CARDIO Flashcards
Oxygen Consumption Rate
CO X (arterial O2 content − venous O2 content)
Can either be measured using a spirometer or by using an assumed value (usually 250 mL O2/min (or 3.5–4.0 mL/kg/min).
↑ Pulse Pressure
Hyperthyroidism
Aortic regurgitation
Aortic stiffening (isolated systolic hypertension in elderly)
Obstructive sleep apnea (↑ sympathetic tone)
Anemia
Exercise (transient)
↓ Pulse Pressure
Aortic stenosis
Cardiogenic shock
Cardiac tamponade
Advanced HF
Loud S1
Mitral stenosis (increased transvalvular pressure gradient)
Tachycardia (short diastole)
Hyperdynamic states (e.g., left-to-right shunts [increased transvalvular blood flow])
Short PR interval (e.g., atrioventricular reentrant tachycardia (AVRT))
S1 is generally not heard in aortic and pulmonary areas. It is considered “loud” if it is as loud as S2 in aortic and pulmonary areas.
Soft S1
Severe mitral stenosis (mitral valves are severely calcified and immobile)
Conditions that impair the transmission of heart sounds to the chest wall → COPD, pneumothorax, pericardial effusion, obesity
Left bundle branch block (LBBB) (delayed onset of systole)
Prolonged PR interval (e.g., first-degree heart blocks)
S1 is considered “soft” if S2 is louder than S1 at the mitral region.
S1 with Variable Intensity
Atrial fibrillation
AV dissociation
Auscultatory alternans → severe LV failure, large pericardial effusion
Loud A2
Arterial hypertension
Coarctation of the aorta
Loud P2
Pulmonary hypertension
Atrial septal defects
P2 is a soft sound and is usually heard only in the pulmonary area; therefore, P2 is considered “loud” when it is clearly heard in the mitral area or when it is louder than A2. A loud P2 is highly specific for pulmonary hypertension.
Signs of ↑ Jugular Venous Pressure (JVP)
Jugular venous distention
Kussmaul sign → distention of the jugular veins during inspiration due to the negative intrathoracic pressure that attempts to pull blood into the right heart, which is restricted by noncompliant pericardium or myocardium (e.g., constrictive pericarditis, restrictive cardiomyopathy, right atrial tumors, ventricular tumors, right HF, massive PE)
Hepatojugular reflux
Causes of ↑ Jugular Venous Pressure (JVP)
Right heart failure Fluid overload Tricuspid valve dysfunction Pericardial effusion Constrictive pericarditis Cardiac tamponade SVC syndrome Pulmonary hypertension
Kussmaul Sign
Distention of the jugular veins (↑ JVP) during inspiration due to the negative intrathoracic pressure that attempts to pull blood into the right heart, which is restricted by noncompliant pericardium or myocardium (e.g., constrictive pericarditis, restrictive cardiomyopathy, right atrial tumors, ventricular tumors, right HF, massive PE)
Kussmaul sign is absent during pericardial tamponade because the negative intrathoracic pressure is still able to ensure filling of the right ventricle.
JVP a wave
First peak caused by atrial contraction
Absent in atrial fibrillation
Prominent in tricuspid valve atresia
JVP c wave
Second peak caused by tricuspid valve closure, contraction of the right ventricle, and bulging of the tricuspid valve into the right atrium
cv wave (merging of the c and v waves; Lancisi sign) → severe tricuspid valve regurgitation
JVP x descent
A drop in JVP caused by atrial relaxation
Absent in:
- Tricuspid valve regurgitation
- Right heart failure
JVP v wave
The third peak caused by venous refilling of the right atrium against the closed tricuspid valve
Prominent in:
- Tricuspid valve regurgitation
- Right heart failure
JVP y descent
A drop in JVP caused by decreased right atrial pressure as blood flows into the right ventricle after opening of the tricuspid valve
The y descent is sharp and deep due to rapid filling in the first half of diastole.
Prominent in:
- Tricuspid valve regurgitation
- Constrictive pericarditis
Absent in:
- Cardiac tamponade
- Tricuspid valve stenosis
Third Heart Sound (S3)
- Early diastolic sound that is heard immediately after S2
- Ventricular gallop → S1 is followed by S2 and S3 in close succession, resembling the cadence of the word “Kentucky” (Ken-TUC-ky) on auscultation. Described as a ventricular gallop because the pattern of S1-S2-S3 on auscultation resembles the sound of a galloping horse.
- Occurrence:
1. Physiological → young individuals (< 40 years of age), athletes, or pregnant women
2. Pathological: - Chronic mitral regurgitation
- Aortic regurgitation
- Heart failure (due to dilated ventricles)
- Dilated cardiomyopathy
- Thyrotoxicosis
- L → R shunt
Fourth Heart Sound (S4)
- The fourth heart sound is often called an atrial gallop because the sound originates in the atria
- S1 rapidly follows S4, resembling the cadence of the word “Tennessee” (Ten-nes-SEE) on auscultation.
Occurrence:
- Physiological → advanced age (due to reduce ventricular compliance)
- Pathological if palpable
- Ventricular hypertrophy (e.g., hypertension, aortic stenosis, cor pulmonale)
- Ischemic cardiomyopathy
- Acute myocardial infarction
Split S1
Occurs when the closure of the tricuspid valve is delayed (e.g., due to an RBBB), resulting in the sound of tricuspid valve closure heard shortly after mitral valve closure Reversed splitting (tricuspid valve closure before mitral valve closure) is rare.
Causes:
Conduction disorders
Hemodynamic cause
S2 Physiological Split
The sound of aortic valve closure (A2) precedes the sound of pulmonary valve closure (P2) during inspiration
Inspiration → fall in intrathoracic pressure → increase in venous return to the right side of the heart → prolonged right ventricular systole → delayed closure of P2
Pooling of blood in pulmonary circulation → shortened left ventricular systole → premature A2
Especially pronounced among young individuals (chest wall excursion and, therefore, the likelihood of hearing a physiological split decreases with age)
S2 Wide Split
An exaggerated physiological split, which is more pronounced during inspiration (A2 precedes P2)
Caused by any condition that increases right ventricular afterload or decreases left ventricular preload
Increased right ventricular afterload → prolonged right ventricular systole
Decreased left ventricular preload → shortened left ventricular systole
Causes: Pulmonary hypertension Pulmonary valve stenosis RBBB Massive pulmonary embolism Severe mitral regurgitation Wolff-Parkinson-White syndrome Constrictive pericarditis
S2 Fixed Split
Does not change with respiration and tends to be wide, i.e., the split is also audible during expiration (since the right and left sides of the heart communicate, the pressure difference that normally exists during respiration evens out; therefore, the duration of the split does not change with inspiration or expiration)
Left-to-right shunt in ASD → RV volume overload → delay in the closure of the pulmonary valve
Cause:
Atrial septal defect (ASD)
Severe RV failure
S2 Paradoxical Split (Reversed Split)
Audible during expiration but not inspiration
Expiration → A2 is heard after P2 during expiration due to delayed closure of the aortic valve (split reversal)
Inspiration → the closure of the pulmonary valve is also delayed, resulting in A2 and P2 occurring simultaneously (i.e., a paradoxical decrease in the split during inspiration)
Cause: Aortic stenosis Left bundle branch block HOCM (LV outflow tract obstruction) Early excitation of the right ventricle (e.g., RV pacing, Wolff-Parkinson-White syndrome)
S2 Absent split
No splitting of S2
Cause:
- Severe aortic stenosis (geriatric) (A2 is absent due to calcification and, in severe cases, immobility of the aortic valves)
- VSD with Eisenmenger syndrome (pediatric) (VSD results in communication between the left and right ventricles. They then essentially function as a single ventricle, leading to A2 and P2 occurring simultaneously, during both inspiration and expiration (fused A2-P2)).