Performing the cardiovascular objective examination: the guide
The cardiovascular objective test is an important step at the intensive care unit level, since many of the diseases that require admission to the ICU on a primary or secondary basis involve the cardiovascular system itself
It can be understood how knowledge of the physical assessment of the cardiovascular system plays an important role in the physiology and, above all, in the pathophysiology.
In this chapter, we do not wish to exhaust the vast field of clinical cardiovascular science, but to provide a tool for systematically analysing the patient with regard to clinical stability and the arterial and venous vascular system.
CARDIOVASCULAR OBJECTIVE EXAMINATION: INSPECTION
During the cardiological objective test, the examiner stands to the right of the patient, while the patient may be supine, lying on the left side, or sitting (on the right side of the bed or with the headboard elevated); generally in the ICU the patient is positioned supine with a narrow margin of mobilisation.
The general assessment is performed with the patient supine, while the left flank is reserved for better evaluation of a punctal icterus or the presence of a mitral valvular murmur; in the sitting position, the characteristics of an aortic murmur are better evaluated.
Breathing: the presence of tachypnoea is one of the most sensitive signs to indicate a cardio-respiratory pathology; the frequency, rhythmicity and depth of the respiratory acts must be assessed (they are assessed unconsciously for the patient, otherwise the tendency is to hyperventilate). The presence of orthopnoea and/or dyspnoea is also assessed.
Skin: In haemodynamics, the skin is one of the organs most visibly assessed for colour, jugular turgor and pressure pulses; see the chapter on shock (Chapter 6) for more details on the usefulness of skin analysis in this regard.
Precordial draft: protrusion from the rib cage of the entire precordial area; indicates congenital heart disease/early life, when the chest is still deformed.
PALPATION IN THE CARDIOVASCULAR OBJECTIVE EXAMINATION
Cardiac palpation in the routine clinical setting appears to be of little use and is therefore poorly performed; it is usually performed using the hand with 2 fingers flat (usually the index and middle fingers) on the normal site of the itto-tip, with the palm of the hand located on the left parasternal line.
Through palpation analysis, the site/size of the itto-tip is assessed.
Until a few decades ago, it could be studied by means of the apicocardiogram (APG), which assessed the positive/negative deflection of the different waves obtained from the transmission of the tip ichthyto on the chest wall.
Ichthyto of the tip: is defined as the transmission of the contraction of the interventricular septum through the chest wall; it generally has dimensions similar to a coin and is positioned anterior to the cardiac apex; through its spatial modifications and the different timing of onset, information on the cardiac chambers can be obtained.
Timing of apex beat:
Systole: In normal cases, the normal pulsation sees a short-duration outward movement of the skin at the beginning of systole, with a return to baseline position at the end of systole.
In the case of a hyperkinetic pulsation, there is a ichthus of greater amplitude and generally due to hyperdynamic cardiovascular situations (such as hyperkinetic syndromes); there can be a protracted pulsation with a lifting ichthus, of protracted duration, which always indicates a cardiac pathology (such as a left ventricular hypertrophy or a ventricular aneurysm) or a re-entrant pulsation defined as a significant re-entry of the punctal ichthus, which is detected at the end of systole; in this case, a differential diagnosis arises between forms of constrictive pericarditis/pleuropericardial adhesions (with extensive re-entry) and ventricular overload (with circumscribed re-entry).
Presystole: A pre-systolic tip ichthis is due to the atrial flutter, which usually represents the tactile equivalent of the IV tone in situations where the ventricular telediastolic pressure is elevated.
Typically these are situations with ventricular hypertrophy, ischaemic heart disease, ventricular aneurysm, arterial hypertension and/or valvular/subvalvular aortic stenosis.
Protodiastole: typically due to overfilling of the ventricle, it is the tactile equivalent of tone III, in situations of severe ventricular pathology such as mitral insufficiency, interventricular/interatrial defects and/or congestive heart failure.
Location of the ictus cordis:
Normal ictus cordis: localised at the 5th intercostal space, 1 cm medial to the left hemiclavicular line, the origin of which arises from an anterior and rightward twisting of the apical region (pertaining to the left ventricle), occurring at the onset of systole (due to spiral arrangement of myocardial fibres).
Left ventricular hypertrophy: if this is considerable, the septum rotates on its major axis counterclockwise (so that the left chambers become more anterior); in the case of concentric hypertrophy, the cardiac yctus becomes more prominent, more extensive than normal, while in the case of eccentric hypertrophy the cardiac yctus shifts to the left and inferiorly.
Right ventricular hypertrophy: the septum rotates on the major axis in a clockwise direction (the right chambers become more anterior), with a left parasternal/epigastric impulse generated by the anterior wall of the right ventricle, which is best palpated by the Tenar eminence of the hand (located at the left parasternal level).
CARDIOVASCULAR OBJECTIVE EXAMINATION, PERCUSSION:
In the cardio-vascular field, the percussive technique is not used as it does not add any additional clinical information to that obtained from a good objective test, it is also inaccurate and of doubtful diagnostic usefulness.
In the cardiovascular field, auscultation focuses on the perception of the turbulent motions of the blood and its vibration against the heart valves and/or arterial walls such that they are perceived with the phonendoscope (at different frequencies).
The auscultation foci are the points of maximum intensity at which sounds coming from a particular valve can be heard; the mitral focus is perceived at the itto of the tip, the tricuspidal focus at the left V intercostal space on the left parasternal line, the aortic focus at the level of the right II intercostal space on the right hemiclavicular line and the pulmonary focus at the level of the left II intercostal space on the left hemiclavicular line.
In addition, there is Erb’s area, located at the level of the left III intercostal space on the left half-clavicular line (immediately below the pulmonary focus), where certain aortic pathologies can be better perceived.
The auscultation areas are the different peripheral districts that are first reached by the different cardiac tones; each noise can extend into the areas of its own competence (especially mitral noises are able to spread widely), so only by subtraction effect can it be deduced that a murmur in the axillary area is of mitral competence and a murmur at neck level is of exclusive competence of the aortic valve.
CARDIOVASCULAR OBJECTIVE EXAMINATION: THE FIRST TONE
The first cardiac tone represents the transformation of acoustic energy of the blood on the mitral/tricuspid valve (according to some authors it is given by the combination of the two valves, according to other authors it is not) which determines the beginning of systole; it is structured by three components: a first low-frequency component, followed by a main component with a high frequency and high amplitude and ending with a last low-frequency component.
The structure of the first tone is called triphasic.
I phase: represents the first movements of the ventricular wall, which rapidly tenses around the incompressible ejection volume;
Phase II: represents the increase in pressure due to ventricular contraction, with associated vibration of the atrio-ventricular valves which generate the high and intense frequencies (in fact, it represents the main component of the first tone);
Phase III: represents the increase in pressure flowing into the large vessels, with oscillation of their roots;
The intensity of the first tone is linked and depends on the inotropism (ΔP/Δt) in a directly correlated manner, on the stiffness of the valve cusps (in the case of mitral stenosis, a closing pop can be generated) and on the valve position, in fact, a greater intensity indicates the presence in telediastole of distant valve leaflets (as during tachycardia) and a lower intensity indicates the presence in telediastole of closer valve leaflets (as in bradycardia).
In fact, it must be remembered that the mitraglio/tricuspidal valvular movement is of maximum opening during the first phase of diastole, and then slowly gets closer in the late phase; this late phase is reduced until it disappears in the case of tachycardia.
Hence the understanding of what was said earlier about the intensity of the former being related to heart rate.
CARDIOVASCULAR OBJECTIVE EXAMINATION, THE SECOND TONE
The second tone represents the transformation of the acoustic energy of the blood on the aortic (or pulmonary) valve, which determines the onset of diastole; the second tone has a higher pitch than the first tone, much more intense in the upper auscultatory foci.
The tone is due to the closure of the semilunar valves generated by the retrograde currents due to the pressure drop in the ventricle during the release phase, resulting in vibration of the vascular walls.
The intensity of the tone depends on the pressure values contained in the different valve segments; therefore, the aortic component is usually much more intense.
Physiological splitting: It is normal that during inhalation the distance between A2 and P2 is approximately 0.04 sec, while in exhalation A2 returns synchronous with P2.
This phenomenon appears to be related to the presence of a greater venous return of blood during the inspiratory phase in the right chambers (see Chapter 2.7.2), thus requiring a longer ventricular emptying time.
Physiological doubling may be accentuated in a constant manner (especially in the case of pulmonary stenosis) or it may be modifiable with breathing, but be increasingly accentuated (as in the case of right branch block).
Fixed splitting: Fixed splitting is defined as when there is a tone distance that remains constant between A2and P2 (generally about 0.03-0.08 sec); this mechanism is linked to the presence of a left-right shunt, with the appearance during exhalation of increased filling of the right chambers (as in the case of patency of the Botallo duct, an inter-atrial defect, etc.).
Therefore, during the inspiratory phase, the ‘classic’ mechanism of physiological doubling occurs, and during the expiratory phase, the lowering of pressure in the right chambers (due to a reduction in venous return) leads to a shunt with a consequent increase in local flow and persistence of the doubling, which remains fixed at auscultation.
Paradoxical splitting: this is defined as a splitting where during inspiration A2 becomes synchronous with P2, while during exhalation the distance between P2 and A2 lengthens to about 0.04 sec.
This is a phenomenon related to delayed closure of the aortic valve as in the case of aortic valve stenosis, marked hypertension, left ventricular decompensation, etc.).
THE THIRD TONE IN THE CARDIOVASCULAR OBJECTIVE EXAMINATION:
The third tone is defined as a low-frequency protodiastolic tone, audible in the ventricular chambers (especially on the left thoracic margin) as a dull noise, occurring approximately 0.12-0.15 sec after the second tone (thus, it is generally well audible), the presence of which leads to the appearance of a protodiastolic gallop (of ventricular origin).
The formation of the third Tone is thought to be related to an atrio-ventricular pressure difference with two possible origins:
Valvular origin: there is a snap of the chordae tendineae due to excess pressure in the opening of the atrio-ventricular valve; this sudden snap (linked to extremely rigid structures or vice versa very loose) would generate the sound.
Muscular origin: vibrations occur in the left ventricular musculature due to rapid and sudden filling (as in diastolic dysfunction or severe systolic dysfunction).
The presence of a third tone may be paraphysiological in young people after physical exertion, whereas in adults it almost always indicates ventricular overload of diastolic origin with ventricular insufficiency.
CARDIOVASCULAR OBJECTIVE EXAMINATION, THE FOURTH TONE:
What is called the fourth tone is a telediastolic (or also presystolic) tone, audible as a low-frequency dull sound, which is generated about 0.06-0.10 sec after the P wave in the ECG, just before the first tone; its presence leads to the appearance of a presystolic gallop (of atrial origin).
The origin of the fourth tone is thought to be produced by the atria due to excessive blood compression, especially during atrial systole with increased contractile activity of the atrium itself (see Chapter 2.7.4).
The main causes are arterial hypertension, severe aortic valve stenosis (with maximum gradients greater than 70 mmHg), hypertrophic obstructive cardiomyopathy, myocardial ischaemia, mitral insufficiency.
Opening Snap: this is the opening snap of the mitral valve, which is often more frequent than the relative murmur; it is a high-frequency sound that appears after 0.07-0.12 sec from the second tone, well audible on the left parasternal region at the insertion of the ipsilateral IV costa, with an intensity independent of the inspiratory phase.
It is thought to be related to a sudden tension of the mitral cusps (like an unfurling of sails in a boat) due to an important pressure difference between the atrium and the ventricle.
The intensity and delay of the sound depend on valvular anatomical changes (such as calcifications) and the magnitude of the trans-valvular pressure gradient.
The opening pop disappears when the leaflets become too rigid and no longer flexible and/or if mitral insufficiency is present.
-mitral stenosis (most frequent condition);
-pervasiveness of the Botallo’s duct;
-ventricular septal defect;
-paraphysiological (after physical exertion due to flow hyperkinesis).
Protosystolic click: it is an ejection click, equivalent to the opening of the aortic and/or pulmonary semilunar valves (in the case of valve stenosis) or from the aortic root (in patients without valve pathology); it is a sound related to the third phase of the first tone component, due to vibration of the root of the large vessels.
It is generally due to aortic valve stenosis, hyperkinetic states (due to accelerated ejection from the left ventricle), aortosclerosis (especially in elderly patients) and/or hypertensive cardiovasculopathy (due to the presence of a tortuous, sclerotic, non-compliant aortic root associated with accelerated ejection from the left ventricle).
Meso-telesystolic click: this is a click that occurs in the meso-telesystolic phase (much later than proto-systolic clicks), often mistaken for a split second tone.
It is generally due to various situations such as asynchronous myocardial dyskinesia/contraction, papillary muscle dysfunction, mitral prolapse (from myxomatous degeneration with cusp protrusion into the atrium).
Pericardial rubbing: pericardial rubbing noise is usually triphasic (consisting of a systolic, protodiastolic and presystolic component), more rarely it is biphasic or monophasic.
It has the characteristic of becoming accentuated with inhalation by diaphragmatic lowering, with the parietal pericardium and anterior visceral pericardium coming together.
It generally has a harsh and strident timbre, which is sometimes perceived as a vibration, transient in character and disappears due to excessive pericardial effusion.
Pacemaker sound: this is considered an ‘extra-sound’ produced by the electric pacemaker, due to the diffusion of the electric current into the nearby intercostal nerves, producing contractions of the intercostal muscles.
It tends to decrease in intensity on the inhale.
It is usually a noise clearly distinguishable from cardiac tones.
Galloping rhythms: three-stroke sequences in which there is an added tone of systolic/diastolic origin (which are respectively the III or IV tone) are defined as such and generally occur with rapid frequency.
They are weak, low-frequency tones (therefore assessable with the bell of the phonendoscope) audible with a patient positioned supine, while appearing weaker if the patient sits or is positioned in orthostasis.
Systolic gallop: this is systolic added sound (which can be either protosystolic, mesosystolic or telesystolic), where the added sound is called click-systolic.
It can vary greatly in intensity, especially depending on the patient’s position and breath acts; it is best heard in the apico-sternal area.
Diastolic gallop: is a diastolic added noise of different origin; it can be of atrial origin(presystolic) where the added tone is the IV tone, of ventricular origin (protodiastolic) where the added tone is the III tone or of summation (usually mesodiastolic) where the added tone is due to the fusion of the III with the IV tone, a condition further favoured by the shortening of the diastole by tachycardia; in those rare cases where there is no complete fusion of the two added tones and a “quadruple rhythm” (locomotive rhythm) occurs.
Blood turbulence is at the basis of the physical explanation of murmurs, defined as the perception of turbulent blood motion; based on the ratio (radius x velocity x density)/viscosity, the Reynold number is obtained; at constant density and viscosity (except in onco-haematological pathologies), the radius of the structure and the velocity of the blood can lead to an increase in the Reynold number, therefore to the appearance of turbulent motion.
It can therefore be said that high velocity, local stenosis, vascular ectasia and the combination of stenosis/ectasia lead to increased turbulent motion of blood, therefore increased blowing.
Location: it appears essential to describe the starting area of the murmur (Mitral, Tricuspidal, Aortic, Pulmonary) and its irradiation (towards the axilla, towards the neck, etc.).
Timing: the timing of a murmur is one of the basic characteristics for classifying a murmur and is in fact based on the phase of the cardiac cycle in which they occur (systolic/diastolic/continuous). In addition to this, they can be stratified according to the sub-phase of the cardiac cycle in which they occur: ‘proto’ when it is an early phase, ‘meso’ when it is an intermediate phase, ‘tele’ when it is a late phase and ‘pan’ when it is the whole phase.
Intensity: classically, the intensity of the breaths is categorised on a scale of 0 to 6, where the breath of 1/6 appears very slight, very quiet, and is generally appreciable not immediately, but only with adequate concentration and silence, the breath of intensity 2/6 appears slight (quiet), but immediately appreciable on auscultation. The breaths of intensity 3/6 are defined as moderately slight, of medium intensity and well audible, while the breaths of intensity 4/6 are defined as intense (loud) with a quiver that appears appreciable when the phonendoscope is fully supported. Intensity 5/6 puffs are intense (loud) with a quiver that is appreciable even with a partially detached phonendoscope and intensity 6/6 puffs are very intense with a quiver that is appreciable even with the phonendoscope totally detached.
Shape: the murmurs can also be defined according to their time course, classically stratified into crescendo or decrescendo shapes, or diamond shapes (when they have a crescendo and a decrescendo phase).
Frequency: breaths are classified according to the sound frequency at which they are perceived into low frequency forms (around 80 Hz), medium frequency forms (around 80-150 Hz) and high frequency forms (over 150 Hz).
Quality: the quality of a breath is a peculiar characteristic that depends on the type of valve involved and the type of damage that is generated, because these two aspects determine the intensity and type of turbulent motion. You can have a rough breath (with a harsh quality), a sibilant breath, a chirping breath, a sweet breath (with a more musical character), or a breath with other peculiar characteristics (seagull cry, etc.).
From ejection: the murmur occurs in systole (before or after the opening of the semilunar valves), with a “diamond” shape, generated by the trans-valvular pressure difference (between the ventricle and the artery). The severity of the valvulopathy correlates with the delay in the peak intensity of the murmur: the later the intensity, the greater the obstruction. Typically from aortic valvular stenosis: (both valvular and subvalvular), from hypertrophic cardiomyopathy (differential diagnosis with valvular stenosis, but usually does not have the second tone because it is covered by the murmur that begins before the valve opens), from high flow conditions (the greater the systolic output, the greater the ‘flow murmur’) and in cases of post-valvular ectasia.
From regurgitation: in these cases the murmur occurs in systole, during isovolumetric contraction (this is why it includes the I tone) and the intensity/duration is parallel to the pressure gradient across the orifice where it originates. It is typically due to retrograde blood flow from the ventricles to the atrium via the AV ostium which is incontinent and/or due to the presence of an interventricular defect; the pan-systolic form is related to the almost constant pressure difference, the quality is generally ‘blowing’ due to the high pressure and narrow orifice. The intensity of the murmur correlates with the severity of the valvulopathy. Typically from mitral insufficiency, interventricular defect, tricuspid insufficiency.
From ejection: the murmur occurs at the end of diastole, telediastolic (sometimes meso/telediastolic), often with a pre-systolic reinforcement due to the atrial systole component.
It is due to stenosis of the valvular ostia (most frequently mitral valve) also due to partial fusion of the two leaflets and/or chordae tendineae.
The shape of the murmur is related to the trans-valvular pressure difference, with a pre-systolic accentuation due to increased intra-atrial pressure.
From regurgitation: the murmur occurs at the onset of diastole, decreasing, of variable duration; it is typically due to aortic insufficiency or pulmonary insufficiency with a trans-valvular pressure gradient arising due to incontinence of the semilunar valves. The severity correlates with the duration of the murmur.
Continuous murmurs are murmurs that persist through systole and diastole without interruption, typically due to the presence of shunts between vessels; the murmur arises in differential diagnosis with valvulopathies.
Typical forms of continuous murmur are patency of the Botallo’s duct (most common condition in the population), the presence of shunts in the aorto-pulmonary window, the presence of high inter-atrial defects with aortic valve insufficiency, rupture of an aneurysm of a sinus of Valsalva in the atrial or right ventricle, the presence of a thyroid murmur (in the case of hyperthyroidism), the presence of a venous buzz (accelerated venous flow) and/or the presence of peripheral morphological abnormalities or surgical anastomoses.
The finding of a murmur is not always an indication of pathology; there are many situations where the finding of a murmur is simply an indication of an increase in turbulent blood flow, without this voluntarily indicating a valvulopathy.
Such murmurs (defined as ‘non-pathological’) are further classified into innocent murmurs, physiological murmurs and relative murmurs.
Innocent murmurs are harmless murmurs that are not associated with structural or functional changes in the heart; in childhood, approximately 50% of patients have an innocent murmur that may persist for years and then suddenly disappear.
Apicosternal murmurs: these are murmurs whose maximum intensity is perceived in the apicosternal region;
TeLesystolic murmur: best perceived at the apex, it may begin after a systolic click and/or a systolic gallop; it must be excluded that it is due to a dysfunction of the papillary muscles and/or mitral prolapse; if so, it is of no clinical and/or prognostic impact.
Apical-musical systolic murmur: this is a murmur that is best perceived at the cardiac apex or the left lower sternal margin (rarely also along the pulmonary area); on the phonocardiogram it presents with a uniform frequency (musical in character). It is a very common murmur in childhood, with no pathological significance.
Straight back syndrome: this is a murmur of 1-3/6 intensity, secondary to the loss of normal dorsal kyphosis, with asymptomatic compression of the heart and large vessels. This anatomical abnormality leads to the formation of a turbulent motion of blood that is perceived along the left sternal margin/III intercostal space, decreasing in inspiration. Pressure on the chest is shown to increase the intensity of the murmur.
2nd intercostal space murmurs: these are non-pathological murmurs whose maximum intensity is perceived at the level of the left 2nd intercostal space;
Pulmonary systolic ejection murmur: this is a very frequent murmur, linked to the presence of a functional stenosis in the right ventricle outflow chamber or in the pulmonary artery, with the formation of whirling motions. It is first of pathological significance.
Pregnancy murmur: this is a continuous noise with diastolic accentuation, often present in the second trimester of pregnancy, in the puerperium and/or during lactation. It is most common on the 2nd intercostal space, and is obliterated by phonendoscope compression; it is thought to be due to high flow between the aorta and the internal mammary arteries.
Straight back syndrome: see previous paragraph.
Cervical murmurs: these are murmurs best perceived at the level of the vessels in the neck;
Venous buzzing: is a continuous noise with diastolic accentuation (present in 95% of children), most intense under the sterno-cleido-mastoid muscle, and best heard with the patient seated. It may sometimes be transmitted to the II-III intercostal space, be obliterated by compression of the neck veins and be accentuated by turning the head contralaterally. It is present in adults with severe hyperkinetic conditions such as anaemia, thyrotoxicosis, pregnancy, etc.
Supraclavicular arterial murmur: this is a murmur heard in the supraclavicular area, which often simulates an aortic/pulmonary murmur from stenosis; it is not a pansystolic murmur, but appears much more intense over the cervical vessels, obliterated by compression of the carotid/succlavicular arteries. It is devoid of pathological significance.
Innocent diastolic murmurs: these are not synonymous with organic murmurs, but are ‘flow murmurs’, auscultated at the cardiac apex in situations that are accompanied by high output (circulatory hyperkinesis/hyperdynamic states). The normality of the ECG/echocardiography allows local pathologies to be excluded; they have no prognostic impact.
2) Physiological murmurs:
Physiological murmurs are turbulent motions found in hyperdynamic states, linked in fact to an increase in the speed of the blood circulation. They can be paraphysiological as in the case of physical exercise and/or emotional reactions (fear, anxiety) or pathological as an indication of extra-cardiac pathology such as in the case of fever, thyrotoxicosis, pheochromocytoma, anaemia (CAVE: blood viscosity is reduced), chronic pulmonary heart; beri-beri, AV fistulas (from pregnancy, liver cirrhosis, bone Paget, fistulas proper), etc.
3) Relative murmurs:
Relative murmurs are murmurs produced by structural alterations that do not affect either the valves or any abnormal cardiac and/or vascular communication; unlike organic murmurs, they tend to disappear following appropriate therapy that improves ventricular inotropism and corrects any cardiomegaly. Examples may be a punctal holosystolic murmur from mitral insufficiency (secondary to left ventricular dilatation), a left parasternal/xiphoid holosystolic murmur from tricuspidal insufficiency (secondary to right ventricular dilatation) or a diastolic murmur from relative mitral stenosis, secondary to dilatation of the ventricle not accompanied by expansion of the valvular fibrous rim.