Cardiovascular Toolbox Flashcards
What is the leading cause of mortality in the US and the world?
Has the death rate for this cause been increasing or declining?
Cardiovascular disease- from 1998 to 2008 it has been declining (by 30%) but it is still the leading cause
About how many Americans die of cardiovascular disease each day?
2200 which is about one every 39 seconds
What is the total and indirect cost for care for cardiovascular disease and stroke in 2008?
297.7 billion dollars
Cancers was (228 billion)
What is “ideal cardiovascular health” as defined by the American Heart Association?
(7 attributes)
the absence of clinical manifestations of cardiovascular disease and optimal levels of:
- lean body mass
- no smoking
- regular exercise
- healthy eating
- untreated cholesterol <100mg/dl
How many American adults over 20 have hypertension?
over 75 million
How many adults have cholesterol levels over 200?
over 240?
100 million, 33million
How many adults have DM?
Pre-diabetes?
Undiagnosed diabetes?
DM-18 million
undiagnosed- 7 million
pre-diabetes- 80 million
What percent of adults meet physical activity guidelines?
High Schoolers?
20%
37%
What percent of adults reach “ideal healthy diet?”
<1%
What percent of people are smokers?
20%
What percent of American adults are overweight or obese?
roughly 70%
What health factors have Americans been improving on?
What factors have plateaued?
What has gotten worse?
Improved: 1.CVD and stroke mortality 2. lowered cholesterol 3. increased physical activity Plateau: 1. HTN 2. smoking Gotten worse: 1. DM 2. obesity
What specific cardiovascular disease kills the most people worldwide?
Where do 80% of the deaths take place?
7 million from coronary heart disease, 6 million from stroke
80% of deaths occur in low and middle-income countries
What are the 4 major non-communicable diseases the WHO are focusing on?
What are the four common risk factors?
- Cardiovascular disease
- chronic lung disease
- Diabetes
- cancer
- tobacco
- inactivity
- alcohol
- unhealthy die
What are the 5 main cardiac complaints when taking a history?
- Chest pain
- Palpitations
- Shortness of breath (dyspnea)
- Syncope
- Edema
Describe ischemic chest pain (angina pectoris).
how does it feel, where is it localized, where does it radiate, “classic” presentation
- tightness, heaviness (“elephant sitting on chest”), pressure, squeezing
- Cannot be localized to one point
- radiates to neck, jaw, upper arm, shoulder (sometimes midepigastric to back)
- nausea, sweating, vomiting, anxious
How does the description of angina pectoris differ for men and women?
Women have more vague symptoms with usually just nausea and midepigastric pain.
What four things can typically provoke ischemic chest pain?
What is the treatment for it?
- Exertion
- Emotional upset
- cold weather
- large meals
Treated with nitroglycerin or rest.
Describe the pain associated with pericardial inflammation.
What aggravates it?
- Sharp, stabbing
2. aggravated by changes in position or deep breaths
Describe the pain associated with aortic dissection.
Where does the pain radiate to?
- Tearing, severe
2. Radiates to the back
What are palpitations?
An unusual awareness of the beating of the heart:
racing, fluttering, pounding, skipping beats
Associated with abnormal rhythm (not always but frequently)
What causes dyspnea with heart failure?
Increased pulmonary pressure from heart failure or left valve dysfunction causes edema to leak into the alveolar space decreasing compliance and increasing resistance to airflow.
What is othopnea?
How is it assessed?
dyspnea in the supine position where gravity redistributes fluid back to central circulation, elevating pulmonary venous pressure.
It is assessed by the number of pillows a patient sleeps with each night
What is paroxysmal nocturnal dyspnea?
A sleeping patient is awakened by sense of dyspnea that is only improved if they sit up
What is syncope?
What are the 4 prodromal symptoms?
transient loss of consciousness due to decreased cerebral blood flow.
Dizziness, visual change, nausea, sweating
What are the two main forms of edema associated with heart disease?
- Systemic edema- usually seen in the legs due to gravity but can progress to the entire body (anasarca)
- Pulmonary edema- fluid accumulates in the interstitial spaces of the lungs
What are the 5 major causes of edema?
- Heart disease
- Renal disease
- lymphatic drainage or venous insufficiency
- obstruction
- decreased colloid
What is the common presentation of volume overload?
- dyspnea on exertion
- PND, orthopnea
- edema
Given the following observations, what is suggested?
- obesity and/or cyanosis
- tall with long arms/fingers
- cachexia
- slender/nervous
- slow, non-pitting edema
- febrile, ill, skin lesion
- right heart failure, sleep apnea
- Marfan’s
- end stage heart disease
- hyperthyroidism
- hypothyroidism
- endocarditis
Normal blood pressure varies by less than ________________ between inspiration and expiration.
If it is greater than that what is potential cause?
10 mmHg
Greater than 12mmHg change is suggestive of pulsus paradoxus where cardiac tamponade is the typical cause.
Describe the physiological mechanism behind the change in BP during inspiration and expiration.
- On inspiration, the intrathoracic pressure decreases which increased RV filling.
- RV pushes septum into LV decreasing LV volume and stroke volume
- Decreased stroke volume decreases systolic BP slightly
What is pulsus paradoxus? What is the predominant cause?
It is an inspirational drop in systolic pressure of 12mmHg or more.
It is usually caused by cardiac tamponade which is fluid and pressure in the pericardial space which impinge upon the ventricles reducing LV stroke volume more.
Also seen with obesity/severe lung disease
What 2 things does the jugular venous waveform give us information about?
- fluid status in the right side of the heart (RA)
2. cardiac rhythm
How is jugular venous waveform measured and reported?
Jugular venous waveform should be measured: supine 45degree angle erect in order to ascertain the meniscus.
The RA is the zero reference level and the height of the waveform is reported as cm of water.
5-10cm is normal.
For venous waveforms, what are:
- a wave
- c wave
- x descent
- v wave
- y descent
- RA contraction
- Tricuspid closes
- RA relaxation
- RA filling
- tricuspid opens and RA empties into RV
What is the affect of respiration on the jugular venous pressure?
Inspiration increases filling in the right sided heart chambers due to negative intrathoracic pressure.
This decreases the blood in the vena cava, decreasing the JVP.
Expiration, intrathoracic pressure increases which inhibits vena cava emptying into the RA. This increases JVP.
What is Kussmaul’s sign?
What are the underlying causes?
It is when there is a paradoxical increase in JVP during inspiration due to right heart not being able to tolerate increased flow.
Caused by restrictive/constrictive cardiac disease like:
1. constrictive pericarditis
2. acute RV infarction
What are situations that could cause large A waves on the jugular venous waveform? (4)
What would cause absent A waves? (2)
A waves mark RA contraction, so anything that would increase RA pressure.
- A-V obstruction - tricuspid stenosis, myxoma
- Compete A-V block - “Cannon” a waves
- Increased RA volume
- Restriction to RV filling- pulmonary hypertension
Absent
- atrial flutter
- atrial fibrillation
What are situations that would cause V wave abnormalities on the hugular venous waveform?
V waves are the filling of the RA so, the V wave will be taller in the case of :
1. tricuspid regurgitation
What is the point of maximal impulse?
When and where can it be palpated?
When you place your palm on the left chest wall you can feel the impulse of the heart (less than the size of a nickel)
It can be palpated during early systole at the fifth intercostal space to the left of the sternum
What is the significance of the PMI being:
- displaced laterally
- inferiorly displaced
- sustained for majority of systole
- Ventricular dilation
- low diaphragm (potential COPD)
- ventricular hypertrophy
What 7 arteries should be assessed when taking pulse?
Which assesses normal arterial pulse best at the bedside?
- carotid- best arterial pulse at the bedside
- brachial
- radial
- abdominal aorta
- femoral
- popliteal
- posterior tibial
What is a bruit?
It is turbulent flow. It is a “swoosh” sound you hear when blood crosses an artery with an obstruction
What arteries are palpated during cardiology physical exam?
Why?
Popliteal and abdominal aorta to assess for peripheral vascular disease such as:
- atherosclerosis
- aneurysm
- congenital vascular disorders
Describe the normal arterial pulse.
- Rapid upstroke
- smaller secondary upstroke (not palpable)
- gradual decline
What is the classic cause of increased amplitude in the carotid upstroke?
What is the other potential cause?
- Aortic insufficiency- LV stroke volume is increased with increases in systolic volume
- decreased peripheral resistance
What is the water-hammer pulse?
Where is it felt?
Aortic insufficiency causes increased LV stroke volume causing:
- rapid upstroke with higher amplitude
- rapid downslope (wide pulse pressure)
What are 6 causes of decreased peripheral resistance that can increase amplitude of the carotid upstroke?.
- sepsis
- patent ductus arteriosus
- fever
- anemia
- thyrotoxicosis
- peripheral A-V malformation
What is parvus et tardus?
What is the major cause?
Aortic outflow obstruction such as:
- stenosis
- supra or sub valve stenosis
Causes the pulse in the carotid to be small volume with a slow rise and fall that is delayed
What is bisferiens pulse?
What is the major cause?
Two systolic peaks during the peak amplitude of the arterial pulse.
Hypertrophic cardiomyopathy with a dynamic outflow obstruction in the LV is the cause.
- Initial upstroke is rapid and high amplitude (like normal)
- Brief decline and plateau
- Transient decrease in degree of LV obstruction allows for another peak
“Spike and dome wave”
What is pulsus alternans?
What is the major cause?
A strong pulse followed by a weak pulse.
Severe LV dysfunction (systolic)
What is pulsus paradoxus?
What is the major cause?
It is when the carotid pulse decreases with inspiration
(arterial pulse should NOT be dependent on respiration. BP and venous waveform depend on respiration)
Major cause : pericardial effusion (fluid surrounding the heart)
What frequencies are the diaphragm used to detect? Which heart sounds are heard at this frequency?
What frequencies are the bell used to detect? Which heart sounds are heard at this frequency?
Diaphragm is higher frequency (>300Hz)- S1, S2, ejection clicks
Bell is low frequency (
What are the 4 precordial sites and where are they located?
- Aortic- 2nd right interspace
- Pulmonary- 2nd left interspace
- Tricuspid- 4th left interspace
- Mitral- cardiac apex
What are the 3 positions the patient should be in for assessing the 4 precordial sites?
- seated
- supine
- left lateral decubitus (on their side)
What is occurring physiologically at S1 heart sound?
The AV valves (tricuspid and mitral) are closing.
This sound is heard prior to the carotid upstroke pulse.
What increases the intensity of S1?
- position of the tricuspid and mitral valve leaflets at onset of systole
- distance of heart from the chest wall
What is occurring physiologically at S2 heart sound?
The aortic and pulmonary valves are closing.
This occurs just after you feel the peak carotid pulse.
A2 closes first because the LV has higher systemic resistance and thus is activated prior to the RV.
What are the 2 components of S2?
How does respiration change their relationship?
A2 closes before P2.
During inspiration, the intrathoracic pressure is negative and RV filling increases. This prolongs the time the pulmonary valve is open and there will be a wider A2 P2 split. (50-90msec)
On expiration, there is less RV filling so P2 will close sooner and there will be less time between A2 closing and P2 closing (10msec)
What affects the intensity of S2?
- leaflet mobility
- pulmonary hypertension
- systemic hypertension
What are the 2 factors that make S2 widely split?
- Delayed P2 due to prolonged RV contraction
2. Early A2 closure due to decreased duration of LV contraction
What is 1 electrical way and 4 mechanical ways that P2 can be delayed?
- Right bundle branch block
- pulmonic valve stenosis (slower emptying of RV)
- RV dysfunction (slower emptying of RV)
- PE (increased afterload so prolonged empty)
- pulmonary hypertension
What are the 2 ways A2 occur prematurely?
- mitral regurgitation (less blood in LV to eject)
2. Ventricular septal defect (less blood in LV to eject)
What is a fixed split? What is the main cause?
Fixed split S2 is pathognomonic for atrial septal defects.
During inspiration: increased blood return decreased volume shunted across the defect from left to right.
During expiration, venous return is reduced but there is a reciprocal increase of shunting LtoR delaying P2
In both inspiration and expiration, the P2 is delayed. Resulting in a “fixed split” between A2 and P2
What is a paradoxical split?
When LV emptying is prolonged resulting in delayed A2 or early P2 closure
What would delay/prolong LV contraction resulting in delayed A2? (1 electric, 3 mechanical)
- LBBB
- Aortic stenosis
- Hypertrophy
- cardiomyopathy
What would cause early P2 closure?
decreased RV filling due to tricuspid regurgitation
What is S3? When is it heard?
It is a low frequency heart sound heard in early diastole during ventricular filling (right after S2)
Children : normal
Adults: CHF
What are the two main causes of pathologic S3 in adults?
- Decreased ventricular compliance (ventricular failure) — dilated cardiomyopathy
- Increased flow across AV valve (increased ventricle volume) – mitral regurgitation, aortic insufficiency, ventricular septal defect
Where do you listen for S3 and S4 heart sounds?
PMI - right over the cardiac apex at the mitral valve
What is S4? When is it heard?
It occurs prior to ventricular activation and is secondary to atrial contraction (just prior to S1)
What is the major cause of an S4 heart sound?
decreased ventricular compliance due to ventricular hypertrophy.
- arterial hypertension
- aortic stenosis
- hypertrophic cardiomyopathy
When are ejection fractions heard?
during early ventricular systole secondary to blood flow across the aortic and pulmonic valves.
When are aortic ejection sounds most commonly heard?
In patients with bicuspid aortic valves
less commonly in aortic root disease or aortic coarctation
When are pulmonary ejection sounds most commonly heard?
- pulmonic stenosis
- pulmonary hypertension
- dilated pulmonary artery
(VARIES WITH RESPIRATION)
What are the 5 pieces of info used to classify a cardiac murmur?
- timing
- location
- quality
- intensity
- pitch
What are the 6 grades of murmur intensity according to the Levine and Harvey scale?
Murmurs under what grade are considered “innocent”
- barely audible
- audible with stethoscope on chest wall
- loud
- loud with thrill
- loudest murmurs heard while still requiring stethoscope
- murmur audible w/o stethoscope
2 and under are innocent –> no significant pathology
_________-sided murmurs get louder with respiration.
Right
What are the 4 causes of a left-sided systolic murmur?
- Aortic stenosis
- Mitral regurgitation
- Mitral valve prolapse
- hypertrophic cardiomyopathy
_________murmurs can be pathogenic or non-pathogenic. ____________ murmurs are always abnormal.
Systolic murmur can be normal but diastolic are always abnormal
Describe the ejection murmur produced by aortic stenosis.
It is a left-sided systolic murmur that is harsh and diamond-shaped (crescendo-decrescendo)
The timing of the peak of the diamond corresponds to the severity of the stenosis. (Later = more severe)
For aortic stenosis, the severity of the obstruction correlates with _______________ NOT the ____________________.
severity of the obstruction correlates with the timing of the peak NOT the intensity of the murmur.
In addition to a left-sided murmur, what other change in heart sounds is associated with aortic stenosis?
It will take longer for LV to empty so there will be delayed A2.
This can result in either one S2 sound (A2 andP2 at the same time) Or a paradoxical split (A2 after P2)
Where does a left-sided murmur due to aortic stenosis radiate to?
It radiates to the carotid as a pulsus parvus et tardus (delayed and low amplitude)
Describe when you would hear mitral regurgitation on auscultation. What are the characteristics of the sound?
What increases the intensity of the murmur?
You hear it in systole (S1 to A2) and it is soft, blowing, high-pitched.
It will be associated with an S3 sound because of the increased flow across the valve
The intensity is increased with isometric exercise
Where does a left-sided murmur due to mitral regurgitation radiate to?
When the regurgitation is due to the anterior leaflet- axilla and thoracic spine
Due to the posterior leaflet-
anteriorly toward the base of the heart
What is mitral valve prolapse?
When would a murmur due to MVP occur? What factors make it earlier or later?
What sounds are associated with it?
It is when the valve leaflets pull back into the atrium.
It is associated with a mid-systolic ejection click and late systolic murmur.
It will be audible earlier if there is less blood in the ventricle ( standing, Valsalva) because there will be larger mismatch between ventricle size and valve leaflets
What is the main problem with hypertrophic cardiomyopathy?
What sounds are associated with hypertrophic cardiomyopathy?
Where and when are the sounds best heard?
Where does it radiate to?
Cardiomyopathy has a dynamic outflow obstruction (so the degree of obstruction can increase or decrease)
Increased intensity of S1 and preservation of both components of S2. S3 or S4 MAY be present
It is heard best at the left sternal border. Does NOT radiate to carotids.
What are factors that increase the intensity of a hypertrophic cardiomyopathy murmur?
- decreased left ventricular dimension (Valsalva, vasodilators)
- Increased ionotropy (PVB, medication)
What are maneuvers that decrease the intensity of a hypertrophic cardiomyopathy murmur?
- increased left ventricle dimension (squatting, Mueller)
2. Increased afterload (isometric exercise, phenylalanine)
What are the two major left-sided diastolic murmurs?
- aortic valve regurgitation
2. mitral valve stenosis
What are the sounds associated with aortic valve regurgitation?
S1= normal or decreased S2 = normal with ejection sounds S3 = due to increased LV volume S4 = due to decreased LV compliance
The sound begins after S2 and is decrescendo in quality
Where does aortic valve regurgitation murmurs radiate?
along the left lower sternal border
When is an aortic valve regurgitation murmur best heard?
with the patient sitting, leaning forward at the end of expiration
What is the most common cause of mitral valve stenosis?
Rheumatic heart disease which affects mitral leaflets and subvalvular apparatus
What sounds are associated with mitral valve stenosis?
- Increased P2 due to pulmonary hypertension
- Opening snap 30 to 120ms after S2 followed by a low rumbling murmur
- Pre-systolic accentuation
How should the patient be positioned to best hear mitral valve stenosis?
left decubitus listening at the apex
What are the four right sided murmurs?
- Tricuspid regurgitation
- Pulmonary stenosis
- pulmonic valve regurgitation
- atrial septal defect
Who is most frequently diagnosed with an atrial septal defect?
How does the murmur sound?
Asymptomatic people with a fixed split S2.
The murmur is heard at the second left intercostal due to increased pulmonic flow.
It has an ejection click followed by crescendo/decrescendo systolic murmur.
What is a typical cause of tricuspid regurgitation?
When is the murmur heard and what are the qualities?
What increases the intensity of the murmur?
The typical cause of a tricuspid regurgitation is dilation of the RV stretching the tricuspid annulus.
It is heard in systole, high pitched and heard at the lower left sternal border.
The intensity is increased by anything that increased the volume of blood on the right side (like inspiration)
When would you hear a murmur due to pulmonic valve stenosis?
What does it sound like?
You hear it during systole and it is harsh crescendo-decrescendo best heard at second left intercostal space.
The later the peak, the more severe the PS.
There is an ejection click due to abrubt cessation of valve movement and a delayed P2.
When would you hear pulmonary valve regurgitation murmurs?
Diastole with a decrescendo murmur heard at the second left intercostal radiating to the low sternal border.
S2 is more intense because of increased intensity of P2 and the S2 split will be wide because of delayed P2
What is the major cause of pulmonary valve regurgitation?
pulmonary hypertension - it is called a Graham Steel murmur
What is a continuous murmur?
A murmur that begins in systole and continues to diastole which means there is communication between arterial and venous circulations.
- AV fistulas
- ruptured Valsalva sinus
- Patent Ductus arteriosus
How is PDA heard?
Patent ductus arteriousus is heard at the left second intercostal space
S1 is normal, S2 may be paradoxically split due to a large left to right shunt
It is a continuous murmur so it begins in systole, peaks at S2 and continues into diastole.
The duration into diastole is determined by the pulmonic hypertension (higher pressure, shorter duration)
What is a Holter monitor, event monitor and implantable monitor?
Holter- outpatient EKG for 24 to 48 hours
Event- outpatient for a month
Implantable- up to 2 years that is in the chest wall to monitor rhythm
What are the 2 types of stress tests?
- Exercise stress tests
2. Chemical stress tests - dobutamine then watch sonography and EKG
What does echocardiography assess?
What are the benefits?
- heart size
- ventricular function
- valve function
It is portable and non-invasive
What is cardiac catheterization?
An invasive procedure where catheter is introduced into cardiovascular system via x-ray to measure pressure, collect blood, inject contrast, balloon vessels.
What is ablation and what can it treat?
Cold temp (cryoablation) and heat (radiofrequency) can damage certain areas of cardiac tissue to treat arrhythmias
