Track 1: Obtaining a Comprehensive Patient History in Cardiac Disease Flashcards
OBTAINING A COMPREHENSIVE PATIENT HISTORY IN CARDIAC DISEASE
6 key features of the history
- Character (+ location, radiation, severity, *anginal equivalent?)
- Timing (including onset, progression)
- Duration
- Associated sxs
*SOB, pain with respiration, orthopnea, edema, diaphoresis, nausea, palpitations, LH, change in functional activities - Mitigating factors
- Alleviating factors
*Lead time (weeks leading up)
*Self treatment
Cardiac physical exam (systematic approach) (8)
- Vital signs
- General appearance
- Head/Neck
- Cardiac Exam
- Lungs
- Abdomen
- Extremities
- Neurological
Physical exam vital signs
- Febrile?
- Rate? Rhythm?
- BP in both arms (especially when dissection is on ddx)
- RR
- O2 sat
Physical exam general appearance
- Diaphoretic
- Distressed
- Cold
- Warm
- Restless
- Sitting up, comfortable?
- Obvious rashes, trauma, wounds
Physical exam head and neck
- Color of face (cyanosis, flushing, jaundice, structural abnormalities)
- Neck (thyromegaly, lymphadenopathy)
(JVD/Bruits are a nice segue into cardiac exam)
Physical exam cardiac
Vascular assessment, inspect and palpate precordium, then auscultate
VASCULAR ASSESSMENT
- JVD (light chin tilt up w/ head to left, 45 degree angle)
Point of reference is RA or sternal angle (5cm), add anything above this point to 5cm. > 9cm is elevated *tip look at ear lobe and jaw line
- Carotid (listen for bruit, evaluate for upstroke: brisk, delayed, normal)
- Abdominal and femoral pules (strength, bruit)
- Peripheral pulses (absent to bounding scored 0-4+, symmetry, irregularity)
*Radial and femoral pulses are especially important if pt undergoing cath or other procedure requiring arterial access. Need to know baseline
INSPECT PRECORDIUM
- Chest wall deformities
- Rashes or wounds
- Scars
PALPATE CHEST WALL
- Chest wall tenderness
- Heave of lift
- Apical impulse (~10cm down from mid-sternal line in 4th-5th ICS) should be gentle and nonsustained
AUSCULTATE
EXTREMITIES
- Capillary refill
- Hair growth
- Nails (clubbing etc)
- Edema
Physical exam lungs
- Respiratory effort, labored? tachypneic
- Retraction
- Symmetry with expansion
- Auscultate for crackles, wheezes, rales, rubs (*See if sounds are resolved by cough)
- Diminished lung sounds
- Cough (productive? non productive? hemoptysis?)
- Lay flat if concern for orthopnea
Physical exam abdomen
- Auscultate before palpating
- Size, shape, soft, distended
- Tenderness
- Ascites
- Hepatojugular reflux (firm pressure over liver, hold for 30 seconds +, good test for RV failure, TR, constrictive pericarditis)
Physical exam extremities
- Rashes, petechiae, ecchymosis, splinter hemorrhages, nodules, erythema nodosum (sarcoid)
- Edema
- Cool or warm
- Clubbing
Physical exam neurological
- Orientation, cranial nerves, motor function
- Focal neurological deficits (especially if ao dissection is on ddx, * chest pain + neuro deficits)
- Establish good baseline, cardiac procedures harbor small stroke risk. Good documentation of baseline can help assess subtle changes after any procedure
Evidence for correlations between history and physical exam findings. and cardiovascular disease severity and prognosis have been developed most rigorously for what conditions? (3)
- Heart failure
- Valvular disease
- Coronary artery disease
Name 3 key physical exam features that contribute to bedside risk assessment in patients with ACS
Vital signs
Presence of MR
Detection of pulmonary congestion
Heart failure in the ambulatory patient
Name 3 basic elements of the history that support dx
Name 6 validated elements of the PE that support dx
- Dyspnea at one flight of stairs
- Orthopnea
- PND
- Displaced apex beat
- Rales
- Irregularly irregular pulse
- Murmur suggestive of MR
- HR > 60
- Elevated JVP
Typical angina should satisfy 3 characteristics. Name them
- Substernal discomfort
- Initiated by exertion or stress
- Relieved with rest or sublingual nitro
*chest discomfort w/ 2 of the 3 criteria is considered atypical angina, pain with 1 or none of these features is considered nonanginal
Name some characteristics that increase or decrease the likelihood for ACS in setting of chest pain
- Sharp, pleuritic, reproducible with palpation- decreased likelihood
- Radiation to both arms or shoulders, precipitated by exertion- increased likelihood
Name some anginal equivalents
- Indigestion
- Belching
- Dyspnea
In what 3 special populations must you keep a high suspicion for ACS despite a “classic” presentation
- Women
- Elderly
- Diabetics
Dyspnea upon standing
Platypnea
Describe characteristics of PND of cardiac origin
- Usually occurs 2-4 hours after onset of sleep
- Severe enough to compel pt to sit upright or stand
- Subsides gradually over several minutes
Regular, rapid-pounding sensation in the neck or visible neck pulsations associated with palpitations
Increased likelihood for:
Atrioventricular nodal reentrant tachycardia (AVNRT)
*Absence of “neck pounding sensation” makes AVNRT less likely
Syncope w/ early warning signs (nausea, yawning), ashen and diaphoretic, slow to revive
Syncope w/ sudden onset, rapid restoration of full consciousness thereafter
More likely neurocardiogenic
More like cardiac
Chest pain diminishes with sitting up, leaning forward or breathing shallowly
Pericarditis
Pursing of the lips, breath quality to voice, increased AP chest diameter
Favors pulmonary etiology
In pt with palpitations, resting heart rate < 60 bpm increases likelihood of
clinically significant arrhythmia
Name some criteria to evaluate fragility (useful tool in eval of pt w/ HF and pre procedural appraisal)
- Unintentional weight loss
- Grip strength
- Gait speed
- Exhaustion (self reported)
- Inactivity
- Serum albumin
- Hemoglobin
Central cyanosis, consider:
- Right to left shunt
- Hereditary methemoglobinemia
Peripheral cyanosis
- Reduced blood flow that accompanies small vessel constriction seen in severe HF, shock, or PVD
Cyanosis affecting the lower but not the upper extremities
- PDA
- Pulmonary artery hypertension (PAH)
- Right to left shunting at the great vessel level
Lace-like purplish discoloration of the skin that imparts a mottled or reticulated appearance
Livedo reticularis
Can occur on exposure to cold in normal individuals
Also observed in a variety of conditions resulting in sluggish cutaneous blood flow (cardiogenic shock, certain autoimmune disorders, polyarteritis nodosum, antiphospholipid etc.)
Telangiectasias
- Scleroderma
- Pulmonary hypertension
- Cirrhosis
Ecchymoses:
Petechiae:
Purpura:
- OAC, antiplatelet use
- Thrombocytopenia
- Infective endocarditis, other causes of leukocytoclastic vasculitis
Tanned/bronzed discoloration of the skin in unexposed areas
- Iron overload
- Bronze discoloration
(*Bronzed diabetic)
Xanthomas
- Various lipid disorders
- Located subcutaneously along tendon sheaths or over extensor surfaces of extremities
Lupus pernio, erythema nodosum, or granuloma annulare
Sarcoid
What head/neck PE component should be assessed both as a source of infection and as an index of general health and hygiene
Dentition
Large protruding tongue
Parotid enlargement
* Carpal tunnel
Amyloidosis
High arched palate
Marfran + other CT disorders
Bifid uvula
Loeys-Dietz syndrome
* CT disorder, enlarged aorta
Blue sclera
MR or AR
Recurrent non traumatic skeletal fractures
Osteogenesis imperfecta
Lacrimal gland hyperplasia my be associated with
sarcoid
“Mitral facies”
- Rheumatic mitral stenosis. Also pulmonary hypertension and reduced cardiac output
- Pink-purplish patches with telangiectasias over the malar eminences
Proptosis, lid lag, stare
Graves hyperthyroidism
Nail clubbing
Central shunting
Arachnodactyly
Long, slender, curved fingers
Marfan
Contender, slightly raised areas of hemorrhage on the palms and soles
Janeway lesions
Tender, raised nodules on the pads of the fingers or toes
Osler nodes
Ulcerations and tissue loss of the fingertips may suggest
thromboangiitis obliterates
Normal JVP
Extensive varicosities, medial ulcers, brownish pigmentation from hemosiderin deposition
Chronic venous insufficiency
Muscular atrophy
Loss of hair
Dependent rubor
Chronic arterial insufficiency
Redistribution of fat from extremities to central abdominal stores
lipodystrophy
(pt with HIV infection related to antiretroviral therapy, insulin resistance, metabolic syndrome)
Cutaneous venous collaterals over the anterior chest
Chronic obstruction of superior vena cava or subclavian vein (especially in presence of indewlling catheters or leads from cardiac implantable electrical devices)
Pectus carinatum or pectus excavatum
May suggest connective tissue disorder
Barrel chest of emphysema or advanced kyphoscoliosis may be associated with
cor pulmonale
Severe kyphosis of ankylosing spondylitis, cardiac abnormalities possible?
- AR
- First degree AV block
“Straight back syndrome”, loss of normal kyphosis of thoracic spine. May accompany what cardiac abnormality?
MVP
Prominence of cardiac impulse in the epigastrium
Emphysema
Liver enlarged and tender
Heart failure
(or other hepatic pathology)
Systolic hepatic pulsations
Severe TR
Splenomegaly
Long standing infective endocarditis
Ascites
Advanced and chronic right heart failure
Constrictive pericarditis
The dx of heart failure is fundamentally made at the bedside from the sxs and signs that reflect (2)
- Congestion
- End organ perfusion
Name 8 history and exam findings suggestive of cardiac syncope
- Known heart disease
- Abnormal CV PE
- Family hx of sudden death or drowning
- Male sex
- Age > 35 years at time of syncope
- ≤ 2 previous episodes
- Palpitaitons
- Chest pain or dyspnea
In evaluating JVP, the estimated height of the venous pressure indicates:
the CVP or right atrial pressure
Venous waveform characteristic features (4)
a wave
c wave
v wave
x descent
y descent
Describe the technique to measure venous pressure/JVP
Estimated by the vertical distance between the top of the venous pulastion and the sternal inflection point (where the manubrium meets the sternum/angle of Louis)
*Distance > 3cm is considered elevated
Define elevated JVP
Venous pulsation > 3cm from angle of Louis
*But note distance between angle of Louis and mid-right atrium varies considerably as a function of body size and position
Distance from right atrium to clavicle
At least 10cm
venous waveforms
reflects right atrial presystolic contraction, occurs just after the ECG P wave and precedes the first heart sound (S1)
a wave
prominent venous a wave suggests
Reduced RV compliance
Cannon a wave
AV dissociation and right atrial contraction against a closed tricuspid valve
The presence of cannon a waves in a patient with wide complex tachycardia identifies the rhythm as
ventricular in origin
Describe the a wave in JVP eval
reflects right atrial presystolic contraction, occurs just after the ECG P wave wave, precedes S1
The a wave is absent in what rhythm
AF
Venous pulsations
Reflects the fall in right atrial pressure after the a wave
Atrial diastolic suction created by ventricular systole pulling the tricuspid valve downward
In normal persons this is the predominant waveform in the jugular venous pulse
X descent
Venous pulsations
Interrupts the x descent as ventricular systole pushes the closed valve into the right atrium
C wave
Venous pulsations
Represents atrial filling, occurs at the end of ventricular systole and follows just after S2
Height determined by atrial compliance and by volume of blood returning to right atrium
V wave
V wave is accentuated in
TR
Describe a and v wave in evaluating JVP
a wave: reflects right atrial presystolic contraction, occurs after P wave, precedes S1
v wave: represents atrial filling, occurs at the end of ventricular systole, follows just after S2
Venous pulsations
Follows the v wave peak and reflects the fall in right atrial pressure after tricuspid valve opening
y descent
Normal venous pressure should fall by at least how many mmHg during inspiration?
3 mmHg
Rise in venous pressure (or its failure to decrease) with inspiration
Kussmaul sign
- Constrictive pericarditis
- Restrictive CMP
- Pulmonary embolism
- RV infarction
- Advanced systolic heart failure
*Seen with right sided volume overload and reduced RV compliance
Kussmaul sign
Describe:
When can this be seen? General and specific.
Rise in venous pressure (or failure to decrease) with inspiration
Seen with right sided volume overload and reduced RV compliance
Constrictive pericarditis, restrictive CMP, PE, RV infarction, advanced systolic HF
Describe the pathophysiology behind Kussmaul sign
Normally the inspiratory increase in right sided venous return is accommodated by increased RV ejection, facilitated by an increase in the capacitance of pulmonary vascular bed
In states of RV diastolic dysfunction and volume overload, the RV cannot accommodate the enhanced volume and the pressure rises
Increased pulmonary vascular resistance may also limit the RV ejection and contribute to phenomenon
Describe technique for proper abdominojugular reflux
What tips should you tell your pt?
Firm and consistent pressure over the right upper quadrant for at least 10 seconds
Refrain from valsalva or holding breath during procedure, can falsely elevate
Postitive abdominojugular reflux
rise in more than 3cm in the venous pressure sustained for at least 15 seconds
+ abdominojugular reflux sign can predict
- heart failure
- pulmonary artery wedge pressure higher than 15 mmHg
On occasion when taking BP, the Korotkoff sounds my disappear soon after the first sound, only to recur later before finally disappearing.
This auscultatory gap is more likely to occur in what population?
Older, hypertensive patients with target organ damage
In what patient populations may you hear Korotkoff sounds all the way down to 0 mmHg w/ cuff completely deflated
- Chronic severe AR
- AV fistula
- Pregnant
- Children
A BP differential between arms of > 10 mmHg may be associated with:
*Note ~20% of normal subjects w/o sxs will have a difference > 10 mmHg
- Subclavian a. disease
- Supravalvular AS (SVAS)
- Aortic coarctation
- Aortic dissection
Systolic leg pressures may exceed arm pressures by as much as 20 mmHg
Measurements > 20 mmHg difference may be seen in
- Severe AR (Hill sign)
- Extensive calcification of LE arterials (severe PAD), arteries are noncompressible
Hill sign
- Systolic leg pressures exceed arm pressures by > 20 mmHg
- Severe AR
Define orthostatic hypotension
Fall in blood pressure of more than 20 mmHg systolic and/or more than 10 mmHg diastolic
If orthostatic hypotension is accompanied by lack of compensatory tachycardia, what might you suspect
autonomic insufficiency (consider diabetes, parkinsons)
In pt’s with POTS does blood pressure usually fall on standing?
Generally no, more about inappropriate heart rate response
Wide pulse pressure
(valvular abnormality)
Aortic regurgitation
Increase in pulse pressure can represent
- Increased vascular stiffness (aging, atherosclerosis)
A bounding pulse may occur in
- Hyperkinetic states (fever, anemia, thyrotoxicosis)
- Pathologic states (ie severe bradycardia, AR, or arteriovenous fistula)
A fall in systolic pressure of > 10 mmHg during inspiration
Pulsus paradoxus
- Pericardial tamponade
- Severe pulmonary disease
- Massive pulmonary embolism, hemorrhagic shock, severe obstructive lung disease, tension PTX
- *Can also occur in obesity and pregnancy without clinical disease
Beat-to-beat variability of the pulse amplitude
Every other phase Korotkoff sound is audible as cuff pressure slowly lowered
Pulsus alternans
- Severe heart failure, severe AR, hypertension, hypovolemic states
- Attributed to cyclic changes in intracellular calcium and action potential duration
Weak and delayed carotid pulse
Appreciated by careful palpation of carotid during simultaneous auscultation of the heart sounds
Pulsus parvus et tardus
- Severe AS
- *Less specific finding in older, hypertensive patients with reduced vascular compliance and stiffer carotid arteries
Abrupt carotid upstroke with rapid fall off
Chronic AR
Left parasternal lift suggests
RV pressure or volume overload
Pt positioning for palpation of heart
Supine, leaning forward 30 degrees
PMI location
Midclavicular line, 5th intercostal space
Best heard at end of exhalation (heart closest to chest wall)
PMI displaced leftward and downward
LV cavity enlargement
Sustained apical impulse
LV pressure overload (AS, HTN)
