Patho Test 3- Cardiac

During the cardiac cycle, what happens during diastole?

- ventricular muscle reestablishes the Na/K/Ca gradient and is relaxing - isovolumic relaxation - AV valves are open, causing a rapid inflow of blood - diastasis: slow flow into the ventricle - atrial systole: p wave, extra blood in, and accounts for 25% of filling volume (lose this with afib since you lose the atrial kick)

How can you treat cardiac shock?

-Digoxin -Increase atrial pressures using digitalis and dobutamine (alpha and beta stimulation) -give volume -dissolve blood clot if that's the cause

Treatment of decompensated heart failure? (6)

-Diuretics -Decrease Na and H2O intake -ACE Inhibitor -Cardiotonic drug like dig (increases quantity of calcium ions in muscle fibers - Breathe O2 -Heart transplant or LV assist

How does hypertrophic cardiomyopathy affect the functioning of the heart?

-Stops the mitral valve from completely closing leading to regurg -LV hypertrophy (w/o obvious cause) -Asymmsetric septal hypertrophy -Systolic anterior motion of mitral valve

Clinical manifestations of hypertrophic cardiomyopathy

-asymptomatic throughout life -some with severe CHF and sudden death d/t ventricular tachydysrhythmias -diastolic dysfunction (stiffness, narrowed subaortic area) -principles symptoms: angina, syncope, tachydysrhythmias, CHF -max wall thickness of 35 mm or more -EF >80%

What is hypertrophic cardiomyopathy?

-complex cardiac disease with unique pathophysiologic characteristics -great diversity of morphologic, functional, and clinical features -affects all ages -common genetic malformation of the heart -may be caused by a mutation in one of four genes that encode proteins in the cardiac sarcomere

Signs and symptoms of pulmonary edema

-decrease CO -increased pulmonary blood volume -decreased PaO2 leading to peripheral vasodilation, increased venous return, increased pulmonary capillary pressure leading to more and more edema -listen for rales- can also be seen on chest xray

Causes of turbulent flow?

-high velocities -sharp turns in the circulation -rough surfaces in the circulation -rapid narrowing of blood vessels

What is restrictive cardiomyopathy?

-least common type -considered in patients presenting with CHF without evidence of cardiomegaly or systolic dysfunction -usually results from increased stiffness of myocardium which causes pressures within the ventricles to increase precipitously with only small increases in volume -impaired ventricular filling, but systolic function usually remains normal

Clinical manifestations of restrictive cardiomyopathy

-more impairment of LV filling than right -all signs of CHF except cardiomegaly -peripheral edema and ascites in advanced stages -A-Fib -No angina except with cardiac amyloidosis

What causes dampening of pulse pressures? (2)

-resistance to blood movement in the vessels -compliance of the vessels degree of damping = (resistance x compliance)

What happens with a left BBB and what ECG changes are evident in V1, V5, and V6?

-septum depolarizes right to left instead of left to right -loss of R wave in V1, lost of Q wave in V6 -Left ventricle prolonged depolarization causes a wide notched R wave in V5 and V6

During the cardiac cycle, what happens during systole?

-ventricular muscle is stimulated by an action potential and contracts - isovolumic contraction - AV valves close, and the aortic valve opens, causing greater pressure in the ventricles than the atria - this is the ejection phase - at the end of systole, the aortic valve shuts

normal time of PR interval

0.16 sec- can also be the PQ interval, indicates the beginning of electrical excitation of the atria and the beginning of excitation of ventricles

Total time of conduction from SA to AV node?

0.16 seconds

How long does it take for the AP to get from the SA node to the ventricles?

0.22 seconds

How long does the refractory period last and what happens during it?

0.25-0.3 sec no re-excitation

normal time of QT interval

0.35 sec- indicates contraction of ventricles

What are the two ways an AP causes release of Calcium?

1- AP traverses the t-tubules causing the release of calcium from the sarcoplasmic reticulum via the longitudinal sarcoplasmic tubules. Calcium then diffuses into the myofibrils causing actin and myosin to slide and perform muscle contraction 2- Extracellular Calcium enters via voltage-gated calcium channels in the t-tubule membrane, which causes the ryanodine receptor to open and Calcium to release from the sarcoplasmic reticulum

Descriptors of cardiac muscle? (6 points)

1- striated 2- contain actin and myosin 3- contains dark circles that are intercalated discs, with cell membranes separating cardiac muscle cells 4- individual cells connect in a series in a parallel fashion 5- gap junctions between disks allow rapid diffusion of ions 6- AP spreads rapidly due to syncytium of heart muscle (cardiac cells are interconnected)

How does the body respond to contractility failure? (3)

1-Renal sodium and water are retained, increasing blood volume and decreasing venous resistance 2- Cardiac recovery (repair of muscle) 3- Atrial Natriuretic Factor causes extra Na excretion

Blood flow through the heart

1-Superior & Inferior Vena Cava 2-Rt Atrium 3-Tricuspid Valve (AV) 4- Rt Ventricle 5-Pulmonary Valve (Semilunar) 6-Pulmonary Artery 7- Lungs-pick up oxygen 8-Pulmonary Veins 9- Lt Atrium 10- Mitral Valve (Bicuspid/ AV) 11-Lt Ventricle 12- Aortic Valve (Semilunar) 13-Aorta 14- Body

Overall percentage of cerebral arterial blood flow?

15%

Heart Rate for Purkinje Fibers

15-40

How far can axis deviations swing while maintaining a normal electrical axis?

20 to 100 degrees

Clinical manifestations of idiopathic dilated cardiomyopathy

20-50 years old CHF most common initial clinical manifestation chest pain on exertion EF <25% LVED dilation and hypokinetic LV PCWP >20 mmHg CI<2.5 L/min/m2

The capacitance of veins is how many times more that of arteries?

24 times

Overall percentage of GI arterial blood flow?

25%

Overall percentage of Skeletal muscle arterial blood flow?

25%

Overall percentage of renal arterial blood flow?

25%

Total surface area of capillaries (largest surface area of all the vessels)

2500 cm

How much can the LV hypertrophy due to aortic regurgitation?

4-5x the normal LV size

Heart Rate for AV Node

40-60

Overall percentage of coronary arterial blood flow?

5%

Overall percentage of skin arterial blood flow?

5%

What is the normal mean electrical axis in ventricles?

59 degrees (sometimes referred generally as 60 degrees)

Heart Rate for SA Node

70-80

Veins are how much more distensible than arteries?

8x

What does the normal vector of 59 degrees positive indicate, and which lead is it most similarly related to?

A negative (base) to positive (apex) flow of depolarization Lead II

What is Wolf-Parkinson White?

A syndrome where there is an accessory pathway known as the bundle of Kent (in between atria and ventricle in addition to AV node), it does not share the rate-slowing properties of the AV node and may conduct electrical activity at a significantly higher rate than the AV node

What is laminar flow?

A way to describe venous or arterial blood flow that moves in a uniform direction and moves in concentric rings, remains the same distance from the wall

Which catecholamine decreases the rate of depolarization and how?

Acetylcholine (PSNS decrease HR) causes the AP to take a longer time to reach TP and causes a more rapid potassium efflux reaching -65 to -75 (decreases the SA node rate and AV excitability)

How are precordial leads arranged?

Across the chest at 30 degree intervals in a transverse plane of the heart

With ST elevation, what happens to the ECG and what does it indicate?

After the j point and t wave the ECG gets more negative indicating flow from positive (good muscle) to negative (bad muscle) T-P is negative

With ST depression, what happens to the ECG and what does it indicate?

After the j point and t wave, the ECG gets more positive. T-P is positive

Hormones that affect volume?

Aldosterone

What principle does depolarization follow?

All or none- once it starts, it cannot be stopped

On the cardiac flow volume loop, where is the period of filling?

Between points A and B (mitral valve opening/end-systolic volume and mitral valve closing/end-diastolic volume)

What happens to the heart when there is decreased contractility and is in heart failure? (LV, SV, ESV, EDV)

Big boggy heart due to less LV peak pressure and inability to pump leading to increased volume. ESV increases along with EDV because the ventricle is unable to empty properly. This leads to decreased SV

What is myocardial contractility?

CHEMICAL the ability of the heart to generate force to a given preload and a given afterload. This is determined by the chemical environment of the cardiac cell

What determines mean arterial blood pressure?

CO and SVR

What is the main determinant of threshold potential and how does hyper- or hypo- effect it?

Calcium Hypercalcemia- Threshold potential becomes more positive Hypocalcemia- Threshold potential becomes more negative

What makes up the chemical environment of the cardiac cell? (6)

Calcium, Magnesium, Oxygen, Acids, Drugs, Hormones

Which nerves are your cardiac accelerators?

Cardiac splanchnic nerves

What can cause changes in preload? increased or decreased?

Change in volume increased- more volume decreased- less volume due to loop diuretics, vasodilators such as NTG, or patho reasons- tamponade, mitral stenosis

High cardiac output failure causes? (4)

Decrease in SVR and Increase in Venous Return -Beriberi (thiamine deficiency) decreases SVR so severely that venous return and CO double -AV shunt decreases PVR and increases VR and CO -Hyperthyroidism causes increased metabolism of major body tissues that leads to increased oxygen use and vasodilation and decreased PVR -Anemia causes reduced viscosity of blood and decreased oxygen delivery lead to decreased PVR

What is the resting membrane potential?

Difference in electrical charge across the membrane at rest

4 classifications of cardiomyopathy

Dilated Restrictive Hypertrophic Obliterative

What is the relative refractory period and how long does it last?

During Phase 3 and if a large impulse comes along, an AP can cause contraction. 0.05 seconds

What happens to EDV, ESV, Blood Pressure, HR, SVR, SV, and EF with a decreased afterload in the normal heart?

EDV- decreased ESV- decreased BP- decreased (decreased SVR) HR- increased d/t baroreceptor SVR- decreased SV- increased (decreased SVR) EF- increased (increased SV and decreased EDV)

What happens to EDV, ESV, Blood Pressure, SV, SVR, and EF with increased contractility in the normal heart?

EDV- decreased (LV shrinks) ESV- decreased BP- increased SV- increased SVR- may decrease (baroreceptor) EF- increased (decreased ESV)

What happens to EDV, Blood Pressure, HR, SVR, and EF with a decreased preload in the normal heart?

EDV- decreased due to decreased filling BP- decreased (reduced output) HR- increased d/t baroreceptor reflex SVR- increased d/t baroreceptor reflex EF- remains mostly unchanged (d/t equal decrease in SV and EDV)

What happens to EDV, ESV, Blood Pressure, HR, SVR, SV, and EF with an increased afterload in the normal heart?

EDV- increased ESV- increased BP- increases (SVR increased) HR- decreased d/t baroreceptor SVR- increases SV- decreases (d/t increased SVR) EF- decreased (SV decreases and EDV increases LV- dilates

What happens to EDV, ESV, Blood Pressure, HR, SV, SVR, and EF with decreased contractility in the normal heart?

EDV- increased (dilated LV) ESV- increased (dilated LV) BP- decreased HR- may increase (d/t baroreceptor) SV- decreased SVR- may increase (d/t baroreceptor) EF- decreased

What happens to EDV, Blood Pressure, HR, SVR, and EF with an increased preload in the normal heart?

EDV- increased due to increased filling BP- increased HR- may decrease d/t baroreceptor reflex SVR- may decrease d/t baroreceptor reflex EF- remains mostly unchanged (d/t equal increase in EDV and SV)

What happens to the EF if SV decreases and EDV increases?

EF decreases

What happens to the EF if SV increases and EDV decreases?

EF increases

What can cause an extreme right axis deviation aka No man's land?

Emphysema, Hyperkalemia, Lead transposition, Ventricular pacing, Ventricular Arrhythmia

What three things are important functions of capillary exchange?

Exchange of O2, Nutrients, Waste Products (C)

Causes of decompensated heart failure? (5)

Failure of the heart to pump sufficient blood to make the kidneys excrete the necessary amounts of fluid every day -Overstretched sarcomeres (fluid retention) -Edema of heart muscle -Norepi in myocardial tissues -Increased RAPs and decreased CO -Longitudinal tubules of SR fail to accumulate enough Ca

What vessels make up coronary venous circulation?

Great cardiac vein, middle cardiac vein, anterior cardiac vein, coronary sinus, and thebesian veins

Signs and Symptoms of Right Heart Failure

Greater decrease in CO than LHF Peripheral congestion Increased pulmonary vascular resistance

What is tachycardia, and what is it caused by?

HR greater than 100 bpm caused by increased body temp, increase SNS activity, or weakened myocardium

What is bradycardia, and what is it caused by?

HR less than 60 bpm an athletic reflex, caused by large SV output, carotid sinus syndrome (baroreceptor reflex) or vagal via Ach

With ECG, what does the R to R interval determine?

Heart rate

Percentage of blood distribution throughout the body (Heart, Pulmonary Circulation, Arteries, Arterioles/Capillaries, Veins/Venules/Venous Sinuses)

Heart- 7% Pulmonary Circulation- 9% Arteries- 13% Arterioles/Capillaries- 7% Veins/Venules/Venous Sinuses- 64%

The SA node is located where?

In the right atrium, below and lateral to the SVC

Low cardiac output failure causes? (6)

Increase in SVR and Decrease in Venous Return -CAD leading to MI -Severe Valve disease -Myocarditis -Cardiomyopathies -Cardiac Tamponade -Cardiac metabolic derrangments

Bipolar limb lead I records the potential difference between which two points and at what degree is the axis?

LA (active) and RA (reference) Axis- 0 degrees

What is indicated by Lead III?

LA to LL (- to +) second most accurate display of true electricity of the heart d/t direction of leads

Which artery runs with the Great cardiac vein?

LAD

What does the LCA divide into?

LAD and left circumflex artery

With an anterior wall infarct, which artery is occluded, and where will you see ST elevation?

LAD is occluded Elevation in I, aVL, V1-V4 (negative after the J point, vector of +150, the negative end will point towards left ventricle and positive end will point towards right ventricle)

Bipolar limb lead III records the potential difference between which two points and at what degree is the axis?

LL (active) and LA (reference) Axis- 120 degrees

Bipolar limb lead II records the potential difference between which two points and at what degree is the axis?

LL (active) and RA (reference) Axis- 60 degrees

What sound does laminar flow make versus turbulent?

Laminar- silent Turbulent- murmurs

With an posterior infarct, which artery is occluded, and where will you see ST elevation and ST depression?

Left Circumflex Artery is occluded Elevation in II, III (negative after J point) Depression in V1, V2 (positive vector towards the anterior wall)

With a lateral wall infarct, which artery is occluded, and where will you see ST elevation?

Left Circumflex artery is occluded Elevation in I, aVL, V5 V6

What is the most common cause of right sided heart failure?

Left sided heart failure

With the SA node AP, why does Phase 0 have a slower uptake than muscle?

Less negativity and inactivation of fast Na channels, so only slow channels open

What happens with a SA block?

Lose your p wave causing a loss of the following QRS

What can lead to myocardial contractility failures? (7)

MI Heart valve damage Pulmonary embolism Anemia Myocarditis Hypertension- severe AV Fistula & Beriberi (high output failure)

What is the J point?

Marks the start of the ST segment (end of QRS) which is the exact point depolarization completes its journey through the heart injury disappears and there is zero voltage

What can cause an decrease in the CO output curve? (5)

Myocardial Infarction Valvular Disease (stenosis or regurgitation) Myocarditis Cardiac Tamponade Metabolic Damage

Is aortic regurgitation isovolumetric?

No, because at the end of systole, there will be back-flow of the blood which will cause an increase in ESV

Which catecholamine increases the rate of depolarization and how?

Norepinephrine (SNS- Beta 1) causes the AP to get to TP more quickly you have increased SA node and AV conduction, along with increased permeability of Sodium and Calcium

Signs and Symptoms of compensated heart failure? (9)

Normal CO increased RAP decreased Cardiac Reserve increased HR pale skin sweating with nausea air hunger weight gain (fluid retention) Orthopnea

Which law affects cardiac output? And what two pressures determine it?

Ohms Law Arterial pressure/total peripheral resistance

What happens with PACs?

P wave occurs too soon and PR interval is shortened compensatory pause between PAC and next beat

What are two types of premature contractions?

PACs and PVCs

Which artery runs with the Middle cardiac vein?

PDA

What happens with a First Degree block?

PR interval is greater than 0.20 seconds (delays conduction of the atria to ventricles)

What is afterload?

PRESSURE the tension in the wall of the heart at the time the aortic valve opens. It is determined by the Systemic Vascular Resistance (SVR). The greater the SVR, the greater the afterload

With the SA node AP, in which phase does slow calcium channels open causing an influx of Ca and depolarization?

Phase 0- Slow depolarization there is some sodium influx, but they close quickly

Which ventricular phase correlates with the ST segment?

Phase 2- Plateau

With the SA node AP, which which phase does potassium channels open more to cause an efflux of potassium and repolarization?

Phase 3- Repolarization

Between what two phases in the SA AP is the threshold potential?

Phase 4 and 0- all or none principle

With the SA node AP, which phase is responsible for autorhythmicity?

Phase 4- Diastole

With the SA node AP, which phase has a slow influx of sodium (leaky), last 1/3 of calcium influx, and an progressive decrease of effluxed potassium, causing spontaneous depolarization to TP?

Phase 4- diastole

Ventricular Muscle- Phase 2

Plateau- L-type calcium channels open more (prolongs depolarization and activates muscle contractile process from SR); Fast voltage-gated K channels close, but slow delayed rectifier potassium channels open and potassium exits but is very minimal

Which law reflects resistance to blood flow?

Poiseulle's Law

What is the main determinant of resting membrane potential and how does hyper- or hypo- effect it?

Potassium Hyperkalemia- RMP becomes more positive Hypokalemia- RMP becomes more negative

What is indicated by the Q and T waves?

Q- ventricle depolarization T- ventricular repolarization

What happens with PVCs?

QRS is prolonged slowing down conduction through the ventricles high voltage, one-sided depolarization of ventricles that causes large potentials T wave is opposite of QRS

What is indicated by Lead I?

RA to LA (- to +)

What is indicated by Lead II?

RA to LL (- to +) most accurate display of true electricity of the heart d/t direction of leads

Which artery runs with the anterior cardiac vein?

RCA

With an inferior infarct, which artery is occluded, and where will you see ST elevation and ST depression?

RCA is occluded Elevation in II, III, aVF Depression in aVL

With the SA node AP, what is the normal RMP and where is the threshold?

RMP -60, TP -40

Ventricular Muscle- Phase 0

Rapid depolarization- Fast voltage gated sodium channels open, slow calcium channels open (-90 to +30), and K inward- rectifier channels close

How does severe hyperkalemia effect the RMP compared to regular hyperkalemia?

Regular increases the RMP making it slower to TP and causing depolarization to happen rapidly. However, severe hyperkalemia (like that which is seen when using cardioplegia for bypass surgery) completely blocks depolarization due to inactivating the sodium channels

Ventricular Muscle- Phase 3

Repolarization- L-type calcium channels close, fast delayed rectifier potassium channels open (efflux) and K inward-rectifier Channels re-open towards the end of this phase

Where does the SA node reside and during which Phase does it fire?

Resides in the right atrium fires during Phase 4

Ventricular Muscle- Phase 4

Resting membrane potential- everything is closed except for potassium leak channels and Sodium/Potassium/ATPase pump, which removes sodium from depolarization and replenishes potassium lost during repolarization. This reverts the cell to baseline (usually -90). Diastole phase, where the ventricles are filling up.

Types of blocks

SA First Degree AV Second Degree AV Type 1 (Mobitz 1/Wenckebach) Second Degree AV Type 2 (Mobitz 2) Third Degree - Complete AV Stoke Adams Syndrome Right BBB Left BBB

Which phases do CCB work on in the SA node and Ventricular Muscle?

SA- Phase 0 Ventricular- Phase 2

How does SNS and PSNS affect coronary blood flow?

SNS- can either increase or decrease pending receptors (Alpha decreases, while Beta increases) PSNS- affects HR which can have negative impact on coronary blood flow if too slow or too fast

Subendocardial injury appears as what on en ECG?

ST depression

Transmural (Epicardial) injury appears as what on en ECG?

ST elevation

Causes of the hypoeffective heart? (8)

Severe HTN Inhibition of NS to excite heart Abnormal heart rate or rhythm Heart attack Valve Disease Congenital heart disease Myocarditis Cardiac hypoxia

What happens to the ventricular function curve with decreased preload?

Shifts down (caused by NTG or Lasix)

What happens to the ventricular function curve with increased preload?

Shifts up (caused by giving fluids like LR)

With the SA node AP, what pump is responsible for re-establishing the RMP?

Sodium Potassium ATPase pump

What should you never give to patients with WPW syndrome?

Sodium channel blockers, such as Local Anesthetics

Which substance of plasma does not contribute to plasma colloid osmotic pressure?

Sodium chloride

How does the body retain renal sodium and water to increase blood volume and decrease venous resistance? (5 steps)

Steps 1- sympathetic constriction of afferent arterioles lead to decreased GFR and decreased UOP 2- Angiotensin II release that leads to sodium retention 3- Aldosterone release (from angiotensin II and increased K) also leads to sodium retention 4- Increased ADH release (water balance? ) 5- Decreased MAP initially that then returns to normal

What happens to the stroke volume when preload increases?

Stroke volume also increases (Frank-Starling Law)

What can cause an increase in the CO output curve? (2)

Sympathetics Heart Hypertrophy

How do you determine your ejection fraction?

Take EDV (120 mL) and subtract the ESV (50 mL), which will give you your stroke volume or ejection volume (70 mL). Divide your SV (70) from your EDV (120). This will give you your EF (58%) simpler way- (SV/EDV) x 100

How do you determine your cardiac output?

Take your heart rate (70 bpm) and multiply it by your Stroke Volume (70 mL) and it will give you your CO (4900 ml/min or 4.9 L/min) CO= HR and SV

With an anteroseptal infarct, which artery is occluded and where will you see ST elevation?

The LAD is occluded Elevation in V1-V4

What happens within the heart when aortic stenosis is present? (LV, SV, Blood volume etc)

The LV fails to empty adequately and causes the LV to become hypertrophied d/t compensation SV is reduced Blood volume increases due to diminished renal output of urine (decreased arterial pressure) and there is an increase in venous return to help overcome deficient SV decreased blood flow during systole reduces coronary blood flow

What does the circumflex artery perfuse?

The left atrium, lateral, and posterior walls of the left ventricle; SA node in 30% of patients

Once the AP reaches the AV node, what path does it take to get to the ventricles and how long does it take for each step?

The purkinje fibers (1.5/4m/sec) cause an instant cardiac impulse through the ventricles via very few myofibrils. This happens through two steps 1- the left and right bundle branches spread the AP throughout the ventricular mass (0.03 sec) 2- the AP spreads through the ventricular muscle fiber from endocardial to epicardial surfaces (0.03 sec) totaling an extra 0.06 seconds

What happens with Stoke Adams Syndrome?

There is ventricular escape causing fainting delays in the ventricular beat after a total AV block, AV distal starts ventricular escape

Which main ventricular arrhythmia has an increased susceptibility when the QT interval is prolonged, what causes it and how do you treat it?

Torsade de Pointes Cause: hypo Mg/K/Ca; excess quinidine, fluoroquinolones, or erythromycin; mutation of sodium or potassium channel genes Tx: Magnesium

Ventricular Muscle- Phase 1

Transient (brief) repolarization- fast voltage-gated sodium channels close, fast voltage-gated potassium channels transiently open (efflux), and chloride influxes into the cell

Colloid osmotic pressure is mainly caused by the presence of large proteins, true or false?

True

Dysrhythmias associated with Hypokalemia?

U waves, ST depression, shallow or flat inverted T waves

How can one break up the cardiac shock cycle?

Use sympathetics or increase the right atrial pressure (starling's law) to prevent further decreased CO and decompensation

How does the Q R and S appear in V1 versus V6

V1- small positive r with large negative S V6- small negative q with large positive R

What are the precordial leads and what do they serve as for electrical flow?

V1-V6 serve as the positive

What happens in V1, V6, and V1-V3 with a right bundle branch block?

V1: rSR' with a broad R (rabbit ears) V6: qRS with a broad S V1-V3: inverted T wave

Which nerve is your cardiac decelerator?

Vagus nerve (CN X)

What happens during the QT interval?

Ventricular Systole (Phase 2- Plateau)

What happens during the QRS complex?

Ventricular depolarization and Atrial repolarization (Phase 0-1)

What is Ohm's Law?

Voltage = (Current)(Resistance) Flow = Pressure at origin of vessel minus pressure at end of vessel divided by resistance

What is hyperpolarization?

When the RMP is far away from TP and makes it more difficult for the cell to depolarize

How does mitral stenosis affect the pressures in the chambers of the heart?

You'll have impeded flow from the LA to the LV causing LAP to increase and be about 25-40. This can cause blood to be back up into the lungs, leading to pulmonary edema and RAP increase up to 60 You will also have low LV volumes during early diastole due to lack of blood being able to get through the mitral valve

Changing the slope of Phase 4 causes what?

a change in heart rate due to the change in depolarization

What are the augmented unipolar limb leads?

aVR, aVL, aVF

How does the QRS appear in aVR, aVL, and aVF?

aVR- negative aVL- positive aVF- positive

What pressures tend to increase venous pressures in the legs?

abdominal pressures

How do you fix WPW?

ablation

What are cardiac arrhythmias?

abnormal rhythmicity of the pacemaker, shifts from SA to another place in the heart, can be caused by blocks in conduction or abnormal pathways. It's a spontaneous generation of impulses

What happens with a Second Degree Type 1 (Mobitz 2) block?

abnormality of His-purkinje system usually a fixed number of Ps for every QRS (2:1, 3:2, 3:1)

What happens with a Second Degree Type 1 (Mobitz 1/Weinkebach) block?

abnormality of the AV node (benign) going, going, going, drop

How much of the SV can flow back into the LV with aortic regurgitation?

about 75% of the 250 mL of output can flow back into the LV

Where is there a large pressure drop in the body's vascular system?

across the arteriolar-capillary junction

When does the infarcted area become electrically silent?

after day or weeks of the infarct, becomes nonconducting zone. Current of injury stops and the ST segment abnormalities subside

Which leads are considered unipolar/precordial?

all V leads

Which has a higher velocity, aortic/pulmonary valves or AV valves?

aortic/pulmonary valves have a higher velocity due to having a smaller opening and they are made up of strong fibrous tissue

Leads V4-V6 are closer to which part of the heart, thus making them

apex, making them positive

What regulations are generally independent of either local blood flow controls or cardiac output control?

arterial pressure regulations

What happens during the p wave?

atrial depolarization (diastole phase 4)

What happens during the PR interval?

atrial systole and AV nodal delay

Leads V1-V2 are closer to which part of the heart, thus making them

base making them negative

Why is their no plateau during Phase 0/Slow Depolarization?

because calcium is already there

On the cardiac flow volume loop, where is the point of isovolumetric contraction?

between points B and C (mitral valve closing and aortic valve opening)

On the cardiac flow volume loop, where is the period of ejection?

between points C and D (aortic valve opening and aortic valve closing)

On the cardiac flow volume loop, where is the point of isovolumetric relaxation?

between points D and A (aortic valve closing and mitral valve opening)

In essence, all pairs of electrodes are what?

bipolar

What happens when there is an increase in RAP?

blood backs up into the venous system thereby increasing venous pressures

What does. the electrical silent area alter?

both the direction and magnitude of the electrical vectors during the cardiac cycle

Where is the apex of the heart?

bottom of the heart

How does compensated heart failure occur?

by SNS acutely and chronically by partial heart recovery and renal retention of fluid

Most common type of aortic stenosis and usual LV pressure when present?

calcified aortic stenosis LV pressure can be as high as 300-400 mmHg

How does the Sympathetic nervous system affect CO?

can cause increase in heart rate and increased contractility with heart rate

How can tachycardia affect cardiac output?

can decrease CO due to lack of time to allow for ventricular filling during diastole

What is the sum of all the local tissue flows?

cardiac output

What does the cardiac output curve measure?

cardiac output relative to right atrial pressure VR must equal cardiac output and RAP is the same for both the heart and the systemic circulation

How does mitral regurgitation affect the pressures in the chambers of the heart?

cardiac output will fall dramatically and have elevated RAP and pulmonary edema can also cause Afib Eccentric LV hypertrophy eventually happens

What is aortic regurgitation caused by and what can it sometimes present itself as?

caused by congenital defects or due to rheumatic fever Chronic AR can present as congestive heart failure

What has changed when the cardiac flow volume loop gets taller or shorter?

change in pressure

What has changed when the cardiac flow volume loop gets wider or skinnier?

change in volume

What is attached to the A-V valves?

chordae tendinae

What happens with a Third Degree block?

complete disassociation of atria and ventricle conduction, P and QRS are acting independently

What factors tend to cause resistance to flow in large peripheral veins?

compressional factors

What does the pressure volume loop look like with mitral stenosis?

concentric d/t pressure (less pressure in LV d/t less volume) loop will shift down and to the left due to decreased preload (EDV is decreased because the LV will fill less) ESV is mostly unchanged

concentric vs eccentric related to the pressure volume loop

concentric- pressure eccentric- volume

What does the pressure volume loop look like with mitral regurgitation?

considered eccentric d/t volume with acute MR- short and to the right with chronic MR- larger and to the right (LV hypertrophies d/t increased volume in LV) leads to larger stroke volumes in chronic MR and smaller LV volumes in acute MR

Role of arterioles

control site for blood flow, major resistance site for circulation

Where does the major of venous blood return to on the heart and where is it located?

coronary sinus, located on the posterior aspect of the right atrium just superior of the tricuspid valve

How quickly does death occur with idiopathic dilated cardiomyopathy and what usually causes death?

death usually occurs within 3 year of diagnosis ventricular dysrhythmias and sudden death common

How to treat hypertrophic cardiomyopathy?

decrease contractility (BB, CCB) increase preload (volume) increase afterload (phenylephrine)

When SV falls due to decrease in afterload or increase in contractility, volume in the LV does what?

decreases

How does the Parasympathetic nervous system affect CO?

decreases the heart rate markedly and decreases cardiac contractility slightly. Vagal fibers go mainly to atria

How does the PSNS affect Phase 4 of SA AP?

decreases the slope

What happens when the QT interval is prolonged?

delayed repolarization

What causes ST-segment depression?

delayed repolarization phase in the ischemic subendocardial zone, it is also often associated with prolongation of the QT interval

How do the ventricles depolarize (direction) and why?

depolarization proceeds from the left septal wall to the right septal wall due to the left ventricle being more electrically predominant

TP segment does not remain isoelectric during which current of injury?

diastolic current of injury

With mitral stenosis, what type of murmur will you have, and where will you hear it?

diastolic murmur (weak, low frequency) best heart at cardiac apex

With aortic regurgitation, what type of murmur will you have and where will it be located?

diastolic murmur that will sound like a blowing murmur at the left sternal border

When are coronary arteries perfused?

during diastole

Where do you see your pulse pressure on the pressure volume loop?

during period of (ventricular) ejection between point C and D (aortic valve opening and closing)

What does the pressure volume loop look like with aortic regurgitation?

eccentric loop d/t to VOLUME (eccentric LV hypertrophy) with acute AR- loop will be small, shorter, and to the right with chronic AR- loop will be large, taller, and to the right

What happens during the TP segment?

entire myocardium is repolarized

Where does the potassium go after it leaves the damaged heart myocardial cells?

extracellular fluid this rise depolarizes the injured myocardial cells, resulting in decreased RMP

How do you determine pressure change?

flow x resistance

How does a cardiac impulse flow around the heart?

from base to apex it first arrives in the ventricles in the septum and then spreads to the inside of the remainder of the ventricles electronegativity on the inside and electropositivity on the outside

How is the ST-segment vector directed with ST-depression?

from epicardial to endocardial, or nonischemic to ischemic zone

What are cardiomyopathies?

group of disorders characterized by myocardial dysfunction unrelated to the usual causes of heart disease

Why are murmurs or bruits important?

help diagnose vessel stenosis, vessel shunts, and cardiac valvular lesions

Where is the highest venous pressure in the body, and where is the lowest?

highest- legs (+90) lowest- head (-10)

What can cause pulmonary vascular resistance?

hypoxia hypercarbia acidosis hypothermia high peep Nitrous Oxide

How can mitral stenosis cause afib?

impedance of the electrical signal through the atrial wall due to increased pressure

Vascular compliance = ?

increase in volume/increase in pressure

Signs and Symptoms of Left Heart Failure

increased LAP pulmonary congestion pulmonary edema RAP may be normal CO may be normal

What factors determine right atrial pressures?

increased blood volume increased venous tone dilation of arterioles decreased cardiac function

What makes hypertrophic cardiomyopathy worse?

increased contractility decreased preload decreased afterload

What can cause an increase in voltage?

increased muscle mass (hypertrophy) increased muscle=increased electricity

How does viscosity affect resistance?

increased viscosity = increased resistance decreased viscosity = decreased resistance

What causes increased or decreased myocardial contractility?

increased- medication (Dig, PDE III inhibitor, Calcium) decreased- patho- CHF

What causes changes in afterload? increased and decreased?

increased- meds such as vasoconstrictors (Neo) or patho issues such as chronic aortic stenosis decreased- medication induced (nitroprusside)

How does the SNS affect Phase 4 of SA AP?

increases the slope

When SV falls due to increasing in afterload or decreased contractility, volume in the LV does what?

increases, and the chamber dilates

Phase II of the cardiac flow volume loop?

isovolumic contraction- LV pressure increases by 80 mmHg

Phase IV of the cardiac flow volume loop?

isovolumic relaxation- decreased pressure

If cardiac contraction increases, what happens to coronary blood flow?

it also increases

What happens to calcium at the end of Ventricular Phase 2?

it is pumped back into the sarcoplasmic reticulum and t-tubules via the Calcium Adenosine triphosphate (ATPase) pump. Sodium and Calcium are exchanged

With the SA node AP, which channels in Phase 4 cause less negativity than in the muscle?

leaky sodium channels

What can cause a left axis deviation?

left ventricular hypertrophy along with HTN, aortic stenosis/regurg, congenital heart conditions, left BBB, normal in kids, COPD, previous Anterolateral MI, PE, ASD/VSD, WPW, pectus excavatum, reversed arm leads

What does the magnitude of the vector depend on?

length of the border (longer border equals greater magnitude of the vector)

What are the purpose of the thebesian veins and where are they located?

located in all four chambers of the heart, only small amount of blood drain into these vessels play a small part in the anatomical shunt of the heart via the left side causing a dilution of paO2

How does length affect resistance

longer increases resistance shorter decreases resistance

What does the pressure volume loop look like for heart failure?

loop is shorter and shifts to the right due to decreased contractility. The baseline increases because of constant LV pressure

Role of capillaries

major site of water and solute exchange between blood and tissues

How can you indicate a left axis deviation on a 12 lead ECG?

more positive QRS in Lead I and aVL more negative QRS in Lead II and aVF

How can you indicate a right axis deviation on a 12 lead ECG?

more positive in lead III and aVF more negative in lead I and aVL

What does the pressure volume loop look like when aortic stenosis is present?

moves up and to the right d/t increased afterload (pressure) and appear taller along with LV volume remaining basically the same, just unable to empty completely so loop will appear skinnier considered concentric d/t to stenosis increasing pressure of the LV. This will lead to hypertrophy

What is the degree of LV outflow influenced by with hypertrophic cardiomyopathy?

myocardial contractility, preload, afterload

Concerning the heart, it is always negative towards the _________ and positive towards the ________ during almost the entire cycle of depolarization

negative towards the base and positive towards the apex

With a normal QRS, Q waves are always

negative- below baseline

With a normal QRS, S waves are always

negative- below baseline

Is mitral regurgitation isovolumetric?

no, it is nonisovolumetric d/t LV starting to empty prior to the aortic valve opening leading to smaller LV volumes

Does preload affect ESV?

no, just EDV

What can cause a decrease in voltage?

old MI's or diminished muscle mass, fluid in pericardium like a pleural effusion or pulmonary emphysema

How does oxygen affect coronary blood flow?

oxygen dilates the coronaries and oxygen demand increases coronary blood flow

What is attached to the chordae tendinae and contracts during systole to help prevent back-flow of blood?

papillary muscle

Dysrhythmias associated with Hyperkalemia?

peaked or tented T waves, flat P waves, widened QRS

What does the posterior descending artery perfuse and where can it originate from?

perfuses the inferior wall can either come from the RCA (70-80% of the time, right dominance) or from the Circumflex (left dominance)

Phase III of the cardiac flow volume loop?

period of ejection- increased systolic pressure, decreased systolic volume

Phase I of the cardiac flow volume loop?

period of filling-increased volume from 50-120, and LV pressure 2-3. This volume makes up the stroke volume

What are ventricular function curves?

plots of some index of ventricular function like SV or SV index versus some measure of EDV like PCWP

What is the aVL lead? is it negative or positive?

positive LA, negative RA and LL lead is positive cause LA is closer to the apex

What is the aVF lead? is it negative or positive?

positive LL, negative RA and RL lead is positive cause LL is closer to the apex

What is the aVR lead? is it negative or positive?

positive RA, negative LA and LL lead is negative cause RA is closer to the base

With a normal QRS, R waves are always

positive- above baseline

Origin of which vessel defines coronary dominance?

posterior descending artery

Where is the AV node located?

posterior wall of the right atrium immediately behind the tricuspid valve

At rest, what electrolyte do nerve cells leak, causing loss of positive charge?

potassium

What is stroke volume determined by?

preload, afterload, contractility

How do you determine resistance?

pressure change divided by flow

What happens to the volume loop with a decreased afterload?

pressure volume loop shifts down (lower pressures) and to the left (smaller volumes)

What happens to the volume loop with decreased contractility?

pressure volume loop shifts down (lower pressures) and to the right (higher volumes)

What happens to the volume loop with increased contractility?

pressure volume loop shifts up (greater pressures) and to the left (smaller volumes)

What happens to the volume loop with an increased afterload?

pressure volume loop shifts up due to increased pressure and right due to greater volumes

What is idiopathic dilated cardiomyopathy?

primary myocardial disease of unknown cause characterized by LV or biventricular dilation, impaired myocardial contractility, decreased cardiac output, and increased ventricular filling pressures

What is common to all types of cardiomyopathy?

progressive, life-threatening congestive heart failure

Dysrhythmias associated with Hypermagnesemia?

prolonged PR, widened QRS

Dysrhythmias associated with Hypocalcemia?

prolonged QT- longer plateau

How does radius affect resistance?

radius increase, decreased resistance radius decrease, increased resistance

What is the greatest factor of blood flow resistance?

radius of vessel

How is angina relieved in hypertrophic cardiomyopathy?

recumbent position (huge indicator of hypertrophic cardiomyopathy)

Why does a u wave sometimes appear in an ECG?

reflects hypokalemia

How is right atrial pressure regulated?

regulated by a balance between the ability of the heart to pump blood out of the atrium and the rate of blood flowing into the atrium from peripheral veins

What happens to the EF if both SV and EDV increase or decrease?

remains mostly unchanged

What is the major determinant of extravascular volume?

renin

What causes a sinus arrhythmia?

respiratory, medullary mediated

Role of Veins, IVC/SVC

returns blood to heart under low pressure and serves as blood reservoir

What type of axis deviations can occur?

right and left

Which type of hypertrophy can be seen with restrictive cardiomyopathy?

right ventricle or left ventricle can be seen, or both

What can cause a right axis deviation?

right ventricular hypertrophy along with pulmonary valve stenosis, congenital heart defect, right BBB, past inferior MI, ventricular pacing, emphysema, hyperkalemia, WPW

What does " R' " denote?

second R wave

What does " S' " denote?

second S wave

What happens to the ventricular function curve with decreased contractility/increased afterload?

shift is down and to the right- which indicates a decrease in stroke volume and increase in size of LV (can be caused by heart failure or phenylephrine)

What happens to the ventricular function curve with increased contractility/decreased afterload?

shift is up and to the left- which indicates an increase in Stroke Volume or a decrease in LV chamber

Dysrhythmias associated with Hypercalcemia?

shortened QT- brief plateau

Role of Pulmonary circulation

site of O2 and CO2 exchange

How will the cardiac volume loop appear with a decreased in stroke volume?

skinny, shorter pressure volume loop due to reduced filling

What does q,r,s denote?

small amplitude waves

Vessel velocity of blood flow from least to greatest

small veins, capillaries, arterioles, aorta

What causes PACs?

smoking, caffeine, coffee, alcoholism, drugs, healthy athletes

For frontal plane ECG, why are 6 leads placed?

so one lead is at every 30 degree interval, so that no matter what angle of the cardiac vector is directed, it will get recorded maximally in at least one lead

What happens to stroke volume when afterload increases?

stroke volume decreases due to the increased pressure

ST segment does not remain isoelectric during which current of injury?

systolic current of injury manifests only after J point

With aortic stenosis, what type of murmur will you have and where will it be located?

systolic murmur at the right second intercostal space the sound may cause a thrill to be felt due to severe turbulence in the root of the aorta

With mitral regurgitation, what type of murmur will you have, and where will you hear it?

systolic murmur that creates a blowing sound (d/t backward flow during systole) that is best heart at the cardiac apex very similar to mitral stenosis in eventual problems

Dysrhythmias associated with Hypomagnesemia?

tall T waves, depressed ST

How does the SA node send the AP to the AV node and how long does it take?

the SA node sends the AP directly through the atrial muscle fibers (0.03 sec) then through 3 internodal pathways with transitional fibers that increase conduction to the AV nodes (0.09 sec) and finally penetrate the AV bundle where it passes into the ventricles (0.04)

What is preload?

the VOLUME of blood in ventricles at end of diastole also known as the tension, or force, in the wall of the left ventricle at end-diastole right before contraction

What is the major determinant of intravascular volume?

the amount of sodium in the body

What does the LAD perfuse?

the anterolateral and apical walls of the left ventricle as well as the anterior two-thirds of the intraventricular septum along with the Bundle of His (in 75% of patients) and Left and Right Bundle Branches

Where do the LCA and RCA arise from?

the aortic root

What happens to the cell when RMP is closer to TP?

the cell is easier to depolarize

What is the pressure in the right atrium and what is the usual range?

the central venous pressure normally 0, but can get as high as 20-30

What vein is cannulated to administer cardioplegia solution during bypass?

the coronary sinus

Cells with the fastest rate determine what?

the depolarization frequency

What determines cell excitability?

the difference between RMP and TP

What determines pulse pressure?

the difference between systolic and diastolic pressures

What is injury potential?

the difference in voltage between the onset of P and zero voltage of j

What is vascular distensibility?

the fractional increase in volume for each mmHg rise in pressure Vascular Distensibility = Increase in Volume / (increase in pressure x original volume)

Which lead will record the maximum amplitude?

the lead that is disposed along the direction of the cardiac vector

Which lead will record nothing?

the lead that is oriented exactly perpendicular to the cardiac vector

What happens to the heart muscle after suffering from coronary ischemia?

the muscle remains totally or partially depolarized all the time (always negative)

What happens during depolarization?

the normal negative potential inside the fiber reverses and becomes slightly positive inside and negative outside

What happens every time the SA node fires?

the rest of the myocytes conduct and fire

What does the RCA perfuse?

the right atrium, right ventricle, interatrial septum, and posterior third of the interventricular septum; SA node in 70% of patients and AV node in 80% of patients

What is velocity of blood flow?

the speed at which blood flows in the circulation (mm/sec) Blood flow/cross sectional area

What determines the plateau of the CO curve?

the strength of the heart (contractility plus increased HR)

What is vascular capacitance?

the total quantity of blood that can be stored in a given portion of the circulation for each mmHg capacitance is approximately equal to distensibility x volume

What happens concerning the injury potential vector with injured heart muscle?

the vector still goes negative to positive, so the negative point towards the damaged portion of muscle and the positive end points towards the normal cardiac muscle

What happens when contractility decreases?

the ventricle empties less and the stroke volume decreases

What happens when contractility increases?

the ventricle empties more and stroke volume increases

What is threshold potential?

the voltage change that must occur to initiate depolarization

What happens to the heart when there is increased contractility and is in heart failure? (LV, SV, ESV, EDV, BP) and how does it affect the pressure volume loop?

there is a decrease in ESV and EDV because the ventricle empties more completely. The LV shrinks and there is an increase in SV. Blood pressure and LV pressure increases at time of ejection loop shifts up and to the left

What happens with ventricular contraction in the presence of hypocalcemia?

there is a slower calcium diffusion that causes a prolonged plateau phase (phase 2) and the TP becomes more negative, which causes it to be closer to the RMP and cells will depolarize more easily

What happens to the heart with aortic regurgitation?

there is an increase in blood volume in the LV, increased intraventricular diastolic pressure (will compress the inner layer of the heart muscle and decrease coronary blood flow), you will have low diastolic pressures in the aorta and increase myocardial oxygen demand.

What happens with ventricular contraction in the presence of hypercalcemia?

there is faster calcium diffusion which causes a shorter plateau phase (phase 2) and the TP becomes more positive pushing it further away from the RMP. This makes the cell more resistant to depolarization and IV calcium can reduce the risk of dysrhythmias in patients with hyperkalemia

Why are myocardial cells capable of automaticity?

they have self generating action potentials (these lead to ventricular contraction)

What are the purpose of the cardiac valves?

they prevent backflow of blood in the heart

Why are Leads I, II, and III considered bipolar?

they use two different sites on the body, one serving as the reference and the other is the exploring or active electrode

What is the absolute refractory period?

time during which another action potential is impossible; limits maximal firing rate; happens during Ventricular Phase 1 when the sodium channels are closed and in an inactive state

Cardiac output is proportional two what two things? Formula?

tissue O2 use & 1/Total peripheral resistance when atrial pressure is constant CO= (MAP-RAP)/TPR CO is the sum of all tissue flows and is affected by their regulation

What determines blood flow to most tissues?

tissue need

Why do we give calcium with hyperkalemia?

to increase the threshold and prevent over-excitation of the cell

What is the direct of vector perpendicular to?

to the border between depolarized and repolarized muscles of the heart

Where is the base of the heart?

top of the heart

How to treat pulmonary edema

tourniquet bleed patients lasix/diuretics breathe O2 digitalis bronchodilator

Role of the aorta and arteries

transport blood under high pressure

What is considered significant in up-sloping and horizontal/down-sloping ST depressions?

up-sloping 1.5 mm horizontal and down-sloping 1 mm

How does laminar flow determine velocity of blood?

velocity in the center of the vessel is greater than that toward the outer edge, creating parabolic profile

What is the major determinant for cardiac output?

venous return (frank-starling)

What determines preload?

venous tone and intravascular volume

What happens during the t wave?

ventricular repolarization (Phase 3)

When is the current of injury called the diastolic current of injury?

when it occurs when the cardiac muscle is in a polarized state

When is the current of injury called the systolic current of injury?

when it occurs while the cardiac muscle is depolarizing or repolarizing

When does elevation of the ST segment disappear?

when the myocardium is completely depolarized (diastolic) or repolarized (systolic) pending when the current of injury occurred

How will the cardiac volume loop appear with an increase in stroke volume?

wider, slightly taller pressure volume loop due to increased filling

At what potential should the ST segment and TP segment be?

zero potential- aka isoelectric