Block 2 Quiz 1 Cardiovascular Stuff

Causes

Drugs: BB, digitalis, CCB
and quinidine.
Ischemia heart disease in
inferior wall.

Clinical presentation

(Same symptoms than Mobitz I)

Fainting, feeling dizzy
Chest pain
Feeling tired
Shortness of breath
Heart palpitations
Rapid breathing

Phase 0 = rapid upstroke and depolarization—

voltage-gated Na+

In contrast to skeletal muscle:
ƒ Cardiac muscle action potential has a
plateau due to Ca2+ influx and K+
efflux.
ƒ Cardiac muscle contraction requires Ca2+
influx from ECF to induce Ca2+ release
from sarcoplasmic reticulum (Ca2+-induced
Ca2+ release).
ƒ Cardiac myocytes are electrically coupled to
each other by gap junctions.

channels open.

Phase 1 = initial repolarization—inactivation of

voltage-gated Na+

channels. Voltage-gated K+

channels begin to open.

Phase 2 = plateau—Ca2+ influx through voltage[1]gated Ca2+ channels balances K+

efflux. Ca2+

influx triggers Ca2+ release from sarcoplasmic

reticulum and myocyte contraction (excitation[1]contraction coupling).

Phase 3 = rapid repolarization—massive K+

efflux due to opening of voltage-gated slow

delayed-rectifier K+

channels and closure of

voltage-gated Ca2+ channels.

Phase 4 = resting potential—high K+

permeability through K+

channels

During a routine physical examination, a 32-year-old female is found to have second-degree heart block. Which of the following ECG
recordings was obtained from the patient during her physical examination?

A rapid succession of identical, back-to-back atrial depolarization
waves. The identical appearance accounts for the “sawtooth”
appearance of the flutter waves.
Treat like atrial fibrillation +/– catheter ablation of region
between tricuspid annulus and IVC.

EF = SV/EDV = EDV − ESV/EDV

EF is an index of ventricular contractility (increase in
systolic HF; usually normal in diastolic HF)

Mean arterial pressure MAP = CO × total peripheral resistance (TPR)

MAP (at resting HR) = 2/3 DBP + 1/3 SBP = DBP + 1/3 PP

The spouse of a 58-year-old-man calls 9-1-1 because her husband complains of chest pain radiating down his left arm. He is transported to
the Emergency Department, where an electrocardiogram and cardiac enzymes indicate a recent myocardial infarction. The man is sent for a cardiac catheterization, including coronary angiography and hemodynamic recordings throughout the cardiac cycle. No valvular defects were present. During ventricular ejection, the pressure difference smallest in magnitude is between which of the following?

Causes

Myocardial infraction.
Thyrotoxicosis.
Mitral valve prolapse.
Hypertension.

Clinical presentation

Shortness of breath.
Fatigue.
Chest pain.
Palpitations

Causes 
Obstructive coronary artery
disease – Most common
cause.

Clinical presentation
Persistent chest pain with
radiation to the neck, lower jaw
or left arm.
Atypical symptoms: Shortness
of breath, nausea/vomiting,
fatigue, palpitations or syncope.

Causes

Mitral valve prolapse.
Metabolic syndromes:
thyrotoxicosis, obesity,
chronic pericarditis,
Excessive alcohol
ingestion (Holiday heart
syndrome).

Clinical presentation

History of rheumatic fever.
Palpitations.
Dyspnea.
Fatigue.
Chest tightness/ pain.
Poor effort tolerance.
Syncope.

The black loop represents normal cardiac
physiology.

Phases—left ventricle:

1. Isovolumetric contraction—period
between mitral valve closing and aortic
valve opening; period of highest O2
consumption

2. Systolic ejection—period between aortic
valve opening and closing

3. Isovolumetric relaxation—period between
aortic valve closing and mitral valve
opening

4. Rapid filling—period just after mitral
valve opening

5. Reduced filling—period just before mitral
valve closing

The image depicts the relationship of left ventricular pressure and volume in the cardiac cycle. The various phases of the cardiac cycle are labeled I through IV. During which phase are the pressures in the left atrium and left ventricle most equal

Phase where no blood enters or leaves the ventricles
when its relaxing
End Systolic Volume
o Amount of blood left in the LV after it contracts
Ventricles are repolarizing and relaxing → ↓ventricular
pressure
The ↓ventricular pressure is still greater than the atrial
pressure keeping the semilunar valves closed
The arteries are extremely elastic
o Allows it to take on a high pressure and stretch
Arterial Pressures higher than Ventricular Pressures
o Causes the SL valves to shut close
o Produces S2
 Second heart sound
 Commonly known as “dub” in “lub-dub”

Atrial pressure < Ventricular pressure o AV vales remain closed Some blood can go back down due to increase in pressure o Ventricles are relaxed and repolarized o ECG: T wave

Aortic stenosis

Increase LV pressure
Increase ESV
No change in EDV (if mild)
decrease SV
Ventricular hypertrophy leads to decrease ventricular
compliance leads to increase EDP for given EDV

Aortic regurgitation

Increase EDV
Increase SV
Loss of dichrotic notch

Mitral stenosis

Increase LA pressure
Decrease EDV because of impaired ventricular filling
Decrease ESV
Decrease SV

Mitral regurgitation

No true isovolumetric phase
Decrease ESV due to Decrease resistance and
Increase regurgitation into LA during systole
Increase EDV due to Increase LA volume/pressure from
regurgitation leads to Increase ventricular filling
Increase SV (forward flow into systemic circulation
plus backflow into LA)

High Yield

Cardiac and vascular function curves

Intersection of curves = operating point of heart (ie, venous return and CO are equal, as circulatory system is a closed system)

Receptors:
ƒ Aortic arch transmits via vagus nerve to solitary nucleus of
medulla (responds to changes in BP).
ƒ Carotid sinus (dilated region superior to bifurcation of carotid
arteries) transmits via glossopharyngeal nerve to solitary nucleus
of medulla (responds to changes in BP).
Chemoreceptors:
ƒ Peripheral—carotid and aortic bodies are stimulated by  Pco2,
 pH of blood, and  Po2 (< 60 mm Hg). ƒ Central—are stimulated by changes in pH and Pco2 of brain interstitial fluid, which in turn are influenced by arterial CO2 as H+ cannot cross the blood-brain barrier. Do not directly respond to Po2. Central chemoreceptors become less responsive with chronically  Pco2 (eg, COPD) Ž  dependence on peripheral chemoreceptors to detect  O2 to drive respiration. Baroreceptors: ƒ Hypotension— arterial pressure Ž  stretch Ž  afferent baroreceptor firing Ž  efferent sympathetic firing and  efferent parasympathetic stimulation Ž vasoconstriction,  HR,  contractility,  BP. Important in the response to severe hemorrhage. ƒ Carotid massage— pressure on carotid sinus Ž  stretch Ž  afferent baroreceptor firing Ž  AV node refractory period Ž  HR. ƒ Component of Cushing reflex (triad of hypertension, bradycardia, and respiratory depression)— intracranial pressure constricts arterioles Ž cerebral ischemia Ž  pCO2 and  pH Ž central reflex sympathetic  in perfusion pressure (hypertension) Ž  stretch Ž peripheral reflex baroreceptor– induced bradycardia

Atrial contraction is triggered by:

a. AV node
b. SA node
c. Ventricular Contraction
d. Arterial Contraction

image is a representation of the pressurevolume (P-V) relationship in the left ventricle
during a typical cardiac cycle. The phases
of the cardiac cycle are labeled I through IV.
Which of the following occurrences alone
would increase the width of the P-V loop?

The electric signal gets slower until AV conduction gets
blocked.
o PR interval gets progressively longer until a QRS
complex disappears.

Cardiac output CO = SV × HR

Fick principle:
CO =                rate of O2 consumption
(arterial O2 content – venous O2 content)

rate of O2 consumption divided by arterial O2 content minus venous O2 content)

In early stages of exercise, CO maintained by
increased HR and increased SV. In later stages, CO maintained
by increased HR only  increased (SV plateaus).
Diastole is shortened with increased HR (eg, ventricular
tachycardia)  leads to decreased diastolic filling time leads to decreased SV
leading to decreased CO.

Represents ventricular repolarization.
o Ventricular membrane cells become more negative.
 → Ventricular relaxation.

Conduction pathway: SA node -> atria

->  AV node -> bundle of His -> right and

left bundle branches -> Purkinje fibers

-> ventricles; left bundle branch divides into

left anterior and posterior fascicles.

SA node—located at junction of RA and SVC;

“pacemaker” inherent dominance with slow

phase of upstroke.

AV node—located in posteroinferior part of

interatrial septum. Blood supply usually

from RCA. 100-msec delay allows time for

ventricular filling.

Pacemaker rates: SA > AV > bundle of His/

Purkinje/ventricles.

Speed of conduction: His-Purkinje > Atria >

Ventricles > AV node. He Parks At Ventura

AVenue.

P wave—atrial depolarization.

PR interval—time from start of atrial

depolarization to start of ventricular

depolarization (normally 120-200 msec).

QRS complex—ventricular depolarization

(normally < 100 msec). QT interval—ventricular depolarization,

mechanical contraction of the ventricles,

ventricular repolarization.

T wave—ventricular repolarization. T-wave

inversion may indicate ischemia or recent MI.

J point—junction between end of QRS complex

and start of ST segment.

ST segment—isoelectric, ventricles depolarized.

U wave—prominent in hypokalemia (think

hyp“U”kalemia), bradycardia

“Phase of Ventricular Ejection”
o Blood leaving the ventricles
Ventricles are still depolarizing and contracting more
intensely  ventricular pressure continue to rise
o ECG is still QRS Complex
o Ventricular pressure has risen enough that it’s greater
than the pressure in the arteries  semilunar valves
open  blood moves from ventricles to arteries 
arterial pressure starts to rise
Ventricular pressure >>> Atrial pressure
o Keeps the AV valves close

F waves (capital F-waves) represent reentry circuits of Pwaves until one reaches the AV node leading to ventricle
depolarization.
o → Characteristic sawtooth wave.
Not life-threatening but can progress to a more serious
condition (atrial fibrillation).

The most important aspects of Figure VI-1-1 are the following:
• → QRS → contraction of ventricle → rise in ventricular pressure above
atrial pressure → closure of mitral valve
• It is always a pressure difference that causes the valves to open or close.
• Closure of the mitral valve terminates the ventricular filling phase and
begins iso-volumetric contraction.
• Isovolumetric contraction—no change in ventricular volume, and both
valves (mitral, aortic) closed. Ventricular pressure increases, and volume
is equivalent to end-diastolic volume.
• Opening of the aortic valve terminates isovolumetric contraction and
begins the ejection phase. The aortic valve opens because pressure in the
ventricle slightly exceeds aortic pressure.
• Ejection Phase—ventricular volume decreases, but most rapidly in early
stages. Ventricular and aortic pressures increase initially but decrease
later in phase.
• Closure of the aortic valve terminates the ejection phase and begins
isovolumetric relaxation. The aortic valve closes because pressure in the
ventricle goes below aortic pressure. Closure of the aortic valve creates
the dicrotic notch.
• Isovolumetric relaxation—no change in ventricular volume, and both
valves (mitral, aortic) closed. Ventricular pressure decreases, and volume
is equivalent to end-systolic volume.
• Opening of the mitral valve terminates isovolumetric relaxation and
begins the filling phase. The mitral valve opens because pressure in the
ventricle goes below atrial pressure.
• Filling Phase—the final relaxation of the ventricle occurs after the
mitral valve opens and produces a rapid early filling of the ventricle.
This rapid inflow will in some cases induce the third heart sound. The
final increase in ventricular volume is due to atrial contraction, which is
responsible for the fourth heart sound.
• In a young, healthy individual, atrial contraction doesn’t provide significant filling of the ventricle. However, the contribution of atrial contraction becomes more important when ventricular compliance is reduced

Measurement of Cardiac Output by Fick's principle

O2 Consumption/O2 pulmonary artery – O2 pulmonary vein=Cardiac Output (Fick’s)

The equation is solved as follows:
1. O2
consumption for the whole body is measured.
2. Pulmonary vein [O2
] is measured in systemic arterial blood.
3. Pulmonary artery [O2
] is measured in systemic mixed venous blood.
■ For example, a 70-kg man has a resting O2
consumption of 250 mL/min, a systemic
arterial O2 content of 0.20 mL O2/mL of blood, a systemic mixed venous O2
content of 0.15 mL O2 /mL of blood, and a heart rate of 72 beats/min. What is his cardiac output?
What is his stroke volume?

250/.20-.15=5000mL/min is Cardiac Output

5000/72=69.4mL/beat is Stroke Volume

A 76-year-old man receives a pacemaker to treat a dangerous form of heart block. His condition is characterized by an ECG with a constant PR interval, with the random absence of QRS complexes. Which of the following abnormalities is the most likely cause of this type
of heart block

Conduction from atrial to ventricles is completely blocked.
There is no relation between P-wave and QRS complex,
each beat on their own rate.
o Complete heart block

a wave
• Highest deflection of the venous pulse and produced by the contraction
of the right atrium
• Correlates with the PR interval (see figure)
• Is prominent in a stiff ventricle, pulmonic stenosis, and insufficiency
• Is absent in atrial fibrillation
c wave
• Mainly due to the bulging of the tricuspid valve into the atrium (rise in
right atrial pressure)
• Occurs near the beginning of ventricular contraction (is coincident with
right ventricular isovolumic contraction)
• Is often not seen during the recording of the venous pulse
x descent
• Produced by a decreasing atrial pressure during atrial relaxation
• Separated into two segments when the c wave is recorded
• Alterations occur with atrial fibrillation and tricuspid insufficiency
v wave
• Produced by the filling of the atrium during ventricular systole when the
tricuspid valve is closed
• Corresponds to T wave of the EKG
• A prominent v wave would occur in tricuspid insufficiency and right
heart failure

y descent
• Produced by the rapid emptying of the right atrium immediately after
the opening of the tricuspid valve
• A more prominent wave in tricuspid insufficiency and a blunted wave in
tricuspid stenosis.
Some abnormal venous pulses are shown in the following figure.

Most common type of ventricular preexcitation syndrome. Abnormal fast accessory
conduction pathway from atria to ventricle
(bundle of Kent) bypasses the rate-slowing
AV node to ventricles begin to partially
depolarize earlier -> characteristic delta wave
with widened QRS complex and shortened PR
interval on ECG. May result in reentry circuit
-> supraventricular tachycardia.

_________________________is an interval in the cardiac cycle, from the aortic component of the second heart sound, that is, closure of the aortic valve, to onset of filling by opening of the mitral valve.^[1] It can be used as an indicator of diastolic dysfunction.

It can be measured by simultaneous Doppler echocardiography and M-mode sonography, or better still, by simultaneous phonocardiogram and transmitral Doppler.^[2]

Prolonged IVRT indicates poor myocardial relaxation. A normal IVRT is about 70 ± 12 ms, and approximately 10 ms longer in people over forty years.^[2] In abnormal relaxation, IVRT is usually in excess of 110 ms.^[2] With restrictive ventricular filling, it is usually under 60 ms.^[2

A 55-year-old male reports several recent episodes of syncope. An
electrocardiogram is performed. Which of the following arrhythmias is
most commonly associated with syncope?

A _____________________, named after its developer, Carl Wiggers, is a unique diagram that has been used in teaching cardiac physiology for more than a century.^[1][2] In the Wiggers diagram, the X-axis is used to plot time subdivided into the cardiac phases, while the Y-axis typically contains the following on a single grid:

• Blood pressure
  • Aortic pressure
  • Ventricular pressure
  • Atrial pressure
• Ventricular volume
• Electrocardiogram
• Arterial flow (optional)
• Heart sounds (optional)

Polymorphic ventricular tachycardia,
characterized by shifting sinusoidal waveforms
on ECG; can progress to ventricular
firillation. Long QT interval predisposes to
torsades de pointes. Caused by drugs, ↓ K+,
↓Mg2+, ↓ Ca2+, congenital abnormalities.
Treatment includes magnesium sulfate.

Drug-induced long QT (ABCDEF):
AntiArrhythmics (class IA, III)
AntiBiotics (eg, macrolides, floroquinolones)
Anti“C”ychotics (eg, haloperidol, ziprasidone)
AntiDepressants (eg, TCAs)
AntiEmetics (eg, ondansetron)
AntiFungals (eg, azoles)
Torsades de pointes = twisting of the points

Goes from the beginning of P-wave until the beginning of
the QRS complex.
Represents conduction through AV node.

Case 2. To take an accurate blood
pressure (BP) reading, place the
sphygmomanometer at the level of the
heart. If the cuff is above the level of
the heart, the reading will be falsely
low; conversely, if the cuff is below the
level of the heart, the reading will be
falsely high.

Congenital condition.
Irregular extra electrical pathway called Bundle of Kent
o Impulse can be bidirectional → reentry
Delta wave

A 32-year-old man with diabetes presents to his
physician with orthostatic hypotension. A deficiency in the normal physiologic response carried out by arterial baroreceptors located in the
aortic arch and the carotid sinus is suspected.
What is the mechanism of the normal physiologic response to hypotension?

Relation between the action potential and the
ECG curve

The electric signal gets slower until AV conduction gets
blocked.
o PR interval gets progressively longer until a QRS
complex disappears.

A 56-year-old male was admitted to the hospital with angina and diaphoresis. A myocardial infarction is suspected, and a 12-lead electrocardiogram (ECG) is ordered. The ECG is most effective in detecting a
decrease in which of the following?

Chaotic and erratic baseline with no discrete P waves in between
irregularly spaced QRS complexes. Irregularly irregular
heartbeat. Most common risk factors include hypertension and
coronary artery disease (CAD). Occasionally seen after episodes
of excessive alcohol consumption ("holiday heart syndrome").
Can lead to thromboembolic events, particularly stroke.
Treatment: anticoagulation, rate and rhythm control,
cardioversion. Definitive treatment is catheter ablation.

Blood from the venous circulation is returning to the heart
and accumulates into the atria
o From the IVC, SVC, Coronary Sinus, Pulmonary
Veins into the atria
Atrial Pressure > Ventricular Pressure
AV valves open
Without contraction, 70-80% of the blood passively flows
down from the atria into the ventricles due to gravity
Arterial Pressures are still higher than the Ventricular
Pressure  SL valves remain closed
o Pressure in the aorta is higher than in the RV
o Pressure in the pulmonary trunk higher than in the LV

Normal Versus Abnormal Jugular Pulses

ST segment elevation indicates transmural ischemia.
The ST segment elevation will be located in the leads
which observe the affected area.

Causes

Prolonged artery occlusion.

Clinical presentation

Usually the same symptoms than
STEMI.

Phase where no blood enters or leaves the ventricles
when its contracting
End Diastolic Volume
o Blood accumulated in the LV before it contracts
Ventricles start to slowly depolarize and contract →
↑ventricular pressure
o Myocardium (cardiac muscle layer) contracts to
squeeze the chambers and slowly push the blood up
into the pulmonary trunk and aorta
Ventricular Pressures are still lower than the Arterial
pressures  semilunar valves remain closed
o Aorta (80 mmHg) > RV (60 mmHg)
o Pulmonary Trunk (10 mmHg) > LV (7 mmHg)
Ventricular Pressures rise above the Atrial Pressure
o Causes the AV valves to shut close
o Produces S1
 The first heart sound
 Commonly known as “lub” in “lub-dub”

is expressed by the following equation:

Cardiac output S = stroke volume x Heart rate

F waves (capital F-waves) represent reentry circuits of Pwaves until one reaches the AV node leading to ventricle
depolarization.
o → Characteristic sawtooth wave.
Not life-threatening but can progress to a more serious
condition (atrial fibrillation).

Goes from the end of the P-wave to the start of the QRS
complex.
Represents the slow electrical signals conducted from SA
node to AV node.
o Isoelectric line on EKG

(i)
Represents atrial depolarization.
o Auricular membrane cells become more positive.
 → Auricular contraction.
Important to know
Atrial repolarization is hidden within the QRS complex
so is not visible on EKG.

Causes

Chronic degenerative
changes.
Drugs: Digitalis toxicity.

Lyme disease.
AMI.

Clinical presentation

Dizziness, fainting
Chest pain
Feeling tired
Shortness of breath
Symptoms in 3º heart block are
more severe than 2º.

Causes

Nicotine or other drugs
Caffeine.
Exercise.

Clinical presentation

Can be asymptomatic.
Palpitations.

Progressive lengthening of PR interval until a beat is “dropped”
(a P wave not followed by a QRS complex). Usually
asymptomatic. Variable RR interval with a pattern (regularly
irregular).

Represents ventricular depolarization.
o Ventricular membrane cells become more positive.
 → Ventricular contraction.

Pulse pressure PP = systolic blood pressure (SBP) – diastolic blood pressure (DBP)

PP directly proportional to SV and inversely
proportional to arterial compliance.
Increased PP in hyperthyroidism, aortic regurgitation,
aortic stiffening (isolated systolic hypertension
in elderly), obstructive sleep apnea
(Increased sympathetic tone), anemia, exercise
(transient).
Decreased PP in aortic stenosis, cardiogenic shock,
cardiac tamponade, advanced HF

The flow of blood in and out of the heart takes an average
of 0.8 seconds performed in 4 phases

42-year-old woman with mitral prolapse is admitted to the hospital for evaluation of her cardiac function. Which of the following values is
the best index of the preload on her heart?

The atria and ventricles beat
independently of each other. P waves
and QRS complexes not rhythmically
associated. Atrial rate > ventricular
rate. Usually treated with pacemaker.
Can be caused by Lym3 disease.

Represents the small period between ventricular
depolarization and ventricular repolarization.
o Isoelectric line on EKG.

(PCG) records heart sounds and murmurs in the form of a plot (also seen on the Wigger's diagragm)

Causes

Normal variant:
Occasionally observed in
highly trained athletes.
Drugs.
Ischemia heart disease in
inferior wall.

Clinical presentation

Fainting, feeling dizzy
Chest pain
Feeling tired
Shortness of breath
Heart palpitations
Rapid breathing

In cardiac physiology,_______________ is an event occurring in early systole during which the ventricles contract with no corresponding volume change (isometrically). This short-lasting portion of the cardiac cycle takes place while all heart valves are closed.

A patient with an inferior MI develops a stable bradycardia of 50/min. The cardiologist orders an ECG to evaluate whether there is sinus node dysfunction or an atrioventricular conduction disturbance. The diagnosis of a first-degree heart block is made in which of the following cases?

Diastole = Relaxation
“Phase of Ventricular Filling”

Atrial vs Ventricular Pressure
Tricuspid valve between RA and RV
Bicuspid valve or Mitral valve between LA & LV
Arterial vs Ventricular Pressure
Atrial-Ventricular Valves
Semilunar Valves
EKG/ECG

The PR interval is prolonged (> 200 msec). Benign and
asymptomatic. No treatment required

Most of the energy consumption occurs during isovolumetric contraction.
• Most of the work is performed during the ejection phase.

Mechanically Altered States

Aortic insufficiency: Increased preload, increased stroke volume, increased ventricular systolic pressure
• All the cardiac volumes are increased (EDV, ESV, SV)

Heart failure (decreased contractility): Decreased ventricular systolic pressure,
increased preload, loop shifts o the right

Essential hypertension (aortic stenosis): Increased ventricular systolic pressure,
little change in preload in the early stages

Increased contractility: Increased ventricular systolic pressure, decreased pre-load, increased ejection fraction, loop shifts o the left
Exercise: Increased ventricular systolic pressure, ejection fraction, and preload.

A completely erratic rhythm with no identifiable waves. Fatal
arrhythmia without immediate CPR and defibrillation.

Ejection Fraction

■ is the fraction of the end-diastolic volume ejected in each stroke volume.
■ is related to contractility.
■ is normally 0.55 or 55%.
■ is expressed by the following equation:

Causes

Electrolyte disturbances:
Hypokalemia,
hypomagnesemia.
Drugs toxicity:
Antiarrhythmic agents
and psychotropic drugs.

Clinical presentation

Heart palpitations.
Dizziness and chest pain.
Cold sweat.
Low blood pressure.
Unconscious patient
Rapid or absence of pulse

■ is the work the heart performs on each beat.
■ is equal to pressure ¥ volume. For the left ventricle, pressure is aortic pressure and volume
is stroke volume.
■ is expressed by the following equation:

Force of contraction is proportional to end increased diastolic length of cardiac muscle fiber
(preload).

Increased contractility with catecholamines, positive
inotropes (eg, dobutamine, milrinone,
digoxin).

Decreased contractility with loss of functional
myocardium (eg, MI), β-blockers (acutely),
nondihydropyridine Ca2+ channel blockers,
HF.

A 36-year-old man presents with sudden-onset
dizziness and chest palpitations. He had been
healthy previously. An ECG is shown in the
image. Laboratory work-up reveals normal levels of RBCs and WBCs and a normal cardiac
panel. The drug commonly used to treat this
condition inhibits which of the following?

Most electrical signals reach the ventricles and then one
doesn’t.
o PR intervals are normal until one QRS complex
disappears.

The "p" wave in an ECG represents which phase of  the cardiac cycle?

c. Reduced Filling Phase

A patient presents to the Emergency Department with intermittent chest pain. The ECG and blood tests are negative for myocardial infarction, but the echocardiogram shows thickening of the left ventricular muscle and narrowing of the aortic valve. Medications to lower afterload are pre-scribed. Which of the following values would provide the best measure of the effectiveness of the medication in lowering left ventricular afterload in this patient?

_________________________-– this begins after left atrial pressure has exceeded the pressure within the LV and the mitral valve opens, allowing passive blood flow into the LV. This phase contributes the largest volume during filling.

Occurs in the SA and AV nodes. Key differences from the ventricular action potential include:

Phase 0 = upstroke—opening of voltage-gated Ca2+ channels. Fast voltage-gated Na+ channels are permanently inactivated because of the less negative resting potential of these cells. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.

Phases 1 and 2 are absent.

Phase 3 = repolarization—inactivation of the Ca2+ channels and increase activation of K+

channels leads to increase K+

efflux.

Phase 4 = slow spontaneous diastolic depolarization due to If (“funny current”). If channels responsible for a slow, mixed Na+/K+ inward current; different from INa in phase 0 of ventricular action potential. Accounts for automaticity of SA and AV nodes. The slope of phase 4 in the SA node determines HR. ACh/adenosine decrease the rate of diastolic depolarization and decrease HR, while catecholamines increase depolarization and increase HR. Sympathetic stimulation increase the chance that If channels are open and thus increase HR.

End-diastolic volume (EDV): volume of blood in the ventricle at the end of
diastole
End-systolic volume (ESV): volume of blood in the ventricle at the end of
systole
Stroke volume (SV): volume of blood ejected by the ventricle per beat
SV = EDV – ESV
Ejection Fraction (EF): EF = SV/EDV
(should be greater than 55% in a normal heart)

Causes

Congenital condition.

Clinical presentation

Asymptomatic.
Palpitations.
Supraventricular tachycardia.
Auricular fibrillation

Heart Sounds
The systolic sounds are due to the sudden closure of the heart valves. Normally
the valves on the left side of the heart close fi st. Valves on the right side open fi st.
Systolic sounds
S1: Produced by the closure of the mitral and tricuspid valves. The valves close
with only a separation of about 0.01 seconds which the human ear can appreciate
only as a single sound.

S2: Produced by the closure of the aortic (A2 component) and pulmonic valves
(P2 component). They are heard as a single sound during expiration but during
inspiration the increased output of the right heart causes a physiological splitting.
The following figu e illustrates several situations where splitting of the second
heart sound may become audible.

• Reduced Ventricular Filling - _______________
• diastole continues in atria
• the longest phase of the cardiac cycle
• marked by slower filling

Causes

Drugs
Age factors: Aged
individuals and children
are vulnerable.

Clinical presentation

Asymptomatic most of the
times.
Commonly presented in
athletes.

Ventricular stroke volume (SV) is often thought of as the amount of blood (mL) ejected per beat by the left ventricle into the aorta (or from the right ventricle into the pulmonary artery). This assumes, however, that all the blood leaving the ventricle is ejected into the outflow tract, but this is not the case when there is atrioventricular valve regurgitation or an interventricular septal defect. Therefore, a more precise definition for SV and one that is used in echocardiography when assessing ventricular function is the difference between the ventricular end-diastolic volume (EDV) and the end-systolic volume (ESV). The EDV is the filled volume of the ventricle prior to contraction and the ESV is the residual volume of blood remaining in the ventricle after ejection. In a typical heart, the EDV is about 120 mL of blood and the ESV is about 50 mL of blood. The difference in these two volumes, 70 mL, represents the SV. Therefore, any factor that alters either the EDV or the ESV will change the SV.

SV = EDV - ESV

For example, an increase in EDV increases SV, whereas an increase in ESV decreases SV.

There are three primary mechanisms that regulate EDV and ESV, and therefore SV.

Preload

Changes in preload affect the SV through the Frank-Starling mechanism. Briefly, an increase in venous return to the heart increases the filled volume (EDV) of the ventricle, which stretches the muscle fibers, increasing their preload. This leads to an increase in the force of ventricular contraction and enables the heart to eject the additional blood that was returned to it. Therefore, an increase in EDV results in an increase in SV. Conversely, a decrease in venous return and EDV leads to a decrease in SV by this mechanism.

Afterload

Afterload is related to the pressure that the ventricle must generate to eject blood into the aorta. Changes in afterload affect the ability of the ventricle to eject blood and alter ESV and SV. For example, an increase in afterload (e.g., increased aortic pressure) decreases SV, and causes ESV to increase. Conversely, a decrease in afterload augments SV and decreases ESV. It is important to note, however, that the SV in a normal, non-diseased ventricle is not strongly influenced by afterload because of compensatory changes in preload. In contrast, the SV of hearts that are failing are very sensitive to changes in afterload.

Inotropy

Changes in ventricular inotropy (contractility) alter the rate of ventricular pressure development, affecting ESV and SV. For example, an increase in inotropy (e.g., produced by sympathetic activation of the heart) increases SV and decreases ESV. Conversely, a decrease in inotropy (e.g., heart failure) reduces SV and increases ESV.

It is important to note that the effects of changes in EDV and ESV on SV are not independent. For example, an increase in ESV usually results in a compensatory increase in EDV. If SV is increased by increasing EDV, this can lead to a small increase in ESV because of the influence of increased afterload on ESV caused by an increase in aortic pressure. Therefore, while the primary effect of a change in preload, afterload or inotropy may be on either EDV or ESV, secondary changes can occur that can partially compensate for the initial change in SV. For a more detailed description of these interactions, see the pages describing preload, afterload, or inotropy.

Stroke volume

is the volume ejected from the ventricle on each beat.
■ is expressed by the following equation:

Causes

Normal variant: Common
in highly trained athletes.
Ventricular hypertrophy

Clinical presentation

Commonly asymptomatic.
Found during a routine ECG.

■ is directly related to the amount of tension developed by the ventricles.
■ is increased by
1. Increased afterload (increased aortic pressure)
2. Increased size of the heart (Laplace's law states that tension is proportional to the radius
of a sphere.)
3. Increased contractility
4. Increased heart rate

Review

Causes

Myocardial infraction.
Thyrotoxicosis.
Mitral valve prolapse.
Hypertension.

Clinical presentation

Shortness of breath.
Fatigue.
Chest pain.
Palpitations

Heart sounds:

S1—mitral and tricuspid valve closure. Loudest
at mitral area.

S2—aortic and pulmonary valve closure.
Loudest at left upper sternal border.

S3—in early diastole during rapid ventricular
filling phase. Best heard at apex with patient
in left lateral decubitus position. Associated
with increased filling pressures (eg, MR, AR, HF,
thyrotoxicosis) and more common in dilated
ventricles (but can be normal in children,
young adults, athletes, and pregnancy).
Turbulence caused by blood from LA mixing
with increased ESV.

S4—in late diastole (“atrial kick”). Turbulence
caused by blood entering stiffened LV. Best
heard at apex with patient in left lateral
decubitus position. High atrial pressure.
Associated with ventricular noncompliance (eg,
hypertrophy). Can be normal in older adults.
Considered abnormal if palpable.

Jugular venous pulse (JVP):
a wave—atrial contraction. Absent in atrial
fibrillation.

c wave—RV contraction (closed tricuspid valve
bulging into atrium).

x descent—atrial relaxation and downward
displacement of closed tricuspid valve during
rapid ventricular ejection phase. Reduced or
absent in tricuspid regurgitation and right HF
because pressure gradients are reduced.

v wave—increase RA pressure due to increase volume against
closed tricuspid valve.

y descent—RA emptying into RV. Prominent
in constrictive pericarditis, absent in cardiac
tamponade.