CM - Cardiovascular A&P - The Heart (Pavlick)

How does the heart get perfused with oxygenated blood?

*Aortic pressure* generated by the heart facilitates perfusion. On Wiggers diagram, it is indicated by the *dichrotic notch*.

What is another name for the *staircase effect*? What is this phenomenon?

*Bowditch staircase* or *treppe* Increased HR increases the force of contraction in a stepwise fashion as the intracellular Ca2+ increases cumulatively over several beats.

___ binds to ___, resulting in ___ being moved out of the way, removing he inhibition of ___ & ___ binding

*Ca+2* binds to *troponin C*, resulting in *tropomyosin* being moved out of the way, removing the inhibition of *actin* and *myosin* binding

What does cardiac contraction absolutely require during the action potential plateau phase?

*Ca2+ influx* through L-type Ca2+ channels

What is an *emergent* complication of pericardial effusion?

*Cardiac Tamponade* Risk of death depends on speed of diagnosis, treatment provided, and underlying cause.

What can happen when a person with Infective Endocarditis has a vegetation that fragments?

*Distal embolization*... can occur almost anywhere and can result in septic infarcts in the brain or other organs.

What is the calculation for *ejection fraction*?

*EJ = SV / EDV x 100%* Where EJ is ejection fraction, SV is stroke volume, and EDV is end diastolic volume.

What happens once blood is ejected (Wiggers Diagram)?

*Entering back into isovolumetric ventricular relaxation* LVP falls below aortic pressure and the aortic semilunar valve shuts; second heart sound produced. Aortic pressure falls as blood runs off to the arteries. T wave produced (repolarization of ventricles). Volume of blood remaining in left ventricle after ejection is ESV.

Frequency of Ischemic Heart Disease (IHD) is increased in what population of patients with a certain syndrome?

*Metabolic syndrome*: - central (truncal) obesity - atherogenic lipid patterns - HTN - insulin resistance (Type 2 DM)

What causes Angina and MIs?

*Myocardial ischemia* commonly as a result of atherosclerosis.

Contrast a Negative Dromotropic effect and a Positive Dromotropic effect.

*Negative - decreases conduction velocity* through the AV node, slowing the conduction of action potentials from the atria to the ventricles and *increasing the PR interval* *Positive - increases conduction velocity* through the AV node, speeding the conduction of action potentials from the atria to the ventricles and *decreasing the PR interval*

What is one way to remove excess fluid from the pericardial sac when someone has a cardiac tamponade?

*Pericardiocentesis* Using a needle to removed the fluid by approaching in subxiphoid or parasternal approach.

What are the first two branches off the aorta? Where do they originate?

*Right Coronary Artery* and *Left Coronary Artery* Originate at the root of the aorta behind the cusps of the aortic valve.

Which node is the pacemaker?

*Sinoatrial (SA) node* located in the right atrium near the entrance of the superior vena cava.

Differentiate the different components of skeletal muscle vs cardiac muscle. A. Striation B. Voluntary or Involuntary muscle C. Thick and Thin filaments D. Sarcoplasmic Reticulum density E. Mitochondria F. Intercalated Disks

*Skeletal Muscle*: A. Striated B. Voluntary C. Thick and Thin filaments D. Sarcoplasmic Reticulum - more dense E. Mitochondria - many F. Intercalated Disks - none *Cardiac Muscle*: A. Striated B. Involuntary muscle C. Thick and Thin filaments D. Sarcoplasmic Reticulum - less dense E. Mitochondria - tremendously numerous F. Intercalated Disks

What are the 2 patterns of myocardial ischemic necrosis?

*Transmural infarction*: entire ventricular wall from endocardium to epicardium *Subendocardial infarction*: limited to the interior 1/3 of the wall of the ventricle

What are the *most common congenital* cardiac abnormalities?

*Ventricular septal defects* Found in 30-60% of all newborns with a congenital heart defect, or about 2-6 per 1000 births. *Can be acquired* a few days post MI due to macrophage remodeling of dead heart tissue before scar tissue forms.

Endocardium

*innermost* layer of the heart - lines inner chambers, valves, chordae tendineae, and papillary muscles

Myocardium

*middle layer* of the heart - *cardiac muscle* - responsible for *pumping action* - *NOT* capable of regeneration (hyperplasia) - is capable of hypertrophy

First heart sound (S1)

- associated w/ closure of *tricuspid* and *mitral (AV) valves* - often referred to as "*lub*" in "lub-dup"

Second heart sound (S2)

- associated with closure of *pulmonic* and *aortic (semilunar) valves* - "*Dup*" in "lub-dup"

Tricuspid valve

- lies between right atrium and right ventricle - consists of three separate leaflets - larger in diameter and thinner than mitral valve

What are some examples of "excitable" cells?

- neurons - muscle cells (skeletal, cardiac, & smooth) electrical potential differences across biological membranes are the basis of the electrical activity of excitable cells

Mitral (Bicuspid) Valve

- only two cusps - lies between left atrium and left ventricle

What two factors are normally, independently present in development of infective endocarditis?

-*A damaged endocardial surface* (presence of valvular disease, prosthetic heart valves, or congenital heart defects provide an environment conducive to bacterial growth) -*A portal of entry by which the organism gains access to the vasculature* (URI, dental procedure, skin lesion, etc.)

What are the complications that may occur post-MI?

-*Arrhythmia*: MCC of death in first several hours -*Myocardial (pump) failure*: lead to CHF and/or shock. likelyhood and severity determined by size and location of lesion. -*Myocardial rupture*: occurs w/in first 4-7 days and may result in death from cardiac tamponade, compression of the heart by hemorrhage into pericardial space. -*ruptured papillary muscle* -*mural thrombosis*: thrombus formation on the endocardium overlying infarct

From where does the right atrium receive blood?

-*Superior Vena Cava*: blood supply from upper body -*Inferior Vena Cava*: blood supply from lower body -*Coronary Sinus*: blood supply from heart

What is the purpose of calcium entering the cardiac muscle cell during an action potential?

-*does not* promote actin-myosin interaction -*induces calcium release* from the sarcoplasmic reticulum (calcium-induced calcium release = CICR), which promotes actin-myosin interaction and contraction via *Ryanodine receptors (RyR2)*

Excluding the autonomic nervous system and hormones, what other factors affect heart rate?

-Age -Gender -Physical fitness -Electrolyte levels -body temperature

What 3 proteins make up the cardiac troponin complex?

-Cardiac troponin C (cTnC) -Cardiac troponin I (cTnI) -Cardiac troponin T (cTnT) T = tropomyosin binding I = inhibitory C = calcium binding

How does the PNS have negative chronotropic effects on the heart?

-Decreases HR by decreasing rate of phase 4 depolarization -fewer action potentials occur per unit time because the threshold potential is reached more slowly, and therefore, less frequently -"main" mechanism is decrease I-f, the inward Na+ current that is responsible for phase 4 depolarization of the SA node.

What factors affect stroke volume?

-Preload (via Frank-Starling mechanism) -Inotropism (cardiac contractility) -Afterload

Where do the sympathetic nerves innervate on the heart? Which neurotransmitter and receptors are involved?

-SA node -AV node -atria -ventricles *Norepinephrine (NE)* act on *B1-receptors*.

Where does the parasympathetic vagus nerve innervate on the heart? Which neurotransmitter and receptors are involved?

-SA node -atria -AV node *Acetylcholine (ACh)* act on *Muscarinic receptors*. Ventricles are not innervated by the parasympathetic vagus nerve.

What key features are in both skeletal and cardiac muscle cells?

-Sarcolemma -T-tubules -Sarcoplasmic reticulum -Terminal cisternae -Mitochondria -Myofibrills -Sarcomeres

What cardiac markers might be elevated when there is cardiac cell death?

-Troponin I -CK-MB -Myoglobin

What are components of the cardiac muscle cell?

-cylindrical branching cells -single central nucleus -intercalated discs

How does the PNS have negative dromotropic effects on the heart?

-decreases conduction velocity through the AV node -action potentials are conducted more slowly from atria to the ventricles -increases PR interval

What are the heart valves function(s)?

-ensure blood flow in one direction through the heart chambers -prevent backflow (*regurgitation*) of blood

How does the SNS have positive chronotropic effects on the heart?

-increases HR by *increasing rate of phase 4 depolarization* -more action potentials occur per unit time b/c threshold potential is reached more quickly and more frequently -*mechanism is increase I-f*, the inward Na+ current that is responsible for phase 4 depolarization in the SA node

How does the SNS have positive dromotropic effects on the heart?

-increases conduction velocity through the AV node -action potentials are conducted more rapidly from the atria to the ventricles, and ventricular filling may be compromised -decreases the PR interval

In Ischemic Heart Disease, what physiological factors cause an increased cardiac demand.

-myocardial hypertrophy -overcoming excessive preload -overcoming excessive afterload

What are 2 normal factors that influence coronary resistance?

-neural (ANS) -metabolic (adenosine, O2, CO2, K+, H+)

What type of cells are excitable and can have electrical potential differences?

-neurons -muscle cells (skeletal, cardiac, & smooth) -cardiac conduction system cells

Who are susceptible to Infective endocarditis?

-people w/ pre-existing heart lesions like *Rheumatic Heart Disease* -*IV drug abusers*: in 75% of IVDA IE, no underlying valvular abnormalities are noted.

What happens during Phase 3 of the Slow Response Cardiac Action Potentials?

-repolarization -caused by an increase in K+ conductance; increase results in outward K+ current that causes repolarization of membrane potential

When does Troponin I and Troponin T rise and peak after injury?

-rise 2-6 hours after injury -peak 12-24 hours after injury They can remain elevated for many days.

What happens during Phase 4 of the Slow Response Cardiac Action Potentials?

-slow depolarization -accounts for automaticity (pacemaker activity of SA node) -caused by increase in Na+ conductance, which results in an inward current called I-f - I-f is "turned on" by repolarization of the membrane potential during the preceding action potential

What happens during Phase 0 of the Slow Response Cardiac Action Potentials?

-upstroke of AP -caused by increase in Ca2+ conductance -ionic basis for phase 0 in SA node is very different from that in ventricles, atria, purkinje fibers (where it is the results of an inward Na+ current)

Describe the pathophysiology of the heart when there is *pericardial effusion*.

1. Fluid around heart compresses heart wall 2. Heart can't expand to fill. 3. Backup into systemic circulation. 4. Decreased blood flow to lungs. 5. Decreased output to body

What are the 2 mechanisms of SNS stimulation via B1-receptors to increase the force of contraction?

1. Increases inward Ca2+ current during the plateau phase of each cardiac action potential 2. Increases the activity of the SERCA pumps; as a result, more Ca2+ is accumulated by the SR and thus more Ca2+ is available for release in subsequent beats.

1. How does an increased afterload affect stroke volume? 2. How does a decreased afterload affect stroke volume?

1. It decreases stroke volume because the ventricle must pump blood against a higher pressure. 2. It increases stroke volume because the ventricle pumps blood against a lower pressure.

1. How does vasoconstriction affect blood flow? 2. How does vasodilation affect blood flow?

1. It increases resistance causing flow decreases. 2. It decreases resistance causing flow increases.

What are the 2 types of cardiac action potentials?

1. Non-pacemaker / "Fast Response" - undergo rapid depolarization - occur in atria, ventricles, and purkinje fibers 2. Pacemaker / "Slow Response" - undergo slow depolarizatin - occur in the SA & AV node

How do the following neurotransmitters alter calcium conductance? 1. Norepinephrine 2. Ca2+ Channel Blockers 3. Beta blockers

1. Norepinephrine increases conductance 2. Ca2+ Channel Blockers decrease conductance 3. Beta blockers decrease conductance

In the following categories, what etiologies can lead to heart failure? 1. Pressure overload 2. Volume overload 3. Loss of Myocardial tissue 4. Decreased Cardiac Contractility 5. Diminished filling

1. Pressure overload: -pulmonary hypertension -systemic hypertension 2. Volume overload: -valvular insufficiency 3. Loss of Myocardial tissue: -acute coronary syndromes 4. Decreased Cardiac Contractility: -cardiomyopathies -myocarditis 5. Diminished filling -pericarditis -cardiac tamponade

What are the 3 phases of Ventricular Filling?

1. Rapid Passive Filling 2. Slow Passive Filling (diastasis) 3. Atrial Systole

What 2 factors does the amount of Ca2+ released from the sarcoplasmic reticulum depend on?

1. Size of inward Ca2+ current during plateau of myocardial action potential [*CICR = calcium induced calcium release* via ryanodine receptors (RyR)] 2. Amount of Ca2+ previously stored in sarcoplasmic reticulum for release

What occurs during *rapid ventricular ejection*?

1. The left ventricle develops enough pressure such that LVP exceeds aortic pressure. 2. Aortic semilunar valve opens and blood is ejected 3. both aortic pressure rises (aortic distension) and Left ventricular pressure continues to rise also (contraction continues).

What happens during isovolumetric ventricular contraction?

1. The left ventricle must *first* be depolarized (QRS complex occurs right before IVC) 2. Ventricles contract and LV pressure steadily rises (aortic valve is still closed); *no ejection of blood occurs* as left ventricular volume remains constant due to all valves being closed.

What are the common sites of coronary artery occlusion?

1. anterior interventricular (IV) branch 2. right coronary artery 3. circumflex branch 4. left coronary artery 5. posterior interventricular branch 6. marginal artery

The heart has parasympathetic innervation via which; 1. nerve 2. neurotransmitter 3. receptor

1. vagus nerve 2. acethylcholine (Ach) 3. muscarinic receptors

How many electrodes are used in a 12-lead EKG? How many precordial leads? How many limb leads?

10 total electrodes, but 12 total views: 6 precordial/chest leads give views V1-V6 4 limb leads give views I, II, III, aVL, aVF, and aVR

What are the 4 major valves of the heart?

2 AV Valves: - Tricuspid (right) - Bicuspid/Mitral (left) 2 Semilunar Valves: - Pulmonic (right) - Aortic (left)

What is a lead on an EKG?

A lead is a particular view of electrical activity of the heart.

What is inotropism?

A modification of cardiac contractility. An increase in cardiac contractility is an increase in contractile strength that is independent of Starling's law. Ex of why the red line in the picture has increased contractility: -the heart has more norepinephrine so it contracts more forcefully -SNS can stimulate the heart to contract independent of volume of blood in ventricle

What is cardiac systole?

A period of contraction and emptying. Atrial systole and ventricular systole

What is Diastole?

A period of relaxation and filling. Atrial diastole and ventricular diastole

What is PTCA?

A revascularization technique PTCA = percutaneous transluminal coronary angioplasty

What is a *CABG*?

A revascularization technique that bypasses the blocked coronary artery with a graft. Grafts used to come from *Saphenous vein*, but now comes from internal mammary arteries.

What is a stent?

A revascularization technique that places a device permanently in the blocked vessel to keep it open.

What is the difference between a 12-lead EKG and a Rhythm Strip?

A rhythm strip is a recording of only 1 lead for a longer period of time.

Characterize the following factors that contribute to the physiology of decreased cardiac supply. A. Hemodynamic factors B. Cardiac factors C. Hematologic factors

A. Hemodynamic factors -increased resistance in coronary arteries (ex: atherosclerotic occlusion) -hypotension B. Cardiac factors -valve disease -increased heart rate C. Hematologic factors -anemias -poisons

What are the 2 main branches of the: A. Right Coronary Artery B. Left Coronary Artery

A. Right Coronary Artery: 1. right marginal (acute) artery 2. posterior descending (interventricular) artery B. Left Coronary Artery: 1. circumflex artery 2. left anterior descending (interventricular) artery

Lies b/n right atrium and right ventricle. Which valve is it? A. Tricuspid B. Bicuspid C. Pulmonic D. Aortic

A. Tricuspid

For the following hormones, describe where they originate and how they affect heart rate. A. Epinephrine/NE B. T3 and T4

A. from adrenal medulla; similar effects as SNS, tend to be important during exercise, stress, and excitement B. thyroid hormones; can elevate HR at rest

How much of the cardiac output goes to the heart?

About 5% of the resting cardiac output goes to the heart.

What protein(s) make up *thin filaments*?

Actin, tropomyosin, and troponin

What happens at the beginning of *isovolumetric ventricular relaxation*?

All 4 chambers of the heart are relaxed and all of its valves are closed. Ventricular volume is constant; ventricular pressure is decreasing. Left atrium is filling with blood that has returned to it via the pulmonary veins; atrial pressure is rising.

What does it mean to have an atrial septal defect?

An interatrial septum that fails to develop properly.

What is the *key difference* between Angina and Myocardial Infarction?

Angina: -*no cell death* -supply and O2 demand equalizes before permanent damage MI: -*cell death* due to O2 supply and demand mismatch for an extended period of time. Myocardial tissue becomes hypoxic. -can result in death of pt

How can you tell Angina chest pain from MI chest pain?

Angina: -related to exertion, emotion, eating, or cold -usually short-lived and relieved by nitroglycerin MI: -spontaneously occurring -long-lasting -not relieved w/ nitroglycerin

Which X-ray test uses a special dye and camera (fluoroscopy) to take pictures of the blood flow in an artery (such as the aorta) or a vein (such as the vena cava)?

Angriogram

What does the tip of the left ventricle form?

Apex

What is the most common cause of death in the first several hours following a cardiac infarction?

Arrhythmia

Has two cusps that look like a bishop's headdress. Which valve is it? A. Tricuspid B. Mitral C. Pulmonic D. Aortic

B. Mitral aka *Bi*cuspid

Where is the heart located in terms of the sternum?

Behind the sternum, b/n the lungs 2/3 of the heart is left of midline of the sternum.

What type of angina occurs during rest or with minimal exercise and frequently occurs nocturnally? A. Classic angina B. Exertional angina C. Variant angina D. Prinzmetal's angina E. Vasospastic angina F. Unstable angina G.Pre-infarction angina

C. Variant angina D. Prinzmetal's angina E. Vasospastic angina These are all the same. Caused by spasms, mostly in the presence of coronary artery stenosis. Many cases are unpredictable and the mechanism is uncertain.

Which cardiac markers were preferred for detecting myocardial cell injury before the introduction of cardiac troponins?

CK-MB isoenzyme False-positive elevations may occur due to existence of isoenzyme in skeletal muscle. Elevations may be due to trauma, heavy exertion, or myopathy.

The stretch of ventricular myocardium by greater ventricular filling (Starling's law) may enhance the affinity of Troponin C for ______ and also may increase _____ uptake and release from the SR.

Ca2+ These effects increase developed force and contribute to increase in contraction when cardiac muscle fiber length increases.

Which cardiac markers are preferred for detecting myocardial cell injury?

Cardiac troponins

What are Dromotropic effects?

Changes in *conduction velocity*, primarily in the AV node.

What is the triad of manifestation of acute pericarditis?

Chest pain Friction rub ECG changes

Dichrotic notch

Closure of the aortic valve causes a brief rise in aortic pressure as backflowing blood rebounds off the closed valve cusps - significant in relation to coronary blood flow

What drug toxicities can cause myocarditis?

Cocaine and Amphetamines

In general, what is the cardiac cycle?

Complex, coordinated sequence of *mechanical* and *electrical* events that repeats with every heartbeat - At a heart rate of 75 beats/min, each cardiac cycle lasts 0.8 seconds

If you have a stroke volume of 88 mL, which is half of the end diastolic volume, what is the Ejection Fraction?

EF = 88/176 x 100% = 50%

Calculate Ejection Fraction from the below data: SV = 95 ml/beat HR = 90 bpm CO = 8.55 L/min VR = 8.55 L/min EDV = 130 ml ESV = 35 ml

EF = SV/EDV x 100 EF = (95/130) x 100 = 73%

What is the End Diastolic Volume of the ventricles? How much is normally ejected?

Each ventricle holds about 150 mL. They eject about 70-80 mL.

What happens during Phase 1 of the Fast Response Cardiac Action Potentials?

Early/Initial Repolarization: -transient outward current as K+ channels open -"Fast" Na+ channels close

What is the *ST interval* of an EKG?

End of QRS complex to end of T wave

Point 2: Aortic Valve opens

End of isovolumetric ventricular contraction and beginning of left ventricular ejection

Point 4: Mitral Valve opens

End of isovolumetric ventricular relaxation and beginning of left ventricular filling

Point 3: Aortic Valve Closes (S2)

End of left ventricular ejection (ESV) and beginning of isovolumetric ventricular relaxation

Point 1: Mitral Valve Closes (S1)

End of left ventricular filling (EDV) and beginning of isovolumetric ventricular contraction

What is the *ST segment* of an EKG?

End of the QRS complex to the onset of the T wave

What effect do the following factors have on cardiac output? - increased preload - increased inotropy - increased heart rate - decreased afterload

Enhanced performance/increased cardiac output

What is another name for Visceral Pericardium?

Epicardium

What is *angina pectoris*?

Episodic chest pain caused by inadequate oxygenation of the myocardium. *There is no cell death*.

What type of angina is considered a clinical syndrome of myocardial ischemia that falls b/n stable angina and myocardial infarction? Why does it occur? A. Classic angina B. Exertional angina C. Variant angina D. Prinzmetal's angina E. Vasospastic angina F. Unstable angina G.Pre-infarction angina

F. Unstable angina G.Pre-infarction angina They are the same. Results from atherosclerotic plaque disruption. High propensity to lead to infarction.

When end diastolic volume is reached, what does contractility directly correlate with?

For a given EDV, contractility correlates directly with *the intracellular Ca2+ concentration*.

How does heart rate relate to the SA node?

Heart rate is the number of times the SA node "discharges" per minute.

Cardiac contractibility is proportional to what?

ICF Ca+2

What causes cardiac ischemic heart disease?

Imbalance b/w supply and demand of oxygen. In disease state: demand > supply

What is a life-threatening condition that affects the *endocardial surface* of the heart, including the heart valves?

Infective Endocarditis (Bacterial Endocarditis)

What is myocarditis?

Inflammation of the heart muscle and conduction system without evidence of MI. - wide range of clinical presentations - causes; viral (#1), drug toxicity, autoimmune, idiopathic, etc.

What separates the right and left atria?

Interatrial septum

What separates the right and left ventricles?

Interventricular septum

What is homeometric regulation?

Intrinsic mechanisms controlling the strength of ventricular contractions that are *independent of the length of myocardial fibers* at the end of diastole.

How does the SNS affect contractility?

It has a *positive inotropic effect* on the heart causing an increase in SV at a constant preload. This type of regulation of SV is *homometric regulation*.

Describe the *pericardial space or cavity*.

It is b/n the parietal and visceral pericardial layers. Contains ~10 mL of fluid that acts as lubricant, preventing friction and cooling heart (heart creates heat as it contracts) as the heart beats.

What is the dichrotic notch? What's its significance?

It is the *measure of back pressure* seen on Wigger's diagram *after the Aortic Valve closes*. This back pressure helps to *facilitate coronary blood flow (CBF)*.

What is *stroke volume*?

It is the amount of blood pumped out by the left ventricle at contraction. About 70-80 mL.

What does it mean to be a *latent* pacemaker? Which heart parts act as latent pacemakers?

It means that it will take over for the SA node if it is suppressed, sometimes even override the SA node. The AV node, Bundle of His, and Purkinje fibers are all latent pacemakers.

What is the parietal pericardium?

It's the rough outer layer of the pericardial sac.

What happens during Phase 3 of the Fast Response Cardiac Action Potentials?

Late or Final Repolarization: - continual efflux of K+ through several types of K+ channels - L-type Ca2+ channels eventually close

Identify the following leads with their corresponding electrode placements on a Basic 3-Lead Electrocardiogram. Lead I Lead II Lead III

Lead *I* --> *l*eft arm (LA) and right arm (RA) Lead *II* --> *l*eft *l*eg and right arm Lead *III* --> *l*eft arm and *l*eft *l*eg

What happens at the end of isovolumetric ventricular relaxation?

Left atrial pressure (LAP) exceeds left ventricular pressure (LVP), resulting in opening of the mitral valve. Ventricular filling ensues.

What are the approximate dimensions of the heart? Length Width Thickness General size

Length: 5 inches (12 cm) long Width: 3.5 inches (9 cm) wide Thickness: 2.5 inches (6 cm) thick About the size of the owner's fist.

Which heart valve is most frequently involved in Infective Endocarditis?

Mitral valve

What protein makes up *thick filaments*?

Myosin

Thick vs. Thin filaments

Myosin --> thick filaments Actin, Tropomyosin, & Troponin --> thin filaments

What are Nitroglycerin tablets used for?

Nitrodilators are used to decrease afterload, thereby decreasing myocardial oxygen demand.

Are cardiac isoforms present in the blood of health people?

No, they are very specific for cardiac injury.

What are the 2 types of cardiac action potentials?

Non-pacemaker or "Fast Response" action potentials: -occur in *atria, ventricles, and purkinje fibers* -"rapid" depolarization Pacemaker or "Slow Response" action potentials: -occur in *SA node and AV node* -"slow" depolarization

How does the inefficiency of Na+ - Ca2+ membrane exchanger (NCX) at higher heart rates affect contractility?

Not as much calcium will be pumped out and will therefore increase stores in the cell.

When is S4 heard?

Not audible in normal adults. May be heard late in diastole in a pt w/ ventricular hypertrophy, where ventricular compliance is decreased.

What is the *PR interval* of an EKG?

Onset of P wave to middle of QRS complex.

What is the *QT interval* of an EKG?

Onset of QRS complex to end of T wave

Trace the flow of oxygenated blood through the left heart.

Oxygenated blood leaves the lungs and enters the left atrium via the pulmonary veins --> mitral valve to the left ventricle --> aortic valve to the aorta --> cardiac and systemic circulation

Permanent anatomical close of the foramen ovale occurs with time in normal infants; failure to close results in a __________?

Permanent anatomical close of the foramen ovale occurs with time in normal infants; failure to close results in a *patent foramen ovale*.

What happens during Phase 2 of the Fast Response Cardiac Action Potentials?

Plateau Phase: -long-lasting (L-type) Ca2+ channels open leading to inward calcium movement -efflux of K+ through several types of K+ channels

What are the 2 major variables that affect blood flow?

Pressure and resistance The *major influence on resistance is the radius* of the artery.

What structures make up the anterior surface of the heart?

Primarily the right ventricle

When a previously healthy young person dies suddenly of heart failure, what is the suspected cause?

Primary Cardiomyopathies In autopsy, they usually have cardiomegaly.

Where is conduction velocity the fastest?

Purkinje system

What is Ohm's Law?

Q (blood flow) = (change in Pressure) / resistance

What is End Diastolic Volume (EDV)?

Quantity of blood remaining in either ventricle at the end of ventricular diastole. Average = 130 ml

What is End Systolic Volume (ESV)?

Quantity of blood remaining in either ventricle at the end of ventricular systole.

What is venous return (VR)?

Quantity of blood returned to the heart per minute. Normally, this equals CO.

What happens during Phase 0 of the Fast Response Cardiac Action Potentials?

Rapid depolarization: -upstroke of the action potential -"fast" Na+ channels open -several K+ channels close

What is conduction velocity?

Reflects the time required for excitation to spread throughout cardiac tissue.

When Ca2+ is reaccumulated by the sarcoplasmic reticulum and moved from ICF to ECF, what happens in the cardiac muscle cell?

Relaxation occurs

What happens during Phase 4 of the Fast Response Cardiac Action Potentials?

Resting Membrane Potential (RMP): - K+ channels remain open - Calcium extrusion mechanisms become highly active

Which cardiac cell receptors are the major mediators for Calcium-Induced Calcium Release (CICR)?

Ryanodine Receptors (*RyR2*) -major mediator for sarcoplasmic release of stored calcium ions

Which heart sound is associated with the closure of the AV valves?

S1 of the first heart sound. Often called *Lub* in "Lub-Dup".

Which heart sound is associated with the closure of the semilunar valves?

S2 or the second heart sound. Often called *Dup* in "Lub-Dup".

Trace the flow of cardiac conduction.

SA Node --> internodal tracts --> AV node --> AV bundle (bundle of His) --> R/L bundle branches --> purkinje fibers SA Node --> interatrial tracts

What are the main ways Calcium Extrusion (returning back to where it came from) occurs?

Sarcoplasmic reticulum (SR) Ca2+ pumps (SERCA) Sarcolemmal Ca2+ pumps 3Na+/Ca2+ exchangers (NCX)

Which vertebrae contain the sympathetic branch that innervates the SA node, atria, AV node, and ventricles of the heart?

T1-T4

Where is the base of the heart?

TOP of the heart, at the level of the 2nd costal cartilages.

What is the danger of Primary Cardiomyopathies?

The *onset is silent*, and symptoms do not occur until the disease is well advanced. May be detected with physical activity particularly in athletes.

What does *Sinus* mean in terms of a Normal Sinus Rhythm?

The SA Node is in charge leading conduction signals.

What is SA node automaticity?

The ability of the SA node to spontaneously initiate its own depolarization without neural input. The SA node has very unstable RMPs and no sustained plateau.

Why can't we/don't we measure cardiac action potentials?

The appearance of cardiac action potentials depends on where it is measured. We would need to measure every individual cardiac cell.

Skeletal muscle cells are independent of one another both structurally and functionally. What allows for cardiac muscles to work together?

The plasma membranes of adjacent cardiac muscle cells interlock at dark-staining junctions called *intercalated discs*.

What do the papillary muscles do?

They are anchors for the AV valves. They help keep the valves opened or closed when they need to be. However, they *do not cause* the valves to open or close.

How is myocardial disease different from cardiovascular disease? What are the 2 major forms of myocardial disease?

They are disorders that originate within the myocardium (heart muscle) not vasculature. 2 Major Forms: *myocarditis* & *primary cardiomyopathies*

What are the "heart strings" of the heart and what do they do?

They are the *chordae tendineae*, and they attach the AV valves to the papillary muscles, serving as anchors.

Describe the shape and function of semilunar valves.

They have 3 half-moon cusps that prevent backflow from the aorta and pulmonary arteries into the ventricles during ventricular diastole.

Why is conduction velocity slowest in the AV node?

This allows time for ventricular filling, as seen on EKG as PR interval.

What would limit the effects of treppe on cardiac contractility?

Time that it takes to fill the ventricles. If heart rate goes above maximum heart rate (~210/220 bpm), HR is increasing contractility, but there is not sufficient time for ventricles to fill up.

What is the *PQ segment* of an EKG?

Time when the impulse is traveling through the AV node, bundle of His, and bundle branches

Which troponin subforms are distinct and have immunoassays that can differentiate skeletal muscle cells and cardiac muscle cells?

TnI and TnT. There are no structural differences for TnC.

What causes heart murmurs?

Valvular regurgitation

What is the quickest way to decrease afterload?

Vasodilation

What ventricular defect can be acquired after a myocardial infarction?

Ventricular Septal Defect (VSD)

What happens if conduction of velocity in the AV node is increased?

Ventricular filling may be compromised.

When does valvular regurgitation/incompetence/insufficiency occur?

When a valve does not close properly -- frequently results in backflow of blood.

When does valvular stenosis occur?

When a valve does not open properly.

When is S3 heard?

When blood flows rapidly from the atria to the ventricles. Normal in children, but *abnormal* in adults. In middle-aged or older adults, S3 indicates volume overload, as in congestive heart failure or advanced mitral or tricuspid regurgitation.

When might you want treppe/staircase effect of cardiac contractility?

When you are exercising you want calcium to build up so you can have increase contractility.

What is the *Frank-Starling Law of the Heart*?

Within limits, the more the ventricles are filled during diastole, the more blood they will eject during systole (i.e. the greater the preload, the greater the force of contraction) - based on the length-tension relationship in the ventricle

How can changes in heart rate be reflected on an ECG?

You will see changes in the R-R intervals

Pericardial effusion

accumulation of excess fluid (exudate) in the pericardial sac

Epicardium

aka *Visceral Pericardium* - external layer - includes blood capillaries, lymph capillaries, nerve fibers, and *epicardial fat*

What is a *myocardial infarction*?

aka Heart Attack Ischemic death of myocardial tissue. - Usually results from rupture or fissuring of atherosclerotic plaque.

Cardiac Tamponade

an increase in pericardial sac pressure caused by an accumulation of fluid or blood in the pericardial sac, resulting in reduced ventricular filling and subsequent hemodynamic compromise MEDICAL EMERGENCY

Myocyte

cardiac muscle cell

Trace the flow of deoxygenated blood through the right heart.

deoxygenated blood enters the right atrium --> tricuspid valve to the right ventricle --> pulmonic valve to the pulmonary trunk --> right and left lung pulmonary arteries to the capillaries

What is the *P wave* of an EKG?

depolarization of the atria

What is the *QRS complex* of an EKG?

depolarization of the ventricles

What are the 3 layers of the heart? i. Innermost ii. Middle iii. Outmost

i. Innermost --> endocardium; lines inner chambers, valves, chordae tendineae, and papillary muscles ii. Middle --> myocardium; pumping action, not capable of regeneration (hyperplasia), is capable of hypertrophy iii. Outmost --> epicardium; aka visceral pericardium, blood capillaries, lymph capillaries, nerve fibers, and epicardial fat

What are characteristics of the heart with Infective Endocarditis?

large, soft, friable, easily detached vegetations consisting of fibrin and intermeshed inflammatory cells and bacteria. May cause ulceration, often w/ perforation, of valve cusps or rupture of one of the chordae tendineae.

Infective Endocarditis (Bacterial Endocarditis)

life-threatening condition of the endocardial surface of the heart, including the heart valves

What must the heart overcome in order to pump blood?

must contract forcefully and overcome *aortic* and *pulmonary pressures* in order to pump blood LVP > AP RVP > PP

What must the right & left ventricles overcome in order to pump blood to the lungs and into the systemic circulation?

must contract forcefully and overcome aortic and pulmonary pressures in order to pump blood

What is the *T wave* of an EKG?

repolarization of the ventricles

What is the resting and maximum cardiac output volume per min?

rest - 5L/min max - 20-25L/min HR x SV = CO

What is the resting and maximum heart rate per minute?

rest - 72 beats/min max - 230 beats/min

What is the resting and maximum stroke volume per beat?

resting - 70 ml/beat maximum - 120 ml/beat

What is the #1 job of the heart?

to maintain cardiac output (CO) so that there is adequate perfusion of all body tissues

Characterize Acute Pericarditis. 1. What does acute mean? 2. Etiology 3. Manifestations

1. Acute inflammation of the pericardium that is *< 2 weeks*. 2. *Infectious* (viral, bacterial, or fungal), but can be autoimmune diseases (ex: RA, SLE), trauma, drug toxicity 3. Triad of *chest pain* (abrupt, precordial, sharp), *friction rub* (rubbing and friction b/n inflamed pericardial surfaces), and *ECG changes*.

Characterize *Left-Sided Heart Failure*. 1. Definition 2. Forward effects 3. Backward effects

1. Definition: left ventricle is mechanically overloaded (aortic stenosis) or weakened (post MI) develop dyspnea and orthopnea as a result of pulmonary congestion/edema. 2. Forward effects --> decrease CO -fatigue -weakness -faint pulses -decreased mentation -decreased GFR 3. Backward effects --> decreased ejection fraction --> increased LV volume --> increased LA volume --> increased pulmonary capillary volume --> pulmonary edema -dyspnea -exertional dyspnea -cough -congestion -cyanosis

Characterize *Right-Sided Heart Failure*. 1. Definition 2. Forward effects 3. Backward effects

1. Definition: right ventricular overload (pulmonary valve stenosis or pulmonary HTN). symptoms resulting from pulmonary congestion such as orthopnea are less common, and *systemic edema and venous distention are more prominent*. 2. Forward effects --> decrease CO -fatigue -weakness -faint pulses -decreased mentation -decreased GFR 3. Backward effects --> decrease ejection fraction --> increased RV volume --> increased RA volume --> increased systemic venous volume and pressure --> systemic edema -hepatomegaly -splenomegaly -ascites (abdominal edema) -peripheral edema -jugular vein distention *no edema in lungs*

1. What are *chronotropic effects*? 2. Negative chronotropic effect 3. Positive chronotropic effect

1. Effects on the heart rate. 2. Decreases heart rate by decreasing firing rate of SA node. 3. Increases heart rate by increasing firing rate of SA node. changes in HR are reflected on the ECG by changes in the R-R intervals

Where is conduction velocity: A. Fastest B. Slowest

A. Fastest in Purkinje system B. Slowest in AV node (seen as PR interval on EKG), allowing time for ventricular filling before ventricular contraction.

What is *heterometric regulation*?

A type of control of Stroke Volume. Intrinsic regulation of the strength of cardiac contraction as a function of diastolic fiber length (volume), independent of afterload, autonomic nerves and other extrinsic influences. Associated w/ Frank-Starling law of the heart.

What are the Intrinsic Firing Rates (impulses/min) of the following locations? A. Sinoatrial node B. Atrioventricular node C. Bundle of His D. Purkinje fibers

A. 70-80 B. 40-60 C. 40 D. 15-20 These can vary from person to person.

What type of Angina is associated with atherosclerotic disease that produces fixed obstruction of the coronary arteries? A. Classic angina B. Exertional angina C. Variant angina D. Prinzmetal's angina E. Vasospastic angina F. Unstable angina G.Pre-infarction angina

A. Classic angina B. Exertional angina They are the same and considered *stable anginas*. Occurs with exertion or stress. Pain is usually precipitated by situations that increase the work demands of the heart.

Describe the *rapid passive filling* phase of ventricular filling.

Blood flows quickly through the mitral valve and into the relaxed ventricle; ventricular volume increases. No muscle contraction occurs. Ventricular pressure remains low, b/c it is still relaxed and compliant. *High compliance* means that volume can be added to it without changing pressure.

Describe the *slow passive filling* phase of ventricular filling.

Blood flows through the mitral valve and into the relaxed ventricle; ventricular volume continues to increase. No muscle contraction occurs.

What effect do the following factors have on cardiac output? - decreased preload - decreased inotropy - decreased heart rate - increased afterload

Depressed cardiac output

What is the *fossa ovalis*?

Depression in the interatrial septum; remnants of foramen ovale.

What makes a heart valve open or close?

Differences in pressure.

What are Primary Cardiomyopathies?

Diseases of the heart muscle that are non-inflammatory and are not associated with HTN, congenital heart disease, valvular disease, or CAD.

What is different about the "plateau phase" of the cardiac muscle excitation-contraction coupling step that does not happen in skeletal muscle cells?

During the "plateau phase" of this action potential, Ca2+ channels open and *Ca2+ enters the cell from the ECF*. Skeletal muscle does not require influx through L-type Ca2+ channels.

Which pathogens often cause Infective/Bacterial Endocarditis?

Staphylococcus and Streptococcus species

On the Ventricular Pressure-Volume Loop -- What does the width between point 4 and point 1 represent?

Stroke Volume

Describe the *atrial systole* phase of ventricular filling.

The left atrium must *first* be depolarized (p wave occurs just before atrial systole). Atria contract. Contribution of atrial contraction to ventricular filling is usually small, *approx. 10-15%* of total ventricular volume. After atrial systole, LVP > LAP and the mitral valve shuts; first heart sound produced. Volume of blood left in the ventricle is EDV.

What is preload?

The load or stretch on the ventricular cardiac muscle *before* it contracts. It is directly influenced by end diastolic volume. Effects are confirmed by Frank-Starling law of the heart.

What is afterload?

The load the heart must overcome during and after contraction. AKA *Back Pressure* exerted on the aortic and pulmonary semilunar valves.

What would happen on the Ventricular Pressure-Volume Loop if there was an increased contractility?

The loop with increase in width towards the left and grow taller.

What would happen on the Ventricular Pressure-Volume Loop if there was an increased preload?

The loop would shift to the right on the x-axis.

What would happen on the Ventricular Pressure-Volume Loop if there was an increased afterload?

The loop would shrink in width towards the right and grow taller.

The magnitude of the tension that develops is proportional to ________.

The magnitude of the tension that develops is proportional to *ICF [Ca2+]*.

Which AV valve is thinner and bigger in diameter?

Tricuspid valve