Cardiac Physiology Flashcards
Vitamin deficiency that can cause heart failure
Vitamin B1 or Thiamine
Which is not targeted in drug therapy for heart failure?
a. Preload
b. Afterload
c. Relaxation
d. contractility
Relaxation
In the ECG, what correlates with the plateau phase (phase 2) of ventricular contraction?
ST segment
What part of the electrical conductance of the heart does the PR interval correlate with?
Conduction velocity through AV node
Formula of MAP and normal value
2/3 Diastole + 1/3 Systole
Diastole + 1/3 PP
Normal value = 100 mmHg
ARTERIES VS. ARTERIOLES
Greatest resistance
Arterioles
ARTERIES VS. ARTERIOLES
Highest pressure
Arteries
How much of the blood volume is contained in the veins?
64%
Fastest blood flow velocity is in?
Slowest?
Aorta
Capillaries
Formula for blood flow velocity
V = Q/A
V = velocity (cm/sec)
Q = blood flow (ml/min)
A = cross-sectional area (cm2)
Velocity is directly proportional to blood flow but inversely proportional to cross-sectional area
Formula for blood flow is derived from?
OHM’S LAW
CO = mean arterial pressure - right atrial pressure/TPR
CO = BP/TPR
BP = CO x TPR
BP = (HR x SV) x TPR
Inc. HR, SV and TPR will all lead to increased BP
3 principal factors affecting venous return
Right atrial pressure
* Inc RAP = dec. VR
* dec RAP = inc. VR
Mean systemic filling pressure
* Inc MSFP = inc. VR
* dec MSFP = dec. VR
Resistance to venous return
*Inc RVR = dec VR
*dec RVR = inc VR
FORMULA
VR = MSFP - RAP/RVR
What is the formula that serves as the basis for resistance to blood flow?
Poiseuille law
R = 8ήl/Πr^4
R = resistance
ή = viscosity of blood
l = length of blood vessel
r = radius of blood vessel raised to the 4th
Resistance is directly proportional to viscosity and blood vessel length, but indirectly proportional to radius
Formula for Reynold’s number (to determine turbulent blood flow)
N = pdv/ή
N = reynolds number (higher number, >2,000 is associated with turbulent blood flow and bruits)
p = density of blood
d = diameter of blood vessel
v = velocity of blood flow
ή = viscosity
Reynolds number is directly proportional with density of blood, diameter of blood vessel, and velocity of blood flow, but inversely proportional with viscosity
Will an atheromatous vessel have an increased/decreased blood flow velocity? How about the turbulence, will it increase/decrease?
Firstly, based on the formula of Blood flow velocity, which is V = Q/A, blood flow velocity (V) is inversely proportional to cross-sectional area (A). An atheromatous vessel will have a decreased cross sectional area than a normal blood vessel.
Next, to determine turbulence of blood flow, we utilize the Reynolds number (>2000 will be turbulent BF). This formula is N = pdv/ή. Reynolds number (N) is directly proportional to velocity of blood flow (V). Thus, a greater velocity = greater turbulence.
Finally, atheromatous vessel —> inc blood flow velocity —> inc turbulence of blood flow
POLYCYTHEMIA VS. ANEMIA
Turbulent blood flow
Anemia
Formula for determining probability of turbulent blood flow
N = pdv/ή
N = reynolds number (higher number, >2,000 is associated with turbulent blood flow and bruits)
p = density of blood
d = diameter of blood vessel
v = velocity of blood flow
ή = viscosity
Reynolds number is inversely proportional to viscosity, this means that with a lesser viscosity (e.g. anemia), the Reynolds number would be higher.
POLYCYTHEMIA VS. ANEMIA
Increased resistance to blood flow (reduced)
Polycythemia
Formula for resistance to blood flow
Poiseuille law
R = 8ήl/Πr^4
R = resistance
ή = viscosity of blood
l = length of blood vessel
r = radius of blood vessel raised to the 4th
Resistance is directly proportional to viscosity (correlated with hct). The greater the viscosity (e.g. polycythemia), the greater the resistance would be
Formula for capacitance of blood vessel
C = V/P
C = capacitance/compliance
V = volume
P = pressure
When does blood flow of coronary arteries occur?
Diastole
Right atrial pressure synonym: _______________________________
Left atrial pressure estimated by:
_______________________________, measured using ______________
Central venous pressure
Pulmonary capillary wedge pressure
Swan-Ganz catheter
Formulas for pulse pressure and normal pulse pressure value
SBP - DBP
SV/AC (Arterial compliance)
40 mmHg
What happens to my pulse pressure when I’m old and have arteriosclerosis? HAHA
Widened. Because decreased arterial compliance. PP = SV/AC
Conditions that increase/widen pulse pressure
Well-conditioned endurance runner
Old age
Aortic regurgitation
Aortic sclerosis
Severe iron deficiency anemia
Arteriosclerosis
Hyperthyroidism
Conditions that decrease/narrow pulse pressure
Heart failure
Blood loss
Aortic stenosis
Cardiac tamponade
AV BLOCKS
All atrial impulses reach ventricles, but PR interval is prolonged (>0.20 secs)
1st degree AV block
AV BLOCKS
Not all impulses conducted to ventricles, ventricular rate < atrial rate, p wave not always followed by QRS
Sporadically occurring with constant PR intervals before block
2nd degree AV block
Mobitz Type II
AV BLOCKS
Not all impulses conducted to ventricles, ventricular rate < atrial rate, p wave not always followed by QRS
ECG shows gradual increase of PR interval before block
2nd degree AV block
Mobitz Type I: (+) Wenkebach phenomenon
AV BLOCKS
Atrioventricular dissociation
May cause fainting, syncope, worsening exercise tolerance from cerebral ischemia
Can be caused by amyloidosis, sarcoidosis, SLE
3rd degree (Complete) AV block
ECG PATTERNS:
Saw tooth appearance
Atrial flutter
ECG PATTERNS:
Flat/inverted T waves
Hypokalemia
ECG PATTERNS:
Prominent u waves (inc susceptibility to Torsades de Pointes)
Hypokalemia
ECG PATTERNS:
Inc amplitude and width of P waves
Hypokalemia
ECG PATTERNS:
ST depression, QT prolongation
Hypokalemia
ECG PATTERNS:
Low P waves, tall-peaked T waves
Hyperkalemia
ECG PATTERNS:
Prolonged QT interval
Associated with long QT syndrome (sudden fainting and death), Torsades de Pointes (ventricullar arrythmias and fibrillation)
Hypocalcemia
ECG PATTERNS:
Shortened QT interval
Hypercalcemia
ECG PATTERNS:
ST Segment elevation
Q-wave infarct/Transmural infarct
ECG PATTERNS:
ST Segment depression
Non-Q-wave infarct/Subendocardial infarct
When can the fetal heartbeat be heard using UTZ? How bout using Doppler?
UTZ - 6 weeks
Doppler - 10 weeks
When does Troponin I levels rise in an MI episode? What about when it peaks? And how long does it remain elevated?
Rise: 6 hours
Peak: 12 hours
Remain elevated: 1-2 weeks
Which of the following is NOT an inferior MI component?
a. Ventricular tachycardia
b. Cardiogenic shock
c. Hypotension
d. Heart block
A. Ventricular tachycardia (myatay na gane ang myocytes, magpapakabilis pa ba siya for the life?)
How long should one do lifestyle modifications only (no meds) for newly diagnoses Stage 1 hypertensives?
3-6 months
Possible cause of sudden onset heart failure
Coronary artery disease
Erratic electrical activity, Vfib, Vtach?
Vfib
Meaning of e wave and a wave in 2D-echo
e wave - early diastolic filling from left atrium to left ventricle
a wave - atrial kick
Isoelectric portion of the ECG that corresponds to complete ventricular depolarization
ST segment
Where is the pacemaker placed when ECG has no P wave but has normal QRS complex and T wave
Atrioventricular (AV) node
Two P waves preceding each QRS in ECG means?
Decreased conductance through AV node
Stable RMP of Cardiac
-90 MV
Inotropes affect
Ventricular contraction (SV)
Dromotropes affect
Cardiac contractility (AV node)
Chronotropes affect
Heart rate (SA node)
INCREASE OR DECREASE SV:
During PVC
Decrease
INCREASE OR DECREASE SV:
Normal beat after PVC
Increased
(Greater Ca influx due to increased ventricular filling time)
FRANK-STARLING MECHANISM
Inc VR —> Inc SV —> Inc CO
(Increased venous return —> increased right atrial pressure —> increased end-diastolic volume —> increased stretch of sarcomeres (inc ventricular fiber length) —> Greater force of contraction —> Increased stroke volume —> Increased cardiac output)
BAINBRIDGE REFLEX
Inc VR —> Inc HR —> Inc CO
(Increased venous return —> increased right atrial pressure —> Stimulation of cardiopulmonary baroreceptors (low pressure receptors) —> Increased heart rate —> Increased cardiac output)
Cardiac preload is equivalent to _______________, which in turn is influenced by _________________. An increased preload will ________________ cardiac output.
End-diastolic volume;
Right atrial pressure;
Increase
Cardiac preload is equivalent to _______________ in the left ventricle and to _______________ in the right ventricle. An increased afterload will ________________ cardiac output.
Aortic pressure;
Pulmonary artery pressure;
Decrease
Which is not affected by stroke volume?
A. Pulse pressure
B. Preload
C. Afterload
D. Contractility
C. Afterload
Definition of SV
Formula for SV
Normal value for SV
Blood ejected by ventricles per heartbeat
SV = EDV - ESV
Normal value = 70 ml
Definition of EF
Formula for EF
Normal value for EF
Percentage of EDV that is actually ejected by ventricle
EF = SV/EDV
Normal value = 55%
Definition of CO
Formula for CO
Normal value for CO
Total blood volume ejected per unit time
CO = HR x SV
Fick equation —> CO = VO^2/a-VO^2
(VO^2 - steady state oxygen consumption; AVO^2 - difference in arterial O2 content and mixed venous O2 content)
Normal value = 5L/min (resting)
*Max CO for non-athletes = 20L/min
*Max CO for athletes = 30L/min
What happens to EF in Hypertrophic Cardiomyopathy?
Preserved Ejection Fraction
Main energy used for stroke work (work of heart in each beat)
Fatty acids
7 Phases of Cardiac Cycle
- Atrial contraction
- Isovolumic contraction
- Rapid ventricular ejection
- Reduced/slow ventricular ejection
- Isovolumic relaxation
- Rapid ventricular filling
- Reduced/slow ventricular filling
Important events in ATRIAL CONTRACTION
ECG:
Atrial pressure:
Ventricular pressure:
Ventricular volume:
Atrial pressure curve:
Heart sound:
- ATRIAL CONTRACTION
ECG: preceded by P wave
Atrial pressure: Increases slightly
Ventricular pressure: Increases slightly
Ventricular volume: Increases sligtly
Atrial pressure curve: a-wave
Heart sound: 4th heart sound
Important events in ISOVOLUMIC CONTRACTION
ECG:
Atrial pressure:
Ventricular pressure:
Ventricular volume:
Atrial pressure curve:
Heart sound:
- ISOVOLUMIC CONTRACTION
ECG: preceded by QRS complex
Atrial pressure: Ventricular pressure > atrial pressure –> closure of AV valves
Ventricular pressure: Increased (Ventricular pressure < Aortic pressure –> no movement of blood from ventricle to aorta/semilunar valves closed)
Ventricular volume: Remains the same
Atrial pressure curve: c-wave
Heart sound: 1st heart sound (closure of AV valves
Important events in RAPID VENTRICULAR EJECTION
Ventricular pressure:
Ventricular volume:
- RAPID VENTRICULAR EJECTION
Ventricular pressure: Ventricular Pressure > Aortic pressure –> opening of semilunar valves –> blood goes from left ventricle to aorta
Ventricular volume: Rapidly decreases
Important events in Reduced/Slow Ventricular Ejection
ECG:
Ventricular pressure:
Ventricular volume:
Aortic pressure:
- REDUCED-SLOW VENTRICULAR EJECTION
ECG: T-wave occurs
Ventricular pressure: Decreases
Ventricular volume: Decreases
Aortic pressure: Decreases (runoff of blood from large arteries to smaller arteries)
Important events in ISOVOLUMIC RELAXATION
ECG:
Atrial pressure:
Ventricular pressure:
Ventricular volume:
Atrial pressure curve:
Heart sound:
- ISOVOLUMIC RELAXATION
ECG: preceded by T-wave
Atrial pressure: Lower than ventricular pressure
Ventricular pressure: Ventricular pressure > atrial pressure –> AV valves still closed –> no blood goes from atria to ventricles; Ventricular pressure < aortic pressure –> semilunar valves close
Ventricular volume: Remains the same
Atrial pressure curve: v-wave
Heart sound: 2nd heart sound
INCISURA/DICROTIC NOTCH - closure of aortic valve causes vibrations in the aorta near the aortic valve –> slight increase in aortic pressure
Important events in RAPID VENTRICULAR FILLING
Atrial pressure:
Ventricular pressure:
Ventricular volume:
Heart sound:
- RAPID VENTRICULAR FILLING
Atrial pressure: Higher than ventricular pressure
Ventricular pressure: Lower than atrial pressure –> AV valves open –> blood flows from atria to ventricles
Ventricular volume: Rapidly increases
Heart sound: 3rd heart sound
Important events in REDUCED/SLOW VENTRICULAR FILLING
Ventricular volume:
- REDUCED/SLOW VENTRICULAR FILLING
Ventricular volume: Reduced increase
Longest phase of cardiac cycle
Phase 7: Reduced/Slow Ventricular Filling (Diastasis)
Meaning of the peak waves in atrial pressure curve
a-wave: atrial contraction
c-wave: ventricular contraction (causes the valves to bulge into the atria –> increased pressure; also carotid pulse)
v-wave: venous return of blood to atria
What phase in the cardiac cycle is the v-wave seen in an atrial pressure curve?
Isovolumic relaxation
What phase in the cardiac cycle is the a-wave seen in an atrial pressure curve?
Atrial contraction
What phase in the cardiac cycle is the c-wave seen in an atrial pressure curve?
Isovolumic contraction
What phase in the cardiac cycle is the dicrotic notch/incisura seen?
Isovolumic relaxation
Heart sounds and their meanings
1st:
2nd:
3rd:
4th:
1st heart sound: S1, closure of AV valves
2nd heart sound: S2, closure of semilunar valves
3rd heart sound: S3, rapid ventricular filling
4th heart sound: S4, atria contracting against stiff ventricles
What phase in the cardiac cycle may the 3rd heart sound be heard?
Phase 6: Rapid ventricular filling
What phase in the cardiac cycle can the 1st heart sound be heard?
Phase 2: Isovolumic contraction
What phase in the cardiac cycle can the 2nd heart sound be heard?
Phase 5: Isovolumic relaxation
What phase in the cardiac cycle may the 4th heart sound be heard?
Phase 1: Atrial contraction
CARDIAC CYCLE PHASES:
Ventricular pressure is high but still lower than aortic pressure, semilunar valves remain closed thus there is no blood flow from left ventricle to aorta. Also, AV valves are closed in this phase
Phase 2: Isovolumic contraction
CARDIAC CYCLE PHASES:
Ventricular pressure is now higher than the aortic pressure, semilunar valves open and there is rapid blood flow to aorta, decreasing the ventricular pressure rapidly
Phase 3: Rapid Ventricular Ejection
CARDIAC CYCLE PHASES:
Atrial pressure is higher than ventricular pressure, leading to opening of AV valves and rapid blood flow from atria to ventricles
Phase 6: Rapid Ventricular Filling
CARDIAC CYCLE PHASES:
Ventricular pressure is now decreasing but still higher than atrial pressure, AV valves remain closed, and there is no blood flow from atria to ventricles. Since the aortic pressure now is higher than ventricular pressure, semilunar valves close
Phase 5: Isovolumic relaxation
CARDIAC CYCLE PHASES:
What phase of the cardiac cycle corresponds to the phase with the highest ventricular volume?
Phase 2: Isovolumic contraction
CARDIAC CYCLE PHASES:
What phase of the cardiac cycle corresponds to the phase with the highest ventricular and aortic pressure?
Between Phase 3 and Phase 4: Between Rapid Ventricular Ejection and Reduced/Slow Ventricular Ejection
CARDIAC CYCLE PHASES:
What phase of the cardiac cycle corresponds to the phase with the lowest ventricular volume?
Phase 5: Isovolumic relaxation
Most common cardiac rhythm disorder with ECG findings of narrow complex “irregularly irregular” pattern with no distinguishable p waves
Atrial fibrillation
Atrial contraction during atrial systole
Atrial kick
Wide QRS complex typically seen in atrial fibrillation
Ashman syndrome
Auscultatory hallmark of Atrial Septal Defect (ASD)
Fixed splitting
Conditions with Wide Split S2/Exaggeration of normal splitting
RBBB
Pulmonic Stenosis
Mitral valve regurgitation
VSD
Paradoxical splitting of the 2nd heart sound has a common ECG finding of
LBBB
Explain mo ba sab sa sarili mo bakit may Physiologic S2 Splitting
Inhale –> decreased thoracic pressure –> HIGOP more of the right, less of the left –> VR is increased in right and VR is decreased in left –> more blood to the right and less blood to the left (going from atria to ventricles) –> Later closure of pulmonic valve and lesser closure of aortic valve –> Physiologic S2 split
THIS MURMUR SOUNDS FAMILIAR
Murmur with wide pulse pressure
Early diastolic murmur
Accentuated when leaning forward in full expiration
Aortic regurgitation
THIS MURMUR SOUNDS FAMILIAR
De Musset Sign (head bobbing in synchrony with heartbeat) is seen in?
Aortic regurgitation/insufficiency
THIS MURMUR SOUNDS FAMILIAR
Early systolic murmur with JVP distention
Tricuspid regurgitation
THIS MURMUR SOUNDS FAMILIAR
Usually associated with RHD
Holosystolic murmur in 5th ICS MCL
Loudest at apex
Radiates to axilla
Enhanced by expiring and making a fist
Mitral regurgitation
THIS MURMUR SOUNDS FAMILIAR
Decreased Pulse pressure
Prominent systolic ejection click
Crescendo-decrescendo murmur over right sternal border
Radiates to carotid arteries
Aortic stenosis
THIS MURMUR SOUNDS FAMILIAR
Opening snap (OS)
Low-pitched diastolic rumble
Loud S1
Presystolic accentuation
Mitral stenosis
THIS MURMUR SOUNDS FAMILIAR
Midsystolic ejection click
Late diastolic accentuation
Mitral valve prolapse
MURMURS AND MANEUVERS
Hand grip
↑ Afterload
↑ AR, MR, VSD
↓ Hypertrophic Obstructive Cardiomyopathy (HOCM) and Mitral valve prolapse
MURMURS AND MANEUVERS
Squatting
↑ preload
↑ AS, MS, AR, MR
↓ HOCM, MVP
MURMURS AND MANEUVERS
Valsalva
↓ preload
↑ HOCM, MVP
↓ AS, MS, AR, MR, VSD
MURMURS AND MANEUVERS
Standing abruptly
↓ preload
↑ HOCM, MVP
↓ AS, MS, AR, MR, VSD
MURMURS AND MANEUVERS
Amyl nitrite
↓ afterload
↑ AS, HOCM, MVP
↓ AR, MR, VSD
Vasomotor area of medulla that serves as the “Excitatory area” (↑HR and ↑BP)
Lateral portion
*Outer - Extrovert
Vasomotor area of medulla that serves as the “Inhibitory area” (dec. HR and BP)
Medial portion
*Inner - Introvert
Last ditch stand before death
CNS Ischemic response
Starts at less than 60 mmHg and optimal at 15-20 mmHg
All systemic arterioles vasoconstrict severely, except CORONARY AND CEREBRAL VESSELS
Cushing reflex triad
Hypertension, bradycardia, irregular respirations
Branch of CN IX that carries signals from the carotid sinus to Nucleus Tractus Solitarius
Hering nerve
To what signals (increased or decreased BP) do carotid baroreceptors respond to?
Increased and decreased BP (nonselective)
BP within 50-180 mmHg
To what signals (increased or decreased BP) do aortic baroreceptors respond to?
Increased BP only (selective)
BP >80 mmHg
Na sensor in DCT
macula densa
↑ Capillary Hydrostatic Pressure - EDEMA
- Arteriolar dilatation
- Venous constriction
- ↑ venous pressure
- Heart failure
- ECF volume expansion
- Standing
↓ Capillary Oncotic pressure - EDEMA
- ↓ Plasma protein
- Severe liver disease
- Protein malnutrition
- Nephrotic syndrome
↑ Filtration coefficient (capillary permeability x surface area)
- Burns
- Inflammation (due to release of histamine, cytokines)
Organs capable of autoregulation
- Brain
- Heart
- Kidneys
What will happen to the brain if there is increased CO2?
Cerebral vessels will vasodilate –> permit wash out of CO2
Angiogenesis occurs in response to?
Hypoxia
Most potent vasoconstrictor
Vasopressin
VASOCONSTRICTOR VS. VASODILATOR
Prostacyclin
Vasodilator
VASOCONSTRICTOR VS. VASODILATOR
Serotonin
Vasoconstrictor
VASOCONSTRICTOR VS. VASODILATOR
Endothelin
Vasoconstrictor
VASOCONSTRICTOR VS. VASODILATOR
PGF
Vasoconstrictor
VASOCONSTRICTOR VS. VASODILATOR
Thromboxane A2
Vasoconstrictor
VASOCONSTRICTOR VS. VASODILATOR
Lactate
Vasodilator
VASOCONSTRICTOR VS. VASODILATOR
Adenosine
Vasodilator
VASOCONSTRICTOR VS. VASODILATOR
Nitric oxide
Vasodilator
VASOCONSTRICTOR VS. VASODILATOR
Acetylcholine
*Generally vasodilator by increasing production of NO in vascular smooth muscle
*Vasoconstrictor during endothelial damage due to decreased NO
VASOCONSTRICTOR VS. VASODILATOR
PGE
Vasodilator
VASOCONSTRICTOR VS. VASODILATOR
Histamine
Vasodilator
VASOCONSTRICTOR VS. VASODILATOR
Bradykinin
Vasodilator
Vasoactive metabolites of coronary vessels
Hypoxia
Adenosine
Vasoactive metabolites of cerebral vessels
CO2
H+
Vasoactive metabolites of muscles
Lactate
K+
Adenosine
Vasoactive metabolites of pulmonary vessels
Hypoxia (vasoconstriction)
At what PO2 level will neuronal activity begin to decline?
Cerebral PO2 <20 mmHg
Cerebral blood is kept constant at a MAP of
60-140 mmHg
RAAS pathway
↓ Na delivery to macula densa in DCT –> stimulation of Juxtoglomerular (JG) cells –> renin release –> liver angiotensinogen is converted to Angiotensin 1 by renin –> Angiotensin I is converted to Angiotensin 2 by lung ACE –> Release of aldosterone –> effect on principal cells and intercalated cells of kidney –> Principal cells: ↑ Na reabsorption, ↑ K secretion; Intercalated cells: ↑ K reabsorption, ↑ H secretion (Net effect is still ↓↓↓ K) –> Na causes water reabsorption –> Increased IVC –> ↑ VR and ↑ CO –> ↑ BP :)
Cardiac AP
Phase 1: Na influx
Phase 2: K efflux = Ca influx
Phase 3: K efflux
Phase 4: Stable RMP
SA node AP
Phase 4: slow Na influx
Phase 0: Ca influx (depolarization)
Phase 3: K efflux (repolarization)