Physio

Non pacemaker cells

Stable resting potential; prolonged depolarization sustained by Ca++ influx

Cardiac output (CO)
- % distribution of blood?

CO LV = CO RV (in steady state)

- distributed among various organs via parallel arteries
25% --> GI
25% --> MSK
25% --> renal
15% --> cerebral
5% --> coronary
5% --> skin

Cardiac arrhythmias
- 3 causes

caused by altered impulse formation, altered impulse conduction, or both altered impulse conduction /formation.

Heart failure
- caused by

caused by defects in mechanical component (pump not functioning)

Ectopic foci
- results from

when other cells become pacemakers
- can be due to disease --> if they fire faster than the SA node ==> rapid abnormal heart rate
- can also be slow (ex. Purkinje fibers can fire APs but heart will beat much slower)

Tachyarrhythmia
- results in:

blood pressure can not be maintained → syncope, sudden death

Cardiomyocyte
- structure/features

striated, + by AP, troponin, involuntary, intercalated discs & gap junctions

Effect of hyperkalemia on heart rate

- Decrease HR
high extracellular K+ depolarizes the cell & decreases the full activation of funny channels

Electrical activity in cardiac cells
- What is it?
- How is it transmitted?

movement of ions & current flow
- transmitted to neighboring cells via intercalated disks

AV node conduction velocity

Slowest of the pacemakers which allows for ventricular filling
~ 0.5 m/s

AV bundle

only tissue continuous between atria and ventricles (everywhere else surrounded by fibrous tissue)

Beta blockers affect on heart rate

Decrease heart rate

Non pacemaker cells

________: Stable resting potential; prolonged depolarization sustained by Ca++ influx.

Steady state

CO= VR
- Cardiac output of LV= cardiac output of RV
- Venous return equal in L and R heart

AV fibrous tissue function

barrier between atria & ventricles
- acts as insulator (prevents passage of impulse between them except through AV bundle)

Venous return (VR) in study state

VR of L heart = VR of R heart in steady state

Arterioles

come off arteries
- blood pressure regulation

Pacemaker cells
- Resting potential
- Comparison to cardiac muscle

- Unstable resting potentials
- More negative than cardiac muscle
- Spontaneous depolarization/repolarization

Non-pacemaker cells
- Resting potential

Stable resting potential
Prolonged depolarization sustained by Ca++ influx

SANS effect on HR

NE → + B1 adrenergic R (Gs/GPCR)→ increase cAMP
- Increased HR, increased rate of conduction through AV node

PANS effect on HR

ACh → +M2 receptors (Gi/GPCR) → decrease cAMP 2 effects
1. decrease HCN → decrease Na+ influx & rate of phase 4 depolarization

2. decrease Ca+ channel phosphorylation → less Ca+ → AP threshold moves away from Vm

OVERALL: decreased HR, decreased rate of conduction through AV node

Anti-arrhythmic drugs mechanism of action

can block Na+, K+, or Ca++ channels

Excitation-contraction coupling in cardiac muscle

Calcium mediated calcium release (Ca++ enters via L type VG Ca++ channels → triggers release of Ca++ from SR → muscle contraction)

Tachyarrhythmia

blood pressure can not be maintained → syncope, sudden death

Physiologic basis for conduction

local currents & gap junctions

Purkinje system conduction velocity

1.5 to 4 m/sec
Fastest!
- gap junctions
- syncytium (ventricular muscle mass contracts together)

Electrical component

regulates timing of mechanical component

AV nodal blocks

most clinically significant heart block (conduction block can also occur @ Bundle of His or at left or right bundle branches)

Pulmonary veins
- number
- pathway

4 (2 from each lung) --> bring oxygenated blood from the lungs to the LA

Pulmonary arteries
- number
- pathway

2; deoxygenated blood travels from right ventricle through the pulmonary semilunar valve into the lungs

Capillaries
- features

where venules & arterioles meet
- single endothelial cell thick
- site of substance exchange
-very high surface area

Passive mechanisms which maintain Em

1. Permeability of K+ >>> Na+ at rest (more K+ channels)
2. K+ concentration gradient
3. Non diffusible intracellular anions from negatively charged proteins

Active mechanisms which maintain Em

Na+-K+-ATPase

SA node
- Intrinsic rate
- Em

60-100 BPM
-55 to -60 mV

NATIVE PACEMAKER --> overdrive suppression

Intrinsic rate of:
AV node

40-60 BPM

Intrinsic rate of:
Bundle of His

40 BPM

Intrinsic rate of:
Purkinje fibers

15-20 BPM

Non pacemaker cell action potential phases

0: Rapid depolarization (VG Na+ open & Na+ influx)
1: Initial repolarization (VG Na+ channels inactivate & K(to) open w/ K+ efflux)
2: Plateau (VG Ca++ open & Ca++ influx) --> ventricles contract
3: Repolarization (VG K+ open, K+ efflux)
4: Rest: outward K+ current

What is responsible for the plateau & why is it important?

- Phase 2: VG calcium channel opens and calcium enters the cell
- Ventricles contract

Pacemaker cells action potential phases

4: Diastolic/spontaneous depolarization: Cation (typically Na+) influx via funny channels
0: Slow depolarization: VG Ca++ channels, Ca++ influx
3: Repolarization: K+ efflux ==> Maximum diastolic potential (-65 mV)

Effect on HR:
Beta adrenergic agonists

Increase HR

Effect on HR:
Beta adrenergic antagonists

Decrease HR

Effect on HR:
Hyperthyroidism

(Elevated T3, T4)
Increase HR

Effect on HR:
Hypothyroidism

(decreased T3, T4)
Decrease HR

Effect on HR:
Catecholamines

Epinephrine primary one
- Increase HR

Effect on HR:
Digoxin

Decreases HR, but makes it pump harder

Propagation & spread of heart cell depolarization

1. Ca++ triggers contraction: spreads through intercalated disks & connexons
2. Excitation-contraction coupling
--> calcium mediated Ca++ release ==> contracted sarcomere

Bradyarrhythmia

- Death of a pacemaker
Blood pressure cannot be maintained --> sudden death

Types of tachyarrhythmia

- V tach
- V fib
- Torsades de pointes

Intercalated disks contain:

- Gap junctions
- Connexins (channels formed by proteins in gap junctions)
- Desmosomes (firm mechanical attachments)

Myocyte conduction pathway

SA node --> Atria --> AV node --> Bundle of His --> Purkinje fibers --> Ventricles

Conduction through the atria

- Ends of SA node fibers --> directly connect w/ surrounding atrial muscle fibers
- Velocity: 0.3 m/s
- Some fibers are faster & are located in the internodal pathways & interatrial band to the left atrium

Conduction through the AV node

AV DELAY = allow for ventricular filling & coronary circulation
- occurs due to decreasing number of gap junctions (increases resistance to flow of ions)
- approx. 0.16 seconds between origin in SA node before traveling to Bundle of His

Conduction through the Bundle of His

Delay of 0.4 seconds
- AV bundle: only tissue continuous between atria & ventricles

Conduction through ventricles

Rapid conduction thanks to gap junctions & Purkinje system
Once impulse reaches the end of the Purkinje fibers --> must travel through the ventricular muscle mass & slows down to 0.3 - 0.5 m/s

Types of cardiac arrhythmias

- Re-entry/circus movements
- Conduction blocks
- Accessory pathways

Circus movements

Re-entry movements - type of arrhythmia

Normal tissue:
Purkinje twig splits into 2 --> AP traveling down each branch (can cancel each other out in the middle)

Diseased tissue: retrograde impulse can travel through diseased/weak tissue & re-excite the tissue

Causes of conduction block

- Ischemia
- Scarred tissue (disease)
- Refractory tissue (disease)

Drug treatment for conduction delay & mechanism:
symptomatic bradycardia

Atropine can treat symptomatic bradycardia
- block ACh @ M2 receptors on nodal tissues

ECG:
P wave

Atrial depolarization

ECG:
PR interval

atria contract, AV node excitation
** AV delay

ECG:
QRS complex

Ventricular depolarization & atrial repolarization
- pushing blood out of the heart

ECG:
QT interval

Covers the:
QRS complex - ventricular depolarization
ST segment - start of ventricular repolarization

ECG:
ST segment

- Correlates w/ phase 2
- Ventricles contracting & emptying (depolarized) = isoelectric
Start of ventricular repolarization

ECG:
T wave

Ventricular repolarization

ECG:
TP interval

Ventricles relaxing & filling

Cardiac cycle

see photo

1st degree AV block

- Delayed conduction thru AV
- Still sinus rhythm

ECG: prolonged PR interval

2nd degree AV block

Some AP do not proceed to ventricles --> ventricular bradycardia
Mobitz type 1: Progressive PR + dropped beats
Mobitz type 2: Fixed PR + dropped beats
* can be treated w/ antiarrhythmics

3rd degree AV block

- P > QRS
- complete dissociation between atria & ventricles
- latent pacemakers (Purkinje fibers) could take over --> ventricular bradycardia

Ventricular depolarization sequence

1. depolarization of the heart from left to right in septum (small negative deflection ~ Q)
2. depolarization towards apex of the heart (~ R upstroke)
3. depolarization of the left ventricle (back to baseline, R downstroke )

MEA

mean electrical axis; net vector of depolarization

effect of ventricular mass on deflection size

larger mass --> larger deflection

LVH on EKG

larger amplitudes

EKG
- U wave

only seen in pathology
ex. could be seen in hypokalemia

Normal intervals:
P wave

0.08 - 0.10 seconds

Normal intervals:
PR interval

0.12 - 0.20 seconds

Normal intervals:
QRS

0.06 - 0.10 seconds

Normal intervals:
QTc

QT/square root of RR
less than or equal to 0.44 seconds

Bipolar standard limb leads

Leads I, II, III

Unipolar augmented leads

aVR, aVL, aVF

unipolar chest leads
& placement

V1-V6
V1 R 4th IC space
V2 L 4th IC space
V4 mid clavicular line 5th IC
V6 mid axillary line 5th IC

Lateral leads
& coronary circulation

I, aVL, V5, V6
LCx

Inferior leads
& coronary circulation

II, III, aVF
RCA and/or LCx

Anterior leads
& coronary circulation

V3, V4
LAD

Septal leads
& coronary circulation

V1, V2
LAD

Normal intervals
MEA of:
- aVR

P = negative
QRS = negative, exaggerated R
T = inverted

Normal intervals
MEA of:
- aVL

P = small
QRS = biphasic
T = normal

Normal intervals
MEA of:
- aVF

P = normal
QRS = positive, exaggerated R, small S
T = normal

MEA moves __ hypertrophy

MEA moves towards hypertrophy

MEA moves __ heart attack

MEA moves away from heart attack

Rhythms which lack a P wave

Atrial fibrillation
Atrial flutter
Sinus arrest with escape rhythm

EKG characteristics of:
Atrial fibrillation

Lacking P wave
Atrial fibrillatory waves
Decreased amplitude & increased frequency

EKG characteristics of:
Atrial flutter

Saw tooth pattern
Coarse fibrillatory waves
Irreg. irreg.

EKG characteristics of:
Sinus arrest w/ escape rhythm

retrograde atrial stimulation
P and QRS synchronized
- Small QRS & no P
Bradycardia

Ventricular problems on EKG

PVC
V tach
V fib

STEMI
- ST segment corresponds with which phase of AP

Stage 3
transmural infarct involving the entire wall thickness of a ventricular region --> ischemic tissue becomes depolarized because of its inability to maintain normal ion gradients across the cell membranes