Ch 11 – Pathophys
Cardio – Heller – 9.29.09
1
Circ Shock = generalized, severe red in tissue bld flowmetabolic needs aren’t met
Shock primary disturb categories: dec pump func (cardiogenic shock) or dec vent filling (hypovol,
pulmonary embolus, or sustained vent dilation)
Primary disturb  compensatory response (know the dif!)
Think: What is the primary disturb? And what of the Sx I am seeing are compensatory to the primary disturb?
Prim. Disturb
Causes
Cardiogenic S.
Pump failure (MI, severe
arrhythmia, abrupt valve
misfunc, coronary
occlusion)
Hypovolemic S.
Fluid loss (hemorrhage,
severe burns,
Vomit/diarrhea)
Vasodilator (type 4
hypersensitivity)
Vasodilator (endotoxin
 NOS I  NO)
 sympt,  para ***
Anaphylactic S.
Septic shock
Neurogenic S.
Shock  dec MAP
MAP = TPR x CO
Key
Charac
 CO
Card. Func Curve
Prim Dist Tx
CO, VR 
CVP
Tx cause
(Don’t give fluids)
 CO
VR  CO
CVP
IV fluids*
TPR**
 CO
TPR
 CO
TPR
 CO
-----
antihistamines,
vasoconstrictors
Antibiotics
----VR  CO
CVP
sympathomemtics
*IV fluids: dextrose containing IV best cuz inc oncotic pressure, keeps fluid in vessels unlike Norm Saline  ECF.
**  TPR cuz histamine release vasodilates ( arterial tone), opens porefluid into tissue
*** Neurogenic Shock:  sympt   art tone   TPR;  venous tone   CO
ANS battle to compensate. Primary dist is  sympt, want to  sympt but cant
Compensatory Mech
-Goal:  MAP
-In all cases Para, sympt (not effective in neurogenic shock)
-Shock is invariably accompanied by a compensatory  in sympt to maintain MAP via augmented CO and VR.
-Heart:  HR,  contractility   CO
-systemic organs:  venous & arterial tone   TRP   organ blood flow
(& inc fluid absorption in caps   CO)
- resp pump via rapid shallow breathing
-  Angiotensin II (vasoconstrictor) via  Renin release from kidney due to  sympt   TPR
-pathway activation promotes Na retention (via aldosterone) & thirst/drinking (via angiotensin II)
- Epi  vasoconstriction
- Cap hydrostatic P from art constriction, same oncotic P  net fluid absorption.
-Epi & NE induce glycogenolysis in liver   glucose,  extracellulary osmolarity so fluid shift from cells  ECF
-release of ADH from post pit due to dec cardiopulmonary barorecp firing  vasoconstrictor & fluid retention by kidney
Decompensatory Processes
-Decomp processes precipitated by shock state are generally caused by inadequate bld flow
& loss of homeostasis & result tissue damage with a progressive and irreversible fall in PA
-Progressive stage (situation progressively degen) Irreversible stage (cant stop collapse of CVS)
-MAP  MAP (positive feedback cycle = BAD)
-Eventually Sympt , vasoconstriction  vasodialate  further MAP  death
-Effect on organs:
GI – factors released from pancreas that directly suppresses the cardiac func curve &
accumulation of toxins in the lumen  leak across (BAD)
-Kidney– electrolyte imbalance  arrhythmias  CO
- both electrolyte imbalances and toxins  venous tone
-Ischemia in organs  acidosis vasodilator release  VR   CVP  CO.
-If art tone affected  TPR; inc cap pressure  inc filtration  promote fluid loss
Ch 11 – Pathophys
Cardio – Heller – 9.29.09
CARDIAC DISTURBANCES
Cardiac Disturbance
Coronary Art Disease
2
Cause
Atherosclerotic Plaques 
stenosis  R,  Q 
ischemia
Systolic Chronic Heart Fail.
(Congestive Heart Failure)
Primary cardiomyopathy
or Sustained challenges
(CAD,  afterload, 
functional cardiac musc
mass post-MI)
Diastolic Chrnic Heart Fail.
Stiff vent  hard to fill
(See list below)
Primary Systemic HTN
Unknown-gentc, lifestyle link
KIDNEYS allow it
Hypertension Pulmonary
lung R  heart work
Effects
-Ok at rest, anginal pain w/exercise cuz cant
meet oxygen needs
-Inadequate flow to meet metabolic needs
-Arrhythmias (irritable from ischemia)
-Clots form on plaques 
infarction/thrombi/emboli
-Myocyte abnormalities**
-Primary Dist is  CO & PA  low exercise
tolerance, fatigue
-sympt  vasoconstriction, fluid retention
 congestion, ascites, SOB, myocyte
responsiveness to sympt stim (down reg
beta recp)
CVP, need high sympt to maintain output
similar Sx to SCHF
TPR, struct changes, reflexes reset
(see below)
PA, R vent hypertrophy
Tx
1. lower bld lipids (diet, drugs)
2. Nitroglycerin, β blockers, Ca
blocker
3. surgery for stenosis: Balloon
angioplasty, Stent, Bypass
(saphenous vein or mammary art)
1. digitalis: improve contractility
2. diuretic & ACE Inhibt,
angiotensin II recp blockers
limited
Lifestyle, diet, diuretics, ACE
inhibitors, β blockers
Poor, – endothelan recp blockers
Coronary Artery Disease:
-CAD, usually assoc w/atherosclerotic plaques in large coronary arteries, results in progressive compromise in coronary bld flow,
inadequate for needs.
-Atherosclerotic plaques form in response to high shear stress  lipid deposition in wall  calcify  reduce bld flow
-*CAD Tx:
-Nitroglycerin: use w/acute angina,
-vasodialate coronary art   oxygen;
-reduce myocardial oxygen demand by:  preload (dilate veins) &  afterload (PA)
- β blockers: oxygen demand by blocking sympt (HR, contractility)
-Ca channel blockers: dilate coronary arteries (block Ca entry into smooth musc, dec
contractions)
Chronic Heart Failure – Systolic Dysfunction (Congestive Heart Failure)
-Heart failure exists when vent func is depressed through myocardial damage, red bld flow, etc
-Systolic Heart failure = red of cardiac musc contractility & results in  CO at all preloads
-lower than normal cardiac function curve (right)
Effects:
-**Myocyte abnormalities:
- intracell Ca (dec Ca sequestering in SR & upreg Na/Ca exchanger),
- troponin affinity for Ca,
-altered substrate metabolism from FA  glucose oxidation,
-resp chain activity
-Compensatory fluid retention mech are evoked in heart failure to improve
cardiac filling, but when fluid retention is excessive, congestive
complications arise (pulmonary edema, acites)
-benefits sympt:
1.  arteriolar constriction  norm Q to kidney, splanchic
2. myocardial oxygen consumption
-when norm CO achieved = compensated
-Neg Effects of fluid retention:
- cardiac dilation (CVP  EDV)
-organs: high venous P   cap filtration, edema, congestion
-L heart failure: pulmonary congestion
-R heart failure: distended neck veins, ankle edema, ascites, liver
congestion/dysfunction
Tx:
-digitalis – shift cardiac func curve up
-Angiotensin Converting Enz Inhibitors:  fluid retention by block whole pathway,
blocks abnormally robust heart scar tissue formation in heart too
Above: Chronic systolic heart failure cardiac function curve:
-Normal (A)  (B) uncompensated CHF (CO, CVP)
-B  C w/sympt 1. cardiac func curve to norm, 2. PVP
via venous constriction  VR. (CO still  norm but better)
But sympt cant remain high long term…
-CDE w/blood vol sympt via renin & fluid retention
 venous func curve (CO norm, sympt)
E: stable, norm sympt,  fluid retention
Nutshell: sympt comp early w/vasoconstriction, longterm
comp via inc blood vol.
Above:
unTx: contractility, ejection fraction
Tx: ejection fraction by SV from
afterload
Ch 11 – Pathophys
Cardio – Heller – 9.29.09
3
Chronic Heart Failure – Diastolic Dysfunction
-Diastolic dysfunc resulting from reduced cardiac compliance often accompanies (and may precipitate) heart failure.
Causes:
1. delayed myocyte relaxation early in diastole due to slow cytosolic Ca removal
2. inadequate ATP to disconnect myofilament crossbridges
3. residual, low-grade cross-bridge cycling during diastole due to Ca leaking from SR
4. Increase myofibrillar passive stiffness due to protein alteration
5. Decrease cardiac tissue passive compliance due to extracellular remodeling, collagen cross-linking & other extracelluar protein alt
Hypertension
Chronic elevation of arterial bp (+140/90) due to unknown causes (essential or primary hypertension) is a common & serious condition
influenced by genetic & environmental factors.
-HTN  risk for CAD, MI, heart failure, stroke, ect
-Primary HTN: Cause is often unknown
-Secondary HTN: cause is known: tumors, renal diseases, thyroid disease, parathyroid disorders
-Primary HTN facts: (from book)
-genetic link,  in males,  in blacks
-environ factors: high salt diet, stress
-structural changes: early L heart hypertrophy, thickening of larger arteries; late:  CT, elasticity, func
-TPR when HTN is established causes:
-density caps, peripheral vasc bed adaptations,  activity of vasc SM, vasc SM sensitivity to vasoconstrictor,  vasodialator
production
-sustained high bp not due to sustained high sympt or other vasoconstrictor
-bp reg reflexes reset to higher level
-KINDEYS ALLOW HTN! NOT A VASC DISEASE, IT IS A KIDNEDY DISEASE
-disturbances in renal func key in development and maintenance of HTN
-sm change in PA  big change in urine production.
-Person w/hypertension has a suppressed renal func curve  need higher than
normal PA to get a given urine output.
Treatment:
-lifestyle alteration (exercise, diet, reduce stress)
-w/restricted fluid intake and salt restrictions (effectiveness depends on slope of curve)
-diuretics to urine output, fluid retention (shift curve up).
-β-adrenergic blockers: block sympt on heart and renin release
-ACE inhibitors: block renin formation
Study Questions:
1. An increase in CVP is seen in which type of shock?
A. Cardiogenic B. Hypovolemic C. Septic
D. Neurogenic
2. An increase in sympt activity is effective in compensation of all the following types of shock EXCEPT:
A. Cardiogenic B. Hypovolemic C. Septic
D. Neurogenic
3. Which of the following cardiac disturbances is STRONGLY associated with atherosclerotic plaques in large coronary arteries:
A. Systemic HTN
B. Pulmonary HTN
C. Coronary Artery Disease
D. Congestive Heart Failure
4. Which of the following are true regarding systemic hypertension:
A. bp reflexes reset to a lower level
B. more common in women
5. Pulmonary Hypertension is:
A. more common than systemic HTN
C. causes R vent hypertrophy
B. Responsive to the same Tx as systemic HTN
D. Kidneys allow HTN
C. leads to R vent hypertrophy
Answers:
1.
2.
3.
4.
5.
A, Cardiogenic shock CO, VR  CVP
D, Neruogenic shock: primary disturbance is a decrease in sympt and increase in parasympt so you cant inc the sympt.
C, Coronary Artery Disease – high shear stress promotes atherosclerotic plaque formation in large coronary arteries  R, Q,  oxygen
D, kidneys allow HTN (see above for explanation)
C, R vent hypertrophy: the heart has to work harder to pump against inc resistance of the lungs