Flashcards in Biochemistry Deck (20)
What are the waveforms of the JVP?
- a: pre-systolic produced by right atrial contraction
- c: bulging of tricuspid valve into RA during ventricular systole (isovolumic phase)
- x: combination of atrial relaxation, downward movement of the tricuspid valve and ventricular systole
- v: occurs in late systole; increased blood in RA from venous return
- y: tricuspid valve opens and blood flows into the right ventricle
What is a grade 4 murmur?
Loud murmur with a palpable thrill
What are murmurs produced by?
- Low viscosity of blood
- Decreased radius of vessel or valve
- Increased velocity of blood through morphogically normal structures
What is the aetiologies of HF?
- Ischaemia (CAD, AMI)
- Diabetes (diabetic cardiomyopathy or CAD)
- Valvular (AS, MR)
- Tachycardia (uncontrolled AF)
- Heart block (bradycardic)
- Pulmonary (COPD, pulmonary fibrosis)
- Toxins/drugs (alcohol, doxorubicin)
- Infective (viral myocarditis)
- Endocrine (thyrotoxicosis, phaeochormocytoma)
- Dilated cardiomyopathy
- Genetic (HOCM)
What is the Frank-Starling curve?
The relationship between the volume of blood in the heart at the end of diastole (pre-load) and the force of contraction of the ventricle.
- Decreased contractility - graph shifted right
- Increased - shifts left
What can decrease the contractility of the heart?
- Negatively inotropic drugs e.g. anaesthetic agents
What can increase the strength of contractility of the heart?
What causes pulmonary oedema?
Failing heart has reduced contractility which increases end diastolic volume. Initially heart will respond by increasing force of contraction but greater end diastolic volume is required for this. Eventually heart cannot respond and it will decompensate - SV will decrease and further increase in end diastolic volume. Increased venous pressure causes fluid to leak out of blood into interstitial fluid.
What are the causes of mitral regurgitation?
- Rheumatic heart disease
- IHD - associated with papillary muscle rupture
- Valvular vegetations - as in patients with endocarditis
- Physiological mitral valve regurgitation due to dilated LA
What is phase 0 of action potential?
Influx of Na (down concentration gradient from blood to cells) through Na voltage-gated channels causes depolarisation of cell (becomes +).
- activation m gate
- inactivation h gate
What molecules affect the other phases of action potential?
- Ca influx (l-type channel) maintains the long plateau
- K efflux through various channels produce repolarisation
What are early after depolarisations (EADs) arrhythmias?
- Prolongs APD
- Decrease in outward K current
- Can lead to reactivation of I(Ca-L)
-Underlies long QT syndrome - genetic (decreased K or increased Ca currents > prolonged AP) or acquired (problem with drug development)
What are delayed after depolarisations arrhythmias?
- Due to cellular calcium overload (HF)
- Spontaneous calcium release from SR
- Activates depolarising membrane currents
What are reentrant arrhythmias?
- Impulses propagate around the heart - one SA node can produce many recirculating arrhythmias
- Unidirect block - allow the impulse to propagate one way and not the other (longer refractory period)
- Needs slow conduction and short AP (leads to shorter refractory periods) - occurs after MI
What is excitation-contraction coupling?
- Ca entry on Ca current triggers SR release
- Uptake by SERCA, when phospholamban is phosphorylated SERCA activity increases (due to sympathetic stimulation)
- Ca removed by 3Na/Ca exchange channel
Describe systolic HF
Inability of the ventricle to contract normally, resulting in decreased CO, EF is < 40%.
Causes: IHD, MI, cardiomyopathy
Describe diastolic HF
Inability of ventricle to relax and fill normally causing increased filling pressures. Typically EF is >50% (HFpEF).
Causes: ventricular hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, obesity
Describe low output HF
Decreased CO and fails to increase normally with exertion
Causes: excessive preload (e.g. MR) > ventricular dilatation > exacerbates pump failure or chronic excessive afterload (e.g. AS, HTN) > ventricular muscle thickening > diastolic dysfunction
What are the causes of high-output HF?
Causes: anaemia, pregnancy, hyperthyroidism, paget's disease, arteriovenous malformation beriberi
Presents as features of RVF, then later LVF