Cardio Flashcards
Drugs which decrease mortality in HF
B-blockers: Carvedilol, Bisoprol
ACEi: Ramipril
Spironolcatone
Hydralazine with nitrates
Drug treatment HF
1st line: ACEi + Bblockers 2nd line: Aldosterone antagonist (spironolactone), angiotensin II receptor blocker (Losartan) Digoxin, Ivrabadine Diuretics Influenza, pneumococcal vaccine
Pericarditis
Inflammation of pericardium. Characterised by chest pain, pericardial rub, ECG changes
Sx: Pleuritic chest pain, SOB
Signs: Pericardial rub, fever
Ix: ECG (Saddle shaped ST elevation, PR depression in most leads), CRP (elevated), Urea (elevated if uraemic cause), CXR (pericardial effusion)
Causes: Cocksackie virus, TB, post-MI, uraemia,
DDx: MI, PE
Tx: NSAIDs, Pericardiocentesis (if Purulent)
HOCUM (Hypertrophic obstructive cardiomyopathy)
Autosomal dominant disorder, defect of B-myosin protein causing diastolic dysfunction
Sx: asymptomatic, exertional SOB, syncope, sudden death
Ix: ECG (LVH changes - long QRS)
Infective Endocarditis
Infection of endocardium. Usually on valvular surface which have damage to turbulent blood flow. Thrombus is formed which is colonised by bacteria and forms vegetation.
Aetiology: Strep. viridans (native) Staph. aureus (IVDU), Coauglase-negative Staph, staph. epidermis (prosthetic) Staph. epidermis (Post-op) Strep. bovis
Risk fx: Valvular disease, IVDU, cardiac surgery, dental surgery/abscess
Classification: Acute (fever, increased HR, Sub-acute - over weeks/months (non-specific e.g. night sweats, fatigue, weight loss)
Clinical features:
Early: 2wk incubation, fever+murmur
Embolic: splinter haemorrhages, haematuria, pulmonary emboli (right sided endo - tricuspid)
Late: Immunological: Osler’s nodes, finger clubbing, Tissue damage: valve destruction/abscess
Signs: Clubbing, Osler’s nodes (painful on fingers/toes), Janeway lesions (painless plaques on palms/soles, splinter haemorrhages, Roth spots (pale, retinal lesions)
Diagnosis: Duke’s criteria
Major:
2 of 3 cultures +ve for typical organism
Echo +ve
Minor:
>38
Vascular (Janeway lesions, splinter haemorrhages, splenomegaly)
Immunological (Osler’s nodes, glomerulonephrotis)
Blood cultures that does not meet major criteria
Ix: Blood cultures, FBC (normochromic, normocytic anaemia), Echo (TTE if native. TOE if prosthetic), Urinalysis (RBC/WBC casts)
DDx: Rheuamtic fever, Atrial myxoma (most common cardiac tumour)
Tx: Native: B-lactam + gent Prosthetic: B-lactam + gent Vanc + gent (if penicillin resistant) Surgery: Indications: severe CCF, sepsis despite abx, recurrent embolic episodes)
Rhythms: Tachycardia
Narrow complex tachy
- SVT (tachy that is not ventricular in origin)
Tx: valsalva manoeuvre, 2nd line: IV adenosine
Difference between angina and unstable angina
Angina: mycoardial ischaemia, predictable, better on rest
Unstable angina: occurs on rest, unpredictable, increasing frequency, no ECG changes/troponin
ECG changes PE
Sinus Tachy
S1Q3T3 (R. heart strain)
BBB
Right axis deviation
ACS
Syndrome of acute myocardial ischaemia and/or infarction
Unstable angina
ACS with no troponin rise, characterised by rest angina, new-onset or worsening of stable angina, or angina post-MI
Pathology: Athersclerotic plaque forming thrombus leading to narrowing of coronary a.
Can also be caused by emboli, coronary spasm
Risk fx: female, diabetic, HTN
Sx: chest pain radiating to jaw, can occur at rest, dyspnoea
Signs: Tachy, mumur
DDx: stable angina, pericarditis, aortic dissection
Ix: ECG (may T wave inversion - ischaemia) Troponin (normal) FBC (anaemia), UEs (risk stratification), lipid profile (risk stratification), glucose CXR (widened mediastinum) Echo (wall motion abnormalities)
Tx:
O2 (If <90%)
Morphine+metoclopramide
GTN spray/sublingual
Aspirin + Ticagrelor
Risk assess (GRACE - risk of future cardiovascular events)-
Low risk: no ECG changes, no recurrent chest pain, neg troponin
If low: discharge + medical therapy (ACEi, Bblockers, Asipirin+Clopidogrel+Statin+Cardiac rehab)
NSTEMI
ACS with increase in troponin levels, may have ECG changes (ST-depression, T-wave inversion). Due to athersclerotic plaque forming thrombus/emboli causing partial occlusion coronary a. and myocardial infarction
Risk fx: CVD, diabetes, obesity
Sx: chest pain/discomfort, retrosternal, radiates to jaw/left arm, mimics heart burn
Ix:
ECG (may show ST depression, T wave inversion)
Troponin (rises in 4 hours, peaks at 18hrs)
FBC, lipid, glucose
CXR (exclude pneumonia, aortic dissection)
Echo (wall motion abnormalities)
GRACE score to assess coronary angio
High risk: inpt coronary angio within 24hrs
Intermediate risk: outpt coronary angio within 1 wk
Low risk: discharge + medical therapy
Tx:
O2, morphine+metoclopramide, GTN, aspirin+ticagrelor
Fondaparineux (inhibits Xa +anti thrombin) or LMWH
If haemodynamically unstable - PCI
Secondary:
ABC(A)S + cardiac rehab
STEMI
Complete occlusion of coronary a leading to myocaridal cell death. Characterised by ST-elevation in >2 continuous leads and rise in troponin
Athersclerotic plaque forming thrombus/emboli
Other cause: coronary spasm, aortic dissection
Sx: Central crushing chest pain, radiates jaw+arm, N+V, dyspnoea
Signs: cardiogenic shock (profound hypotension, reduced GCS)
DD: aortic dissection, US/NSTEMI, PE, pneumonia
Ix: ECG, troponin, glucose, lipid profile, CXR (exclude other causes), coronary angiogram
Tx: O2 (if <95%), Morphine+metoclopramide, GTN (not hypotensive), Aspirin+Ticagrelor
PCI (within 12hrs symptoms, or 120 mins till PCI)
Thrombolysis (tenecteplase)
CABG
Ind improve mortality: Left main stem disease or triple vessel disease involving LAD
Ind improve symptoms: angina where meds failed, angioplasty failed
Saphenous vein, internal mammary, radial a.
Post-MI: ACEi Bblocker Clopidogrel+aspirin Statin Eplerenone (diabetic, HF) Cardiac rehab
Complications MI
Arrythmias, HF, Valvular disease (MR), Depression
Angina
Symptomatic, reversible myocardial ischaemia
Caused by atheromatous plaques leading to obstruction of coronary a.
Other causes: anaemia
Clinical features: Chest pain, bought on by exertion, relieved by rest/GTN
3=typical angina, 2=atypical angina, 3=non-anginal pain
Ix: ECG, troponin
FBC (low)
Glucose
Exercise stress test
Tx: Lifestyle changes
PRN relief: GTN spray/sublingual
Anti-anginal: Bblockers (carvedilol)/Calcium Ca blockers (amlodipine) (2nd line), isosorbide dinitrate (long acting nitrate), ivrabadine
Aspirin Statin Anti-hypertensives Blood sugar control PCI, CABG (if medical therapy failed)
HF
Decreased CO compared metabolic demand
HF-RF (systolic) - decreased ventricular contraction leading to decreased CO. Causes: IHD, MI
HF-pEF (diastolic) inability ventricles relax leading to increased filling pressures. Causes: ventricular hypertrophy, cardiac tamponade
Chronic HF: develops slowly from acute HF, or new
Acute: new or decompsenated chronic HF
LVF: pink frothy sputum, dyspnoea, orthopnoea, PND, reduced exercise tolerance
RVF: pulmonary oedema, ascites, epistaxis, nausea. Causes: LVHF, lung disease (cor pulmonale)
Signs: raised JVP, peripheral oedema, ascites, RV heave (pulm HTN)
Diagnosis: Framingham criteria: acute pulm oedema, orthopnoea, cardiomegaly
Ix: ECG (may show MI, LVH) B-natruretic peptides CXR (Alveolar oedema, kerley B lines, Cardiomegaly, Upper lobe Distribution, pulmonary Effusion) FBC (anaemic) UEs (N/high) - fluid status LFTs (abdo congestion) Ferritin (HH) Transthoracic Echo (LV systolic dysfunction)
DD: pneumonia, COPD, PE
New York HF classification I: HF but aysymptomatic II: symptoms upon activity III: symptoms limiting activity IV: symptoms at rest
Tx:
ACEi/ARB (2nd line: Sacubitril/Valsartan:)+ Blbockers + lifestyle changes
+Spironolactone
+Diuretics, Digoxin, Isosorbide dinitrate, Ivrabadine, ICD
Annual influenza, one off pneumococcal vaccine
Acute HF:
Causes: post-MI
DD: PE, pneumonia
Ix: ECG, troponin, CXR, BNP, Cardiac monitor
Tx:
High flow O2 (if low)
IV morphine
IV furosemide
GTN spray
IV isosorbide dinitrate (if BP >100, keep<90)
Tachyarrythmias
Sinus tachy causes: pain, infection, exercise, drugs (caffeine, cocaine), fever, hyperthyroidism
Narrow complex tacy: >100 bpm, QRS <120ms
Ventricles depolarised via normal conduction pathways
- AF, atrial flutter, SVT
Acute tx: vasovagal/carotid sinus, IV adenosine
AF
Disorganised atrial electrical activity.
Paroxysmal, persistent or permanent.
Causes: IHD, HTN, valvular disease, PE
Risk fx: HF, diabetes, valvular disease
Sx: palpitations, dizziness, SOB (if HF)
Signs: irregular pulse, hypotension, valvular disease - murmur (MS)
Ix:
ECG (no P waves, irregularly irregular, no isoelectric baseline)
TFTs (thyrotocixosis, low TSH, high T3/4)
UEs (low K+)
Troponin (AF can cause or be a complication of MI)
Echo (left atrial enlargement, mitral valve disease)
Acute AF: Haemodynamically unstable (shock, chest pain, SOB): DC cardioversion
Haemodynanically stable <48hrs: rate+rhythm control
Rate: Blocker: Bisoprolol, Ca+ channel blocker:
(Verapamil, Diltiazem), Digoxin
Rhythm: Flecainide (Contra: heart disease), Amiodarone, or DC cardioversion
Haemodynamically stable > 48hrs: Rate+ anticoagulation
Bisoprolol + DOAC/warfarin
DOACs not to be used with prosthetic heart valve
Chronic AF:
Paroxsymal: <7 days, recur
Persistent: >7 days
Permament: Long-term, sinus rhythm cant be achieved
Unstable Persistent, Paroxsymal: DC cardioversion
Stable persistent, paroxsymal: Rate control + DOAC
Anti-coagulation assess CHA2DS2VASC
CCF, HTN, Age (>65: 1, >74: 2 points), Diabetes, Previous Stroke (2), Vascular disease, Sex (Female)
Anticoagulate if Male: 1, Female:2
Atrial flutter
Organised electrical activity, but circular movement round atria, causing atrial rate: 300 bpm. May be so fast, AVN passes some of the impulses causing 150bpm (AV 2:1 block), 100bpm (AV 3:1)
Ix: ECG (saw tooth pattern, regular) Tx: unstable: cardioversion stable: 1st line: Rate control+anticoagulation, 2nd line: cardioversion Refractory: radiofrequency ablation
Broad complex tacy: <60bpm, QRS >120,ms
VT (commonest), VF (chaotic)
DDx: VT, VF, Torsades de pointes (polymorphic VT),
Causes: IHD, electrolye disorders (low K+), drugs: digoxin, TCAs
Regular: (assume VT/VF) O2 if <90%, IV access, ECG Adverse signs: shock BP<90), chest pain, HF, syncope)? Yes: Sedation Up to 3 synchronised DC shocks Correct electrolyte abnormalities Amiodarone IV
No:
Correct electrolyte abnormalities
Amiodarone
DC shock if fail
Irregular:
AF+BBB= treat as narrow complex tachy
Torsades = IV Mg
VF/pulseless VT:
Arrest protocol
Narrow complex tachy:
Wolf-Parkinson White syndrome
Congenital accessory conduction pathway between atria and ventricles.
ECG: short PR interval, QRS may be widened due to slurred upstroke (delta wave)
Tx:
Carotid sinus massage or valsalva manouvre
IV adenosine
Bradyarrythmias
<60bpm
Sinus brady
Causes: Physical fitness, drugs - Bblockers, amiodarone, hypothyroidism, hypothermia
Heart block: disrupted electrical passage through AV node
1st degree: prolonged PR interval
2nd degree:
Mobitz 1: progressively prolonged PR until dropped beat
Mobitz 2: constant PR interval, regular dropped beat (non-conducted P wave)
3rd degree: no relationship between p wave and QRS
Causes:
1st/2nd: normal variant, IHD, drugs (digoxin, Blbockers, non-dihydropyridine Ca+blockers, e.g. Verapamil)
3rd: IHD (esp inferior MI), aortic valve calcification, digoxin toxicity, cardiac surgery/trauma
Risk fx: use of AV nodal blocking drugs, cardiovascular disease, recent cardiac sugery
Sx: syncope, fatigue, chest pain, palpitations, high (sometimes low) BP
Treatment:
1st: none
2nd/3rd:
Treat Digoxin toxicity: Digoxin immune Fab, Bblockers: glucagon, Ca channel blocker: Calcium chloride
No reversible cause: permanent pacemaker
Severe symptoms (e.g. syncope): temporary pacing
HTN
Most important risk fx for premature death and CVD. Increases risk of coronary a. disease, stroke, HF.
BP >140/90
Essential HTN (95%): no cause Secondary HTN (5%): Renal - Glomerulonephritis, polycystic kidney disease, Endocrine disease - Cushing's, Conn's, phaeochromocytoma
Risk fx: >65, family hx, obesity, Afro-Carribean, alcohol
Sx: aymptomatic
Ix: Confirm with 24hr ambulatory BP readings, or home monitoring (1wk)
Assess cardiovascular risk
Check retinopathy (seen in longstanding HTN)
Fasting glucose, lipid profile (quantify risk)
ECG (LV hypertrophy? previous MI?
Special tests: renal US (renal stenosis), plasma renin+aldosterone, 24hr-urine catecholamines (phaeochromocytoma)
Tx:
>135/85 (stage 1): <80yrs + high risk of CVD, renal disease: lifestyle advice + drug tx
low risk: lifestyle advice 3-6mnths, if not controlled then drug tx
>150/95: lifestyle advice + immediate drug treatment (aim to control within 3mnths)
Stg 1: Clinic BP >140
Stg 2: Clinic BP >160
Stg 3: Clinic BP >180
1st line: <55yrs/diabetic: ACEi >55 yrs/black: Ca channel blocker 2nd line: <55 yrs/diabetic: A+C/D >55 yrs/black: C+A/D 3rd line: A+C+D 4th line: Spironolactone (K+ <4.5) Alpha/Bblocker K+ >4.5
Aim:
<80yrs: Clinic BP <140, ABPM: <135
>80yrs: Clinic BP <150, APBM: <145
Postural/Orthostatic hypotension
BP drop >20 or 30 systolic in those with HTN or 10mmHg diastolic within 3 mins of standing
Causes: drugs (Bblockers, alpha-blockers (tamsulosin), PD, diabetes (peripheral neuropathy), dehydration
Sx: sx of cerebral hypoperfusion - light-headedness when standing, syncope, fatigue, visual changes
DDx: vasovagal syncope, vertigo
Ix:
Measure BP sitting/supine and then standing within 3 mins
Tilt-table test (BP+HR measured when pt supine and during head tilt up. Decrease in BP when head tilted up)
24-hr BP monitoring
BP falls, and HR doesn’t rise = Impaired autonomic cardiovascular reflex:
Fall in BP+rise in HR = dehydration, drugs
Tx:
eliminate causes e.g. drugs
lifestyle changes e..g pts should sit before going supine to standing
Fludrocortisone+sodium chloride: increases BP when given with salt
