Unstable angina - Unpredictable - dont have to have a trigger and can continue despite rest.
What is Stable ischeamic Heart disease (SIHD) ?
0 Inability to provide adequate blood supply to the myocardium.
Manageable & not rapidly progressive.
- no recent infarction , procedural intervention or signs of significant ongoing necrosis.
CAUSES
- Primarily atherosclerosis of coronary arteries.
SIGNS/SYMPTOMS
- Typical angina
0 provoked by stress or exercise
0 Chest pressure or squeezing (last several mins)
0 Relieved by GTN or rest. - Atypical angina ( only 2 of three criteria for typical angina - less indicative of SIHD)
- Non anginal pain ( one or none of criteria - but should be evaluated in consideration with age & risk factors - less predicitive)
- Normal examination
- normal/ unchanged ECG
RISK FACTORS
Age - Older patients (high index of suspcion even in those with atypical angina or excertional symptoms)
- Smoking - (2nd most important)
- Hypertension
- Elevated LDL cholsterol
- Isolated Low HDL cholesterol (HDL is good , LDL is bad)
- Diabetes
- Inactivity
- obesity (linked with Hypertension , diabetes)
- Illicit drug use (e.g cocaine , methamphetamine increases myocardial oxygen demand)
- Male sex.
Diagnsosis of SIHD?
ECG - often normal (but can have ST-T changes suggestive of ischeemia , Q waves suggesting prior infarction.
0 Haemoglbin - (severe anaemia cause angina without any obstructive coronary lesions )
0 Lipid profile (dyslipidaemia - risk factor for IHD)
0 Fasting glucose or HbA1c - diabetes a risk factor.
CAN CONSIDER :
00 Cardia CT angiography (- for diagnosis
0 excercise ECG
0 excercise or pharmalogical stress with imaging
0 TSH - hyperthyroidism can excaberate angina, hypothyroidism associted with dyslipidaemia , IHD.
CXR - can reveal other causes - usually normal in SIHD
0 rest echocardiography
Treatment of SIHD?
Lifestyle education
+ antiplatelet therapy
0 Aspirin
0 Clopidogrel ( if contraindication to aspirin)
0 Aspirin & clopidgrel
+ Sublingual GTN (Prophylaxis & after excercise)
+ Anti - anginal medicine
(Beta blockers (B) - 1st , calcium channel blockers (C), Nitrates (D) (3rd - if beta blocker , calcium channel not possible)
or Nicorandril (potassium channel activator) , Ivabradine , ranolazine. Possible combinations:
B
or B + C or C
or B + C+ D or B +D or C +D or D
ex of Beta blocker :
Metaprolol
bisoprolol
timolol
nadalol
ex of CAB
amlodipine
felodipine
nifedipine
isradipine
ex of long acting nitrates
- Isosorbide mononitrate
- glyceryl trinitrate transdermal
What is ACS ?
Acute coronary syndrome - consist of Unstable angina , Non ST elevation MI , ST elevation MI.
NSTEMI is differentiated from unstable angina by a dynamic elevation of troponin above the 99th percentile. A patient with NSTEMI may also be clinically unstable (e.g., low blood pressure, shock, left ventricular failure) which is not a feature of unstable angina.
What is Unstable angina?
0 Unstable angina - Unpredictable - dont have to have a trigger and can continue despite rest.
SIGNS/SYMPTOMS
Chest pain - New onset of severe angina
- prolonged > 20 mins
- Increasing frequency , duration
- lower threshold
- occurs after recent episode of MI.
RISK FACTOR
- Diabetes
- Hyperlipidaemia
- Hypertension
- Metabolic syndrome
- Renal impairment
- Peripheral arterial disease
- A history of ischaemic heart disease and any previous treatment
- Obesity
- Advanced age
- Smoking
- Cocaine use
- Physical inactivity
- Family history of premature coronary artery disease (<60 years of age).
Investigation of unstable angina ?
ECG - recording within 10 mins of medical contact (if non STEMI , STEMI activate STEMI protocol)
Cardiac troponin (hs - cTnT/cTn - high sensitive troponin ) - done within 60 mins to rule out MI.
- Should be below 99th percentile <14n/gl.
(should be certain that symptoms started more than 12 hours ago - Hs - cTn peaks at 12 hours)
If higher sent for second sample 6 hours later.
0 FBC
0 U & E , creatinine
( chronic kidney disease - may have chronically raised troponin & electrolyte abnormalities can cause ECG changes.)
0 Liver function tests
(assess bleeding risk prior commencing anticoagulation
0 Blood glucose - in known diabetes or hyperglyceamia.
Treatment or Unstable angina?
Suspected or confirmed
P
1ST LINE
0 Dual Antiplatelet therapy
- Aspirin + (P2Y12 inhibitor - Ticagrelor - 1st , clopidogrel , prasugel)
PLUS
0 Antithrombin therapy
Fondaparinux – used in those without high bleeding risk )
or UFH (heparin ) - in those with sig renal impairment.
+ Manage Hyperglycaemia
(keep levels <11mmol/l while avoiding hypo.
(if clinically indicated - insulin infusion & glucose with/out K - regular monitor glucose levels)
CONSIDER - Coronary angiography with PCI - IF unstable angina getting worse or high risk of cardiovascular events.
0 GTN (Translingua/sublingual - if 3 doses dont work IV. )(monitor BP - can cause hypotension) 0 Morphine - GTN does not work. 0 Anti - emetic (ondasetron , Metoclopramide , cyclizine ) - if giving morphine or vomiting
Treatment of Unstable angina - post stabilisation ?
Secondary prevention
similar as stable angina
( continue dual anitplatelet therapy)
+
-ACE or ARBs ( if ACE intolerant)
+ Beta blcoker ( CAB - Verapmil , diltiazem - if Beta intolerant )
do cardiac rehabilitation. , lifestlye changes etc.
Treatment of Non - STEMI ?
Clinically unstable
similar to unstable angina
- Dual antiplatelet - aspirin + another.
+ other things from unstable angina
(Only difference is 1ST LINE - is refer for immediate invasive angiography + revascularisation
(Fondaparinux - not used if immediate coronary angiography)
-
Treatment of Non - STEMI ?
Clinically stable
Same as unstable angina
- decision btw conserative management & surgery (CA & Revasccularisation)
look at unstable angina.
What is Non STEMI ?
Comprimised blood flow to myocardium beavuse of partial or near complete occulsion of coronary artery—-> damages heart.
SIGNS/SYMPTOMS
- Chest pain
0 > 15 mins
0 with nausea and vomiting 0 marked sweating,
0 and/or breathlessness,
0 haemodynamic instability
0 new in onset or occurs as sudden worsening of known stable angina (i.e., recurrent episodes of chest pain > 15 mins , not associated with excretion/stress) - Marked sweating
- Nausea & vomiting
*(Men & women can present different
Men - chest pressure/discomfort lasting at least several minutes,
Women - Middle/ upper back pain or dyspnoea
both can be accompanied by sweating, dyspnoea, nausea, and/or anxiety.) - not set in stone.
- Arrythmias - don t wait for troponin.
- Can be cardiogenic shock - clinically unstable.
( dont wait for troponin to arrange CA.
RISK FACTORS
- same as unstable angina.
+atherosclerosis (history of angina, myocardial infarction, stroke, transient ischaemic attack, peripheral vascular disease)
Diagnosis of NSTEMI ?
same as unstable angina
Hs - cTn - above 99th percentile (>14?)
ECG - indicative of NSTEMI
0 ST depression; (this indicates a worse prognosis)
- Transient ST elevation
- T-wave changes.
What is a STEMI?
lack of blood flow to heart due to complete occulsion of coronary artery.
SIGNS / SYMPTOMS
0 Crushing Heavy central chest pain (pressure / squeezing) - can radiate the left arm , jaw – can happen on rest or activity.
0 Dyspnoea
0 - Pallor (pain) 0 Diaphoresis (marked sweating) 0 nausea & vomiting 0 dizziness /light headedness 0 distress or anxiety 0 palpitations
if in cardiogenic shock :
0 BP <90mmHg
0 bradycardia
0 reduced conciousness
RISK FACTORS
Similar to unstable angina , NSTEMI.
Which groups may present atypically - pain - STEMI?
Be aware of patient groups who are more likely to present atypically.[29]
Women, older patients, and patients with diabetes are more likely to present with atypical features.
Atypical chest pain might be described by the patient as ;
- burning, throbbing, tight, or a feeling like trapped wind.
- The patient may describe indigestion rather than chest pain.
In the absence of chest pain, there may be epigastric pain, back (interscapular) pain, neck or jaw pain, or arm pain (typically left-sided).
Clinical suspicion is key to making the diagnosis. It is, therefore, vital to make a full assessment based on the history, examination, and serial ECGs.
Diagnosis of STEMI?
0 ECG -new or increased and persistent ST - segment elevation > or equal to 1 mm in at least two contingous leads (lie next to each anatomically - so indicate specific cardiac territory
Exception in this cases - V2-V3 :
- ≥2.5 mm in men <40 years old
- ≥2 mm in men >40 years old
- ≥1.5 mm in women regardless of age)
(Note that the presence of left ventricular hypertrophy, LBBB, or a paced rhythm does not preclude a diagnosis of STEMI if the patient presents with typical symptoms of myocardial ischaemia.)
When diagnosed : Coronary angiography with follow on PCI (primary percatenous coronary intervention. ) - if patients presents within 12 hours of onset of synmptoms.
0 Cardiac troponin 0 Glucose 0 FBC 0 electrolyte (avoid arryhtmias) , urea , creatinine , eGFR) 0 CRP 0 Serum lipids.
CONSIDER - CXR - exclude other causes.
Treatment of STEMI?
Offer aspirin , then assess eligilbilty for reperfusion therapy —> if not possible offer medical management.
Eligible ( if PPCI can be given within 120 mins and patients presents 12 HOURS after symptom onset)
Aspirin + Primary percantous coronary intervention)
(if having PPCI offer :
- (Dual antiplatelet - aspirin & prasugrel - if not on any oral anticoagulant)
- ( aspirin & Clopidogrel - if on anticoagulant )
- if over 75 - if sig risk of bleeding give clopidgrel or ticagrelor.
if not possible PPCI within 120mins - Fibrinolysis indicated. (give antithrombin at the same time
)
(- if fibronlysis - antithrombin therapy should occur at the same time :
- alteplase,
- reteplase, streptokinase or tenecteplase
Then offer Ticagrelor with aspirin unless high bleeding risk.
(clopidgrel with aspirin ,aspirin or aspirin alone - if high bleeding risk)
(do ECG after fibrinolysis- if residual ST elevation suggesting failure offer Coronary angiography with PPCI - dont repeat fibrinolysis)
Manage Hypoglycemia
Treatment - post STEMI?
1ST LINE
- Continue dual antiplatelet therapy
+ start beta blocker or CAB (verapamil) - indefintely (for at least 12 months if reduced left ventricular ejection fraction.)
+ start ACE or ARBs
+ Statin
+ Cardiac rehabilitation.
Consider - aldosterone antagonist - for any patient wirh reduced LVEF or symptims of heart failure.
