Cardiac Flashcards
Cardiac muscle contraction
Heart muscle is stimulated by nerves and is self-excitable. (automaticity)
Contracts as a unit has a long
absolute refractory period.
Autorhythmic cell function
- Initiate action potentials
- Have unstable resting potentials called pacemaker potentials.
- Use calcium influx (rather than sodium) for rising phase of the action potential.
Electrical activity of the heart
- SA node and AP spreads throughout right and left atria.
- Simultaneously, impulse goes down internodal pathway to excite the AV node.
- Impulse passes from atria into ventricles through the AV node ( the point of electrical contact for the chambers). Fibrous ring separates chambers.
First two components to cardiac excitation
SA node - generates impulses 75x/pm
AV node - delays impulse 0.1 sec
SA nodal rise to threshold and AP
- Rising phase of the action potential is due mainly to slow Ca2+ channels (L)
- Many voltage-sensitive Na+ channels would be in an inactivated state due to the node’s depolarized state.
Ventricular muscle action potential
Phase 0. fast Na+ channels, like skeletal
1. fast Na+ channels inactivated, ( Gated- Cl- increase, while gated K+ decrease)
- Slow Ca2+ channels or Na+-Ca2+ channels. (slower to open and stay open for 200 msec), decrease in G-K+ so repolarization is not as fast.
- When Ca2+ channels close, G-K+ increases
- Resting state
Excitation-contraction coupling in cardiac contractile cells
Sequence of excitation
- Impulse passes from atria to ventricles via atrioventricular bundle
(Bundle of His)
AV bundle splits into two pathways in the interventricular septum (bundle branches)
- Bundle Branches - carry the impulse toward the apex of the heart.
- Perkinje Fibers - carry the impulse to the heart apex and ventricular walls.
Spiral arrangement of cardiac muscle
Arranged spirally around the ventricles. They “wring” blood from the apex to the base where the major arteries exit.
ECG components
- P wave - atrial depolarization
- PR segment - AV node delay
- QRS complex - ventricular depolarization - simultaneous atrial repolarization
- ST segment - Ventricular contraction and emptying
- T wave - ventricular repolarization
- TP interval - ventricles are relaxing and filling.
Cardiac cycle part I
Filling of ventricles
- 1st 1/3 of vent. diastole - period of rapid filling - blood from atria rushes into vent.
- 2nd 1/3 of diastole - diastasis - only blood coming back to the heart goes from the atria to the ventricles.
- 3rd 1/3 of diastole - atria contract: dump 20-30% of final ventricular volume into ventricle.
(the heart can operate without this 20-30% in most cases. Has 300-400% more capacity to pump than required at rest. )
Cardiac cycle - part II
Period of isovolumic (isometric) contraction- leads to ventricle emptying during systole.
As ventricular contraction begins, ventricular pressure increases greatly causing AV closure. Before vent. P is sufficient to push open semilunar valves open, both entrance and exit valves are closed and contracting.
(no change in overall volume or length)
Cardiac Cycle III
Period of ejection - vent P sufficient to push open semilunar valves -
- Period of rapid ejection - 1st 1/3- 70% of emptying
- Period of slow ejection - 2nd 2/3 - 30% of emptying
- Period of isovolumic (isometric) relexation- no volume change
Drop in intraventricular pressure back to low diastolic values and AV valves open to fill again.
HR abnomalities
- Tachycardia - Rapid rate of more than 100 beats per minute.
- Bradycardia - slow rate of fewer than 60 beats per minute.
Cardiac Rhythm abnormalities
Arrhythmia - variation from normal rhythm and/or sequence of excitation of the heart.
ex. Atrial flutter - 200-350 bpm
Afib - random, uncoordinated excitation and contraction
Ventricular fibrillation - “bag of worms”
Heart block
block somewhere in the excitatory and conducting pathway - AV is common. (pacemaker might be required)
Ectopic focus
PVCs
PSVT
paroxysmal supraventricular tachycardia
Damage to the heart muscle
- Myocardial Ischemia - inadequate delivery of oxygenated blood to heart tissue.
- Necrosis - death of heart muscle cells.
- Acute myocardial infarction - heart attack, occurs when blood vessel supply becomes blocked.
When HR increases…
Diastole shortens, SV is less, CO output is less and less O2 to tissues.
Isovolumetric contraction
All four heart valves closed.
Factors affecting S1 - part I
- Long PR -
longer diastolic filling - LV P gradually increases - mitral valve leaflets slowly drift together and there is a smaller distance between leaflets. (soft s1) - Very short PR -
(ventricle and atrial systole coincide with each other) Mitral leaflets are farther apart at the onset of ventricular systole - closes with a high velocity. (Loud S1)
Factors affecting S1 - part II
- Increased myocardial contractility increases rate of LV pressure ( loud S1, exercise_
- Decreased contractility - (MI, myocarditis) Soft S1
Factors affecting S1 - part III
- Heart Rate - Tachycardia - Loud S1 - shorter PR interval -
– wide open valves due to short diastole and increased myocardial contractility.
Factors affecting S1 - part IV
1.Transmission characteristics of thoracic cavity and chest wall.
[obesity, emphysema, pericardial effusion decrease the intensity of ausculatory events. ]
A thin chest wall increases intensity
S4 presentation
Ususally associated with a stiffened ventricle and is therefore heard in patients with ventricular hypertrophy and myocardial ischemia.
[Ameloidosis,sarcoidosis]
Rubs
1.Pericardial rub - pericarditis
(velcro sound heard throughout the cardiac cycle)
- Pericarditis - upper resp. tract infection; chest pain that is better with leaning forward and worse with laying down.
** IV- NSAIDs
Timing and frequency of S1
Frequency - 50-60 Hz
Time - 0.15 sec.
Timing and frequency of S2
Frequency - 80-90 Hz
Time - 0.12 sec.
(short and sharp)
Timing and frequency of S3
Frequency - 20-30 Hz
Time - 0.1 sec
Occurs beginning of middle third of diastole. rush of blood from atria to ventricle during rapid filling phase of cardiac cycle, causes vibration in blood.
Frequency and Timing of S4
Frequency < 20 Hz
Occurs at the last one third of diastole (just before S1). Rapid blood flow from atria to a noncompliant ventricle - vibration in blood.
Heart Murmurs
abnormal sounds from turbulent blood through abnormal heart valves.
Incompetent valves
valves that do not close properly and remain open.
Whistling murmur
Occurs when blood is forced through a stenotic valve
Gurgling or swishing murmur
Blood flows backward through an incompetent valve.
Systolic murmur organization
Lub - murmur- Dup
Diastolic murmur organization
lub- dup - mumur - lub
Systolic murmur etiology and volume quality
(crescendo-decrescendo)
1. Aortic Stenosis
2. pulmonic stenosis
3. “Innocent”murmur
Holosystolic murmur
- Mitral regurg
- Tricuspid regurg
- VSD
Late Systolic murmur
- MVP
Diastolic Murmur
- Aortic regurg
- Pulmonic Regurg
- Stenosis of mitral or tricuspid
Sound of murmur and its significance
Can be little correlation between sound and severity and most will worsen with a smaller orifice.
ex.
Large VSD - minimal pressure gradient and small murmur but has a v. large physiological consequence.
Small VSD - has turbulent blood flow and loud murmur, yet has a lower hemodynamic significance.
Grading murmurs
I-faintest murmur that can be heard (with difficulty)
II- murmur is also a faint murmur but can be identified immediately
III- moderately loud
IV- loud with a palpable thrill
V- very loud, but still need stethoscope
VI- loudest and can be heard without stethoscope
Where murmurs are heard
- RUSB= (may radiate to neck)
- LUSB=Pulmonic (may radiate to back)
- LLSB=Tricuspid (usually doesn’t radiate)
- Apex=Mitral (may radiate to axilla)
Systolic mumur causes
- having trouble getting out of the ventricle through a tight door (aortic stenosis)
- You fall out through a door which should be closed tight but isn’t (mitral reg)
- A hole exists where it shouldn’t in the ventricular septum and blood crosses from high pressure side to low pressure side (VSD)
Innocent mumurs
- Usually ‘diamond shaped’, brief, little radiation. Common in children and young adults
- ALWAYS: systolic, < III/VI intensity, other heart sounds and pulses are normal.
Diastolic Murmurs
(really bad)
Same “swoosh” but at a different time
You hear it right after S2 and before S1
Blood is having trouble leaving the atrium to the ventricle b/c door is partly shut (mitral stenosis)
Ventricular outflow tract can not stay shut (aortic regurg)
Aortic Regurg - physical manifestation and auscultation.
(Upper Sternal)
1. radiates inferiorly;
best heard with patient sitting up and leaning forward (in expiration)
Mitral stenosis
- Mitral valve is tight so blood can not get out of the atrium
- When the mitral valve area goes below 2cm, the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve. Pressure=turbulence=murmur
- Causes: Rheumatic heart dz, damage from endocarditis
- Sound: A mid-diastolic rumbling murmur will be heard after an opening snap. The murmur is best heard at the apical region and doesn’t radiate.
Mitral stenosis causes
- Rheumatic - 99.9%!!!
- Congenital Prosthetic valve stenosis
- Mitral Annular Calcification
- Left Atrial Myxoma
Acute Mitral Regurg causes
- Infective endocarditis
- Ischemic Heart disease
- Papillary ms rupture
Mitral Valve Prolapse causes
- Chordal rupture
- Chest trauma
Mitral Regurg patho
Leakage of blood into LA during systole
- 1 degree Abnormality -Loss of forward SV into LA
- Compensatory Mechanisms
a. Increase in SV (& EF)
b. Forward SV + regurgitant volume
c. LV (LA) dilatation
d. Left Ventricular Volume Overload (LVVO)
Acute v chronic mitral regurg
- Acute -
Normal (noncompliant) LA
Increase LA pressure
Acute Pulmonary Edema - Chronic -
Dilated, compliant LA
LA pressure normal or slightly increased Fatigue
Atrial arrhythmias- a. fib
Most Pts. fall between these two.
Mitral Valve Regurg
Mitral valve is incompetent and does not close properly (door won’t close)
- Result: abnormal leaking of blood from the LV, through the mitral valve, and into the left atrium
- Causes: myxomatous degeneration, MI, dilated LV
- Sound: holosystolic (swoosh lasts throughout systole) radiates to axilla
Physical findings of mitral regurg
- Auscultatory Findings
S1 – soft or normal
P2 – increased - Holosystolic blowing murmur @ apex
MVP – mid-systolic click
IHSS – murmur increases with Valsalva
- Acute MR – descrescendo systolic murmur, S3 gallop & diastolic flow rumble
- Hyperdynamic Left Ventricle
Brisk carotid upstrokes
Hyperdynamic LV apical impulse
LA lift; RV tap
VSD
- Congenital defect - hole between ventricles.
Left side pressure > right heart
In systole, when heart contracts, the blood in the left goes across the “window” into the right side
- Holosystolic murmur, just like mitral regurgitation. Only difference is that it is usually over the sternal border
Mitral Stenosis -Pathophysiology
- Restriction of blood flow from LA -> LV during diastole.
- As HR increases, diastole shortens disproportionately and MV gradient increases.
- MV gradient - Incr. LA Pressures
- Pulmonary HTN
Passive
Reactive- 2nd stenosis - RV Pressure Overload
RVH
RV failure
Tricuspid regurgitation
Systemic Congestion
Mitral Stenosis- Clinical Symptoms
- Symptoms unrelated to severity of MS-
a) Atrial fibrillation
b)Systemic thromboembolism - Symptoms due to Pulmonary HTN and RV failure-
a) Fatigue, low output state
b) Peripheral edema and hepato-splenomegaly
c) Hoarseness –recurrent laryngeal nerve palsy
Mitral Stenosis: Physical Findings, and how the murmur sounds.
- Auscultatory findings -
S1 – variable intensity; increased early, progressively decreases
OS –opening snap, variable intensity
Low-pitched diastolic rumble @ apex
Duration of murmur correlates with severity of MS - Increased P2
- Body habitus – thin, asthenic, female
- Low BP
- LA lift & RV tap
Mitral Valve Disease – Echo Findings
- Mitral Stenosis
Thickened, deformed MV leaflets
Doppler Gradient
Associated LAE, RVH, PHTN, TR,MR, LV function - Mitral Regurgitation
Determine etiology – leaflets, chordae, MVP, MI
Doppler severity of MR jet
LV function
MVP
- Displacement of an abnormally thickened mitral valve leaflet that gets displaced into the atrium in systole
Mid-systolic click with late systolic murmur.
You can get mitral regurg if severe
Aortic stenosis
- The aortic valve narrows
Creates turbulent blood flow across the narrowed valve. - Result- the heart has to work hard by creating pressure to get blood across the stenotic valve.
- Causes: congenitally bicuspid valve, wear and tear from age, Rheumatic fever
Sound: crescendo-decrescendo murmur in systole, radiates to carotids bilaterally - RUSB with diaphragm
Aortic regurg
- Aortic valve can not close fully
Some blood that should go forward to the body now comes back into the heart
Causes:congenitally bicuspid valve
You hear the turbulence in diastole after aortic valve should have fully closed (after S2)
Acute Aortic valve insufficiency causes
Infective endocarditis
Acute Aortic Dissection
Marfan’s Syndrome
Chest trauma
Chronic Aortic valve insufficiency causes
Aortic leaflet disease
Infective endocarditis
Rheumatic
Bicuspid Aortic valve
Prolapse & congenital VSD
Prosthetic
Aortic Valve Disease: Etiology
Aortic root disease
Aortic aneurysm/dissection
Marfan’s syndrome
Connective tissue disorders
Syphilis
HTN
Aortic Stenosis: Natural History & Clinical Symptoms
Classic Symptom Triad
Angina pectoris – 5 years
CHF 1-2 years
Syncope 2-3 years
Sudden Death
Aortic Insufficiency- Pathophysiology
- one degree abnormality – LVVO (LV Volume Overload)
Severity of LVVO
Size of regurgitant orifice
Diastolic pressure gradient between Ao & LV
HR or duration of diastole
- Compensatory Mechanisms
LV dilatation & eccentric LVH
Increased LV diastolic compliance
Peripheral vasodilation
Acute vs Chronic AR Pathophysiology and Clinical Presentation
- Acute - Sudden AoV incompetence
Noncompliant LV
Acute Pulmonary Edema - Chronic -
Long asymptomatic phase
Progressive LV dilatation
DOE, orthopnea, PND
Frequent PVC’s
Chronic Aortic Regurgitation: Physical Findings
Widened Pulse Pressure > 70mmHg (170/60)
Low diastolic pressure <60mmHg
Hyperdynamic LV –
DeMusset’s signs
Corrigan’s pulse
Quincke’s pulsations
Durozier’s murmur
- DeMusset’s Sign
Rhythmic bobbing or nodding of the head in synchrony with the hear beat Causes include Syphillic aortitis; Rheumatic Fever; Aneurysm - Corrigan’s pulse
A carotid pulse that is forceful and suddenly collapses (Rapid Upstroke) - Quincke’s pulsations
Pulsations in the capillary bed of the nail - Durozier’s Murmur
An audible diastolic murmur which can be heard over the femoral artery when it is compressed by the bell of the stethescope
Acute vs Chronic AR Pathophysiology and Clinical Presentation
Auscultation:
Diminished A2
Descrescendo diastolic blowing murmur @ LSB
Austin-Flint murmur – diastolic flow rumble @ apex
S4 when heard and why
- Vibration of the ventricular wall during atrial contraction.
- Usually associated with stiffened ventricle (low compliance) so heard in pts with vent hypertrophy and Myo ischemia.
Compensatory mechanisms in Aortic Stenosis
- Concentric LVH
- Stiff noncompliant LV
- Diastolic and Systolic pressure increase
** all to keep EF in normal range.
*** once this can’t happen anymore, valve needs replacing.
Hyper dynamic heart factors
- SNS
- Exercise
- Sepsis
- Fever
Thyroid hormones
High output states
Beri Beri
Anemia
Av fistula
Murmur quality of Stenosis, and regurg
- Stenosis - Rumbling/Harsh - AS, MS
- Regurg- Blowing - AR, MR
