The systemic circulation and the left side of the heart operate at higher pressures than the right side of the heart and the pulmonary circulation. In contrast, vascular resistance is lower in the pulmonary circulation than in the systemic circulation. Left atrial pressure can be measured indirectly using the pulmonary capillary wedge pressure (PCWP).
| Site | Mean pressure (mmhg) |
| Aorta and big vessels | 120/80 |
| Left atrium | 2-5 |
| Right atrium | 0-2 |
| Pulmonary artery | 25/8 ; mean 15 |
| PCWP | 2-14 |
Systolic pressure is the arterial pressure produced when blood is ejected during ventricular contraction (systole). Diastolic pressure is the arterial pressure during ventricular relaxation (diastole). Pulse pressure is the difference between systolic and diastolic pressure.
Pulse pressure changes mainly when either stroke volume or arterial compliance changes.
Mean arterial pressure = diastolic pressure + ⅓ of pulse pressure.
Pulse depends on the elasticity of the large arteries. When a large artery fills with blood, it expands; when the pressure falls, it recoils. This expansion and recoil is what you feel as the pulse.
Metabolism of the heart muscle: The heart has a comparatively high oxygen demand, even at rest. This demand can increase tenfold during strenuous exercise. Cardiac muscle relies mainly on oxidative metabolism to generate ATP. It contains many mitochondria and, under normal conditions, preferentially uses free fatty acids as its main fuel source. Because of its vital function, the heart can also adapt to use other substrates for ATP production, including amino acids, glucose, glycogen, lactic acid (during exercise), and ketone bodies (fasting, diabetic ketoacidosis).
Myocardial oxygen consumption is determined using Fick’s principle:
MVO2 = F X (Ca O2 - Cv O2)
Where:
This equation represents how much oxygen the heart extracts per minute.
Cardiac muscle contraction: A sarcomere is the functional unit of muscle. It is the region between two Z lines. Sarcomeres contain thick myosin filaments and thin actin filaments.
Each myosin filament has two heads that bind to actin and ATP. The myosin head has myosin-ATPase activity, meaning it hydrolyzes ATP to ADP and iP. This provides the energy needed for actin-myosin cross-bridge formation.
The regulatory proteins troponin and tropomyosin are associated with actin filaments. Troponin has three subunits:
When intracellular calcium is low, troponin T holds tropomyosin in a position that blocks actin-myosin interaction, so the muscle does not contract. When intracellular calcium is high, calcium binds to troponin C, causing a conformational change that shifts tropomyosin away and exposes the myosin-binding sites on actin.
The cross-bridge cycle proceeds as follows. ATP binds to the myosin head and is hydrolyzed to ADP and iP, producing a conformational change in the neck region of myosin that activates the head. The activated myosin head binds to actin. ATP then binds again to the myosin head, and the cycle repeats (hydrolysis → conformational change → sliding → ATP binding again) until intracellular calcium returns to normal.
With each cycle, the myosin head attaches to a new site on actin and moves from the bent (“cocked”) position back toward its resting position, producing the “power stroke.” This pulls the actin filament so that the myosin filament slides forward along actin.
Muscle contraction requires an increase in intracellular calcium. Action potentials travel along the sarcolemma and into the transverse tubule (T-tubule) system, causing depolarization. Voltage-sensitive L-type calcium channels (dihydropyridine receptors) open, allowing calcium to enter the cytosol. This calcium influx triggers further calcium release from the sarcoplasmic reticulum through ryanodine receptors.
Calcium is then removed from the cytosol and sequestered back into the sarcoplasmic reticulum by SERCA (sarco-endoplasmic reticulum calcium ATPase) and by the Na/Ca exchanger pump. This process - where excitation of the muscle membrane leads to contraction - is called excitation-contraction coupling.
Endocrine function of the heart: The atria and ventricles secrete several hormones with local and systemic effects. The major ones are atrial natriuretic peptide (ANP, also called ANF) and brain natriuretic peptide (BNP). Together, they are called cardiac natriuretic peptides (cNPs).
Other polypeptide hormones expressed in the heart likely act on the myocardium in a paracrine or autocrine manner. These include C-type natriuretic peptide, adrenomedullin (AM), and endothelin-1.
ANP and BNP are co-stored in atrial-specific granules. Mechanical stretch of atrial muscle increases the rate of peptide secretion. Their biological effects are mainly mediated through the NPR-A guanylyl cyclase-coupled receptor, which is widely distributed throughout the body (including kidneys, vascular smooth muscle, adrenals, brain, and heart). Activation of this receptor increases intracellular cGMP.
ANP and BNP:
Blood levels of ANP and BNP increase in several pathological conditions, including heart failure, myocardial infarction, hypertension, left ventricular hypertrophy, and pulmonary hypertension.
Carperitide is a recombinant form of human ANP. It can be used in congestive heart failure and acute myocardial infarction, and it also has renal protective effects in contrast-induced nephropathy. Nesiritide is a recombinant form of BNP that improves heart failure but has serious renal adverse effects.
Adrenomedullin (AM) is a peptide resembling calcitonin. AM has a wide range of biological actions, including vasodilation, natriuresis and diuresis, and inhibition of cardiac fibroblast proliferation and extracellular matrix production. Plasma AM increases in pathological conditions such as essential hypertension, acute coronary syndrome, congestive heart failure, and septic shock.
Endothelin 1 produces potent and long-lasting vasoconstriction, increasing blood pressure. It also has direct positive inotropic and chronotropic effects on heart muscle.
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