One complete cardiac cycle = “lub dub”.
Atria and ventricles each have a systole and diastole:
- Systole is contractile phase
- Diastole is relaxation phase
De-oxygenated blood enters the Rt side via vena cava and is pumped to the lungs.
Oxygenated blood enters the Lt side of the heart via pulmonary veins and gets pumped to the body.
Normally the volume ejected by RV and LV is the same.
At end-atrial and ventricular diastole, the tricuspid valve is open b/w Rt atria and ventricle and blood flows simultaneously into both chambers. Ventricle receives up to 85% of blood during this period.
Prior to ventricular systole, atrium contracts and contributes additional 15-35% to ventricle (atrial kick). As we age, atrial kick contributes more to CO. A fib causes complete loss of atrial kick.
After ventricular end-diastole ventricle enters systole and contracts -> pressure in ventricle increases -> tricuspid valve closes -> pulmonic valve opens -> blood ejected into pulmonary artery -> pressure falls in ventricle -> pulmonary valve closes to prevent back flow.
During diastole ventricles resume their pre-contractile size, the pressure drops below vena cava’s and blood is drawn into ventricle.
The conclusion of atrial systole coincides with the end of ventricular diastole.
Without a sufficient period of diastole, systole is ineffective.
The amount of blood ejected by Left ventricle (LV) in one minute (average 5-8 Lpm; up to 25 L with activity).
Body’s blood flow and pulse are provided by the LV.
Calculated by a formula:
CO = SV x HR
- SV = amount of blood ejected by LV with each contraction (adults 50-80ml).
- HR = beats per minute.
Adequate perfusion is needed for energy supply, delivery of nutrients, removal of wastes, transport of hormones, glucose and continuous flow of O2.
ATP is the primary energy molecule needed for every activity (thinking, moving, contraction, protein formation)
- Aerobic metabolism uses O2 to produce ATP. O2 + Glucose = H2O + CO2 -> 36 ATP. Water is used by body, CO2 gets blown off.
- Anaerobic metabolism takes over when there is lack of oxygen supply due to hypoxia, obstruction, anemia or decreased cardiac output. It is not an efficient energy producer. Glucose = Lactic Acid -> only 2 ATP produced. Only buys some time (i.e. during exercise not enough O2 to muscle cells, lactic acid accumulates -> sore muscles!
- Ischemia is inadequate blood flow to tissues, therefore decreased O2 supply. Body compensates by extracting more from blood. Most tissues use only 1/3 of O2 avail. The heart uses ¾ of O2 thru coronary arteries (even at rest), so adequate blood flow is very important. Heart has very little reserve, coronary arteries must dilate to increase blood flow.
Low CO may cause ischemia -> anaerobic metabolism -> weaker contractility -> further decreased CO -> increase in catecholamines (i.e.norepinephrine) -> dysrrhythmia.
As HR increases so does CO but only to a point!
HR of 100 = 6500 L (SV i.e. 65 x 100)
HR of 80 = 5200 Lpm. So 20% increase in HR yields a 20% increase in CO.
HR of >150 results in a reduced CO due to inadequate filling time. Ventricle receives less blood, SV and CO fall.
HR of < 50/min results in decreased CO because no sufficient HR. (SV 80 x HR 40 = 3200 ml).
Both can lead to shock! (SOB, CP, hypotension, altered LOC).
HR is result of 3 factors:
- intrinsic control by heart’s pacemaker
- sympathetic stimulation
- parasympathetic stimulation
Major contributor to CO.
Varies with changes in preload, afterload, catecholamine release.
Blood supply to the ventricle OR technically, the volume or pressure in ventricle at the end of diastole.
Frank-Starling law states that the more stretch of heart’s chambers (cardiac muscle fibres), the more forceful the contraction (greater SV). Blood filling the chambers increases pressures/volumes, causing fibers to stretch therefore increasing contractility. This is true for healthy heart. The diseased heart (i.e. cardiomyopathy) needs increased pressures to maximize contractility.
During strenuous activity catecholamine release increases force of contraction.
There is a limit to VEDP (ventricular end diastolic pressures) on contractility, with high VEDP, contractility begins to fall. The higher the preload the higher myocardial workload.
Ejection fraction is % of volume ejected from left ventricle.
Usually LV has 100ml blood before contraction, about 50-80 mls is normally ejected with each SV.
Resistance to ejection of blood by ventricle.
LV must create sufficient pressures during systole to overcome diastolic arterial pressure and systemic vascular resistance before blood is ejected.
Affected by size of ventricle, wall tension, arterial BP (if increased BP then increased resistance and work demand and decreased CO) –> hypertrophy
Patient’s DBP is a good indicator of resistance. In general, the higher the DBP the higher the afterload.
It’s like trying to open a door when there is a hurricane outside.
SV and CO decrease with increased afterload -> increased myocardial workload and O2 demand for LV.
Decreased CO = decreased perfusion, decreased LOC, decreased urine output, weak peripheral pulses, chest pain, wet lungs, SOB, cool, clammy skin.
Pressures in systemic circulation are higher than in pulmonary circulation so LV becomes 3x thicker than RV. Hypertrophy occurs as resistance to chamber contraction increases -> accumulation of increased fiber in myocardial cells -> cells bulk up -> thicker chamber walls -> decreased contractility, reduced SV, dysrhythmias.
3. Sympathetic Innervation
HR and contractility are influenced by releases of epinephrine and norepinephrine thru alpha effect (peripheral vasoconstriction) which provides more preload by shunting blood to core organs and beta 1 (increases HR and force of contraction).
Pain, fear, stress increase epinephrine -> increase HR
Main effect of catecholamines (epinephrine & norepinephrine) is increased CO.
4. Parasympathetic Influence
Mediated by Vagus nerve (acetylcholine).
Decreases contractility of atria and causes peripheral vascular dilation. Limited to mainly SA node, atria, AV node. Stimulation of vagus nerve -> decrease in rate of SA firing -> slowed impulse of AV node -> decrease in contraction.
Vagal stimulation can be caused by “bearing down”, carotid sinus massage, immersing head in cold water, change in position.
All forms of vagal stimulation can slow HR significantly!
|Abdominal, peripheral, coronary blood vessels||Arterial, venous constriction|
Increases HR, enhances contractility, increases cardiac irritability
|Cardiac muscle||Inceased HR|
Strengthened force of contraction
|Acetylcholine||Cholinergic receptors||SA node, AV node|
Atria, coronary vessels
|Slows HR, conductivity|
Weakens atrial contraction
Dilates coronary vessels