PNB 2775 Quiz 2: Cardio/Heart

Heart function

- blood circulates/delivers nutrients/removes waste

- need pressure to flow! resistance --> pump

- our blood must function as 2 pumps for 2 capillary beds

Pericardium

dense connective tissue surrounding the heart, fluid filled

fibrous pericardium

serous pericardium:

- visceral (lined directly on heart)

- parietal (outer membrane associated with fibrous)

- gap between visceral and parietal holds fluid

function of pericardium

- support heart/large vessels

- lubrication

- mechanical barrier to infection

cardiac tamponade

increase in pericardial fluid (pericarditis or hemorrhage)

- interferes with filling of heart, specifically compressing RA during diastole

- causes decreased venous return and SV

- TX includes needle to drain fluid

- leaky capillaries/increased fluid/inflammation/buildup causes pressure

Heart Wall

Epicardium (outer) - visceral pericardium

Myocardium (middle) - muscle tissue

Endocardium (inner) - endothelial cells

Coronary Circulation

- coronary arteries

- aortic sinuous

- elastic rebound

- cardiac veins drain into coronary sinus which opens into R Atrium

Coronary Artery Disease

coronary ischemia caused by atherosclerotic plaque

- plaque embedded into smooth muscle covered by endothelium which increases chronic inflammation

- TX: diet, exercise, drugs (vasodilators), Ca2+ channel blockers, surgery

Heart Skeleton

Consists of plate of fibrous connective tissue between atria and ventricles

Fibrous rings around valves to support

Serves as electrical insulation between atria and ventricles

Provides site for muscle attachment

Source of Ca2+ for cardiac vs skeletal muscle

Skeletal source: source is intracellular from SR

Cardiac source: source is extracellular -- T/L channels allow Ca2+ to flow in cell from action potential

Intercalated Disks (Intercellular Junctions)

1) Fascia Adherens and Desmosomes: structural components; myofibrils continue across muscle ignoring cell boundaries

3) Gap Junctions: low resistance electrical connections between myocytes allows for synchronized contraction

Channel Types

Voltage-gated: open or close in response to membrane potential changes

Ligand-gated: open or close in response to agonist binding

Background channels: important determinants in RMP (neither ligand nor voltage)

Conducting System

SA and AV nodes, bundle branches, purkinje fibers

Pacemaker potential

a spontaneously occurring graded potential change that occurs in certain specialized cells (cardiac conductive)

What contributes to the pacemaker potential?

- activation of HCN channels

- activation of Ca2+ channels

- inactivation of K+ channels

- Ca2+ leak from SR and activation of Na+/Ca2+ exchanger

--> Ca2+ clock hypothesis

Action Potential Steps (Pacemaker)

1) Threshold (-40mV)

- activate voltage dependent Ca2+ channels

2) Peak (20mV)

- open K+ channels

- inactivate T-type Ca2+ channels

3) Repolarization

- outward K+ current

Source Sink Mismatch

- avoided through upregulation of Na+ channels, higher conduction gap-junctions

Internodal Pathway

1. Stimulus spreads across contractile cells of L/R atrium by cell-cell contact.

2. Also activates cells in AV node which relay impulse through non-conducting 'heart skeleton' to ventricles.

3. Preferred path through interatrial septum called Bachmann's Bundle.

4. provides 50 msec delay time for atria to contract.

Pacemaker Problems

- theoretical max is 300-400 bpm but CO drops at 180 bpm

- Damage to SA node: AV node can keep heart going at 40-60 bpm

- Damage to both nodes: purkinje fibers can keep heart beating at 20-40 bpm

Lethal Injection

Ischemia --> increase extracellular K+ --> decrease gradient --> depolarizing cell rapid/random --> sodium/calcium channels become blocked --> stops action potentials

Cardiac Myocyte Action Potential

0. Fast Na+ channel (sodium flows in!)

1. Transient K+ channel (K+ flows out!)

2. Ca2+ and K+ channels offset each other (plateau phase)

3. K+ channels open and continue to repolarize (K+ flows out)

4. fully repolarized at rest (K+ flows out still)

Refractory periods prevent...

summation of contractions --> tetanus

defibrillator works to...

pause everything at once (absolute refractory period!) help restabilize heart rhythms

absolute refractory period exists because...

Na+ inactivation will not be removed until cells are hyperpolarized

Why do P and T waves deflect on an ECG in the same direction despite being electrically opposite events?

The way the bipolar leads are make it so that depolarization towards a positive lead results in a positive deflection, and repolarization towards a negative lead also results in a positive deflection, so it just depends on the placement of the leads in an ECG.

ECG basic anomalies

bradycardia

tachycardia

AV Heart Block, no electrical connection between atria/ventricles

long PR interval, P and QRS no longer coordinated (purkinje keeps it going)

Long QT syndrome

caused by loss of K+ channels or increase in Na+ channels

Atrial Fibrillation

ventricles can depolarize but uncoordinated

Ventricular fibrillation

erratic uncoordinated depolarization --> cardiac arrest

Hyperacute T-Wave

increase in extracellular potassium --> linked to early warning sign on ECG of impending MI

Pressure Volume Cycle

1. Late Diastole

- both sets of chambers are relaxed and ventricles fill passively.

2. Atrial Systole

- atrial contraction forces a small amount of additional blood into ventricles.

3. Isovolumetric Ventricular Contraction

- First phase of ventricular contraction pushes AV valves closed but doesn't create enough pressure to open semilunar valves.

4. Ventricular Ejection

- As ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected.

5. Isovolumic Ventricular Relaxation

- As ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves/snaps them shut.

Stroke Volume

Amount of blood ejected from ventricles (SV)

Ejection Fraction

SV/EDV is the percentage of filled ventricle that was ejected; usually 60%

End Systolic Volume

Amount of blood remaining in ventricle at the end of V systole (ESV)

Sympathetic Activity increases

contractility!

Increase in afterload/hypertension causes....

increase in ESV --> decrease SV --> stretching

Heart rate variability is...

good! less variability could indicate a health complication

Hypertension causes...

- enlarged heart

- heart failure

- aneurysms

- hardening of arteries (MI/stroke/kidney failure)

Heart failure (left vs right)

Left - pulmonary congestion/edema

Right - peripheral edema

When pressure in the R Atria drops below zero...

you cannot increase cardiac output without a supplemental increase in venous return

Preload

degree of ventricle stretching during diastole

Frank-Starling Principle

sarcomere has optimal length, stretching increases contractile force by increasing affinity of troponin for Ca2+

Factors that increase preload

- increase in venous blood volume/venous return

- increase in ventricular compliance

- increase in venous pressure/ decrease in venous compliance

- decrease in HR

Afterload

force that must be produced to pump blood into the aorta

How do Ca2+ channel blockers treat hypertension?

Ca2+ channel blockers decrease contractility which decreases afterload

Autonomic Innervation

Sympathetic - cardiac nerve, norepinephrine

Parasympathetic - vagus nerve, achytelcholine

Gi