Physiology Flashcards
2 populations of cardiac cells
Conducting tissue
- modified non-contractile (autorhythmic) cells
- generate and conduct impulses
- lead to electrical activation of myocardial cells
Working myocardial cells
- involuntary, striated cells with contractility properties
- modulte pumping activity of heart
4 properties of cardiac muscle
- Automaticity (Autorhythmicity)
- Conductivity
- Excitability
- Contractility
Action potentials per minute of the conducting system of heart
- SA node: ~100 (normal: ~70)
- AV node: 40-60
- Bundle of His & Purkinje fibers: 20-40
Why is the SA node the normal pacemaker of the heart?
Because its discharge rate is the fastest
The other autorhythmic tissues cannot assume their own rates, because they are activated by the action potentials originating in the SA node before they can reach firing level at their own slower rhythm.
What is sinus rhythm?
If the heart is beating according to the SA nodal rythm, it is also called a sinus rhythm.
Development origins: Sino-atrial = sinus venosus + atria
What is an anatomical syncytium?
a tissue where cell membranes of individual cells disappear - multinucleated cell mass with no boundaries among the cells
What is the functional syncytium?
Although heart is made up of many cells with intact cell membranes, the heart behaves as if it were a single cell, it acts as a functional syncytium.
- this is due to presence of ‘gap functions’ (low resistance intercellular connections) between the cardiac cells (myocytes)
- the current (flow of positive charges) spreads through the gap junctions from one cell to another - rapid cell to cell conduction of impulse (action potential) to all atrial or ventricular myocytes - all or none response
What is the significance of AV nodal delay?
It ensures that ventricles are activated only after atrial activation for complete ventricular filling with blood
What is the significance of AV bundle?
Because of the fibrous skeleton between the atria and the ventricles, cell to cell conduction cannot occur between atria and the ventricles. AV bundle is the only electrical link between the atria and the ventricles.
What is the significance of Purkinje fibers?
It is the fastest impulse conduction.
For rapid transmission of impulse throughout ventricles to obtain simultaneous contraction of all ventricular muscles.
Relaxation of heart
Removal of Ca2+ from intracellular fluid, ICF by
- Ca2+ pump in the longitudinal portion of sarcoplasmic reticulum (into the SR storage)
- Na-Ca exchange in cell membrane (into ECF)
Why tetanus does not affect myocytes?
Due to prolonged absolute refractory period. Myocytes has longer refractory period than skeletal muscles to make sure muscle has relaxed before it can respond.
Effects of hyperkalemia
Decrease in Resting membrane potential - depolarization which is not followed by repolarization - defective conductivity and graual loss of excitability - heart block and decreases heart rate - dilated and flaccid heart and finally stoppage of heart in diastole
Effects of hypercalcemia
Increase in calcium concentration in ECF - increases myocardial contractility; with marked increase in serum calcium, heart relaxes less in diastole and finally stops in systole (calcium rigor)
Effects of hypernatremia
Increase in sodium concentration in ECF - decreases myocardial contractiliy because sodium competes with calcium in contractile process
What is cardiac cycle
Sequence of electric and mechanical events occuring in heart during a single beat.
What is systole & diastole and their duration
Systole: period of ventricular contraction
- 0.3s
Diastole: period of ventricular relaxation
- 0.5s
Total duration: 0.8s one cycle
What is “lub” & “dup” sound
“Lub”: closure ot tricuspid and mitral valve
“dup”: closure of aortic & pulmonary valve
What are the pericordial leads located at
- V1: right to the sternum, 4th ICSpace
- V2: left to sternum, 4th ICSpace
- V3: 5th ICS, between V2 & V4
- V4: 5th ICS, left midclavicular line
- V5: 5th ICS, left anterior axillary line
- V6: 5th ICS, left mid axillary line
What does p, pr segment, q, r, s, t, st segment in ECG means?
p wave: atrial depolarization
PR segment: atrial depolarization but no net movement
q wave: septal depolarization
r wave: ventricular depolarization
s wave: ventricular depolarization (up to base)
ST segment: whole heart depolarized
t wave: ventricular repolarization
What are the 12 leads and which area they indicate?
Lead I: high lateral wall of left ventricles
Lead II: inferior wall of heart
Lead III: inferior wall of heart
avR: right ventricle + basal septum
avL: high lateral wall of left ventricles
avF: inferior wall of heart
V1: right ventricle
V2: right ventricle / basal septum / anterior wall of heart
V3: right ventricle / basal septum / anterior wall of heart
V4: Anterior wall of heart
V5: lateral wall of left ventricle
V6: lateral wall of left ventricle
ECG basics
Positive charges towards + : upward deflection
Positive charges away from + : downward deflection
Negative charges towards - : upward deflection
Negative chages away from -: downward deflection
— on ECG: no net movement / electrical activity is perpendicular to the axis of lead
Duration of PR interval, QRS complex QT interval
PR interval: <0.2s (1 large box)
QRS complex: <0.12s (3 small box)
QT interval:
- male: <0.43s
- female: <0.45s
R wave and S wave pattern through V1 - V6
R wave getting bigger from V1 to V6
S wave getting smaller from V1 to V6
What is cardiac output and its equation
Cardiac output is the volume of blood pumped out by each ventricle in one minute (mil/min)
CO = HR X SV
HR = number of ventricular contractions per minute (beats/min)
SV = volume of blood pumped out by each ventricle per contraction (mil/beat)
Cardiac output of 2 ventricles are equal
systemic blood flow = pulmonary blood flow
5L/min
What is the normal heart rate in infants, adults, elderly. Heart rate of tachycardia and bradycardia?
Normal heart rate: 60-100 beats/min
Infants: 130/min (120-140)
Bradycardia: <60/min
Tachycardia: >100/min
What is the effect of vagal tone & vasomotor area
Vagal tone (cardiac inihibitory centre): parasympathetic (vagus) - Acth - muscarinic - decreases HR
Vasomotor area: sympathetic - NE, Epinephrine - beta 1 - increases HR
What is chronotropic effect
+ve chronotropic effect: increase heart rate
(sympathetic tone)
-ve chronotropic effect: decreases heart rate
(vagal tone - PSNS)
Factors influencing the heart rate
Factors acting reflexly on SA node
1. sympathetic nervous system (+ve chronotropic) - vasomotor area
2. parasympathetic nervous system (-ve chronotropic) - vagal tone - cardiac inhibitory centre
Factors acting directly on SA node
1. T3 & T4 - thyroid hormones (+ve chronotropic)
2. body temperature (+ve chronotropic)
3. increase Ca (+ve chronotropic)
4. decrease Ca (-ve chronotropic)
5. increase K (-ve chronotropic)
6. peripheral chemoreceptors - increase HR (+ chronotropic) due to decrease PO2, increase PCO2, decrease pH
7. Age (fetus, infants, elderly)
8. Atrial Bainbridge reflex (+ve chronotropic): increase venous return, increase stretch, SA node, increase HR
9. Pressure on the eyeball (-ve chronotropic): increase vagal tone
10. punching the abdomen (-ve chronotropic): increase vagal tone
What is inotropic effect
+ve inotropic effect: increases contractility
-ve inotropic effect: decreases contractility
What is Frank-Starling law
The energy contraction is proportional to its initial length of the cardiac muscle fiber (the muslce length just before contraction)
- greater the stretch, greater the force of contraction, increase preload, increase stroke volume
What is heterometric and homometric regulation
Heterometric regulation: regulation of cardiac output by changing the cardiac muscle fiber length
Homometric regulation: regulation of cardiac output by changing the contractility independent of cardiac muscle fiber length
Frank-starling curve association with inotropic effect
+ve inotropic agent: shift curve upward and left
-ve inotropic agent: shift curve downward and right
What are the factors regulating Stroke volume
- Preload: degree to which the myocardium is stretched before it contracts
- Contractility (inotropic)
- Afterload: resistance that needs to be overcome for ventricles to pump blood
- preload increases stroke volume
- contractility increases stroke volume
- afterload decreases stroke volume
What is the equation of stroke volume
SV = EDV - ESV
70ml = 120ml - 50ml
Factors affecting preload
preload is the ‘stretch’ of the heart
Increase EDV increases preload
- venous return (skeletal muscle pump, respiratory pump, venomotor tone - venoconstriction, gravity)
- atrial contraction
Filling time
- increases HR - decreases filling time - decreases preload
Filling capacity (ventricular compliance or distensibility)
- myocardial hypertrophy
- infarction
- infiltrative diseases (cancer)
- end diastolic volume - blood in ventricles before pump
Factors affecting contractility
Sympathetic nervous system (+ve inotropic)
- Epinephrine, Norepinephrine - B1 adrenergic receptors - increase Ca - increase contractility
Hormones
- T3, T4 (+ve)
- glucagon (+ve)
Drugs
- Digitalis (+ve)
- Dopamine (+ve)
- Dobutamine (+ve)
- Atropine (+ve)
- beta-blockers (-ve)
- Ca channel blockers (-ve)
Ions
- increase Ca (+ve)
- decrease Ca (-ve)
- increase K (-ve)
- decrease Na (-ve)
- increase protons H+ (-ve)
Factors affecting afterload
- aortic valve dysfunction
- plaque (occlusion)
- increase BP (increase systemic vascular resistance)
What is ejection fraction
Ejection fraction of EDV that is ejected
Ejection fraction = stroke volume = SV / EDV
- increase EDV - increase preload - increase SV - decrease ESV
Measurement of cardiac output
-
Fick principle
amount of substance taken up by an organ = A-V difference of substance X blood flow -
Dye dilution
CO = amount of indicator injected / average concentration in arterial blood after a single circulation through the heart - Echocardiography combined with Doppler technique
- Electromagnetic flow meter
Probability of turbulence
Re = (density of fluid x diameter of vessels x velocity of flow) /
viscosity of fluid (RBC & plasma proteins)
Re directly proportional to 1/n (viscosity)
Re directly proportional to V (velocity of flow)
decrease viscosity (anaemia) - increase Re - Increase probability of turbulence - sounds (murmurs)
Obstruction - increases velocity beyond it - increases Re - increases probability of turbulence - sounds
Average velocity of blood flow
V = Q/A
V= average velocity
Q = flow
A = total cross-sectional area
Resistance (Ohm’s law)
Flow (Q) = (Pa - Pb) / R
R = (Pa - Pb) / Q
Q = flow, P = pressure, R = resistance
Resistance of blood flow
R = (8 x viscosity x Length of tube) /
(pi x radius of tube^4)
Viscosity directly proportional to R
Viscosity depends on
1. Packed cell volume
2. plasma proteins
3. red cell resistance to deformation
Law of LaPlace
The larger the radius of vessel, the larger the wall tension required to withstand a given internal fluid pressure
What are the microvessles
- precapillary arterioles
- capillaries
- postcapillary venules
- In resting tissue, most of capillaries are collapsed
- Blood flows mostly through the throughfare vessels
- In active tissue, metarterioles and precapillary sphincters dilate
- Intracapillary pressure rises to overcome the critical closing pressure
- Blood flows through the capillaries
- If blood flows through all the capillaries in the body, it is incompatible with life
- Body would bleed to death into its own capillaries
Transport across the capillary walls
Across pores
1. slit-pores
2. fenestration
3. sinusoids
Across the cells
1. vesicular transport (transcytosis)
2. diffusion (flow-limited, diffusion-limited)
3. filtration
Regulation of blood flow
- caliber of arterioles
- vascular tone
- precapillary sphincters
Formula of formation of tissue fluid (ISF)
Fluid movement across the capillary wall =
k [ (Pc - Pi) - (πc - πi)]
k = capillary filtration coefficient
Pc = hydrostatic pressure of capillary blood
Pi = hydrostatic pressure of interstitial fluid
πc = oncotic pressure of capillary blood
πi = oncotic pressure of interstitial fluid
(Pc - Pi) = filtration pressure (driving force)
(πc - πi) = osmotic pressure gradient (drawing force)
Factors influencing ISF volume
Increased filtration pressure
- arteriolar dilation and venular constriction
- increased venous pressure:
- gravity
- venous obstruction
- incompetent venous valves
- heart failure
- total ECF volume increases (salt retention)
Decreased oncotic pressure
- decreased plasma protein level:
- starvation
- poor protein diet
- maldigetion & malabsorption
- decreased protein synthesis by liver
- protein loss through kidney diseases
- osmotically active particles in ISF (immediately after muscular exercise)
Increased capillary permeability
- substance P
- Histamine
- Kinins
- Allergic reactions
- Inflammatory reactions
- insect bites (local edema)
Inadequate lymph flow
- removal of lymph node (breast cancer surgery)
- obstruction of lymphatics (filariasis & elephantiasis)
- Lymphedema (non-pitting edema)
What is blood pressure
Blood pressure refers to the force exerted by circulating blood on the walls of blood vessels
What is pulse pressure
Pulse pressure = SBP - DBP
Mean arterial BP and equationn
It is the average pressure throughout the cardiac cycle. It is slightly less than the value half way between SBP and DBP because systols is shorter than diastole.
Mean arterial BP = DBP + 1/3 (SBP - DBP)
Systemic arterial BP
Systemic arterial BP = CO X TPR
Cardiovascular control (CV) centre
- located in medulla oblongata
- helps regulate heart rate and stroke volume
- also controls neural, hormonal, and local negative feedback systems that regulate blood pressure and blood flow to specific tissues
- groups of neurons regulate heart rate, contractility of ventricles, and blood vessle diameter
- Cardiostimulatory and cardioinhibitory centres
- vasomotor centre control blood vessel diameter
- receives input from both higher brain regions and sensory receptors
Input & output of CV centre
4. From chemoreceptors: monitor blood activity (
Input
1. From higher brain centres: cerebral cortex, limbic system, hypothalamus
2. From proprioceptors: monitor joint movements
3. From baroreceptors: monitor blood pressure
4. From chemoreceptors: monitor blood acidity (H+, CO2, O2)
Output
1. vagus nerve (PSNS) to heart = decreased HR
2. cardiac accelerator (SNS) to heart= increased HR and contractility
3. vasomotor nerves (SNS) to blood vessles = vasoconstriction
3 main types of sensory receptors
- Proprioceptors: monitor movements of joints and muscles to provide input during physical activity
- Baroreceptors: monitor pressure changes and stretch in blood vessle wall
- Chemoreceptors: monitor concentration of various chemicals in the blood
Regulation of Blood pressure
(short term & long term)
Short term
1. Baroreceptor reflex
2. Chemoreceptor reflex
3. Hormones
* epinephrine & norepinephrine
* ANP (Atrial natriuretic peptide)
* ADH
Long term
1. Renin Angiotensin Aldosterone (RAA) system
Location of baroreceptors
- Baroreceptors sense stretch and rate of stretch by generating action potentials
- located in highly distensible regions of circulation to maximise sensitivity
- Carotid sinus (ICA): carotid bodies
- Aortic arch: aortic bodies
Other stretch receptors
- Coronary artery baroreceptors: respond to arterial pressure but more sensitive than carotid and aortic ones
-
Veno-atrial mechanoreceptors: respond to changes in central blood volume
lie down, lift your legs and cause peripheral vasodilatation -
Un-myelinated mechanoreceptors: responod to distention of heart
ventricular ones during systole, atrial ones during inspiration
Other receptors
- Heart chemosensors: cause pain in response to ischaemia (K+, lactic acid, bradykinin, prostaglandins)
- Arterial chemosensors: stimulated in response to hypoxaemia, hypercapnia, acidosis, hyperkalemia (regulate breathing)
- Lung stretch receptors: cause tachycardia during inspiration
BP regulation mechanisms
-
Neural CV reflexes
Baroreceptor reflexes
Chemoreceptor reflexes
Brain (CNS) ischaemic response -
Hormonal
Catecholamines
RAA system
Vasopressin - Renal-body fluid control system
Baroreceptor reflexes
- pressure sensitive receptors in internal carotid arteries and other large arteries in neck and chest
- carotid sinus reflex regulate blood pressure in the brain
- aortic reflex regulates systemic blood pressure
Pathway
1. Blood pressure in brain:
Baroreceptors in carotid sinus - glossopharyngeal nerves (9th CN) - CV centre in medulla oblongata (tractus solitarius)
2. Systemic blood pressure
Baroreceptors in arch of arota - vagus nerve (10th CN) - CV centre in medulla oblongata (tractus solitarius)
3. Sympathetic output:
Nerve from medulla oblongata - spinal cord - sympathetic trunk ganglion - cardiac accelerator - SA node / AV node / Ventricular myocardium
4. Parasympathetic output:
Nerve from medulla oblongata - vagus nerve (10th CN) - SA node / AV node
When blood pressure falls, baroreceptors stretches less, slower rate of impulses from CV - CV decreases parasympathetic stimulation and increases sympathetic stimulation
Chemoreceptor reflexes
- Receptors located close to baroreceptors of carotid sinus (carotid bodeis) and aortic arch (aortic bodies)
- Detech Hypoxia (low O2), Hypercapnia (high CO2), acidosis (high H+), and send signals to CV
- CV increases sympathetic stimulation to arterioles and veins, producing vasocontrction and an increase in blood pressure
- receptors also provide input to respiratory centre to adjust breathing rate
- Homeostasis (Normal O2, pH, CO2 levels in blood and CSF)
- Homeostatis disturbed (Decreased O2, pH, elevated Co2 levels in blood and CSF)
- Reflex response: chemoreceptor stimualted
-Cardioacceleratory centres inhibited - increased cardiac output & BP
-Cardioinhibitory centres inhibited - increased cardiac output & BP
-Vasomotor centres stimulated - vasocontriction occur - increased cardiac output & BP
-Respiratory centres stimulated - respiratory rate increases - Increased O2, pH, decreased CO2 levels in blood
- Homeostatis restored
RAA system
Decreased BP (hypotension)
1. Juxtoglomerular cells in kidney produces prorenin
2. Prorenin is cleaved to renin and released into the blood
3. Renin converts angiotensinogen produced by liver into angiotensin-I
4. Angiotensin-I converts into angiotenin-II by Angiotensin converting enzyme predominantly flound in lungs and kidneys
5. Angiotensin-II binds to angiotensin-II receptors in tissue to exert various effects
6. Increase sympathetic activity
7. Increase water retention by tubular Na & Cl reabsorption and K excretion
8. Increase aldosterone secretion from adrenal cortex to promote water retention (Na,Cl,K) in kidneys
9. Increase arteriolar vasoconstriction - increase BP
10. acts on hypothalamus to stimulate thirst and encourage water intake
- induces posterior pituitary gland to release ADH which promotes water retention in kidneys
- reduces baroreceptor sensitivity response to increase BP so that this response does not counteract with RAAs
Catecholamines in hormonal regulatinon of BP
Epinephrine & norepinephrine
1. adrenal medulla releases in response to sympathetic stimulation
2. increase cardiac output by increasing rate and force of contractions
ADH / vasopressin in hormonal regulation of BP
Antidiuretic hormone / vasopressin
1. produced by hypothalamus, released by posterior pituitary gland
2. reponse to dehydration or decreased blood volume
3. causes vasoconstriction which increases blood pressure
- enhances water retention
- causes vasoconstriction
Atrial natriuretic peptide in hormonal regulation of BP
- secreted by atria of the heart
- secreted in response to increase in blood volume
- targets kidneys and decreases sodium reabsorption - increases sodium excretion - water follows sodium by osmosis - fluid volume decreases - blood volume decreases - Bp decreases
- inhibits RAAS system
- reduces aldosterone secretion
- causes vasodilation and lowers BP:
- vasodilates afferent arterioles of nephrons - increase glomerular filtration rate - increases amount of water and sodium excreted in the kidneys - lower BP
Dromotropic effect
Dromotropic - speed of electrical impulse
+ve dromotropic: enhances electrical impulses to heart
What is vascular tone
refers to degree of blood vessel constriction relative to its maximally dilated state
* vasoconstriction and vasodilation of the resistance arteries
* venoconstriction and venodilation of veins
Types of vascular tone
- arteriolar tone
- tone of precapillary sphincters
- venous tone
Effects of increased arteriolar tone
- decreased radius of arteriole
- greatly increased resistance to bloof flow
- greatly decreased blood flow across the arteriole
- effects on blood volume:
- increased upstream (in artery)
- decreased downstreatm (in capillaries)
- decreased capillary blood flow - decrease capillary hydrostatic pressure (HPc) (pust out) - decreased interstitial fluid formation
Effects of increased venous tone
- generalized venoconstriction in systemic veins
1. increased venous pressure
2. increased venous return to heart
3. increased ventricular filling and EDV
4. increased stretch of muscles in ventricular wall
5. increased force of contraction (Starling’s law - greater stretch, greater FOC)
6. increased stroke volume
7. increased cardiac output
8. increased BP
Effects of decreased vascular tone
-
generalized venodilation in systemic veins
1. decreased venous return to heart
2. decreased EDV
3. decreased force of contraction (starling’s law)
4. decreased stroke volume and cardiac output
5. decreased BP -
generalized systemic arteriolar dilation
1. decreased total peripheral resistance
2. decreased BP
Factors causing vasoconstriction (local, endothelin, neurohumoral ag., neural factors)
Local factors
1. decreased local temperature
2. autoregulation
Endothelin products
1. endothelin-1
2. locally release platelet
3. serotonin
4. thromboxane2
Circulating neurohumoral agents
1. epinephrine (excepts in skeletal muscle and liver)
2. norepinephrine
3. arginine vasopressin
4. angiotensin II
5. endogenous digitalis-like substance
6. neuropeptide Y
7. dopamine
8. calcium ions
Neural factors
1. increased discharge of sympathetic nerves
Factors causing vasodilation (local, endothelin, neurohumoral ag., neural factors)
**Local factors
1. increased CO2 - Hypercapnia
2. decreased O2 - Hypoxia
3. increased K - Hyperkalemia
4. adenosine
5. lactate
6. decreased local pH - acidosis
7. increased local temperature
Endothelin products
1. Nitric oxide
2. kinins
3. prostacyclin
Circulating neurohumoral agents
1. epinephrine in skeletal muscle and liver
2. calcitonin G-related protein
3. substance P
4. Histamine
5. atrial natriuretic peptide
6. vasoactive intestinal polypeptide (VIP)
7. Dopamine (kidney)
Neural factors
1. Decreased discharge of sympathetic nerves
2. activation of sympathetic cholinergic vasodilator nerves to vasculature of skeletal muscles of limbs
Vascular action of NO
- modulates the vasoconstrictor action of endothelin (ET-1)
- anti-thrombotic effect: inhibits platelet adhesion to the vascular endoehtlium
- anti-inflammaotry effect: inhibits leukocyte adhesion to vascular endothelium
- anti-proliferative: inhibits smooth muscle hyperplasia
NO deficiency
-
vasoconstriction
coronary vasospasm
elevated TPR (systemic vascular resistance) - hypertension - thrombosis due to platelet adhesion and aggregation to vascular endothelium
- inflammation due to upregulation of leukocyte and endothelial adhesion molecules
- vascular hypertrophy and stenosis
Autoregulation & theories
Autoregulation: capacity of tissues to regulate their own blood flow
* well developed in heart, brain, kidneys, exercising skeletal muscles
Theory 1: Myogenic theory
* intrinsic contractile response of smooth muscle to stretch
* increased pressure - increased stretch of muscles - stretched muscles contract - smaller radius - greater resistance
Theory 2: Metabolic theory
* accumulation of vasodilator substance in active tissue
* whenever the blood flow is reduced (decreased supply) or tissue metabolism is increased (increased demand). Accumulation of Vasodilator metabolites reduces the vascular tone, and increases the vessel radius, small increase in radius greatly increases blood flow
Hyperaemia (causes, type)
Vasodilator metabolites cause hyperaemia (increased blood flow in the tissues)
1. Active hyperaemia: VDMs maintain the increased blood flow during increased metabolic acitivity of the tissues (exercising muscle)
2. Reactive hyperaemia: increase in blood flow in a tissue when its circulation is reestablished after a period of occlusion. More to compensation for a decrease in blood flow that has occured during occlusion
Causes of heart failure
- diabetes
- hypertension
- anemia
- valve defects
- arrhythmia
- coronary artery disease
- congenital heart disase
- cardiomyopathy, myocarditis
- lung disorders
Describe physiological response of heart failure
Decreased cardiac output
1. increased sympathetic nervous system (increased contractility, increased heart rate, vasoconstriction)
2. increased renin-angiotensin system (vasoconstriction, increased circulating volume)
3. increased antidiuretic hormone (increased circulating volume)
Acute heart failure
- circulatory reflexes like baroreceptor reflex, chemoreceptor reflex are activated
- reflexes that originate in the damaged heart activates the sympathetic nervous systme
- Effects of sympathetic stimulation:
1. strengthens damaged musculature
2. contractility of normal muscle is increased
3. tone of most the blood vessel is increased therby raising the mean systemic filling pressure
Chronic heart failure
- reduced renal blood flow
- renal retention of fluid
- increase in blood volume
- moderate increase in body fluid and volume increases the venous return
- however excess fluid retension can increase the workload of damaged heart
Effects of excess fluid retension
1. over stretching of heart
2. filtration of fluid into the lungs causing pulmonary edema
3. development of extensive edema in most parts of the body
Recovery of myocardium
- new collateral blood supply begins to penetrate the peripheral portions of the infarcted area of the heart
- the undamaged portions of heart musculature hypertrophies
- the degree of recovery depends on the type of cardiac damage
- it varies from no recovery to almost complete recovery
- recovery rapidly occurs during the first few days and weeks
- final state of recovery occurs within 5-7weeks
compensated heart failure
- the maximum pumping ability of hte heart is still depressed to less than one half normal
- increase in right atrial pressure occurs
- this can maintain the cardiac output at a normal level
- but the cardiac reserve is reduced
Decompensated heart failure
- cardiac output cannot rise high enough to make the kidneys excrete normal quantities of fluid
- fluid continues to be retained
- more and more edema occurs
- this can eventually lead to death
- it is the state in which the failure continues to worsen
Treatment of decompensation:
1. strengthening the heart by administrating cardiotonic drug like digitalis
2. administering diuretic drugs
Decompensated heart failure
- cardiac output cannot rise high enough to make the kidneys excrete normal quantities of fluid
- fluid continues to be retained
- more and more edema occurs
- this can eventually lead to death
- it is the state in which the failure continues to worsen
Treatment of decompensation:
1. strengthening the heart by administrating cardiotonic drug like digitalis
2. administering diuretic drugs
