Cardiac, Pulmonary, and PV Exam Flashcards
S1 & S2
S3 gallop
S4 gallop
aortic stenosis
pulmonic stenosis
mitral regurgitation
tricuspid regurgitation
aortic regurgitation
mitral stenosis
S1 & S2
S1- loudest over the mitral and tricuspid valve areas.
S2- loudest over aortic and pulmonic valve areas.
Shortened time between S1 and S2 than time between S2 and S1.
S1- closure ofmitral valve, tricuspid valve may contribute (systole between S1 and S2)
S2- closure of aortic valve, pulmonic valve closure may contribute (diastole between S2 and next S1 lasts longer).
Diaphragm used to listen for S1 &S2 higher pitched sounds, murmurs of aortic and mitral regurgitation and pericardial friction ribs
Splitting Sounds
Splitting of S2: May be physiologic or pathologic.
Inspiration- Aortic (A2) first then Pulmonic (P2) due to pulmonic valve closure delay.
Expiration- Sounds are closer together and heard as a single S2.
S3 gallop
Diastolic Sound
Best heard with bell at the apex lying in left lateral decubitis bringing closer to it.
Volume overload in early diastole, rapid filling phase will fill up quickly tensing chordae tendinae creating sounds attributed to rapid ventricular filling or diminished ventricular compliance.
Sounds like Ken-Tucky
May be physiologic in well conditioned athletes, children, 3rdtrimester of pregnancy.
Older patients usually pathologic.
If diffuse PMI + S3 May suggest heart failure look for elevated JVP and carotid pulse
Women pregnant,too much vloodalready adding ventricle to what is already filled hearing sound after S2.
S4 gallop
Generally pathologic- caused from hearing atria contract. Ventricular tissue hypertrophy (larger than it should be)can cause sudden death.
Hypertension heart contracts against high bood pressure causing muscle increase in side inward making it stiff. Sound is when atria contracts into a very stiff ventricle end of diastole just before S1 component best heard in left lateral decubitis.
Diastolic Sound: atrial diastolic gallop.
Best heard with bell at the apex.
Abnormal and considered pathologic.
Attributed to atrial contraction due to diminished left ventricular stretch.
Sounds like Tenne-ssee
Left ventricular hypertrophy is present secondary to hypertension, aortic stenosis, hypertrophic cardiomyopathy (fibrotic tissue w/ deadly rhythm inverted t wave).
aortic stenosis
Location: Right 2ndand 3rdintercostal spaces aortic area . Timing: Midsystolic murmur. Intensity: Often Loud. Pitch: Medium. Quality: Harsh. Configuration: Crescendo-Decrescendo. Positioning: Heard best with patient leaning forward. systolic ejection murmur, Most common valvular lesion in the elderly. May radiate to carotids. Left sided heart stuff happens a bit before right. Mitral valve closes before aortic opens so delay then sound heart with turbulent flow through valve upward movement of leaflets that then stop because they are not functioning properly first creating ejection click small amount of blood then more and more flow then as relaxes less and less flow. Pulmonary closes before aortic- stenosis where forward blood being impeded w/ restrictions of forward blood, turbal atherosclerosis thickening cholesterol or old and valves are worn out so thickened leaflet of valves. Mitral valve regurgitation goes from ventricle back to atria
pulmonic stenosis
Location: Left 2ndand 3rdintercostal spaces. Timing: Midsystolic murmur. Intensity: Soft to Loud. Pitch: Medium. Quality: Harsh. Configuration: Crescendo-Decrescendo. Commonly heard in congenital heart disease. Aortic valve closer prior to pulmonic cant hear pulmonic closure because of stenosis. ejection click not radiating to carotids and heard in pulmonic area instead of aortic
mitral regurgitation
Location: Apex, Timing: Pansystolic murmur. Intensity: Soft to Loud. Pitch: Medium to high. Quality: Harsh. Configuration: Plateau . Radiation: Left Axilla. Unlike Tricuspid Regurgitation there is no change with respiration. Holosystolic- throughout systole continuous rectangular type of shape, soft to loud,pitch medium to high, variation of plateua radiate to left axilla. As the pressure starts to build int he ventricle w/ the aortic valve closed blood gets through valve right as S1 occurs or tries to occur. Higher in ventricle then atrium so keeps going back up into atrium causing atrial hypertrophy accepted blood volume coming back at a lower pressure doesnt change in intensity until reopens flat or doesnt change forcing back up towards arm.
mitral valve prolapse
from leaflets ballooning into left atria causing click not associate w/ ejection of blood. mid-to-late systolic click. left ventricle contract would close valve tensing of chordae or vlave as it shoots up intro atria as pressure builds making that click not closing completely correctly will then have murmur of blood returning heard best at apex. Standing decreasing venous return to heartprolonging it, squatting increase to return of heart and with preload stretching to accomadateblood and pressure.
TRICUSPID REGURGITATION
Location: Lower left sternal border (4thand 5thICS). Timing: Pansystolic murmur. Intensity: Variable. Pitch: Medium. Quality: Blowing. Configuration: Plateau. Radiation: Right sternum, xiphoid. Increases intensity with inspiration. Venous return more pressure to right side of heart same thing as mitral regurgitation but in a different location.
aortic regurgitation
pulmonic regurgitation
Location: Left 2ndto 4thintercostal spaces. Timing: Diastolic. Intensity: Usually grade 1-3. Pitch: High. Quality: Blowing. Configuration: Decrescendo. Radiation: Apex or Right sternal border.Positioning: Lean forward. Respiration: Hold breath after exhalation. blood coming back and be able to listen along left sternal border blood flows either way. aortic valve not fully close pressure greater on outside of valve in aorta than in ventricle causing it to flow back in ventricle as well as blood in ventricle filling there as well. Loudest at beginning because of high pressure as blood fills ventricle early diastolic decrescendo.
Diastolic murmur. Insufficneicy blood is refluxed back form area of high to low pressure. Hear on left side having them lean forward on left side of heart w/ radiation of sounds stenosis on right intercostal spaces. More severe it gets decrease in length due to incompetency of the valve.
same thing as aortic just heard along upper left side of sternum
mitral stenosis
Location: Apex. Timing: Diastolic. Intensity: Usually grade 1-4. Pitch: Low. Quality: Rumble. Configuration: Decrescendo. Radiation: None.Positioning: Left lateral decubitus. Respiration: Exhalation. Left lateral decubital position bring chest closer to wall. Mitral valve snaps opens (opening snap) after S2 with a not fully open valve and so in beginning most blood coming from atrium to left ventricle w/ rapid filling more beginning than end decrescendo as pressure equal atria then contracts with pre-systolic accentuation heard in mitral area/apex middiastolic rumble
Hear opening snap. Shouldn’t hear valve trying to move. Can cause the atria to become hypertrophied resulting in atrial fibrillation.
tricupsid stenosis heard in tricuspid area
systolic murmurs- pathological or innocent?
What are they and what do they look like?
Can be innocent or pathological
aortic stenosis, pulmonic stenosis
mitral (mitral valve prolapse from regurgitation) or tricuspid regurgitation
Left sided conditions: aortic stenosis, mitral regurgitation and valve prolapse
right sided conditions: pulmonic stenosis, tricupsid regurgitation
clicks: ejection clicks (aortic stenosis) non-ejection click (late systole mitral valve prolapse
opening snap: mitral stenosis
diastolic murmurs? pathological or innocent? what are they and what do they look like?
always pathological
aortic or pulmonic regurgiation
mitral stenosis and tricuspid stenosis\
Left sided aortic regurgitation and mitral stenosis
- Discuss the following common or concerning symptoms, the etiology, presentation, as well as appropriate history questions to aid in the evaluation of patients presenting with such complaints. Discuss the significance of responses.
Chest pain
does the pain occur with climbing stairs? How many flights? How many steps? How about with walking—50 feet, one block, more? What about carrying groceries, making beds, or vacuuming? How does this compare with these activities in the past? When did the symptoms appear or change? Point out the pain, is it relate to exertion? What kind of activities bring on the pain? How intense if the pain1-10? Does it radiate to shoulder, back, or down your arm? Any other symptoms like SOB, sweating, palpitation, or nausea? Does it wake you up at night? Pain Location most important- abdomen back,Quality- pressure, heaviness, sharp, stabbing, achy, burning, numbness (herpes zolster shingles),Radiation/Referral- upper extremity, jaw, back, Severity- pain scale, Onset- when, length, setting, frequency. (come and go or steady,Alleviating and Aggravating Factors-pleuritic (breathing fractured rib), rest, movement, post-prandial (after eating),Associated symptoms- dizziness, syncope, diaphoresis, cough, fever, palpitations, SOB, anxiety, nausea, vomiting, fatigue, neck or shoulder pain. Where patient feels pain isnt often where problem is. Women will come in w/ jaw pain, nausea, fatigue- when having major heart attack. always consider life- threatening diagnoses such as angina pectoris, MI, dissecting aortic aneu- rysm, and pulmonary embolus and pneumonia.gasstro- peptic ulcer disease, refluxm food poisoning. musculosketeal- disc herniation, costochdritis, psycj0 anxiety/panic, neurologica-heroes, or cancer. MI- classically exertion pain, pressure, or discomfort in chest, shoulder, back, neck, or arm found in Angina pectoris. Atypical descriptions like cramping, gridding, pricking or, rarely tooth or jaw pain. Acute coronary syndrome- clinical syndromes caused by acute myocardial ischemia including unstable angina, non-ST elevation MI and ST elevation infarction. Chest pain not caused by CAD- micro vascular coronary dysfunction and abnormal cardiac nocioception, require specialized testing ½. Women w/ chest pain have this. Acute aortic dissection-Anterior chest pain tearing or ripping radiating into back of neck
- Discuss the following common or concerning symptoms, the etiology, presentation, as well as appropriate history questions to aid in the evaluation of patients presenting with such complaints. Discuss the significance of responses.
Palpitations
unpleasant awareness of heartbeat not necessarily heart disease or dysrhythmiasEx. Skipping, racing, fluttering, pounding, or stopping of heart may be irregular, rapidly slow down or accelerate, or arise from increased forcefulness of cardiac contraction. Commonly felt by people who are anxious or have hyperthyroid. If signs or symptoms of irregular heartbeats obtain ECG including atrial fibrillation causing irregulary irregular pulse. Can be caused by transient skips and flip-flops (possible premature contractions), rapid regular beating of sudden onset and offset (possible paroxysmal supraventricular tachycardia), rapid regular beat of 120+ if gradually starting and stopping). Are you ever aware of your heartbeat? What is it like? Ask them to tap out rhythm? Was it fast or slow, regular or irregular? How long did it last? If episode of rapid heartbeats, did they start and stop suddenly or gradually? Palpations- heartbeat awareness (fluttering, skipping, racing, pounding) caused by Arrhythmias, Anxiety, Medications, Smoking, Caffeine, Acute illness, Anemia, Endocrine- hyperthyroidism, hypoglycemia.
- Discuss the following common or concerning symptoms, the etiology, presentation, as well as appropriate history questions to aid in the evaluation of patients presenting with such complaints. Discuss the significance of responses.
Shortness of breath: dyspnea, orthopnea, paroxysmal nocturnal dyspnea
f the patient is short of breath, does this occur at rest, during exercise, or after climbing stairs? Dyspnea- uncomfortable awareness of breathing that is inappropriate to a given level of exertion complaint is common in patients with cardiac or pulmonary problems. Orthopnea- dyspnea that occurs when patient is supine and improves when patient sits up ask number of pillows and how they sleep. PND- episodes of sudden dyspnea and orthopnea awaken patient from sleep 1-2 hours forcing to stand up or get air. W/ associated wheezing and coughing subsides but usually reoccurs. Sudden dyspnea occurs in pulmonary embolus, spontaneous pneumothorax, and anxiety. Orthopnea and PND- occur in left ventricular HF and mitral stenosis, obstructive lung disease. PND mimicked by nocturnal asthma attacks.
- Discuss the following common or concerning symptoms, the etiology, presentation, as well as appropriate history questions to aid in the evaluation of patients presenting with such complaints. Discuss the significance of responses.
Edema (swelling)-
)- Can absorb up to 5L of fluid before pitting occurs can be systemic or local. Have you had any swelling anywhere? Where (ankles)? When does it occur? Worse in morning or at night? Do your shoes get tight? Rings tight on fingers? Eyelids puffy or swollen in morning? Let out your belt? Clothes gotten tight? Associated symptoms (infection) Ask to record daily weight. Frequently cardiac causes (right or left ventricular dysfunction, pulmonary hypertension or pulmonary (obstructive lung disease). Can be nutritional (hypoalbuminemia), and/or positional. Dependent edema appears in lowest body parts: feet and lower legs when sitting or sacrum when bedridden. Anasarca severe generalized edema extending to sacrum and abdomen. Look for perioorbital puffiness and tight rings of nephrotic syndrome and an enlarged waistline from ascites and liver failure. right/left ventricular dysfunction, pulmonary hypertension, hypoalbuminemia (changing oncotic pressure from bad nutrition), allergic reaction, infection, liver/renal disease, lymphatic dysfunction (lympadema, damage to lymphatic tissue), dependent/positioning. 1+-4+. If immediately refills-1+, after 15-20seconds 2+, 3+ 1 minute, 4+ anything longer.
- Define, describe, or discuss the following, and associate PE findings with underlying conditions:
apical impulse
Most of anterior portion of heart is right ventricle. Listening for apical pulse at point of maximal intensity around 4ht-5th intercostal space midclavicular line. Braciocephalic vein (internal jugular becoming subclavian and external jugular vein). Aortic arch (brachiocephalic trunk (right common carotid right subclavian, common carotid left subclavian)
PMI larger than 3cm indicated ventricular enlargement. young adults may have hyperkinetic impulse when excited or after exercise occur in hyperthyroidism, severe anemia, pressure overload of left ventricle from hypertension or aortic stenosis, or volume overload of left ventricle from aortic regurgitation. Sustained high-amplitude impulse increased LVH from pressure overload seen in hypertension. diffuse sustained low-amplitude hypokinetic impuslse seen in heart failure and dialted cardiomyopathy.
Define, describe, or discuss the following, and associate PE findings with underlying conditions:
base of the heart
top of the heart located at the second intercostal interspace above the left atrium
- Define, describe, or discuss the following, and associate PE findings with underlying conditions: cardiac apex
try locating when patient lays supoine finding vertical location and distance from midclavicular at the 5thor 4thinterspace. ex. pregnancy or high left diaphragm may shift upward and to left. lateral displacement toward axillary from ventricular dilation in heart failure, cardiomyopathy, ischemic heart disease, thoracic deformities, and mediastinal shift. in left lateral decubitis diffuse
diastole- period of ventricular relaxation where blood flows from atrium to ventricle, ventricular pressure rises late in this cycle due to atrial contraction. aortic valve closed preventing regurgitation of blood from aorta to LV, mitral open allowing blood from left atrium to LV. Pulmonic valve closes and tricuspid opens.
- Define, describe, or discuss the following, and associate PE findings with underlying conditions:
dyspnea
difficulty breathing caused by asthma attack, COPD, CHF etc.
- Define, describe, or discuss the following, and associate PE findings with underlying conditions: edema
efers to accumulation of excessive fluid in extravascular interstitial space can be caused by CHF, infection
- Define, describe, or discuss the following, and associate PE findings with underlying conditions:
insufficiency
-to blood vessels caused by hypertension, cardiac hypertrophy other degenerative cardiac ofr vascular disease
- Define, describe, or discuss the following, and associate PE findings with underlying conditions:
murmur
Heart murmurs are distinct heart sounds distinguished by their pitch and their longer duration. They are attributed to turbulent blood flow and are usually diagnostic of valvular heart disease.
- Define, describe, or discuss the following, and associate PE findings with underlying conditions:
orthopnea-
difficulty breathing when laying down relived by sitting up ex. caused by edema
- Define, describe, or discuss the following, and associate PE findings with underlying conditions\
paroxysmal nocturnal dyspnea-
episodes of difficulty breathing particularly at nighttime that wake you up from sleep
- Define, describe, or discuss the following, and associate PE findings with underlying conditions: point of maximal impulse
- left ventricle tapered inferior tip, cardiac apex and is the point of maximal impulse. Locates left border of heart found in 5thintercostal space at or or just medial to left midclavicular line (7-9cm) not always palpable on a healthy patient w/ a normal heart. detection affected by pt’s habitus and position. diameter should be up to quarter or 1-2.5 cm,
- Define, describe, or discuss the following, and associate PE findings with underlying conditions: regurgitation-
valve that does not fully close letting blood flow back from where it came as seen in mitral and aortic regurgitation.
- Define, describe, or discuss the following, and associate PE findings with underlying conditions: stenosis-
when valve narrows prevent valve from opening fully reducing or blocks blood flow from heart into body as seen in mitral and aortic stenosis
Define, describe, or discuss the following, and associate PE findings with underlying conditions: systole-
period of ventricular contraction, pressure in LV rises from 5mmhg to 120mmhg pressure falls. aortic valve open allowing ejection of blood from LV to aorta, mitral close preventing regurgitation. Pulmonic valve opens tricuspid closes.
- Define, describe, or discuss the following, and associate PE findings with underlying conditions: venous hum
- found in the jugular venous is found in children up to adulthood and has both systolic and diastolic components benign sound produced by trubulence of blood
- Define, describe, or discuss the following, and associate PE findings with underlying conditions: ventricular hypertrophy
found by PMI >2.5 cm from hypertension or aortic stenosis if the PMI is displaced to midclavicular line or >10cm lateral to midsternal line also an indicator as well as ventricular dilatation MI or CHF. COPD pt’s PMI in xiphoid or epigastric area also due to this phenomenon
- Given a diagram of the heart, identify the following structures:
aorta- curves upward from left ventricle to level of sternal angle, arching posteriorly to left and downward.
aortic valve
apical impulse- PMI
inferior vena cava- medial border of sternum
left ventricle
mitral valve
pulmonary artery
pulmonary artery
pulmonary veins
pulmonic valve
right atrium
right ventricle
superior vena cava- medial border of sternum
tricuspid valve
- Describe the sequence of blood flow through the valves and chambers of the heart.
Blood that has been through systemic circuit returns by superior & inferior venae cavae to right atrium through AV (tricuspid) valve into right ventricle. When right ventricle contracts, ejects blood through pulmonary valve into pulmonary trunk or artery (only arteries in body carrying deoxygenated blood to lungs) exchanging CO2 and O2 at lungs. Blood returns from lungs by two pulmonary veins (only veins carrying oxygenated blood) on left and two on right where they empty into left atrium. Blood flows through left AV (mitral valve) to left ventricle w/ contraction ejecting blood through aortic valve into ascending aorta and through systemic circuit.
- Describe the cardiac cycle (systole/diastole) in terms of pressure changes, valve positions, contraction-relaxation, and blood flow.
During diastole, pressure in the blood- filled left atrium slightly exceeds that in the relaxed left ventricle, and blood flows from left atrium to left ventricle across the open mitral valve. Just before the onset of ventricular systole, atrial con- traction produces a slight pressure rise in both chambers. During systole, the left ventricle starts to contract and ventricular pressure rapidly exceeds left atrial pressure, closing the mitral valve. Closure of the mitral valve produces the first heart sound, S1. As left ventricular pressure continues to rise, it quickly exceeds the pressure in the aorta and forces the aortic valve open. In some pathologic conditions, an early systolic ejection sound (Ej) accompanies the opening of the aortic valve. Normally, maximal left ventricular pressure corresponds to systolic blood pressure. As the left ventricle ejects most of its blood, ventricular pressure begins to fall. When left ventricular pressure drops below aortic pressure, the aortic valve closes. Aortic valve closure produces the second heart sound, S2, and another diastole begins. Semilunar valves- semilunar valves open when ventricular pressure higher than aortic pressure close when aortic pressure higher than ventricle as blood is pumped out beginning S2 ventricular lower than atrial pressure AV valves open for relaxation.
- Identify the physiological events corresponding with normal and abnormal heart sounds.
S1 lub (valvular closure of AV valves, blood flow): Left ventricular Systole- ventricular contraction blood pumped into pulmonary artery to get oxygenated. Right ventricular systole- ventricular contraction blood pumped to body, Mitral valves open. S2- diastole dub blood entering through AV valves through pulmonary veins into left atrium into ventricle. Right side comingin from superior and inferior vena cave semilunar not open. In diastole, left ventricular pressure con- tinues to drop and falls below left atrial pressure. The mitral valve opens. This event is usually silent, but may be audible as a pathologic opening snap (OS) if valve leaflet motion is restricted, as in mitral stenosis. After the mitral valve opens, there is a period of rapid ventricular filling as blood flows early in diastole from left atrium to left ventricle. In children and young adults, a third heart sound, S3, may arise from rapid deceleration of the col- umn of blood against the ventricular wall. In older adults, an S3, sometimes termed “an S3 gallop,” usually indicates a patho- logic change in ventricular compliance. Finally, although not often heard in nor- mal adults, a fourth heart sound, S4, marks atrial contraction. It immediately precedes S1 of the next beat and can also reflect a pathologic change in ventricular compliance.
- Describe splitting of S1 and S2 in terms of individual valves, where it can be heard best and any variation with respiration.
Right ventricular and pulmonary arte- rial pressures are significantly lower than corresponding pressures on the left side. Mitral component: louder and earlier. Tricuspid component: softer and later. S1 splitting does not vary with respiration. Note that right-sided cardiac events usually occur slightly later than those on the left. Instead of a hearing a single heart sound for S2, you may hear two discernible components, the first from left-sided aortic valve closure, or A2, and the second from right-sided closure of the pulmonic valve, or P2. The second heart sound, S2, and its two components, A2 and P2, are caused pri- marily by closure of the aortic and pulmonic valves, respectively. During inspira- tion, the right heart filling time is increased, which increases right ventricular stroke volume and the duration of right ventricular ejection compared with the neighboring left ventricle. This delays the closure of the pulmonic valve, P2, splitting S2 into its two audible components. During expiration, these two com- ponents fuse into a single sound, S2. Note that because walls of veins contain less smooth muscle, the venous system has more capacitance than the arterial system and lower systemic pressure. Distensibility and impedance in the pulmonary vascular bed contribute to the “hangout time” that delays P2. Of the two components of the S2, A2 is normally louder, reflecting the high pressure in the aorta. It is heard throughout the precordium. In contrast, P2 is relatively soft, reflecting the lower pressure in the pulmonary artery. It is heard best in its own area, the 2nd and 3rd left interspaces close to the sternum. It is here that you should search for the splitting of S2. S1 also has two components, an earlier mitral and a later tricuspid sound. The mitral sound—the principal component of S1—is much louder, again reflecting the higher pressures on the left side of the heart. It can be heard throughout the precordium and is loudest at the cardiac apex. The softer tricuspid component is heard best at the lower left sternal border; it is here that you may hear a split S1. The earlier louder mitral component may mask the tricuspid sound, how- ever, and splitting is not always detectable. Splitting of S1 does not vary with respiration.
- Compare and contrast the characteristics of internal jugular pulsations with characteristics of the carotid pulse.
Jugular venous pressure ( JVP) reflects right atrial pressure, which in turn equals central venous pressure and right ventricular end-diastolic pres- sure. The JVP is best estimated from the right internal jugular vein, which has the most direct channel into the right atrium. Changing pressures in the right atrium during diastole and systole produce oscillations of fill- ing and emptying in the jugular veins, or jugular venous pulsations (Fig. 9-20). Atrial contraction produces an a wave in the jugular veins just before S1 and systole, followed by the x descent of atrial relaxation. As right atrial pressure begins to rise with inflow from the vena cava during right ventricular systole, there is a second eleva- tion, the v wave, followed by the y descent as blood passively empties into the RV during early and middiastole. With each contraction, the left ventricle ejects a volume of blood into the aorta that then perfuses the arterial tree. As the ensuing pressure wave moves rapidly through the arterial system it generates the arterial pulse. Internal jugular pulsations: rarely palpable, soft biphasic undulating quality, usually w/ two elevations and characteristic inward deflection, pulsations eliminated by light pressure on veins just above sternal end of clavicle, height of pulsations changes w/ position, normally dropping as patient becomes more upright, height of pulsations usually falls with inspiration. Carotid pulsations: palpable, more vigorous thrust w/ single outward component, pulsations not eliminated by pressure on veins at sternal end of clavicle, height of pulsations unchanged by position, height of pulsations not affected by inspiration.
Look for carotid artery medially superior to sternal notch between sternocleidomastoid for the carotid artery pulsation vigorous thrust w/ visible outward component almost always palpable and doesn’t change w/ position. Lateral to that between sternocleidomastoid and clavicularhead should be the internal jugular venous pulsation are soft undulating pulsations with three elevations per heartbeat and 2 troughs per beat and is rarely palpable eliminated by light pressure above clavicle and change with position in euvolemicpatient level dropping as patient becomes more upright level falls w/ inspiration.
Internal Jugular:
Rarely palpable
flicker wave
Soft and eliminated with light pressure.
Height changes with position and respiration. (when sit them up goes lower)
Carotid:
Palpable
Vigorous and not eliminated with light pressure.
Height unchanged with position or respiration.
Carotidpulse asses valvularheart disease detects aortic stenosis and insufficiency. Palpation to asses amplitude and contour of carotid upstrakeand ausculatationfor the presence or absence of bruits from turbulent blood flow. Don’t press on both at once. Increase pressure until you feel maximal pulsation then decrease pressure until you sense the arterial pressure wave and contour asses amplitude of pulse (pulse pressure speed of upstroke brisk smooth and rapid following S1 immediately. Summit is smooth round and roughly at systolic, downstrokeis less abrupt than the upstroke) can detect bounding upstroke etc.
Shouldn’t move,change w/ movement.
- Given a diagram of the heart, identify the following structures of the heart’s conduction system:
· Atrioventricular (AV) node- low in atrial septm
· Bundle of His
· Left bundle branch
· Right bundle branch
· Sinoatrial (SA) node-in RA near junction of vena cava
- Describe the sequence of the electrical impulses through the heart.
The small P wave of atrial depolarization (duration up to 80 milliseconds; PR interval 120 to 200 milliseconds)
The larger QRS complex of ventricular depolarization (up to 100 milliseconds), consisting of one or more of the following
the Q wave, a downward deflection from septal depolarization
the R wave, an upward deflection from ventricular depolarization
the S wave, a downward deflection following an R wave
A T wave of ventricular repolarization, or recovery (duration relates to QRS)
- Describe and demonstrate appropriate techniques for the cardiac examination to include:
measuring jugular venous pressure (JVP)-
JVP accurately predicts elevations in fluid volume in heart failure, prognostic value for heart failure outcomes and mortality is unclear. Parallels pressure in right atrium, or central venous pressure, relating to volume in venous system best assessed from pulsations in right internal jugular vein in line with superior vena cava and right atrium. Able to detect volume status, right and left ventricular function, patency of tricuspid and pulmonary valves, pressure in pericardium, and arrhythmias caused by junctional rhythms and AV blocks falling with loss of blood or decreased venous vascular tone increases with right or left heart failure, pulmonary hypertension, tricuspid stenosis, AV dissociation, increased venous vascular tone, and pericardial compression or tamponade. Find highest point of oscillation in internal jugular vein using tangential lighting or where external jugular vein collapsed measured in vertical distance above sternal angle. If patient hypovolemic JVP will be low causing you to lower head of bed to see it, if patient is volume-overloaded hypervolemic JVP will be high cuaisng you to raise it. Seen in tricuspid stenosis, chronic pulmonary hypertension, superior vena cava obstruction, cardiac tamponade, and constrictive pericarditis. First eleveation, presystolic a wave (abnormally prominent a waves in increased resistance to right atrial contract-tricuspid stenosis, 1st,2nd,3rddegree AV block, supraventricular tachycardia, junctional tachycardia, pulmonary hypertension, and pulmonic stenosis signal atrial fibrillation) is slight rise in atrial pressure accompanies atrial contraction prior to S1 before carotid upstroke, trough x descent, starts w/ atrial relaxation continues as RV, contracting during systole pulls floor of atrium downward, ends before S2. during ventricular systole, blood continues to flow into right atrium from venae cavae. tricuspid valve closed and chamber begins to fill and right atrial pressure begins to rise again, creating second elevation v wave (increased in tricuspid regurgitation, atrial septal defects, and constrictive pericarditis) when opens early in diastole blood in right atrium JVP parallels pressure in the right atrium or primary volume in the venous system. Measurement of pulsations in the right internal jugular vein provides best accuracy. Highest point of pulsation in the internal jugular or external jugular vein. Jugular Venous Distension (JVD): Visualization of jugular vein. Is a sign of increased central venous pressure which may commonly suggest right sided heart failure, pulmonary hypertension. flows passively into RV and right atrial pressure falls again creating second trough. Measurement of the highest oscillation point (“meniscus”) of jugular venous pulsations, reflects pressure in the right atrium (ventral venous pressure). Provides information about volume status and cardiac function. Pillow just above shoulders. Examine both sides of neck and turning to the left on right side.
Patient is placed in supine position with head of examination table elevated to 30 degrees.
Ruler placed in the vertical plane with zero at the sternal angle.
Place additional straight edge at the top of the jugular pulsation.
Normal is less than or equal to 3 cm or 7-8cm in total distance above right atrium.
Vertical distance in centimeters above sternal angle where your card crosses ruler
How much pressure is required to force a column of water x number of centimeters up. Force require to move column of water up the head.
Use cardor something flat from meniscus highest point of pumping line up on sternal angle at right angle
Important for us to test in euvolemic, hypervolemic(ex. CHF or renal failure) (as high as angle in jaw), or hypovolemic patients (ex. GI bleed, marked dehydration) below sternal angle.
- Describe and demonstrate appropriate techniques for the cardiac examination to include:
locating the key palpation areas on the chest wall and appropriate technique in assessing impulses
After examining the JVP and carotid pulse, inspect and palpate the precordium: the 2nd right and left interspaces; the RV; and the LV, including the apical impulse (diameter, location, amplitude, duration). Left sternal border in 3rd, 4th, and 5thinterspaces w/ patient supine and head elevated ask patient to exhale and briefly stop breathing, plcing fingers to palpate systolc impulse of RV assessing LAD may detect systolic tap in thin individuals or S3 and S4 right sided movements time against upstroke. sustained left parasternal movement beginning at S1 points to pressure overload from pulmonary hypertension and pulmonic stenosis or chronic ventricular volume overload of atrial septal defect sustained movement later in systole seen in mitral regurgitation.
Palpation:
Heaves/Lifts (can see heart pumping through chest wall- Use palm and or fingertips. Ventricular pulses heave and lift fingers suggesting ventricular delitation. Thrills (underlying turbulent blood flow change grading of heart) ball of hand revealing a loud murmur.
Right Ventricular Area (systolic impulse)-Left sternal border.
Epigastric Area. Should not be feeling impulses there could be because of an enlarged ventricle
Pulmonic Area.
Aortic Area.
PMI- Left Mid-clavicular line, 4thand 5thinterspaces. Just below the nipple. 2.5 cm. Measure less than.Underneath nipple can feel PMI, can see movement underneath. Percuss for resonant should hear for lungs filling. Percuss medially until you get to border and you can feel and measure the border of the heart shouldn’t be larger than 2.5cm. Would be further right if they have hypertrophy
Thrills-over the cardiac valve points.- 3, 4, and 5thintercostal spaces should not be feeling impulses at all. Feel for right ventricular impulse at lower left sternal border while keeping one finger in 3rdinterspace then feel for right ventricular impulse in subxiphoid area. If patient’s chest has increased anteroposterior diameter palpate for right ventricular impulse high in epigastric area where it is easier to feel found in COPD due to increased right ventricular pressure and hypertrophy from pulmonary hypertension.
locating the key auscultation areas on the chest wall and appropriate technique in assessing heart sounds
All patients eventually trust me.
Pulmonic (right intercostal space sternal border. Left atrium is posterior, right atrium is superior right netierh examined directly. Pulmonary artery arising from right ventricle quickly bifurcates into left and right branches aorta from left ventricle. Anterior surface of heart right ventricle. . Left ventricle behind and to the left of right ventricle producing tapping apical impulse in left 5th interface measures about size of quarter 1-2.5 cm in diameter. Enlarged right ventrical may produce more prominent impulse than the apical, apical impulse noting location, diameter, and amplitude.. Location from midsternal line if difficult ask patient to roll onto side measure diameter and amplitude. Diffuse apical impulse suggest left ventricualr dilatation found in heart failure. Sustained tapping impulse lifting finger off chest wall suggests left ventricular hypertrophy in hypertension and aortic stenosis. Note cardiac rate and rhythm, S2 louder than S1 in aortic area and pulmonic area.
S2 diminishes and S1 gets louder through 3rd interspace becoming louder as you proceed down the chest into the tricuspid and mitral area. Switch to bell along sternal border of left 4th and 5th interspaces next to sternum and down laterally. S3, S4, and mitral sinus place patient in left lateral decubitis position.
aortic valve- right 2ndintercostal space to apex
pulmonic valve- left 2ndand 3rdintercostal space close to sternum, but at higher or lower levels
tricuspid valve- at or near lower left sternal border
mitral valve- at and around cardiac apex
- Describe the criteria used to classify murmurs.
Heart murmurs are distinct heart sounds distinguished by their pitch and their longer duration. They are attributed to turbulent blood flow and are usually diagnostic of valvular heart disease. A stenotic valve has an abnormally narrowed valvular orifice that obstructs blood flow, as in aortic stenosis, and causes a characteristic murmur. So does a valve that fails to fully close, as in aortic regurgitation. Such a valve allows blood to leak backward in a retrograde direction and produces a regurgitant murmur Distinct heart sounds attributed to turbulent blood flow. Pathologic (systolic and diastolic) vs Innocent (all systolic- functional like pregnancy, infection, anemia) (changes w/ movement) Distinguished by: Duration (how long it lasts for), Configuration (sound based on shape Crescendo-louder increasing intensity, decrescendo- quieter decreasing intensity over time, or crescendo-decresceno: increases then decreases. plaeteau-same throughout), Pitch (high, medium, low) and Quality (Quality- harsh, blowing (aortic regurgitation), musical (murmurs of mitral valve prolapse), dull, booming, scratchy and rumbling (mitral stenosis). Intensity- low hard to hear graded on six point scale, Grade 1- faint, not heard in all, Grade 2- quiet but heard immediately, Grade 3 (moderate w/ palpable thrill), 4 (loud w/ palpable thrill), 5 (loud w/ thrill w/ stethoscope off chest wall), 6 (loudest thrill heart w/ stethoscope off chest wall) increasingly loud and palpable thrim. Location, Respiration and positioning (right sided valves increase w/ inspiration increasing venous return putting more pressure on heart determined by site of origin, explore where murmur is loudest relative to sternum, apex, midsternal, midvlacivluar and axillary lines. If see diastolic pathological. systolic murmur- between S1 and S2 along with carotid upstroke. Early mid or late systolic, pansystolic Carotid upstroke right after S1 blood sent to aorta and throughout palpate while listening to chest. If happens at same time it is systolic, if after it is diastolic. For systolic murmurs must concur with carotid upstroke right after S in systole if after it is after diastolic. Ex. Midsystolic- phsyiologic flow crescendo-decrescnendo murmur of aortic stenosis after S1 before S2 brief gaps between beat and sound, Some systolic murmurs can last throughout systole which are referred to as holosystolic or pansystolic. Diastolic murmur- falling between S2 and S1 before or after carotid upstroke. Mitral regurgitation- starts w/ S1 and stops at S2 without a gap between murmur and heart sounds. Mitral stenosis- starts after S2 following opening snap. Shape of murmur depending upon intensity over time. Radiation based on transmission from point of maximal intensity, reflects site of origin, and intensity of murmur, and direction of blood flow determining where else you can here it. Diastolic- sitting up and leaning forward for aortic regurgitation moving it closer to left wall exhale completely holding breath out, diaphragm left second interspace and sternal border of apex listening for descrendo diastolic murmur of aortic regurgitation. Mitral stenosis- left lateral decubitis more subtle opening snap and diastolic rumble of stenosis. Have to move patient to hear it better
- Describe other heart sounds including rubs, gallops, clicks, opening snaps, and ejection sounds, and associate each with common underlying pathologies. S3 gallop-
Diastolic Sound, Best heard with bell at the apex, Attributed to rapid ventricular filling or diminished ventricular compliance. Sounds like Ken-Tucky. May be physiologic in well conditioned athletes, children, 3rdtrimester of pregnancy. Older patients usually pathologic of heart failure. May suggest heart failure. Women pregnant, too much vlood already adding ventricle to what is already filled hearing sound after S2. If diffuse PMI + S3 suggests congestive heart failure look for elevated JVP and carotid pulse
- Describe other heart sounds including rubs, gallops, clicks, opening snaps, and ejection sounds, and associate each with common underlying pathologies.
S4 Gallop-
Diastolic Sound: atrial diastolic gallop caused from hearing atria contract Best heard with bell at the apex. Abnormal and considered pathologic. Before S1 component Attributed to atrial contraction due to diminished left ventricular stretch. Sounds like Tenne-ssee. Left ventricular hypertrophy is present secondary to hypertension, aortic stenosis, hypertrophic cardiomyopathy (fibrotic tissue w/ deadly rhythm inverted t wave) (larger than it should be) can cause sudden death.
- Describe other heart sounds including rubs, gallops, clicks, opening snaps, and ejection sounds, and associate each with common underlying pathologies. Aortic stenosis-
- Location: Right 2ndand 3rdintercostal spaces. Timing: Midsystolic murmur. Intensity: Often Loud. Pitch: Medium. Quality: Harsh. Configuration: Crescendo-Decrescendo. Positioning: Heard best with patient leaning forward. Most common valvular lesion in the elderly. May radiate to cartoids. Left sided heart stuff happens a bit before right. Pulmonary closes before aortic- stenosis where forward blood being impeded w/ restrictions of forward blood, turbal atherosclerosis thickening cholesterol or old and valves are worn out so thickened leaflet of valves. Mitral valve regurgitation goes from ventricle back to atria
- Describe other heart sounds including rubs, gallops, clicks, opening snaps, and ejection sounds, and associate each with common underlying pathologies.
Pulmonic stenosis-
Location: Left 2ndand 3rdintercostal spaces. Timing: Midsystolic murmur. Intensity: Soft to Loud. Pitch: Medium. Quality: Harsh. Configuration: Crescendo-Decrescendo. Commonly heard in congenital heart disease. Aortic valve closer prior to pulmonic cant hear pulmonic closure because of stenosis.
- Describe other heart sounds including rubs, gallops, clicks, opening snaps, and ejection sounds, and associate each with common underlying pathologies.
mitral regurgitation
Location: Apex, Timing: Pansystolic murmur. Intensity: Soft to Loud. Pitch: Medium to high. Quality: Harsh. Configuration: Plateau . Radiation: Left Axilla. Unlike Tricuspid Regurgitation there is no change with respiration. Holo throughout systole continuous rectangular type of shape, soft to loud,pitch medium to high, variation of plateua radiate to left axilla.
- Describe other heart sounds including rubs, gallops, clicks, opening snaps, and ejection sounds, and associate each with common underlying pathologies.
Mitral valve prolapse-
from leaflets ballooning into left atria. Standing decreasing venous return to heart prolonging it, squatting increase to return of heart and with preload stretching to accomadate blood and pressure.
Cardiac System Abnormalities
- Describe other heart sounds including rubs, gallops, clicks, opening snaps, and ejection sounds, and associate each with common underlying pathologies.
tricuspid regurgitation
Location: Lower left sternal border (4thand 5thICS). Timing: Pansystolic murmur. Intensity: Variable. Pitch: Medium. Quality: Blowing. Configuration: Plateau. Radiation: Right sternum, xiphoid. Increases intensity with inspiration. Venous return more pressure to right side of heart
Cardiac System Abnormalities
- Describe other heart sounds including rubs, gallops, clicks, opening snaps, and ejection sounds, and associate each with common underlying pathologies.
aortic regurgitation
- Location: Left 2ndto 4thintercostal spaces. Timing: Diastolic. Intensity: Usually grade 1-3. Pitch: High. Quality: Blowing. Configuration: Decrescendo. Radiation: Apex or Right sternal border. Positioning: Lean forward. Respiration: Hold breath after exhalation. Diastolic murmur. Insufficneicy blood is refluxed back form area of high to low pressure. Hear on left side having them lean forward on left side of heart w/ radiation of sounds stenosis on right intercostal spaces. More severe it gets decrease in length due to incompetency of the valve.
- Describe other heart sounds including rubs, gallops, clicks, opening snaps, and ejection sounds, and associate each with common underlying pathologies.
mitral stenosis
- Location: Apex. Timing: Diastolic. Intensity: Usually grade 1-4. Pitch: Low. Quality: Rumble. Configuration: Decrescendo. Radiation: None. Positioning: Left lateral decubitus. Respiration: Exhalation. Left lateral decubital position bring chest closer to wall. Hear opening snap. Shouldn’t hear valve trying to move. Can cause the atria to become hypertrophied resulting in atrial fibrillation.
crackles (rales)
egophony
hemoptysis
rhonchi
stridor
wheezing
Bronchial breath sounds
Vesicular Breath sounds