Cardiac A & P & P (& P)

Or Cardiac Physiology,
Pathophysiology, and some
Pharmacology

Hugh Jarrard, PhD, NREMT-P

 Objectives for this Lecture
• To understand:

– External/Internal Anatomy of the heart

– CO and Influencing Factors
• Including heart rate, EDV, contractility
– Cardiac Impulse conduction
• Source and path, channels and ionic currents
– Controlling the Heart
• Autonomic n.s., Pharmacological Classes
– Cardiovascular Disease (CAD)
• What it is, what it does, why we get it, how many of us have it
– Role of Paramedic as a Patient Advocate

• Pages: Pulled from Brady Vol 3: Ch 1,2

– Website: http://www.cvphysiology.com/
http://www.cvpharmacology.com/
 Gross Anatomy
• Location in Chest
– Inferior wall, parallel to diaphragm
– Anterior wall, parallel to chest wall
– Apex points to left hip
• No muscular attachment
– Hangs from the aorta
• Implications for rapid deceleration
– Cardiac contusion, aortic dissection
• Encased in the pericardium
• Implications for bleeding
– Cardiac tamponade
http://www.med.yale.edu/intmed/cardio/imaging/anatomy/coronal_section/index.html
Gross Anatomy

6
 Myocyte Diversity

• 3 types of cardiac muscle

– intermediate sized
• strongly contractile, bulk of heart
– small
• weakly contractile, auto-rhythmic, slow AP
conduction
– large
• weakly contractile, specialized for fast electrical
conduction
 Differential in Pressures . . . Why?
• 2 – stage pump
– Right heart
• Low pressure,
mean ~14 mmHg
• ventricle 3-4 mm
thick
– Left heart
• High pressure,
mean ~ 90 mmHg

• Implications?
– Pulmonary hypertension: R heart works harder, enlarges (cor pulmonare)
– Systemic hypertension: L heart works harder, enlarges (LVH)
 Pressure-Volume Relationships
• Things to note:
– pressure in left >> right
ventricle
• systemic vs. pulmonary

– aortic pressure >> atrial

– atrial contraction makes

small contribution to
ventricle filling
• but remember Starling
Mechanism

– ventricle pressure >>

aortic (transiently)
• higher pressure opens
semilunar valve allowing
blood to enter aorta
 Homeostasis: Maintaining Cardiac
Output
HR X SV = CO
beats/min ml/beat ml/min

Rest: 75 70 5250
EDV - ESV
end-diastolic volume –
end-systolic volume
Basically, amt of blood in the ventricle before and
after it contracts!
 Stroke Volume (SV)
• Is determined by 3 variables:
– End diastolic volume (EDV) = volume of blood in ventricles
at end of diastole
• Or, how full ventricles are before contraction
• More full = more stretch = more preload

– Total peripheral resistance (TPR) = impedance to blood flow

in arteries
• Afterload, right? force to overcome during contraction

– Contractility = strength of ventricular contraction

• Modified by amt of stretch and inputs to the heart
• remember Frank-Starling? ↑ stretch = ↑ force of contraction
14-9
Fig 14.5
14-14
14-45
Fig 14.20

14-46
Electrical Impulse
Pathway
• SA node  Atria
– atria contract

• AV node
– delay mechanism

• Bundle of His (R & L)

 purkinje fibers in
ventricles
– ventricles contract
– occurs as near single
event http://www.heart-valve-
• (due to speed of Bundle surgery.com/Images/cardiac-conduction-
system.jpg
of His)
 Pacing of the Heart

SA NODE
Purkinje Fibers 60 – 100 bpm
30 – 40 bpm AV NODE
40 - 60 bpm

Reduced CO Reduced CO Normal CO

 Action Potentials of the Heart
• Autorhythmic cells: AP self-generating
– due to unstable resting membrane potential
– membrane depolarization due to Ca2+ influx
• Contractile cells: AP generated by cation leak through gap
junctions
– Stable resting potential
– membrane depolarization due to Na+ influx
– Ca2+ influx at peak prolongs contraction
 Cardiac Muscle Trigger:
Pacemaker Cells
• Small, weakly contractile specialized cells
– initiate AP in neighboring cells through gap
junctions
– present in SA (sinoatrial) and AV (atrioventricular)
nodes
 SA, AV Pacemaker Action Potential
onsists of 3 Phases:
• Phase 4: Spontaneous Depolarization
– Na+ channels allow leak in (slow), Na+ in, cell
reaches threshold (-40 mV)
• Phase 0: Full depolarization
– Ca2+ channels open and Ca2+ rushes in (slow),
cell fully depolarized, Ca2+ channels close
• Phase 3: Repolarization
– K+ channels open, K+ out, cell repolarizes
– Na+ / K + - ATPase reestablishes gradients
 Contractile Cell APs
• AP spreads along membrane of muscle cell
– descends T tubule to cause contraction
– cytosol depolarization also enters next cell through
gap junctions
 Contractile Cell Action Potential
onsists of 4 Phases:
• Phase 4: Stable Resting Potential
– Open K+ channels ( - out, cell kept negative)
– Ca2+ enters from neighboring cell (+ in),
threshold reached
• Phase 0: Full depolarization
– Na+ channels open (+ in fast), cell fully
depolarized, Na+ channels close, slow Ca2+
channels start opening (+ in  plateau)
• Phase 1: Initial Repolarization
– Na+ channels close, K+ channels open (+ out)
• Phase 2: Calcium Plateau
– slow Ca2+ channels fully open (+ in)
• Phase 3: Repolarization
– slow Ca2+ channels close
– K+ channels open (+ out), cell repolarizes
– Na+ / K + - ATPase reestablishes gradients
(hi Na out, hi K in)

http://www.mfi.ku.dk/ppaulev/chapter11/images/11-2.jpg
 Points from last slide:
• Calcium influx (at plateau) aids contraction of
myocyte
– helps trigger contractile machinery
• Effective Refractory Period (a.k.a. absolute)
prevents additional APs from causing
contraction
– Essentially it limits the frequency of depolarization
and therefore heart rate

http://www.cvphysiology.com/
Arrhythmias/A006.htm
 Can a non-pacemaker become a
pacemaker cell?
• Under certain pathological conditions, YES!

• If a cell becomes hypoxic, the membrane depolarizes

• Think of it: less ATP, reduced function of Na+/K+ ATPase, less membrane
potential
• This closes fast Na+ channels (at –50 mV, all are inactivated)
• APs can still be elicited, but the inward current are carried by slow inward
Ca2+ channels
• APs then resemble those found in SA and AV nodes
• can sometimes display spontaneous depolarization and automaticity
– mechanism behind certain types of ectopic beats and arrhythmias
– as in ischemic heart disease and following myocardial infarction
 One other period of concern . .
• a.k.a. “Vulnerable Period”
• Coincides with the middle & terminal
phases of the T-wave (last part of phase
3 and the first part of phase 4)
• During this period the heart is particularly
susceptible to the induction of VF by an
electrical stimulus

• During Cardioversion . . .
– When an electrical current used to
depolarize all abnormal pacemakers thus
allowing the SA node to resume initiation
of the heart rhythm.
• the impulse is synchronized with the R
wave of the ECG to avoid the ‘vulnerable
period’ of ventricular repolarization

• What if stimulus does occur?

http://www.perfusion.com.au/CCP/Biomedical%20electronics/biomed/Vulnerable%20period.htm
Lake Oswego, Oct 15, 2008
• Lets take a break . . .
 Controlling the Heart: Neural
Influences
• The SA node has an intrinsic rate
• Actually 100-110 action potentials ("beats") / min
• Rate strongly influenced by autonomic nerves
• Vagus nerve dominant over sympathetic influences at
rest
• This "vagal tone" brings the resting heart rate down to
60-80 beats/minute

http://www.cvphysi
ology.com/Arrhyth
mias/A005.htm
 Too much tone?

• Syncope
– Due to
bradycardia?
– Too much
vagal tone . . .
or other
etiology?
 Neural Mechanism: Autonomic
N.S.
• Heart receives
extensive innervation
from parasympathetic
and sympathetic
nervous systems
– parasympath. releases
____, slows HR

– sympath. releases
____, increases HR,
• also increased
contractility  increased
SV http://www.colorado.edu/intphys/Class/
IPHY3430-200/012cardiovascular.htm
14-8
 Control of Heart Function: Rate
Parasympathetic:
• ACh – slows heart rate
– SA node: increases interval between
pacemaker APs
– AV node: slows pacemaker signal passage to
ventricles
– MECHANISM: increases permeability to K+,
leaks out, cells hyperpolarize (more negative),
less likely to fire AP
Sympathetic:
• Norepinephrine (and Epinephrine) – speed
heart rate and force of contraction
– SA node: increases rate of pacemaker APs
– AV node: speeds signal passage
– MECHANISM: decreases resting K+ flow out,
increases slow inward Ca++ and Na+
– Cell spontaneously depolarizes more quickly
(slope of phase 4 increased)

– Myogenic effect: increases strength of

contraction in all heart muscle
Controlling the Heart: Other Influences

• Hormones affect heart rate:

– hyperthyroidism  tachycardia
– hypothyroidism  bradycardia
– Circulating epinephrine  sympathetic effects

• Serum ion concentrations affect rate:

– Hyperkalemia  bradycardia or SA node arrest
– Hypokalemia  tachycardia (↑ rate of phase 4 depolarization)

• Cellular hypoxia
– Cellular hypoxia depolarizes the membrane potential 
bradycardia, SA node arrest
 Treating a Bad Heart: Arrythmias
• Arrythmias may • Drugs act on
be due to: channels and can:
– altered rate – - / + conduction
• brady, tachy velocity
– alter excitability by
– premature beats changing duration of
• Caused by ectopic refractory period
foci – suppress abnormal
automaticity
– altered conduction
• Blocks in
conduction
– Or influence
system sympathetic input
 Na+ . . . Slow Down!
• Effects on depolarization

• Sodium-channel blockers
– block the fast sodium channels that are
responsible for the rapid depolarization
(phase 0)
• non-nodal, cardiomyocytes
• Decrease slope and amplitude of AP
• have no direct effect on nodal tissue
– Main effect: Decreases conduction velocity
in non-nodal tissue (atrial and ventricular
muscle, purkinje conducting system)

• Ex. Lidocaine
– Used for VT, PVCs
 K+ . . . Slow Down!
• Effects on action potentials: repolarization

• Potassium-channel blockers
– block the potassium channels responsible for phase 3
repolarization
– slows repolarization, increasing AP duration / refractory period
– cell less excitable
• Useful in quieting tachyarrhythmias caused by reentry
mechanisms
– Reentry occurs when an AP enters normal tissue when tissue
able to fire
– New premature AP is generated and a circular, repeating pattern
of early activation can develop, which leads to a tachycardia

• Ex. Amiodarone
– We use it for severe supraventricular and ventricular arrhythmias
 Ca++ . . . Slow down and
more!
• Effects on Vascular Smooth Muscle, Myocardial Force
Generation, Rate, and Conduction Velocity!

• Calcium Channel Blockers:

• Block channels located on the vascular smooth muscle,
cardiac myocytes, and cardiac nodal tissue (SA, AV
nodes)
– regulate influx of calcium into muscle cells, which in turn
stimulates smooth muscle contraction and cardiac myocyte
contraction.
• In nodal tissue
– channels create pacemaker currents and phase 0 of AP

• By blocking calcium entry into the cell:

  vascular smooth muscle relaxation (vasodilation)
  decreased myocardial force generation
  decreased heart rate
 decreased conduction velocity within the heart (AV node)

• Ex. Diltiazem (Cardizem), Verapamil

– We use to control rapid ventricular rates assoc. with a-fib, a-
flutter, and SVT
 And Lastly . . .
• Effects Reducing Sympathetic
Stimulation

• Beta-blockers
– Block action of norepinephrine at
Beta-1 sites in the heart
– cause decreases in heart rate,
contractility, and conduction velocity

– also reduce vasoconstriction leading

to reduced BP

• Ex. Metoprolol
– We don’t give it, but many of our pts
are on it for HTN, angina, or
arrythmias
The Final Stretch . . .
Dying of a Broken Heart?
 Deaths from CV Disease, 2006
Coronary Heart
Disease
Coronary Heart
14 Disease
Stroke
7 4 14 Stroke
7 4
HF*
Heart Failure*
HF*
7
52 High Blood
7 High Blood Pressure
17 Pressure
52 Diseases
Diseases of the
of the
Arteries
Arteries
17
Other
Other

Percentage breakdown of deaths from cardiovascular diseases

(United States: 2006 preliminary)
* - Not a true underlying cause. Source: NCHS and NHLBI.
 What is Coronary Heart (Artery)
Disease?
• CAD reduces coronary blood flow and
oxygen delivery to the myocardium.
– leads to myocardial hypoxia and impaired
function
– Can lead to infarction

– Plaque buildup due to:

• Fat / Cholesterol deposits
• Calcium deposits

http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_All.html
 Process of Clot Formation
1. abnormal deposition of lipids in the vessel wall
2. leukocyte infiltration and vascular inflammation
3. plaque formation
4. thickening of the vessel wall

http://www
.nia.nih.go
v/HealthIn
formation/
Publicatio
ns/AgingH
eartsandA
rteries/cha
pter04.ht
m
 Supersize those fries, please!
• A coronary artery plaque . . .

Original
diameter
of vessel

http://www.uphs.u
penn.edu/news/Ne
ws_Releases/jan0
7/MTP-inhibition-
reduce-high-
cholesterol-
photo.htm
 Coronary
Circulation
• Coronary arteries
– Arise from aortic
root
– Fill during diastole
– Flow is due to
diastolic
backpressure
– Located in the
epicardium, small
capillaries into the
pericardium
– No oxygenation
from ventricle

https://www.clevelandclinic.org/heartcenter/pub/guide/heartworks/coronaryartery.htm
Territorial Supply of Coronary Arteries

http://www.med.yale.edu/intmed/cardio/echo_atlas/references/myocardial_segs1.html
 A Simpler View . . .
• Using 12-lead ECG, we can determine
regions that are ischemic  infarcted
• Remember inferior, septal, anterior, lateral (ISAL)
• Inferior? Check for R-sided MI
 CHD, What are the Risk Factors?
The More you Have, the Higher your Risk:

• Unhealthy blood cholesterol levels.

– high LDL cholesterol (bad) and low HDL cholesterol (good).
• High blood pressure.
– At or over 140/90 mmHg consistently?
• Smoking
– Damages/tightens blood vessels, raises cholesterol levels, and raises blood pressure.
– also induces hypoxia
• Insulin resistance  hyperglycemia
• Diabetes
• Overweight or obesity.
• Metabolic syndrome.
– group of risk factors  increased CHD, diabetes, and stroke.
– Symptoms include: central/abdominal obesity (spare tire), HTN, High triglycerides (a type of
blood fat), Insulin resistance, Low HDL ("good") cholesterol

• Lack of physical activity.

• Age.
– In men, the risk for CAD increases after age 45.
– In women, the risk for CAD risk increases after age 55.
• Family history of early heart disease
– Increased risk if father / brother was diagnosed with CAD before 55 years of age
– or if mother/ sister diagnosed with CAD before 65 years of age
 Adult Obesity in Last 40 yrs
40
34
Percent of Population

30.2
30
26
20.6
20 17.1
15.7 16.8
10.7 12.2 12.8

10

0
Men Women

1960-62 1971-74 1976-80 1988-94 2001-2004

Age-adjusted prevalence of obesity in Adults ages 20-74 by sex

and survey. (NHES, 1960-62; NHANES, 1971-74, 1976-80, 1988-
94 and 2001-2004). Source: Health, United States, 2007. NCHS.
Note: Obesity is defined as a BMI of 30.0 or higher.
 Child Obesity by Race, 2007
24 21.4
20 17.9
Percent of Population

18.3
16.6
15.7
16
12.8
12

0
Ma le s Fe m a le s

N H W h ite s N H B la cks H is p a n ics

Prevalence of overweight among students in grades 9-12 by

race/ethnicity and sex (YRBS: 2007). Source: MMWR. 2008 57:
No. SS-4. BMI 95th percentile or higher by age and sex of the CDC
2000 growth chart. NH – non-Hispanic.
 Physical Activity in Kids
60
48.9
Percent of Population

50

40 34.7

30

20
11.9 10.0
10 3.4 5.4

0
Male Female

6-11 12-15 16-19

Prevalence of children ages 6-19 who attained sufficient

moderate-to-vigorous physical activity to meet public health
recommendations of >60 minutes/day on >5 of 7 days by sex
and age. (NHANES: 2003-04). Source: MSSE 2008;40:181-8.
 Adult Smoking in 2008

Prevalence of current smoking for Adults age 18 and older

by race/ethnicity and sex (NHIS:2006).
Source: MMWR. 2007;56:1157-61. NH – non-Hispanic.
 Youth Smoking in 2008
35
30
Percent of Population

23.8 22.5
25
18.7
20
14.9 14.6
15
8.4
10
5
0
NH Whites NH Blacks Hispanics

Males Females

Prevalence of students in grades 9-12 reporting current cigarette

smoking by race/ethnicity and sex. (YRBS:2007). Source: MMWR.
2008;57:SS04. NH – non-Hispanic.
 Cost of Managing CVD/Stroke
2 0 0
1 6 5 . 4
1 6 0
B illio n s o f D o lla rs

1 2 0

6 8 . 9 7 3 . 4
8 0

3 7 . 2
4 0

0
C o r o n a r y H Se at r r o t k e H y p e r t e n sH i ve ea r t F a ilu r e
D is e a s e D is e a s e

Estimated direct and indirect costs (in billions of dollars) of

major cardiovascular diseases and stroke
(United States: 2009). Source: NHLBI.
 Overall Costs of CVD/Stroke
Cardiovascular 340-459 31 3.8
Digestive System 520-579 2 18 .4
Mental 290-319 1 72.5
Nervous System 320-389 1 72
Injury and Poisoning 800-999 16 6.8
Respiratory System 460-519 1 55 .3
Musculoskeletal system 710-739 1 22 .3
Neoplasms 140-239 99
Genitourinary System 580-629 91 .1
Endocrine System 240-279 85

0 50 100 150 200 250 300 350

Direct Costs of the 10 Leading Diagnostic Groups

(United States: 2009). Source: NHLBI.
 QUESTION . . .
• We are our patient’s advocate
FIRST and ALWAYS . . .

• Should we encourage / pressure

them to make healthy lifestyle
choices?
– Should we be advocates for their
health beyond our call?
• Even if it is something they don’t want to
hear? Is this `self-righteous’?
• What is the balance between `service to
the public’ and `health care
responsibility’?
 One last thing . . . .
Let me know if you need someone to talk to
for review / discussion of material you have
had this term . . .

• hjarrard@gmail.com