Cardiovascular system Flashcards
Atrial fibrillation, Heart failure, CAD, Valvular heart disease, Cardiogenic syncope, Hypertension, Myocarditis, IE, Rheumatic fever, Congential heart diseases, Aortic dissection, DVT, PE
What is the classification of AF rhythm?
AHA guidelines
What are the causes of AF beat?
What Ix for AF beat?
What Ix for LA thrombus?
What is the triad for treatment principle for AF?
Rate control +rhythm control + prevention of thromboembolism
Rate control = blocking the AVN to slow conduction through the AVN
What is the pharmacological rate control of AF?
What is target for symptomatic and asymptomatic rate control
Symptomatic: resting HR <80bpm
Asymptomatic + LVEF>40%: HR <100bpm
What is non pharmacological rate control of AF?
What is the pharmacological rhythm control for AF?
- None or minimal underlying heart disease = Flecainide/ Propafenone/ Dronedarone/ Sotalol
- Patients with post-MI/ CAD = Amiodarone/ Dronedarone/ Dofetilide/ Sotalol
- Patients with heart failure = Amiodarone/ Dofetilide
o Dronedarone increases mortality in patients with recently decompensated HF and depressed LV function and is contraindicated in patients with NYHA class III or IV HF - Patients with hypertension with LVH = Amiodarone
What is non pharmacological rhythm control for AF?
Direct current (DC) cardioversion
Indications: haemodynamically unstable patients, refractory to pharmacological cardioversion, rapid control of ventricualr rate during AF is required
Delivery of electrical shock synchronized with QRS complex to avoid inducing VF which can occur by a shock applied during ventricular repolarization of T wave
AF<48 hours of duration: pre and post cardioversion anticoag required only in patients with high risk of thromboembolism
AF >48 hours of duration or unknown duration: precardioversion anticoagulation > 4 weeks. Post cardioversion anticoagulation >4 weeks
Urgent cardioversion: need for restoration of SR takes precedence over need for protection from thromboembolism. Can be anticoagulated acutely with heparin and proceed directly to anticoagulation if no atrial thrombus seen on pre-cardioversion TEE
Catheter ablation
Indicated in patients with symptomatic paroxysmal/ persistent/long standing persistent AF who are refractory or intolerant to >1 class I or III anti arrhythmic drugs when a rhythm control strategy is desired
RFA and cryoballoon ablation. Anticoag required for RFA ablation.
Complications: cardiac tamponade (most common), stroke, TIA or pulmonary veins tenosis
Surgical maze procedure (surgical ablation): indicated in selected patients undergoing cardiac surgery for another indication such as valvular replacement or CABG
What are the indications for anticoags in AF?
What scoring system used
Indications for anticoagulation
* ALL valvular AF (since stroke risk is very high)
* Non-valvular AF with CHA2DS2-VASc score ≥ 2
* Prior stroke or transient ischemic attack
What scoring system for quantification of bleeding risk for anticoagulants use?
What are the antithrombotic options for AF?
Compare NOACs to warfarin in preventing thromboembolism in AF?
What is non pharmacological prevention of thromboembolism in AF?
Complication of AF?
What is the classification of HF severity (NYHA)?
New York Heart association (NYHA)
Quantiy degree of functional limitation impsoed by HF
Classification depends on degree of effort needed to elicit symptoms
What is the staging of heart failure (AHA)?
What are the types of heart failure?
Low output heart failure (more common): decreased CO but increased filling pressure
High output heart failure: increased SV and normal or even increased CO, body responds by increasing fluid retention and preload e.g. sepsis/anemia, thyrotoxicosis/AVF or shunting
Left vs right heart failure
Left heart failure (increased left heart filling pressure)
Symptoms: orthopnea, paroxysmal nocturnal dyspnea, dyspnea on exertion, nocturnal cough, palpitation
Signs: tachycardia, presence of S3/S4, cardiomegaly, lung crepitations
RHF
Symptoms: abd distension, ankle swelling
Signs: elevated JVP, hepatojugular reflex, pleural effusion, hepatomegaly, ascites, bilateral ankle pitting edema
HF with reduced ejection fraction <40%: decreased LVEF due to impaired systolyc function, increased LV dilatation
HF with preserved ejection fraction >50%: increased filling pressure but anormal LV filling due to impaired diastolic function. No or niminal LV dilatation
Heart failure according to haemodynamic profile
Presence of congestion = wet vs dry
Adequacy of peripheral perfusion = warm vs cold
What are the causes of heart failure in adults?
Causes of heart failure in children and infants?
What are the causes of pressure overload and volume overload in causing heart failure (LV and RV)?
What is the law that guides heart failure?
Frank starling law: SV of heart increases in response to an increase in volume of blood filling the ventricles (preload)
Length-tension relationship in preload phase
When ventricles filled up with larger volume of blood it stretches the ventricular muscle cells and increases sarcomere length
Reduces overlapping of actin and thus increasing cross bridge formation to optimize stroke volume
Overstretching of ventricular wall will lead to actin and myosin being out of reach –> decrease cross bridge formation and decreasing stroke volume
Before optimal point: increased venous return (preload), increased SV and thus CO
After optimal point: increased venous return (preload), decreased SV and thus CO, increasde LV end diastolic pressure, increased LA pressure, increased pulmonary venous pressure
How does the heart compensate for heart failure?
What is decompensation?
What is clinical, CXR and ECG findings of pressure overload in heart failure
Primary response is ventricular hypertrophy (increased myocardial O2 consumption) but not ventricular dilatation. Imbalance between myocardial O2 demand and coronary flow results in relative myocardial ischemia and myocardial fibrosis. Fibrotic ventricles will eventually dilate (volume overload).
* Clinical
o LV hypertrophy = Strong apical impulse but NO displacement of apex beat
o RV hypertrophy = Left parasternal impulse
* Radiological (CXR)
o LV hypertrophy = NO abnormality seen
o RV hypertrophy = Uptilting of cardiac apex
* Radiological (ECG)
o LV hypertrophy = Left axis deviation/ Deep S wave in V1/ Tall R wave in V6/ T wave inversion in V6 and I (strain pattern)
o RV hypertrophy = Right axis deviation/ Tall R wave in V1/ Deep S wave in V6
What is clinical, CXR and ECG findings of volume overload in heart failure
Increased end diastolic volume of ventricles. LV or RV dilates to accomodate the increased amounnt of blood
* Clinical
o LV overload = Strong apical impulse/ Displaced apex beat
o RV overload = Left parasternal impulse
* Radiological (CXR)
o LV overload = Cardiomegaly with apex extending laterally and downwards
o RV overload = Cardiomegaly with apex displaced laterally and tilting upwards
* Radiological (ECG) (similar to hypertrophy)
o LV overload = Left axis deviation/ Deep S wave in V1/ Tall R wave in V6/ T wave inversion in V6 and I (strain pattern)
o RV overload = Incomplete RBBB (rsR’ pattern) (common)/ Right axis deviation/ Tall R wave in V1/ Deep S wave in V6
What are the symptoms of HF in adults?
- Dyspnea (fluid accumulation)
- Orthopnea: quanity with number of pillows used (redistribution of fluid from splanchnic circulation and LL into central circulation during supine with increase in pulmonary capillary pressure leading to pulmonary congestion
- Paroxysmal nocturnal dyspnea (PND)
- Cheyne-Stokes respiration: cyclic breathing in which apnea is followed by gradual increase in RR and TV and then gradual increase in RR and TV until next apneic period. Apenic phase decreases arterial pO2 and increases pCO2 which stimulates the respiratory center resulting in hyperventilation and hypocapnia followed by recurrence of apnea
- Nocturnal cough
- Edema (decreased CO –> activation of RAAS, sympathetic nervous system)
- Fatigue
- Night sweats
- Decreased excercise tolerance (decreased CO)
- Other associateing symptoms: RUQ discomfort (acute hepatic congestion), palpitations, anorexia (poor perfusion of splanchnic circulation)