PREIOAD Caving pressure) CHRONOTROPY cheat rate )
Determinants are cardiac output : ionic basis of pacemaker action p
yµ µ 1g
4. heart rate 9 . Slow depolar
↳ decrease
2. myocardial connectivity
↳
3. Preload increase
4 . Afterload
I ↳ increase
2.
Voltage gated Ca channels open
Preload →
pressure snatching cardiac muscle ↳ Ca moves in → more voltage
during timing .
cntdnnels ac
Frank starving law → energy of contraction of cardiac muscle 3 .
Depolarisation of K
↳
fibre initial fibre nest
↳ K moves out
relationship a
length at
.
.
between VEDV
→
increased ventricular end diastolic volume Ionic basis of ventricular action p
>
2
µ |g
- 0
e. sv .
↳ increased exposure of myosin heads .
Rapid depola
↳ force
increased one connection .
' '
Venous Return → rate of blood flow back to heart . 9 . Notch → d
4 4
↳ some
Factors -1
→
Affecting Venous Return : -
K
' '
^
Volume of blood 2 . Plateau
2. Distribution of blood ↳ slow inward current → L t
3. Gravity t movement ↳ outward K current .
4 . Venous tone (sympathetic nerve activity) 3 . Repatriation
Reflex Responses : ↳ inward channels deac
-
Hypervotdemird (4 blood volume ) ↳ outward K channel dom
↳ ' '
Arterial barovecepiov mlllex -
Depressor velvet Regulation of Heart Rate by Autonom
↳
decreases sympathetic outflow Parasympathetic : VAGUS NERVE → S
↳ outflow ↳ Acn
increases parasympathetic .
release ↳ at re
↳ ↳ opens fewer
Ariel receptors the channels -
slow
↳ Inhibit sympathetic vasconsricwrp.am to kidneys .
Sympathetic :
ADRENERGIC FIBRES →
↳
Inhibits ADH secretion from post pituitary.
.
↳
release noradrenaline (nonepin
Hypothermia ( t ) ↳
-
blood volume more Na channels
opens
-
'
↳ Arterial Baronecepwr Reflex - Presser ' neliex .
↳
increases sympathetic outflow SYMP : Effects of Norepinephrin
↳ decreases parasympathetic outflow .
↳ NAD →
By aarenoreceptors →
↳ ↳
Atrial Receptors No channels activated earlie
↳ More
to
kidneys CRAAS) phosphoryl
↳ increase sympathetic pathway ca channels
↳ increase ADH from ↳ K
secretion post pituitary
-
. channels activated earlie
Atrial Natriunehc Peptide CAMP) defends against Vol overload -
:
=
Increased HR .
-
released in response to aerial pressure increase (arterial stretch ) PARA : Effects of Acn via vagus
Nat Mz (muscarinic)
↳
stimulates excretion of Hzot ↳ Ach → receptors
↳ Vasodilation (by stimulating comp) ↳ Ach → M2 receptor → 6k → Kt
↳ ↳
inhibits RAAS .
=
Decreased HR .
(WOTROPT fsnengm of connection at a given EDV ) origin of EC6 main features :
Intracellular Cd regulates cardiac contractility : P wave = Atrial depolarisation
connection; qpg comp, = ✓ enn.am depolarisa
-
ca enters an via L type voltage sensitive channels .
T wave -- Ventricular nepoiansavion .
Ca induced Ca release from sarcoplasmic reticulum(via RyR2)
-
-
Cd binds to Troponin C connection Excessive
-
= .
HRS can compromise car
Relaxation: 9 HR (tachycardia) → inadequate
Remove elevated Ca ↳
hyp
:
long term :
-
7. Ca pump -
energy dependant 1 HR (bradycardia → decreased
, AFTERLOAD ( peak ventricular tension during systole ,
determined
by MAP)
MAP = Cox TPR
Afterload → amount of resistance heart must overcome to open aortic valve t expel blood .
Factors that influence Arterial Blood pressure :
Physical Factors :
9. Blood volume
2 . Arterial Compliance
Physiological Factors :
7 .
Cardiac output
2. Total peripheral resistance .
Age , gender , disease, postne eat . . .
Baronecaptors in the reflex control of Arterial Blood pressure:
Baronecaptors in Carotid sinus, root of Aortic Arch .
Chernoreceptovs in cavon.at Aortic bodies .
↳
depressor Ipnessor reflex .
pressure increase →
artery diameter increase → baronecepwrssnetchctumcaadvenn.me) → ap discharge →
Mechanisms regulating vascular tone:
a. Metabolic -
Oz cone . CK02 =
vasodilation )
2. Neural -
a adnenoneceptors = vasoconstriction
Bz daren receptors = vasodilation .
3. Hormonal -
epinephrine Inonepinephnine , angiotensin 11 , ADH = Vasoconstriction .
ANP , histamine vasodilation
-
.
4. Endothelial -
Nine oxide = vasodilation .
Lymph Formation :
starting forces move fluid into capillary bed
Opposing .
xs fluid which is not reabsorbed →
lymphatic vessels back to Cvs .
Determinants are cardiac output : ionic basis of pacemaker action p
yµ µ 1g
4. heart rate 9 . Slow depolar
↳ decrease
2. myocardial connectivity
↳
3. Preload increase
4 . Afterload
I ↳ increase
2.
Voltage gated Ca channels open
Preload →
pressure snatching cardiac muscle ↳ Ca moves in → more voltage
during timing .
cntdnnels ac
Frank starving law → energy of contraction of cardiac muscle 3 .
Depolarisation of K
↳
fibre initial fibre nest
↳ K moves out
relationship a
length at
.
.
between VEDV
→
increased ventricular end diastolic volume Ionic basis of ventricular action p
>
2
µ |g
- 0
e. sv .
↳ increased exposure of myosin heads .
Rapid depola
↳ force
increased one connection .
' '
Venous Return → rate of blood flow back to heart . 9 . Notch → d
4 4
↳ some
Factors -1
→
Affecting Venous Return : -
K
' '
^
Volume of blood 2 . Plateau
2. Distribution of blood ↳ slow inward current → L t
3. Gravity t movement ↳ outward K current .
4 . Venous tone (sympathetic nerve activity) 3 . Repatriation
Reflex Responses : ↳ inward channels deac
-
Hypervotdemird (4 blood volume ) ↳ outward K channel dom
↳ ' '
Arterial barovecepiov mlllex -
Depressor velvet Regulation of Heart Rate by Autonom
↳
decreases sympathetic outflow Parasympathetic : VAGUS NERVE → S
↳ outflow ↳ Acn
increases parasympathetic .
release ↳ at re
↳ ↳ opens fewer
Ariel receptors the channels -
slow
↳ Inhibit sympathetic vasconsricwrp.am to kidneys .
Sympathetic :
ADRENERGIC FIBRES →
↳
Inhibits ADH secretion from post pituitary.
.
↳
release noradrenaline (nonepin
Hypothermia ( t ) ↳
-
blood volume more Na channels
opens
-
'
↳ Arterial Baronecepwr Reflex - Presser ' neliex .
↳
increases sympathetic outflow SYMP : Effects of Norepinephrin
↳ decreases parasympathetic outflow .
↳ NAD →
By aarenoreceptors →
↳ ↳
Atrial Receptors No channels activated earlie
↳ More
to
kidneys CRAAS) phosphoryl
↳ increase sympathetic pathway ca channels
↳ increase ADH from ↳ K
secretion post pituitary
-
. channels activated earlie
Atrial Natriunehc Peptide CAMP) defends against Vol overload -
:
=
Increased HR .
-
released in response to aerial pressure increase (arterial stretch ) PARA : Effects of Acn via vagus
Nat Mz (muscarinic)
↳
stimulates excretion of Hzot ↳ Ach → receptors
↳ Vasodilation (by stimulating comp) ↳ Ach → M2 receptor → 6k → Kt
↳ ↳
inhibits RAAS .
=
Decreased HR .
(WOTROPT fsnengm of connection at a given EDV ) origin of EC6 main features :
Intracellular Cd regulates cardiac contractility : P wave = Atrial depolarisation
connection; qpg comp, = ✓ enn.am depolarisa
-
ca enters an via L type voltage sensitive channels .
T wave -- Ventricular nepoiansavion .
Ca induced Ca release from sarcoplasmic reticulum(via RyR2)
-
-
Cd binds to Troponin C connection Excessive
-
= .
HRS can compromise car
Relaxation: 9 HR (tachycardia) → inadequate
Remove elevated Ca ↳
hyp
:
long term :
-
7. Ca pump -
energy dependant 1 HR (bradycardia → decreased
, AFTERLOAD ( peak ventricular tension during systole ,
determined
by MAP)
MAP = Cox TPR
Afterload → amount of resistance heart must overcome to open aortic valve t expel blood .
Factors that influence Arterial Blood pressure :
Physical Factors :
9. Blood volume
2 . Arterial Compliance
Physiological Factors :
7 .
Cardiac output
2. Total peripheral resistance .
Age , gender , disease, postne eat . . .
Baronecaptors in the reflex control of Arterial Blood pressure:
Baronecaptors in Carotid sinus, root of Aortic Arch .
Chernoreceptovs in cavon.at Aortic bodies .
↳
depressor Ipnessor reflex .
pressure increase →
artery diameter increase → baronecepwrssnetchctumcaadvenn.me) → ap discharge →
Mechanisms regulating vascular tone:
a. Metabolic -
Oz cone . CK02 =
vasodilation )
2. Neural -
a adnenoneceptors = vasoconstriction
Bz daren receptors = vasodilation .
3. Hormonal -
epinephrine Inonepinephnine , angiotensin 11 , ADH = Vasoconstriction .
ANP , histamine vasodilation
-
.
4. Endothelial -
Nine oxide = vasodilation .
Lymph Formation :
starting forces move fluid into capillary bed
Opposing .
xs fluid which is not reabsorbed →
lymphatic vessels back to Cvs .
