Ventricular Dysfunction In
Assessment of CV Dysfunction
• Cardiac pump function - the relationship of cardiac output
to RA pressure (Pra).
• Measurement of cardiac output - thermodilution technique
(pul. a. catheter), nuclear medicine imaging, or Doppler
• Measurement of Pra - distension of the jugular veins, CVP.
• Cardiac dysfunction - LV dysfunction, RV dysfunction, or
external compression (cardiac tamponade)
Definition of Cardiac Function and Its
Relation To Venous Return
The cardiac function curve relates RA pressure (Pra) or EDP to cardiac output. As EDP
increases CO increase, but at high EDP further increases cause less increase in CO.
When EDP = mean systemic pressure (Pms), there is no pressure gradient (Pms-Pra) driving the
blood flow back to the heart so venous return is zero. As EDP (Pra) decreases the gradient from
the veins to the heart to drive blood flow back to the heart increase
The intersection point defines the operating point of the circulation. The interrupted cardiac
function curve illustrates decreased cardiac function, causing reduced cardiac output at a
Control of Ventricular Pumping
• The ventricular pump function curve can be altered by
changes in contractility, preload, afterload, heart rate and
rhythm, and valvular function.
• ESPVR - end systolic pressure-volume relationship;
- ↑ contractility → ESPVR shifts to the left
- ↓ contractility → ESPVR shifts to the right
• Stroke volume = EDV - ESV
• Cardiac output = HR x Stroke volume
1. During diastole the ventricle fills along a diastolic pressure-volume relationship
2. At the onset of systole LV pressure ↑ with no change in volume
3. When LV pressure > aortic P., the AV opens and the LV ejects blood to an end-systolic
4. The LV then relaxes isovolumically
∗ Emax - end-systolic pressure-volume relationship (ESPVR), a good index of ventricular
contractility independent of changes in preload and afterload.
↑ Pressure afterload
↑ Diastolic filling
Measurement of Ventricular Function
• Clinical examination - perfusion status, mean BP, pulse
pressure, HR., distention of jugular v. (↑ RV filling p.),
dependent pul. crackles (↑ LV filling p. ≥ 20mmHg), S3
• Rt heart catheter - a thermistor -tipped catheter with a
distal port at the tip and a proximal port 30 cm from the
tip, can accurately determine C.O. (thermodilution
• Gated radionuclide ventriculography and
Mechanism and Management of LV
∀ ↓ Contractility
∀ ↑ Diastolic stiffness : ↓ preload volume
∀ ↑ Afterload
• Abnormal heart rate and rhythm
• valvular dysfunction
• Myocardial ischemia - O2 demand > supply; ↑ O2 demand :
↑ HR, contractility, afterload, preload, and basal metabolic
• Myocardial hypoxia - sepsis, anemia, etc. ↑ ↑ hypoxic →
anaerobic metabolism → lactic acid ↑ → ↓ contractility
(vicious cycle) (occurred when SaO2 ≤ 75%); Tx.- keep
SaO2 > 90% and normal Hct.
• Myocardial acidosis - resp. and metab. acidosis
• Resp. acidosis → intracell. acidosis → ↓ the effect of
intracell. Ca. on the contractile proteins → ↓ contractility
(can be countered by β agonists)
• Metab. acidosis - less effect on ↓ LV contractility, organic
acids not easily cross into the intracell. compartment.
• Ionized hypocalcemia - septic shock, blood transfusion
(citric acid), lactic acid → extracell. ionized Ca → ↓ flux
and ↓ contractility.
• Side effects of common drugs - ethanol, β-blockers, Ca
blockers, and antiarrhythmics
• Identify and correct acute reversible causes - coronary
vasodilation, blood transfusion, O2, iv calcium,
bicarbonate, correct electrolyte abnormality.
• Managing the depressed heart - optimizing of ventr.
filling p., ↓ afterload, IABP etc.
• Inotropic or vasoactive agents -
1. Dobutamine- acts mainly on β1-receptors
- ↑ contractility, peripheral vasodilation
- 2-15 µg/kg
Table 115-3 Effect of Direct-Acting Vasodilators
Drug Route Dosage Onset Duration Large a. Arterioles Veins
Nipride IV 25-400 µg/min immediate - + +++ +++
Nitroglycerin IV 10-200 µg/min immediate - ++ + +++
Isodil P.O 20-60 mg 30 min 4-6h ++ + +++
Hydralazine P.O 50-100mg 30 min 6-12h 0 +++ ±
Hydralazine IV or IM 5-40 mg 15 min 4-8h 0 +++ ±
Minoxidil P.O 10-30 mg 30 min 8-12h 0 +++ 0
Diazoxide IV bolus 100-300 mg immediate 4-12h 0 +++ ±
Nifedipine P.O 10-20 mg 20-30min 2-4h +++ +++ ±
S.L 10-20 mg 15min 2-4h +++ +++ ±
Increased Diastolic Stiffness
• Increased diastolic stiffness reduces SV because ↓ EDV
(depressed systolic function reduces SV because ↑ ESV)
• much more difficult to treat
• Dx is suggested by finding depressed ventr. pump function
unresponsive to fluid loading, inotropic agents, and
• Nondilated cardiomyopathies - HCM, concentric LVH,
HCVD and restrictive myocardial disease (amyloidosis,
hemochromatosis, sarcoidosis, endomyocardial fibrosis
• Disease of the pericardium - constriction and effusion, and
other processes which ↑ intrathoracic pressure.
• Regional or global ischemia - delayed systolic relaxation
→ ↑ diastolic stiffness
∀ ↑ intrathoracic or intrapericardial pressure - positive-
pressure mechanical ventilation, pericardial effusion
• Hypovolemic shock and septic shock
• Hypothermia (BT < 35o
• Management - treat underline disorder.
Abnormal Heart Rate and Rhythm
• Normally HR and contractile states are matched to venous
return and afterload to maximize the efficiency of the CV
• Excessively high or low HR may limit C.O.
• Afib, AF, VT, VF, PSVT, MAT (pul. dz)
• Management included correcting potential contributing
Mechanism and Management of RV
• RV pump function also depends on contractility, afterload,
preload, HR, and valve function.
• RV, a thin-walled pump, not suited as a high pressure
Decreased RV Systolic Function
• Many causes reduce the LV contractility also decrease
contractility of the RV.
• RV ischemia in the absence of CAD is very important
during critical illness (↑ RV p. → ↑ RV intramural p. →
↓ gradient for RV coronary blood flow → RV ischemia)
Disorder of RV Preload, Afterload,
Rhythm, and Valves
• Pra is heavily influenced by intraabdominal, intrathoracic,
and intrapericardial pressure; a poor indicator of RV
• RV also depends on normal rate and rhythm to attain
• RV valvular dz is less common and less important than LV
• Endocarditis (tricuspid valve) is common in critically ill
pts (preexisting valve dz or medical instrumentation)
• The afterload of the RV is the pulmonary a. pressure.
Table 115-4 Causes of Elevated RV Afterload
Recurrent pulmonary embolism
Primary pulmonary hypertension
Associated with connective tissue diseases
Chronically elevated LA pressure (MS, LV failure)
Hypoxic pulmonary vasoconstriction
Acidemic pulmonary vasoconstriction
Acute elevation in LA pressure
Positive-pressure mechanical ventilation
• Combined pump dysfunction of RV and LV is more
common than isolated RV or LV pump dysfunction.
Acute on Chronic Heart Failure
• CHF - poor prognosis with a survival rate of only 50%
after 5 years.
• Mortality is highest during the first 2 years with worsened
functional status, often related to episodes of acute
• NYHA class III or IV - survival rate ≅ 50 % after 1 yr and
30 % after 2 yrs.
Table 115-5 Common Precipitating Factors of Acute on Chronic Heart Failure
Poor compliance with medications
Dietary indiscretion (salt load, alcohol)
High environmental temperature
Effect of a new medication (β-blockers, calcium channel blockers,
Arrhythmia (typicallly, new atrial fibrillation)
Ischemia or infarction
Valve dysfunction (endocarditis, papillary m. dysfunction)
Surgical abdominal event (cholecystitis, pancreatitis, bowel infarct)
Worsening of another disease (DM, hepatitis, hyperthyroidism, hypothyroidism)
• Often anxious, tachycardiac, and tachypneic with
hypoperfused extremities and possibly cyanosis.
• Jugular veins distended and hepatojugular reflux
• Apical impulse lateral to the midclavicular line or > 10 cm
from the midsternal line
• Apical diameter > 3cm indicates LV enlargement
• S3 or summation gallop
• Crackles (+) in dependent lung fields, dependent edema
• Wheezing, hepatomegaly (may be pulsatile esp. TR)
• CXR - upper zone redistribution of vasculature,
perivascular and peribrochial cuffing, perihilar filling and
pleural effusion, azygos vein enlarge.