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(4) Cardiovascular (Pathology (Heart Failure: Does not follow Frank…
(4) Cardiovascular
Pathology
Cardiac hypertrophy
: Heart grow big
Hyperkalemia
: High K+ levels in blood
Diagnosis
: ECG
ST Segment
ST
Elevation
Hypokalemia
: Low K+ levels in blood
Ishemic
: Insufficient blood supply to organ
Diagnosis
: ECG
ST Segment
Infarction
: Obstruction of blood supply
Diagnosis
: ECG
ST Segment
ST
Elevation
Hypoxia
: Insufficient Oxygen to organ
Diagnosis
: ECG
ST Segment
Heart Failure
: Does not follow
Frank Starling Law
(VR/EDV=CO/SV)
Lower ejection fraction
Blood stuck in venous system / circulation
Heart does not pump all the blood it receives
Resistance
Hypertension
Contractility/Rate
Myocardial Infarction (Obstruction)
Bradycardia (Slow heart rate)
Preload (Frank-Starling)
Hemorrhage
Responses
Long Term
:
Fluid Retention (Kidneys)
Increase VR
Acute (Increase CO):
ANS (HR)
RAAS
Narrowing systemic blood vessels
Edema
Accumulated/excess fluid
2) Increased Venous Pressure
(R) Heart failure
3) Increased capillary permeability
Inflammation
Most Important
1) Reduced capillary oncotic pressure
Plasma proteins (Albumin)
Liver faillure / Nephrotic syndrome
Unable to produce albumin
Unable to reabsorb albumin
4) Decreased lympathic flow
LN Metastasis
Hyperaemia
: Excess blood reaching an organ (Flow)
Congestive Heart Faillure
Fluid build up around heart
Pump inefficiently
Hypovolemic
:
Low volume
Sympathetic
Central Venous Pressure
: Differentiates Cardiogenic from Hypovolemic
Atherosclerosis
: Scarring of blood vessels
Diagnosis
ECG
Detect
Cardiac rhythm
Conduction
Size of heart chambers
Electrolyte concentration
Bipolar - Unipolar
Lead 2
:
P Up Wave
: Depolarization of Atrium
Q Down Wave
: Depolarization of Interventricular Septum
Left bundle branch activated before Right
Depolarization occurs
away
from Lead 2
RS Up Wave
: Depolarization of Ventricle
S1 sound (Closing of AV Valves)
T Wave
:
Repolarization
of Ventricle
Away
from Lead 2
S2 sound (Closing of Semilunar Valves)
ST Segment
: Isoeletric segment representing
plateau phase
Diagnosis of Ishemia / Hypoxia
QT Interval
: Ventricular action potential
ECG wrt
Systole / Diastole
Cardiac Cycle
1)
Late
Ventricular Diastole / Atrial systole
Passive: Ventricular Filling (70%)
Active: Atrium contract fill ventricle (30%)
AV Valves: Opened
Semilunar Valves: Closed
2)
Isovolumetric
Ventricular
Contraction
Unchanging volume
Contraction
Closes AV valves
Contraction Insufficient to
Open Semilunar valves
AV: Closed
Semilunar: Closed
3) Ventricular Ejection
Blood into great arteries
AV: Closed
Semilunar: Opened
Repolarization of ventricles
Semilunar valves close
AV valves still closed
4)
Isovolumetric
Ventricular
Relaxation
and Ventricular Diastole
Passive atrial filling (?)
Blood flow stops (?)
AV Valves: Closed
Semilunar Valves: Closed
Auscultation Points
1)
Aortic Area
2nd (R) intercostal space
2)
Pulmonary Area
2nd (R) intercostal space
3)
Mitral Area
5th (L) intercostal space
4)
Tricuspid Area
(L) Lower sternal border
Heart Sounds
Lub
: Closure of the AV valves at the start of systole
Dub
: Closure of semilunar valves at the end of systole
Murmurs
Narrowed valves
: Produces turbulence
Incompetent valves
: Blood flowing back
A.P
Depolarization
1) SA Node (R to L Atrium)
2) AV Node (In fibrous ring)
3) Bundle of His
4) Purkinje Fibres
Atrial: Gap junctions
Ventricular: Conductive tissue + Gap Junctions
Ventricular
Sustained depolarization
K+ efflux
But Ca2+ influx continues
Ventricular Muscle A.P (-
90mV
)
(1) K+ efflux
(2) Na+ / Ca2+ influx
ER Ca2+
Extracellular Ca2+
(3) K+ efflux & Ca2+ influx
Artrial
Atrial Muscle A.P (
-70-75mV
)
No sustained depolarization
No Ca2+
No plateau phase
Pacemakers
Autorhythemicity
Cells with autorhythmicity
Able to generate heartbeat
Cardiac Pacemarkers
Decreasing resting membrane potential
Fastest suppresses other pacemakers
SA Node (90-100 bpm)
AV Node (40-60 bpm)
Bundle of His (15-30 bpm)
Purkinje (Fastest conduction speed)
Ectopic beat (Ventricle)
Calculation Things
Formulas
CO
=
SV
x
HR
Preload
Heart as pump
Contractility
Rate
Peripheral Resistance
Heart Rate
Physiological State
Parasympathetic tone - Vagus
Natural Rhythm of the heart
More active K+ channels
Determinants
Chronotropic (Rhythm) Agents
Positive Chronotropic
Sympathetic Neurons
Adrenaline
Noradrenaline
b-adrenegric receptors
1) Na+ / Ca2+ influx
2) Increase rate of depolarization
3) Increase HR
Negative Chronotropic
Parasympathetic Neurons
Acetylcholine
M-cholinergic (Muscarinic receptors)
1) K+ efflux
2)
Decrease
Ca+ influx
3) Hyperpolarization of cells
4) Decrease HR
Stroke Volume
Determinants
1)
Pre-load (Volume)
Intrinsic Regulation
Venous Return (
Frank-Starling Law
)
Increase cardiac muscle stretch
Increase pressure generated
Constant ejection fraction
(3)
Inotropic Agents
Extrinsic Regulation
Extrinsic
Drugs
Hormones
Sympathetic (
Contractility
)
Increase force of contraction
Without stretching muscles
Calcium
Key determinant of strength
CA - calmodulin
Required for smooth muscle contraction
2) After-load (Resistance)
CO = MAP / TR
MAP determined by CO & TR
Blood Pressure
Pulse Pressure (PP)
= SP - DP
What you can feel over major arteries
Mean Atrial Pressure
= 2/3 DP + 1/3 SP
= DP + 1/3PP
Standing phenomena
:
Gravity
Lower on extremities
Vein greater compliance
Higher BP / blood pool at extremities
Decrease Venous Return
Sense BP
Baroreceptors
Aortic Arch
Carotid Sinus
Chemoreceptors (Respi)
Carotid Sinus
Aortic Arch
Medulla Oblongata
Regulation
Short Term
ANS
Parasympathetic (Increase HR; CO)
Sympathetic (Increase Contractility; CO)
Sympathetic (Increase Vaso-constriction; MAP)
Long Term
Volume
Fluid absorption by kidney
Total Resistence
= 8 nL/ Pi . r^4
Determinants
Radius
Paracrine
RAAS
Hormones
Autonomic Nervous System
Sympathetic
Continually constrict arterioles
Exercise decrease Sympathetic, vessels dilate
Parasympathetic
Fun Facts
EDV
: 130ml
ESV
: 50ml
SV
: 80ml
EF
: SV/EDV
Normal Range
: 55 - 75%
CO / Venous Return
= 5-5.5 Litre / min
Volume of blood out of (L) ventricle / min
GIT: 20-25%
Kidney: 20%
Brain: 15%
Controlled by
metabolic mediators
Little response to
ANS / hormones
Muscle: 15-20%
Low at rest
Reduced during contraction (compression)
Controlled by
metabolic mediators
Coronary
:
Reduced in systole (Compression)
Increased during diastole
Controlled by
metabolic mediators
Adenosine
Little response to
ANS / Hormone
Cannot use annaerobic
Skin
:
Completely regulated by sympathetic system
HR
: 70bpm
Venous
: High
capacitance
/volume, Low resistance
Arterial
: High resistance; Low
capacitance
/volume
Stores pressure
Maintains flow
Atherosclerosis (elastic loss)
Capacitance
vs
Compliance
Same thing
Blood vessels
Blood Flow
Determinants
Pressure Difference
Directly proportionate
Ohm's Law
Q = Flow
P1 = Start pressure
P2 = End pressure
R = Resistance
Flow (Q)
= (P1 - P2) / Resistance
Vessel Resistance
Inversely proportionate
Arterioles
Control blood entering capillary
Small vessels resistance > Large vessels
Poiseuille-Hagen Formula
R = Resistance
n = Viscosity
L = Length
r = Radius
Resistance
= 8 . n . L / pi (r)^4
Starling Equilibrium
Capillary Pressure
: Higher than Interstitial
Capillary Oncotic
: Higher than Interstitial
Over length of vessel
: Decreasing hydrostatic pressure
Regulation
Metabolic Mediators
Vasoconstrictors
Oxygen
High oxygen
Smooth muscle contract
Decrease blood flow
Low oxygen
Smooth muscle dilate
Increase blood flow
Except pumonary
Glucose
Vasodilators
Adenosine
CO2
Except pulmonary
H+
K+
Contraction Regulation
Extrinsic
Effect of ANS
1)
Chronotropism (Para & Sympa)
At Rest
:
Sympathetic
:
Inotropic & Chronotropic
Maintain contractility
Parasympathetic
:
Dampen SA Node (90-100bpm)
Chronotropic only
2)
Contractility (Sympa only)
Increase force of contraction
Without stretching muscles
Denoted by
Decrease in End Systolic volume, same End Diastolic
Drugs
Hormones
Intrinsic
Venous Return
Gives constant ejection fraction
Excitation-Contraction Coupling
A.P
Voltage gated Ca2+
Extracellular Ca2+ enters
Ca2+ released from sarcoplasmic reticulum
Ca2+ bind to troponin to intiate contraction
Relaxation, Ca2+ unbinds
Ca2+ back in sarcoplasmic reticulum
Ca2+ exchange with Na+
