Physiology # 22: Cardiac Output BP Shock

• MAP
• maintain at a constant level of ~100mmHg

• the V of blood that is pumped by the heart over a period of time
• cardiac output = stroke V x heart rate

amount of blood that is ejected by each ventricular contraction

• 1. Preload (amount of blood returning to the heart)
• 2. Contractility (how hard the heart is contracting)
• 3. Afterload (how much resistance the heart has to pump against)

Preload: for the left ventricle is measured by looking at "ejection fraction" - the amount of end-diastolic V that is pumped during one contraction (normally ~50%)

for the left ventricle is the end-diastolic V (venous return to the left side)

for the left ventricle is aortic P, since that is the force it has to pump against to eject blood

• the "work" the heart performs on each beat
• cardiac output represents "V work"
• aortic P (after load) represents "P work"

• For the left ventricle:
• Work = cardiac output x aortic P

myocardial oxygen consumption

**P work is more costly than V work: it is harder for the heart to pump against a P, than it is to move a V of blood

L ventricle works harder than right one (that's why its bigger)

myocardial hypertrophy results when the ventricles need to pump against an increased force ie aortic stenosis causes left heart enlargement

• Blood P = resistance x cardiac output
• (BP = resistance x [heart rate x stroke V])

vascular tone, heart rate, venous return, contractility

• Neurally-mediated
• -eg baroreceptor reflex
• -restores BP values to normal within seconds
• Hormonally-mediated
• -eg renin-angiotensin-aldosterone system
• -regulates BP more slowly by affecting blood V

• 1. Baroreceptors
• 2. Chemoreceptors
• 3. Atrial reflexes
• 4. CNS ischmia reflexes

These respond almost immediately (seconds) to changes in systemic BP

• BP neutrally-mediated system 
•  
• *Pressure sensors are located in the walls of the:
• --Carotid sinus (responds to increases and decreases in P, uses CN IX)
• --Aortic arch (responds mainly to increases in P, uses CN X)

Both systems relay info to the brain stem where responses are immediately initiated to correct the abnormality

• Changes in MAP results in stretching/relaxation of baroreceptor nerve endings
• are sensitive not only to absolute P, but to changes in P and the rate of changes

Sends impulses to the vasomotor centre in the medulla and pons to elicit changes in output of the sympathetic and parasympathetic systems

• Heart rate
• Vascular tone
• Cardiac contractility
• *BP* ultimately

• Much of the body's blood V is in the venous system at any time
• Sympathetic stimulation that results in constriction of veins will "shrink" the dimensions of the CV system
• This mechanism can maintain near-normal CV function even when as much as 25% of the blood V has been lost

• Chemosensitive cells are located in carotid bodies and aortic body
• -role in responding to low arterial oxygen P
• Whenever BP and blood flow decrease below a critical level, chemoreceptors are stimulated by decreased availability of oxygen and accumulation of CO2 and H+
• stimulates activity in vasomotor center to increase sympathetic tone to return BP back to a normal level
• *are more important for regulating the respiratory  system than the cardiovascular system

Atria contain low-P stretch R's similar to baroreceptors in large arteries

Important for both short-term and long-term control of BP

• occurs when blood flow to the medullary vasomotor centre is decreased, causing ischemia or hypoxia
• when this occurs there is an intense outpouring of sympathetic NS activity, resulting in profound increases in BP
• becomes active when MAP <50mmHg, and reaches max activity when MAP is 15-20mmHg
• Last ditch effort to improve BP before death

seconds - minutes

• relies on HORMONAL responses not neural
•   -catecholamine induced vasoconstriction
•   -renin-angiotensin induced vasoconstriction
•   -ADH-induced vasoconstriction

All of these mechanisms attempt to increase BP by increasing vascular resistance

Delay onset (hours to days) but has a sustained effect on BP

Kidneys regulate Na+ and water to adjust blood V

Changes in Blood V leads to alterations in cardiac output (venous return) and BP

Relies on renin-angiotensin-aldosterone system

• Blood flow to a specific organ or system can increase or decrease depending on its metabolic needs
• *Occurs independent of the systemic arterial P
• Changes in blood flow to an organ are achieved by altering arteriolar resistance
• 1. Local control
• 2. Neural or hormonal control

• Changes in blood flow to an organ are achieved by altering arteriolar resistance
• 1. Local control
• 2. Neural or hormonal control

Primary mechanism for matching blood flow to the metabolic needs of a tissue

Based on the need for oxygen or other nutrients (such as glucose) by the tissue

• Exerted through the direct action of "vasodilator metabolites" (eg adenosine, lactate, CO2, K+)
• When these substances accumulate, they induce vasodilation of arterioles, decrease resistance, and increase flow to meet the increased O2 demands of the tissue  

Local autoregulatory responses to sudden changes in BP typically occur within 1-2 mins

allows an organ or tissue to maintain relatively constant blood flow over a wide range of systemic arterial blood pressures

• characterized by rapid response time (1 sec)
• conveys the ability to regulate blood flow to certain tissues at the expense to others
• SYMPATHETIC nervous system is the most important component of the ANS for regulating blood flow
• parasympathetic has little to no role in BP

• Sympathetic NS transmits impulses via the spinal cord to all blood vessels in the body -->produces a continuous, sustained state of partial vasoconstriction in the body
• Impulses are also sent to the adrenal gland to stimulate release of epinephrine and norepinephrine into circulation where they act directly on adrenergic R's in vascular smooth muscle
• NE stimulates alpha1 receptors to induce vasoconstriction of small arterioles, affecting resistance to blood flow through all tissues

• There are many hormones that may influence local tissue blood flow:
• -Constrictors: epinephrine, norepinephrine, angiotensin, ADH
• -Dilators: bradykinin, serotonin, histamine, prostaglandins, H+, K+, CO2

• Circulatory shock is characterized by inadequate oxygen delivery to cells, resulting in generalized deterioration of organ function
• Due to inadequate tissue blood flow for whatever reason -I.e. hemorrhage, hypovolemic, neurogenic, septic
• end result is the same- if left untreated the patient will die

Delivery of O2 = CO x CaO2

• Physical examination findings will depend on how-long standing the process is and how the patient is able to respond--- don't get fooled if they look like they are doing OK
• Compensated: normal blood pressure
• uncompensated: low blood pressure
• terminal: patient is about to die