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Cardiovascular physiology Flashcards

1
Q

Pericarditis

what does it restrict

What is it caused by?

A

inflammation of the pericardium. Fluid accumulation in pericardial activity

may restrict hearts movement and filling. Results in cardiac tamponade. Heart unable to pump

-viruses, bacteria, fungi

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1
Q

What is the pericardium

Visceral vs Parietal…

What is the pericardial fluid

A
  • Tight constraint around the heart. Tough inelastic sheet covering heart (anchor). Helps adjust bp

Visceral = up against heart
Parietal = surrounding heart

lubricant that allows heart of move freely inside

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2
Q

structure of the heart, what’s on surface?

A

Coronary arteries on surface (LCA and RCA)
- Prevent compression during contraction
- important not in muscle and its on surface of heart

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3
Q

Heart valves job

types of heart valves

A

prevent black flow of blood. Pressure has to be higher in ventricle for atrium to allow flow

  • can never have all 4 open at once. Two max

Atrio-ventricular valves
-Tricuspid (R)
- Mitral (L)

Aortic (L)
Pulmonary (R)

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4
Q

AV valves job

Chordae Tendinae and Papillary muscles role ( only in ventricles)

AV valves are open and closed in….

A

-Prevent back-flow from ventricles back to atria
-Open in Diastolic (filling) (relaxed)

  • Chordae Tendinae anchor AV valves to
    papillary muscle . Prevents back-flow

-As heart contracts, papillary muscle contracts. Control tension on chordae tendinae

-Open in filling (diastole)
-Closed during contraction (systole)

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5
Q

Pulmonary/Aortic valves

Pulmonary/Aortic valves are open and closed in….

A

-prevent backflow from aorta and pulmonary artery back into ventricles
- Open in systole (contraction) (ejection)

-Open during systole (contraction)
-Closed during diastole (relaxation)

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6
Q

Valve problems/heart murmurs

Stenosis

Insufficiency or Regurgitation

Ex: of valve Regurgitation

treat:

A
  • Narrowing of the heart valve leading to faulting opening and decreased ejection. increased HR
  • When should be open there is whistling
  • Faulty closure of valve leading to back flow of blood and decreased forward ejection. leaky valve
  • When should be close there is a whirring/swishing sound
  • due to rheumatic heart disease. auto immune issue if antibiotics are not fully finished

valve replacement

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7
Q

Ventricular torsion

what does it do

A
  • heart untwisting shape
  • allows for more efficient ejection of blood from the heart
    -produces diastolic suction (lower pressure). More efficient filling
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8
Q

Cardiac muscle

Short muscle fibre

Gap junctions

desmosomes

A

Short muscle fibres, gap junctions, desmosomes

-for contraction and relaxation of cardiac muscle

  • allow movement of ions and electrical impulses
  • withstand stress
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9
Q

Types of myocardial/cardiac cells,
-autorhythmic

  • contractile

Action potentials

A

Autorhythmic Cells
-Generates and spreads action potentials
-Pacemaker cells (SA + AV NODE)
-Conducting cells (impulse)

Contractile cells
-99% of cardiac cells
-Mechanical work of contraction and ejection

-Each myocardialcell has a distinct
action potential
-AP’s are initiated at the pacemakers

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10
Q

Nerve electrical excitation

Heart muscle electrical excitation

A

Depolarization -influx of Na+
Repolarization -efflux of K+

-Pacemaker cells
Events:
Na+ influx
Ca++ influx
K+ efflux

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11
Q

Pacemaker potential

Events in pace maker potential
First half

Second half

After threshold reached (rapid depolarization)

After peak (reploarization)

A
  • the slow rise in membrane potential
    (depolarization) prior to an AP in the SA node

Slow depolarization phase of SA node (first half)
-K+ permeability (PK+ )decreases
- Na+ permeability (PNa+) increases due to increased leakiness (slow influx)

Ca++ channels open – voltage sensitive
* Calcium moves in
* Don’t stay open long
pacemaker potential continues to rise toward threshold

L-type (Not T) Ca++ channels open
-Calcium moves in
-rapid depolarization and action potential

-L-type Ca++ channels close
-K+ (rectifier) channels open
-K+ moves out of SA node cells

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12
Q

SA node

Another pace makers:
Av node

Purkinje fibres

A

SA node is autorhythmic
-Self-generated
-events repeat (~ 70 times / minute)

-40 beats / min

~20 beats / min
Ectopic beats (extrasystoles), too excited

-Both are depolarized by SA node before they depolarize themselves
-Av runs the show

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13
Q

Action Potential of the Myocardial
Contractile Cells

Stage 0-1

stage 1-2

stage 2-3

Membrane permeabilities

A

refer to model

Depolarization
Na+ moves in

Plateau
Ca++ moves in
Stays depolarized

Repolarization
K+ moves out

tell us of gates opened or closed

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14
Q

Cardiac Muscle
Excitation-contraction coupling and
relaxation in cardiac muscle

A
  1. AP enters cell
  2. Voltage gated calcium channels open. Ca enters cell
  3. Ca induces Ca release through sarcoplasmic reticulum
  4. Ca binds to troponin to initiate contraction
  5. Relaxation occurs when Ca unbinds
  6. Ca2+ is pumped back into the sarcoplasmic reticulum for storage
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15
Q

Myocardial contractile cells

Refractory period

A
  • Long Refractory period in cardiac muscle
  • Can’t send second AP
  • always get relaxation (filling)

-Long Action potential means long
refractory period
-Prevents tetanus (back flow)

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16
Q

AP: contractile vs autorhythmic myocardium

A

Contractile:
-stable at -90mv
- depolarizes via gap junctions
- Na+ entry in depolarization
-plateau in reploarization
-no hyper polarization
-long ap, long refractory

Autorhythmic:
-unstable pacemaker, -60mv
- Na enters and then Ca+
-Ca+ main AP threshold reacher
- Rapid reploarization
- no hyper polar either (usually)
- can be achieved again

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17
Q

Modulation of heart rate by the sympathetic nervous system

Modulation of Heart Rate by the
Parasympathetic Nervous System

A

Pacemaker cells are more depolarized
-Closer to threshold
-Will reach threshold faster
-Increased heart rate

Hyperpolarizes pacemaker
-Further from threshold
-Takes longer to reach threshold
-Slower heart rate (normal resting condition)

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18
Q

Specialized Conduction System of
Heart

The order in which the electrical signals travel by

A

SA node
Internodal pathway
AV node
Bundle of HIS
-Or AV bundle
-Bundle branches
Purkinje Fibres

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19
Q

what is Electrocardiogram (ECG)

Electrical changes of Atria
Electrical changes of ventricles

Three majors waves of ECG

A

-External recording of electrical events

-Waves of the ECG can be correlated to
specific electrical events

p -> R
R -> T

P-wave
* Atrial depolarization
* Initiates atrial contraction

QRS complex
* Ventricular depolarization
and atrial repolarization
* Initiates ventricular contraction

T-wave
* Ventricular repolarization
* Initiates ventricular relaxation

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20
Q

Conduction of impulses
Stage 1:

Stage 2:

Stage 3:

A

P-wave (atrial Depolarization)
-Initiated in SA node
* Spreads via gap junctions throughout atria
-Initiates atrial contraction
-Impulse moves to AV node
Delay of signal (~100 ms)

QRS Complex (Ventricular Depolarization)
-Impulse moves to Bundle of HIS, to Bundle branches and then to Purkinje fibres
-Initiates ventricular contraction
* Includes atrial repolarization

T-wave (Ventricular repolarization)
-Reversed repolarization wave (from apex)
-Initiates ventricular relaxation

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21
Q

REVIEW SLIDE 65 AND 66

A

very helpful!

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22
Q

ECG leads

A

Simple 3 lead – “Einthoven’s Triangle”

  • also 6 and 12 leads
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23
Q

Abnormalities in rate

sinus rhythm

tachycardia

bradycardia

A

(normal)
* 60 to 120 b/min

Rapid heart rate of more than 100 beats per minute. extra beat
E.g. heart disease, anxiety, fever

low heart rate (less than 60 beats per minute)
* Can be normal in athletes; or abnormal (eg thyroid issue)
-Risk of fainting

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24
abnormalities in rhythm Arrhythmias other examples of arrhythmias PVC (extra beats) Atrial flutter Heart block Ventricular Tachycardia
-can cause sudden death, fainting, heart failure, dizziness, palpitations or no symptoms at all -Causes include hypoxia, caffeine, smoking, alcohol, ectopic excitable cell, damage to conducting path -Premature ventricular contraction - Extra p waves -Impulses from SA node doesn’t reach AV node -Abnormal electrical cycling
25
Atrial fibrillation what is symptoms risks/causes treated by
No organized electrical pattern in atria -No P waves -Can affect ventricular filling -Chest discomfort -Fainting -Risk of clotting * Caffeine, stress, genetics -Electric conversion -Ablation -Anti-coagulants * Risk of clotting
26
PVC
Premature Ventricular Contractions, not usually serious Often caused by ectopic foci -Excitable cells (eg. Some purkinje cells) -Trigger extra beats -Atrial or ventricular Risk factors Stress, sleeplessness Caffeine, medications
27
Supra-ventricular Tachycardia
Abnormally fast heart rhythm -Originating in the atria E.g. Wolff–Parkinson–White syndrome * Extra pathway from atria to ventricle so extra beats -Symptoms include palpitations, fainting, sweating, shortness of breath, or chest pain
28
Heart block what is symptoms risks/causes treated by
Interruption in conduction system -Impulses from atria can’t always reach ventricles -Normal P waves, fewer QRS Fatigue, fainting, chest pain -Aging, heart disease -Stress, caffeine, alcohol -pacemaker
29
Ventricular Fibrillation
Causes include -Arrythmias -Ischemia (heart attack) No organized pattern of depolarization -No organized contraction -No ejection -Leads to death
30
Cardiac cycle slide 79 MUST REVIEW
31
Volumes/ pressures in the heart Thickness in areas of heart - correlates to peak pressures Systole = Contraction Diastole = Relaxation
Aortic pressure = 120/80mmHg Atrial Pressure = 3-10 mm/Hg LV pressure = 3-125 mm/Hg -much more pressure for ejection of blood from heart RV pressure = 2-35mm/Hg
32
Mechanical events 1. Late diastole 2. Atrial systole 3. Isovolumic ventricular contraction 4. Ventricular ejection 5. Isovolumic ventricular relaxation
1. both sets of chambers are relaxed and ventricles fill passively 2. atrial contraction forces a small amount of additional blood into ventricle 3. first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves 4. as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected 5. as ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them close
33
LOOK AT PG 86, WIGGERS DIAGRAM
34
Cardiac cycle 4 stages Electrical event always proceed mechanical events
1. Diastolic Filling 2. Isovolumic Contraction 3. Ejection 4. Isovolumic Relaxation -Left and right sides contract simultaneously + Right side at lower pressures -Pressure changes due to changes in volume or changes in contractile state
35
Cardiac cycle - Diastolic filling Isovolumic contraction
LAP>LVP - Mitral valve open LVP< AP - Aortic valve closed QRS – LV contracts - LVP increases Once LVP>LAP - Mitral valve closes Both valves closed -Pressure still increasing
36
ejection Isovolumic Relaxation
Once LVP> AP -aortic valve opens -Blood ejected into aorta T-wave -Relaxation - LVP decreases Once LVP< AP Aortic valve closes Both valves closed -No movement of blood
37
Completing the cardiac cycle
LVP still decreasing -Once LVP< LAP Mitral valve opens - Blood moves into ventricle - filling
38
Stroke volume (SV) calculating
- amount of blood pumped in 1 beat - average stroke volume = 70 ml SV=EDV-ESV - EDV = end-diastolic volume (after filling) -ESV = end-systolic volume (after ejection)
39
regulation of stroke volume - 3 stages pre load contractility after load
the amount of myocardial stretching - filling of the heart. greater pre load means greater stretch - the amount of force produced during a contraction at a given preload – the tension required for the left ventricle to force open the aortic semilunar valve
40
stroke volume Venous return end diastolic volume (relax) end systolic volume (contraction)
- amount of blood entering heart (greatly increases with exercise) - affected by venous return and filling time (ie, duration of diastole) - the amount of blood still in the chamber after a contraction; is influenced by contractility (force of contraction) and afterload
41
what affects venous return? What is contraction affected by?
-Skeletal muscle pump -Respiratory pump -Sympathetic innervation -Sympathetic tone -Length of muscle fibre
42
Frank starling law Inotropic effect
- Stroke volume increase as EDV increases (filling) -Whatever goes in – goes out the next beat -The effect of increased sympathetic tone on contractility of the heart (anxiety)
43
Role of Epinephrine or Norepinephrine Cardiac output How much average How calculated cardiac out put is dependant on...
increases both contractility and heart rate - harder and faster contractions - seen in higher emotional and physical states - Cardiac Output (CO) = amount of blood pumped per minute -Average Cardiac Output = 5 L -Cardiac Output = Stroke Volume x Heart Rate venous return and sympathetic tone
44
factors affecting HR Autonomic nervous system Others
-Sympathetic NS increases HR -Parasympathetic NS decreases HR -Hormones (E/NE increase HR; Ach decreases HR) -Age (older people → higher HR) -Gender (females have faster HR than males) -Physical fitness (low fitness → increased HR) -Body temperature (increased Tb → increased HR)
45
Variables that affect HR Thyroid hormone- Caffeine Nicotine Cocaine
-↑ number of β1-adrenergic receptors on SA node cells - Inhibits breakdown of cAMP - ↑ release of norepinephrine - Inhibits reuptake of norepinephrine -remains in cleft longer – longer response
46
In exercise.. Increased in epinephrine leads to... Increased in cardiac out for regular vs elite athletes
- Higher demand for O2 and blood flow -Higher contractility and stroke volume -Faster heart rate -Increased venous return Casual athletes – increase by up to 5X * ~25 L/min Elite athletes increased to 35 or 40L/min
47
Heart muscle metabolism - since the heart is highly oxidative what does that mean coronary circulation - during exercise
- abundant mitochondria and myoglobin -Gets oxygen from coronary circulation -heart rate is ↑ * filling time (diastole) is ↓ * heart still gets adequate blood supply * due to dilation of coronary arteries, via adenosine
48
Long term benefits of exercise and fitness bigger heart, doesn't have to work as hard
 Stroke Volume -Resting Heart rate can decrease  Coronary artery diameter - increased blood flow increased Collateral Blood vessels decreased ischemia
49
cardiac remodelling Pathological remodeling Physiological remodeling
-Consequence of disease * High BP, heart failure, infarct -Consequence of training or pregnancy
50
cardiac myopathies - damage to heart muscle -myocardial ischemia (heart attack) -necrosis acute myocardial infraction (heart attack)
-Inadequate delivery of oxygenated blood to heart tissue * Death of heart muscle cells * Occurs when blood vessel supplying area of heart becomes blocked or ruptured
51
Ischemia and infarct Symptoms:
-Blocked coronary artery -Decreased blood flow and oxygen to heart muscle due to plaque or clot Poor muscle function -decreased stroke Volume -increased cardiac Output Chest pain * diaphoresis (sweating) * Nausea, “indigestion” * Referred pain - neck, arm, jaw
52
Ischemia Infarct treatment
-Transient, "angia" -No permanent damage to heart muscle -Symptoms occur when cardiac demand increases beyond what the heart can match -Permanent blockage -Muscle cells are permanently damaged Symptoms remain and worsen “Heart Attack” -Coronary artery bypass graft (CABG) - Vasodilators -Angioplasty Reduce risk factors: ⬧ Diet ⬧ Exercise ⬧ Smoking
53
Atrial hypertension causes: leads to increase arterial pressure meaning... treatments
-Higher risk of heart failure, haemorrhage, and stroke Smoking * Stress * Diet * Age / genetics -LV pressure must exceed this to open aortic valve and eject blood Shorter ejection time -decreased Stroke Volume - decreased Cardiac Output Exercise Diet – reduced caffeine and salt Medications * ACE inhibitors * Beta blockers * Ca channel blockers
54
Heart failure compromised heart - leading to what happens in heart failure eventually...
-Valve stenosis, not a lot of forward ejection - Ischemia or Infarct, muscle not working well - Hypertension, increased pressure -decreased Stroke Volume -Heart compensates with increased heart rate - meaning shorter filling time and more fatigue and worse contractions Muscle is so fatigued it barely contracts - bad stroke volume - increased Blood volume -Excess blood backs up into lungs – Pulmonary edema
55
effect of after load Afterload: Afterload increases with With higher afterload, In heart failure
– force heart works against to eject blood - high blood pressure valve stenosis stroke volume decreases - Harder to eject
56
conjestive heart failure (CHF) symptoms: - dysfunctional/ fast breathing
- Gradual dyspnea and tachypnea * Tachycardia * Neck vein distention * Edema in ankles and lower legs * Right-sided ⬧ congestion of liver and spleen * Left-sided - congestion of lungs
57
heart failure treatments - can't stop but can slow down
Reduce fluids - diuretics Digitalis or similar drugs -to increase contraction strength Diet and exercise – to strengthen muscle Heart transplants -Expensive -Average post-transplant survival: 15 years Temporary -Artificial heart, ventricular assist device
58
Pulmonary hypertension Cardiac aneurysm
RV Pr > LV Pr -Eg. Pulmonary stenosis Septum inverts, pushed down flat Myocardial compression decreased coronary blood flow Bulge of ventricular wall - Muscle weakness -Congenital or from infarct
59
Cardiac testing
Blood pressure / pulse - Catheterization Blood work - Enzymes Ausculation - valves X-Ray MRI Echocardiography Stress Testing

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