Cardio Flashcards
Summarise stable angina
Pathophysiology: coronary arteries are narrowed so when there is increased demand of blood supply (e.g, exercise). Angina is triggered.
Causes: CVD RF e.g. age, Fhx, male, smoking, alcohol, low exercise, obese, stress, htn, DM, CKA, RA, antipsychotics
Presentation: constricting CP which may radiate to jaw/ arms. Relief with GTN or rest.
Investigations: CT coronary angio is gold standard. Also consider ECG, FBC, U+Es (before starting meds), lipids, TFT, HbA1c
Management: Refer to cardiology (urgently if unstable), secondary prevention (aspirin, statin, ACE-i), GTN, beta blocker/ CCB
Summarise ACS
Pathophysiology: Thrombus forms in the coronary artery, made up of platelets
STEMI: St elevation/ new LBBB
NSTEMI: Troponin raised/ ST depression/ TWI/ Q waves
Unstable angina: Trop and ecg normal but have sx
Presentation: Central, tight CP +/- N+V, sweating, SOB, palpitations, radiation jaw/ arms. Continue 20 mins after rest.
Ix: Troponins at baselines and 6/12 hrs. Ecg. FBC (anaemia), U+E (before start ACE-i), LFT (before statins), lipids, HbA1C. +/- CXR, echo, CT angio.
Mx:
STEMI: Primary PCI, thrombolysis with alteplase if PCI not available in next 2 hrs and is 12 hrs since sx began.
NSTEMI: BB, DAT, morphine, nitrates, fondaparinux. Use GRACE score to assess for need to have PCI.
Secondary prevention: 6 As –> Aspirin, Another antiplatelet, atorvastatin, ACE-i, Atenolol. Lifestyle.
Complications: Heart failure, arrthymia, aneurysm, dresslers,
Types MI:
1) ACS
2) secondary to increased demand for/ reduced supply oxygen e.g. anaemia
3) sudden cardiac death
4) secondary to PCI/ CABG
What are causes of raised troponins (not ACS)?
Chronic renal failure Sepsis Myocarditis Aortic dissection Pulmonary embolism
Summarise pericarditis
Pathophysiology: Local immune response causing inflammation of the pericardium. In effusion there is fluid that prevents the heart from expanding in diastole. In tamponade the effusion is so large the pressure reduces CO on systole.
Causes: Can be due to infection (commonly enterovirus); MI (happens 2-3 weeks later); autoimmune (e.g. RA, SLE); injury; uraemia, cancer, methotrexate, HF
Presentation: Pleuritic CP that is worse on lying flat and better on leaning foward, low grade fever, pericardial rub. Can lead to pericardial effusion and rarely cardiac tamponade.
Tamponade: Becks triad (falling BP, rising JVP, muffled heart sounds). pulsus paradoxus (decrease systolic >10mmHg during inspiration), Kussmaul’s sign (paradoxical rise JVP on inspiration).
Ix: ECG shows global saddle shaped ST elevation and PR depression, echo shows pericardial effusion, CRP and ESR raised
Mx: NSAIDs, if more severe may need steroids and pericardiocentesis
Summarise acute heart failure
Pathophysiology: LV cannot adequately move blood through the body. Blood backlogs into the pulmonary veins and lungs. Vessels become big and leaky –> pulmonary oedema
Causes: IV fluids, sepsis, MI, arrthymias
Presentation: Rapid SOB, worse lying and better on sitting up, T1RF. Cough up pink, frothy sputum. Bibasal crackles. Hypotension if develop cardiogenic shock.
Ix: THINK CAUSE: ECG (ischaemia and arrthymias), ABG, CXR, bloods (infection, kidneys, trop if worried about MI)
Mx: Stop fluids, sit up, oxygen, IV 40mg furosemide. Monitor fluid intake and UO.
Summarise chronic HF
Pathophysiology: impaired ventricular relaxation or contraction, so blood backs into the rest of the body/ lungs
Causes: IHD, valvular disease, htn, arrthymia
Presentation: SOB (PND, orthopnoea), fatigue, peripheral oedema, pink forthy cough, S3 gallop, raised JVP (R sided), hepatomegaly, displaced apex beat
Ix: NT proBNP (BNP relaxes smooth muscles so is response to vascular resistance), echo, ECG, CXR (cardiomegaly, upper lobe venous diversions due to back pressure, pleural effusions and fluid in the septal lines (kerley lines) due to oedema)
Mx: Refer (BNP >2000 = urgent referral), manage underlying cause, flu and pneumococcal vaccine, ACE-i + BB, hydralazine and nitrates, ivabradine, lifestyle
NYH Classification:
Stage 1 = heart disease present but no undue dyspnoea from activity
Stage 2 =comfortable at rest, dyspnoea during ordinary activities
Stage 3 = less than ordinary activities cause dyspnoea – limiting!
Stage 4 = dyspnoea present at rest, all activities cause discomfort
Summarise cor pulmonale
Cor pulmonale is right sided heart failure caused by respiratory disease. The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries. This leads to back pressure of blood in the right atrium, the vena cava and the systemic venous system.
Causes: COPD!!, PE, ILD, CF, primary PH
Mx: silfenafil for pulmonary htn
Summarise hypertension
Definition:
stage 1: >140/90 in clinic or 135/85 ambulatory
Stage 2: >160/100 in clinic or 150/95 ambulatory
Stage 3: >180/120 in clinic
Causes: Essential mostly, secondary (ROPE: renal, obesity, pregnancy, endocrine)
Ix: albumin: creatinine ratio for proteinuria, U+Es, lipid, HbA1c, consider specialist referral if secondary cause or <40 yrs
Mx: Start medication if stage 2 htn or stage 1 + DM/ Q risk 10%+/ renal disease/ CVD
ACE-i: diabetic or <55. Use ARB in afro-carribeans.
CCB: afro-carribean or >55
Diuretic: K+ <4.5 consider potassium sparing diuretic
Aim for 140/90 in <80 yrs and >150/90 in >80 yrs.
Summarise mitral stenosis
pathophysiology: narrow mitral valve makes it difficult to push blood from L atria to ventricles
Causes: RF, IE, calcification
Presentation: mis diastolic, low pitched murmur, loud S1, malar flush, louder with pt on left side
Ix: Echo is gold standard for all valvular issues, ECG may show LA enlargement (P-mitrale) and AF
Mx: replacement of valve, IE prophylaxis, monitoring
Summarise mitral regurgitation
Pathophysiology: valve allows blood to leak during systolic contraction of L ventricle –> HF, because the leaking valve causes a reduced ejection fraction
Causes: age, IHD, IE, RF, EDS/ marfans
Presentation: pansystolic high pitched murmur, radiates L axilla, heart failure signs
Ix: Echo, P-mitrale or AF on ecg
Summarise aortic stenosis
Pathophysiology: A pressure gradient develops between LV and aorta; there is increased afterload, difficult to pump blood through narrowed valve. LV compensatory hypertrophy. When compensatory mechanisms are exhausted - dilation, weakness.
Causes: calcification, RF, bicuspid valve
Presentation: ejection-systolic murmur, high pitched, crescendo-decrescendo, radiates to carotids, slow rising pulse, narrow pulse pressure. TRAID = Exertional syncope, SOB, CP.
Ix: P-mitrale ecg, LBBB/ poor R wave progression, echo
Summarise aortic regurgitation
Pathophysiology: Leakage of blood into the LV during diastole – very common and present mildly in 80% of the population. Combines pressure and volume overload. Compensatory mechanisms - LV has to increase EF, tries to work harder, dilation and hypertrophy
Causes: bicuspid valve, RF, IE, age, EDS/ marfans
Presentation: Wide pulse pressure, early diastolic rumbling murmur at left sternal border, collapsing/ waterhammer pulse
Summarise AF
Pathophysiology: Atria contraction is rapid, irregular and uncoordinated, as abnormal electrical activity overrides SAN. The elctrical activity can also spread to the ventricles resulting in HF, tachycardia and clot formation.
Causes: sepsis, mitral stenosis/ regurgitation, IHD, thyrotoxicosis, htn
Presentation: palpitations, SOB, syncope, sx of stroke, sepsis or thyrotoxicosis
Ix: ECG shows absent P waves, tachycardia and irregularly irregular.
Mx:
Rate control unless reversible cause for AF; <48 hrs onset; HF or sx persist.
BB –> CCB –> Digoxin (sedentery)
Rhythm control: cardioversion –> immediate if <48 hrs onset or unstable. Otherwise anticoagulate for 3 weeks prior.
Flecanide –> amiodarone or electrical with defibrillator
Long term rhythm control: BB –> drondarone –> Amiodarone
Flecanide is used for paroxysmal AF and the pill in the pocket approach
Anti-coagulate depending on their CHADVASC and ORBIT
Ablation if severe
Summarise atrial flutter
Pathophysiology: Re-entrant rhythm due to an extra electrical pathway, stimulating atria at around 300bpm which stimulates the ventircles every second lap –> 150 bpm.
Causes: htn, thyrotxicosis, IHD, cardiomyopathy
Ix: ECG shows sawtooth appearance of P wave after P wave
Mx: same as AF
Summarise SVT vs VT/ VF
SVT –> narrow complex tachy. valsalva -> carotid massage -> adenosine
VT/ VF –> broad complex tachy, give amiodarone or shock if unstable
Summarise brugada
Pathophysiology: RBBB, ST elevation in precordial leads. Early repolarisation. Shortened QT.
Presentation: Sudden death. Autosomal dominant – young, previously fit male. Increased in Asian population. Syncope tachyarrhythmias.
Ix: Give sodium channel inhibitor before ecg to reveal st elevation (e.g. ajmaline).
Mx: Implantable cardiac defibrillator.
Summarise heart blocks
First degree: PR >200 ms.
Second degree:
Mobitz 1: longer, longer, longer, drop!
Mobitz 2: unpredictable loss AV conduction, risk asystole.
Third degree: There is no relationship between the P waves and the Q waves. Risk of asystole.
Mx:
Stable: monitor this. Look at U+Es, stop BB and CCB.
Risk asystole: Atripine 500mcg (rpt up to 6 doses)–> temporary and then permanenet implantable defibillator
Summarise wolf-parkinson-white syndrome
Pathophysiology: Due to an aberrant accessory pathway (Bundle of Kent) - congenital remnants.
Sx: Intermittent racing. Sudden onset but can last up to an hour. Sometimes associated with sudden death.
Ix: Chaotic, irregular, fast ECG. Shows delta wave - small P wave and then no clear isoelectric PR interval - QRS starts straight away (no delay between SA and AV conduction). Narrow QRS complex - AV re-entrant from middle to sides, orthodromic (more common). Broad QRS complex - AV re-entrant from sides to middle.
Mx: Avoid drugs that slow AV conduction. Ablation. Use amiodarone or soltalol.
Summarise patent ductus arteriosus
Pathophysiology: ductus arteriosus fails to close. Pressure aorta > pressure pulmonary –> left to right blood shunt –> blood meant to be going around body instead goes to pulmonary vessels –> pulmonary htn –> R ventricular hypertrophy –> L ventricular hypertrophy –> eisenmengers (cyanosis, polycythaemia - need heart-lung transplant)
RF: prematurity, infections e.g. rubella
Presentation: continuous crescendo-decresndo machinery murmur, SOB, FTT, lower RTI
Ix: Echo
Mx: monitor until 1 year, then close surgically. Treat earlier if sx/ HF
Summarise ASD
Pathophysiology: foraman ovale/ septum primum or secondum fails to close and there is a hole between atria, creating left to right shunt –> pulmonary htn –> Eisenmengers (shunt reverses - cyanotic)
Presentation: mid systolic crescendo-decresndo murmur in UL sternal border, fixed split second heart sund, later in life can have dyspnoea, SOB, FTT, LRTI/ present with complications
Mx: if small watch and wait, if large close with tranvenous catheter
Complications: Stroke secondary to DVT as clotcan travel to rest of body due to shunt; AF; RHF, eisenmengers
Summarise VSD
Pathophysiology: Hole in septum between ventricles, left to right shunt –> pulmonary htn –> eisenmengers
RF: Downs, Turners
Presentation: FTT, SOB, tachypnoea, pan-systolic mumur, LL sternal border, thrill
Mx: watch and wait if small, otherwise transvenous cathteter closure, IE prophylaxis
Summarise coarctation of the aorta
Pathophysiology: congenital narrowing of the aortic arch, usually where ductus arteriosus was located, pressure increases proximal to narrowing and reduces distally
RF: Turners!!
Presentation: weak femoral pulses, difference in BP between limbs, systolic murmur infraclavicularly, tachypnoea, FTT, left ventricular heave, underdevlopment limbs with reduced blood flow
Mx: If severe need surgery shortly after birth, otherwise, prostaglandin E open ductus arteriosus before surgery
Summarise pulmonary stenosis
RF: tetralogy of fallot, williams, noonan, rubella
Presentation: Often incidental pick up: ejection systolic murmur in left sternal border, thrill, right ventricular heave, raised JVP, SOB, syncope
Mx: Echo, watch and wait, valvuloplasty
Summarise tetralogy of fallot
Pathophysiology: overriding aorta just to the right of normal, next to the VSD, so deoxygenated blood from the right side of the heart enters the aorta. Pulmonary stenosis then creates resistance against RV creating RVH and further encourages deoxygenated blood into the aorta. Right to left shunt created.
RF: rubella, age mother, alcohol, downs syndrome, diabetes mother
Presentation: ejection systolic murmur, syanosis, clubbing, FTT, tet spells (may squat to resolve)
Ix: echo with doppler dlow to see severity of stenosis. CXR shows boot shaped heart due to RVH.
Mx: during tet spell give ozgen, BB, fluids, sodium bicarbonate (for acidosis). In neonates can use PG until surgery.
Summarise ebsteins anamoly
Pathophysiology: congenital condition where tricuspid valve is lower than normal –> bigger RA and smaller RV –> poor blood flow to lungs. Assocaiated with ASD –> R to L shunt –> cyanosis
Presentation: HF sx, gallop rhythm, cyanosis, SOB, FTT, syncope, deteriorate few days after birth once Ductus Arteriosus closes
Ix: echo
Mx: treat HF and arrthymias, prevent IE, definitive surgery
Summarise transposition of the great arteries
Pathophysiology: Aorta and pulmonary artery are swapped to create two closed circuits where blood doesnt mix. PDA/ VSD/ ASD can initially compensate.
Presentation: very cyanotic at birth unless have the above compensations.
Mx: PG to create DA and balloon septostomy in foramen ovale to create ASD until surgery on a bypass machine
Summarise infective endocarditis
Pathophysiology: bacteria form vegetation on valves, commonly s.aureus, virdans, s.epidermidis
RF: mitral valave prolapse, IVDU, immuncompromised, prosthetic valves, diabetes, RF, elderly, poor dentition
Presentation: systemically unwell, septic, embolus (stroke/ MI, PE, kidney dysfucntion, blindness), murmur, splinter haemorrhages, osler nodes (tender, purple, on ulp digits) janeway lesions (erythema, macular, non tender on finger/ palm/ sole), roth spots on fundoscopy
Diagnostic criteria: DUKES: 2 major criteria (blood cultures yield positive results, evidence of endocarditis on an echo, or a new valve leak)
5 minor criteria (predisposing factor, fever, vascular phenomena, immune phenomena, equivocal blood culture)
Definite IE = 2 majors or 1 majors + 3 minors, or 5 minors
Mx: abx, operate if recurs after treatment or CRP doesn’t fall
