A site for medical students - Practical,Theory,Osce Notes

Showing posts with label heart. Show all posts
Showing posts with label heart. Show all posts

Normal Second heart sound (Identify the abnormalities of S2)

The most difficult thing in auscultation is to identify the abnormalities of S2.

Physiology of Second heartsound
Two components for 2nd heart sound are- aortic and pulmonary

Aortic component it is the 1st component and loud one heard in all areas.

Pulmonary component - 2nd component and soft, heard only over pulmonary area.

Normal second heart sound
It is a high pitched sound with normal split - 2 components are separately heard during inspiration and as single component during expiration over the pulmonary area.
Distance between the 2 components during inspiration is 0.04 sec, during expiration is 0.02 sec. Human ear can appreciate, when the distance between the 2 components is 0.03 or more. Normal second heart sound is expressed as - normal in intensity and normal split with respiration.

Things to look for in S2:
A2 heard over aortic area and pulmonary area and the apex.
P2 heard over pulmonary area and 2-4 LICS only and not at the apex.
P2 heard over the apex only in pulmonary artery hypertension and in young.
Best site for S2 in COPD - epigastrium.

Cardiac electrical activity –salient features

Cardiac cells can contract without Nervous Stimulation
  • Cardiac muscle, like skeletal muscle & neurons, is an excitable tissue with the ability to generate action potential.
  • Most cardiac muscle is contractile (99%), but about 1% of the myocardial cells are specialized to generate action potentials spontaneously. These cells are responsible for a unique property of the heart: its ability to contract without any outside signal.
  • The heart can contract without an outside signal because the signal for contraction is myogenic, originating within the heart muscle itself.
  • The heart contracts, or beats, rhythmically as a result of action potentials that it generates by itself, a property which is called auto rhythmicity (auto means “self”).
  • The signal for myocardial contraction comes NOT from the nervous system but it is from specialized myocardial cells also called auto rhythmic cells.
  • These specialised cells are also called pacemaker cells of heart because they set the rate of the heart beat. 
The myocardium
Two specialized types of cardiac muscle cells exist
Each of these 2 types of cells has a distinctive action potential.
Electrical Activity of the Heart
Myocardial Auto rhythmic cells (1%)
These cells are smaller and  they contain few contractile fibers or organelles. Because these cell do not have organized sarcomeres, they do not contribute to the contractile force of the heart.
Myocardial Contractile cells (99%) -Contractile cells include most of the heart muscle
  • Atrial muscle
  • Ventricular muscle
These cells contract and are also called as the working myocardium
Action Potential of the Autorrythmic cardiac cells
  • The auto rhythmic cells do not have a stable resting membrane potential like the nerve and the skeletal muscles.
  • Instead they have an unstable membrane potential that starts at – 60mv and slowly drifts upwards towards threshold.
  • Because the membrane potential never rests at a constant value, it is called a Pacemaker Potential rather than a resting membrane potential.
What causes the membrane potentials of these cells to be unstable?
  • Auto rhythmic cells contain channels different from other excitable cells.
  • When cell membrane potential is at -60mv, channels are permeable to both Na and K.
  • This will leads to Na influx and K efflux.
  • The net influx of positive charges slowly depolarizes the auto rhythmic cells. It will leads to opening of Calcium channels.
  • This moves the cell more towards threshold. When threshold is reached, many Calcium channels open leading to the Depolarization phase. 
Ionic basis of action potential of autorrythmic cells
Phase 1: Pacemaker Potential:
Opening of voltage-gated Sodium channels called Funny channels  (If or f channels ).
Closure of voltage-gated Potassium channels.
Opening of Voltage-gated Transient-type Calcium (T-type Ca2+ channels) channels .
Phase 2: The Rising Phase or Depolarization:
Opening of Long-lasting voltage-gated Calcium channels (L-type Ca2+ channels).
Large influx of Calcium.
Phase 3: The Falling Phase or Repolarization:
Opening of voltage-gated Potassium channels
Closing of L-type Ca channels.
Potassium Efflux.
Action potential of a contractile myocardial cell:a typical ventricular cell
Unlike the membranes of the autorrythmic cells, the membrane of the contractile cells remain essentially at rest at about -90mv until excited by electrical activity propagated by the pacemaker cells
Action potential of a contractile myocardial cell:a typical ventricular cell
  •   Opening of fast voltage-gated Na+ channels.
  •    Rapid Influx of Sodium ions leading to rapid depolarization.
Small Repolarization
  • Opening of a subclass of Potassium channels which are fast channels.
  • Rapid Potassium Efflux.
Plateau phase
  •  250 msec duration (while it is only 1msec in neuron)
  • Opening of the L-type voltage-gated slow Calcium channels & Closure of the Fast K+   channels.
  • Large Calcium influx
  • K+ Efflux is very small as K+ permeability decreases & only few K channels are open.
  • Opening of the typical, slow, voltage-gated Potassium channels.
  • Closure of the L-type, voltage-gated Calcium channels.
  • Calcium Influx STOPS
  • Potassium Efflux takes place.
Summary of Action Potential of a Myocardial Contractile Cell
  • Depolarization= Sodium Influx
  • Rapid Repolarization= Potassium Efflux
  • Plateau= Calcium Influx
  • Repolarization= Potassium Efflux