Heart Failure and Shock
DEFINITION
- It is the pathophysiologic state in
which an abnormality of cardiac
function is responsible for the
failure of the heart to pump blood
at a rate commensurate with the
requirements of the metabolizing
tissues and/or can do so from an
abnormally elevated diastolic
volume.
- A consequence of myocardial O2
supply and demand imbalance
Heart Failure and Shock
Determinants of Normal Cardiac Performance
A. Preload (Ventricular End Diastolic Volume)
a. Blood Volume = intra/extrathoracic
b. Body position – upright/supine
* Intrathoracic pressure – less intrathoracic
pressure like inspiration more venous return
increased intrathoracic pressure less venous
return
* Venous tone – venoconstriction as in
exercise, fright/flight increases preload
* Skeletal muscle tone
Heart Failure and Shock
c. Atrial contraction – contributes
30% of cardiac output (decreased in
atrial fibrillation, AV dissociation)
B. Myocardial Contractility (Inotropicity) –
intrinsic viable myocardial
cells/sympathetic adrenergic activity
C. Ventricular Afterload – peripheral
resistance, left ventricular wall resistance
Heart Failure and Shock
Case 2
A 65 y/o M known hypertensive who came in
due to hypertensive emergency presenting
with 2 day history of headache, chest pain,
PND, and orthopnea with PE finding of BP
220/120 mmHg, loud S1, crackles all over
and distended neck veins
Heart Failure and Shock
Case 3
A 55/M, smoker, hypertensive who came in
with STEMI of the inferior and right sided,
chest leads presenting as chest pain,
dizziness, and generalized weakness with
PE finding of BP 70/50 mmHg, CR of 44
bpm, distended neck veins and clear
breath sounds
Heart Failure and Shock
Case 4
A21/F, diagnosed of RHD with severe MS,
MR, with severe pulmonary hypertension
came in due to palpitations and
progressive DOB, orthopnea, bipedal
edema of 2 weeks duration. PE finding
showed BP of 100/60, tachycardic,
tachypneic, icterisia, crackles from mid to
base and neck vein distension
Heart Failure and Shock
Case 1
A 68 y/o M, diabetic hypertensive diagnosed
of ischemic cardiomyopathy a month ago
came in because of 2 week history of
recurrent chest pain, PND, orthopnea,
ascites and bipedal edema with PE finding
of BP 80-90/60 mmHg, distended neck
veins, mid to basal crackles and a soft S1
with S3 on auscultation
Congestive Heart
Failure
Precipitating causes
- Infection
- Anemia
- Thyrotoxicosis in pregnancy
- Arrhythmia
- Dietary, fluid and electrolyte excess
- Systemic hypertension
Heart Failure and Shock
Pathophysiologic mechanism of heart
failure depends on the derangements of
Preload, Afterload and Contractility.
Any derangements of the above 3 major
determinants will translate into an
imbalance of myocardial O2 supply and
demand
There are two types of heart failures:
Systolic dysfunction or failure
This type of heart failure is the most common type. It
occurs during the systolic or contraction phase, and
affects the left side of the heart. Here, the left ventricle is
usually enlarged and fluid accumulates in the lungs.
Diastolic dysfunction or failure
This type of failure occurs during the diastolic or
relaxation phase, and usually affects the right side of the
heart. It is usually caused by thickened heart muscle
which prevents the heart to relax completely. As a result,
blood cannot efficiently enter the heart and backs up in
the veins and surrounding heart tissue.
Other forms:
High output vs low output
- Low output (DCMP, AMI, valvular heart disease)
- High output (anemia, Hyperthyroid, Pregnancy)
Acute vs chronic
- acute; usually sudden without bipedal edema or
evidences of right heart failure while chronic usually
shows evidence of right heart failure
Right-sided vs left-sided heart failure
Clinical Manifestations
Left sided
Paroxysmal nocturnal dyspnea (PND)
Orthopnea
Fatigue and weakness
Insomnia, impaired mentation
Pulmonary rales
Soft S1 and left sided S3
Left sided heart failure
Right-sided
Jaundice
Hepatomegaly
Ascites
Pleural effusion
Bipedal edema
Pure, right sided congestive failure; note the dilated sinusoids in zone 3
with some degree of atrophy of the hepatocyte cords. Most of the blood
has drained from the biopsy
Right sided heart failure
Major Goals:
Removal of precipitating cause
Correction of the underlying cause
Control of the congestive heart failure
state
Reduce of cardiac
workload=preload/afterload
Control of fluid/salt retention
Improve myocardial contractility.
Management:
Preload “unloaders”
Non-pharmacologic
Fluid and salt retention
O2 delivery
Adequate/appropriate rest and activity-moderate
to high back rest
Laxatives
*** afterload non-pharmacologic management
same with “preload”
Pharmacologic (PRELOAD)
Nitrates
Morphine/diazepam
Diuretics-furosemide/aldactone
Ace-inhibitors/ARB’s
Pharmacologic (afterload)
ACE inhibitors
Hydralazine
Sodium nitroprusside
Management:
Enhancement of myocardial contractility
Cardiac glycosides-lanoxin
Intoropes (sympathomimetic amines)
dobutamine/dopamine/norepi/epinephrine
Phosphodieterase inhibitors-Milrinone
Prognosis
Outcomes depends on the nature of
underlying heart disease and on the
presence/absence of a precipitating factor
that can be treated.
Mortality is about 30-80% in those whose
precipitating factors and underlying causes
of heart failure were untreated and
unrecognized as against 5-105 to those
who were.
Shock
It is the state in which failure of the
circulatory system to maintain adequate
cellular perfusion results in widespread
reduction in deliver of oxygen and other
nutrients to tissues.
Derangement in maintaining homeostasis
leading to probable multi-organ failure.
Management:
Basic principle is to treat the underlying cause
Cardiogenic- vasodilators (dobutamine)/IABP
Septic- vasoconstrictors(levophed/dobutamine)
fluid resuscitation.
Hypovolemic-fluid retention.
Heart Failure and Shock
Case 1
A 65/M who came in with chest pain of
few hours duration, hypotensive at
palpatory 80, tachypneic, tachycardic
with cold clammy extremities, neck
vein distention and crackles all over
Heart Failure and Shock
Case 2
A70/M DM came in due to altered
sensorium and with wet gangrene of
the left foot 5 days duration. He is
hypotensive at palpatory 80, afebrile,
tachycardic and tachyneic. His breath
sounds are clear with flat neck veins
and warm extremities.
Heart Failure and Shock
Case 3
A 35/F has been having UGIB for 5
days and eventually had syncope few
hours PTA. She was noted to have
palpatory BP, tachycardic,
tachypneic, flat neck veins, clear
breath sounds and cold clammy
extremities.
Heart Failure and Shock
Hemodynamic Parameters of use in
differentiating the classes of SHOCK
1. Cardiac output = (SVxHR) 4-8L/min
2. Cardiac index = (CO/BSA) 2.8-4L/m2
3. SVR = (MAP-CVP)/CO x 80) 800-1200
dynes s/cm2
4. PCWP=8-12 mmHg
Heart Failure and Shock
Clinical State CO/CI SVR PCWP/
CVP
Distributive Hyperdynamic
(septic) “Vasodilated”
Cardiogenic Volume loaded
Myocardial
dysfunction
Vasoconstriction
Hypovolemic Volume depleted
Vasoconstriction
Heart Failure and Shock
Management:
Basic principle is to treat the underlying
cause
1. Cardiogenic – vasodilators (dobutamine),
IABP
2. Septic – vasoconstrictors
(Levophed/dopamine), fluid resuscitation
3. Hypovolemic – fluid resuscitation
