Cardiology Flashcards
Diagnostic classification HTN
1: clinic BP 140/90 - 159/99 and home BP >135/85
2: clinic BP 160/90 - 180/120 and home BP 150/95
3. Clinic BP 180+ systolic, or clinic diastolic120+
Target clinic BPs
age <80: <140/90, home < 135/85
in >80s: <150/90, home below 145/85
If postural hypotension, then target should be based on standing BP
frailty & multimorbidity: make clinical judgement
investigations for HTN
If clinic BP high, ofer ABPM or home BP monitoring
Assess for target organ damage: urine dip (haematuria), urine albumin: creatinine, HbA1x, U&Es, retinal fundi, 12 lead ECG
Assess cardiovascular risk: blood lipids, calculate QRisk
If BP > 180/120 + ANY of:
- retinal haemorrhage/papilloedema
- life threatening symptoms
- suspected phaeochromocytoma
–» refer for same day specialist review
HTN management
Do not forget conservative
If <55 not black African/afro-caribbean OR anyone w diabetes-> ACEi or ARB
Otherwise CCB
+other one
+ thiazide diuretic
+ consider starting spiro or alpha or beta blocker
Mx stable angina
Beta blocker or CCB first line
Consider antiplatelet treatment eg low dose aspirin
consider ACEi if also diabetes
Review 6mo-1 year
Pump failure causes of heart failure
- Impaired systolic function
- following ischaemia/MI
- dilated cardiomyopathy
- hypertension
- myocarditis - Impaired diastolic function (impaired filling)
- pericardial effusion or tamponade
- cardiomyopathy restricted or hypertrophic
3, arrhythmias
- bradycardiac or heart block
-tachycardias
-anti-arrhythmics eg beta block/verapamil
Excess pre load causes of heart fialure
Aortic regurg/mitral regurg
Fluid overload
Excess afterload causes of heart failure
Aortic stenosis
Hypertension
HOCM
high output causes of heart failure
Anaemia
Thyrotoxicosis
Pregnancy
Pathophys of heart failure
Reduced output then heart dilates to increase contractility
Remodelling leads to hypertrophy
RAS and ANP/BNP release
Sympathetic activation
= compensated phase
THEN…
dilation increases, so contractility impaired and functional valve regurgitation
hypertrophy -> relative myocardial ischaemia
RAS activation -> sodium and fluid retention, increased venous pressure
Sympathetic excess incr afterload -> reduced cardiac output
= progressive decrease in CO and decompensation
Symptoms and signs of R heart failure
Anorexia
Nausea
Incr JVP
Jugular venous distension
Tender smooth hepatomegaly
Pitting oedema
Ascites
Symptoms and signs of left heart failure
Fatigue
Exertional dyspnoea
Orthopnoea ad paroxysmal nocturnal dyspnoea
Nocturnal cough
Weight loss and muscle wasting
CXR changes in heart failure
Alveolar shadowing
Kerley B lines
Cardiomegaly
upper lobe Diversion
Effusion
Fluid in the fissures
Mx heart failure
Prescribe ACE
Then beta blocker
2nd line therapy: aldosterone antagonist eg spironolactone and eplenerone (monitor K as both this and ACEi both potential hyperkalaemia)
incr role for SGLT-2 inhibitors if reduced ejection fraction
3rd line: specialist treatment eg ivabradine, sacubitril-valsartan and digoxin
Adverse signs indicating need for shock
Hypotension <90
pallor, sweating, cold, clammy extremities, confusion, impaired consciousness
syncope
myocardial ischaemia
heart failure
What to do if irregular broad complex tachycardia?
seek help!
Possibly AF with bundle branch block, or AF with ventricular pre-excitation or torsade de pointes
Mx regular narrow complex tachycardia
Vagal manoeuvres
IV adenosine
If unsuccessful consider dx atrial flutter and control rate eg w beta block
Mx regular broad complex tachycardias
Assume VT
Loading dose of amiodarone, followed by 24h infusion
Mx irregular narrow complex tachycardia
Probably atrial fibrilaiton
If onset <48h consider electrical or chemical cardioversion
Otherwise rate control, beta block first line unless contraindication
ECG features of hypokalaemia
Small/absent T waves (occasionally inversion)
Prolonged PR interval
ST depression
Long QT
Secondary prevention drugs post MI
Dual antiplatelets eg aspirin + ticagrelor
ACE inhibitor
Beta blocker
Statin
Amiodarone action
Potassium channel blocker
So inhibits repolarisation and prolongs action potential
Also blocks Na channels
USed in treatment of atrial, nodal and ventricular tachycardias
Problems with amiodarone
Very long half life (20-100 days), so loading doses freq give
Causes thrombophlebitis so ideally should be given central veins
Lengthens QT interval
p450 inhibitor, so interacts w many drugs, eg decr metabolism of warfarin
Many adverse effects
Adverse effects of amiodarone
Thyroid function (both hypo and hyper)
Corneal deposits
Pulmonary fibrosis/pneumonitis
Liver fibrosis/hepatitis
Peripheral neuropathy, myopathy
Photosensitivity
Slate-grey appearance
Thrombophlebitis
Bradycardia
Long QT interval
