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What is the difference between primary and secondary cardiomyopathy?
- Primary: Those that are predominantly confined to heart muscle. Can be genetic, mixed, acquired.
- Secondary: demonstrate the cardiac abnormality as part of multisystem disorder
what are the causes of primary cardiomyopathy?
- Hypertrophic cardiomyopathy
- Arrhythmogenic right ventricular cardiomyopathy
- Glycogen storage disease
- Ion channelopathies (long QT syndrome, etc.)
- Dilated cardiomyopathy
- Primary restrictive nonhypertrophied cardiomyopathy
- Myocarditis (inflammatory cardiomyopathy): viral, bacterial, etc.
- Stress cardiomyopathy
- Peripartum cardiomyopathy
What are causes of secondary cardiomyopathies?
- Infiltrative: Amyloidosis & Gauchers’s disease
- Storage: Hemochromatosis
- Toxic:(Drugs, alcohol, chemotherapy, radiation)
- Inflammatory: Sarcoidosis
- Endomyocardial: Endomyocardial fibrosis
- Endocrine: DM, Pheochromocytoma,
- Thyroid disease (hyper or hypo) Acromegaly
- Neuromuscular: Duchenne-Becker dystrophy Neurofibromatosis
- Autoimmune: SLE, RA, Scleroderma
DCM: anatomic and physiologic changes
- LV chamber enlarged
- Systolic dysfunction
- LV wall thickened
- Diastolic dysfunction
- Stiffened myocardium
- Diastolic dysfunction
RCM sounds like HCM at first (Stiff LV and diastolic dysfunction), what is different?
stiff myocardium is d/t fibrosis or some infiltrative process (not from build up from muscle fibers themselves. Something went in and broke up myocardium w/less pliable tissues
Causes of DCM
- Inflammatory :Infectious (especially viral), Noninfectious (Connective tissue diseases-other inflammatory conditions, Peripartum, Sarcoidosis)
- Toxic: Chronic alcohol ingestion, Chronic hypocalcemia or hypophosphatemia
- Neuromuscular: Muscular or myotonic dystrophy
Acute viral myocarditis occurs in young or old ppl?
Various viruses implicated (coxsackie, adenovirus, parvovirus) viral is usually self limited and recovery is complete but some unknown reason some pt. will progress to dilated cardiomyopathy Immunosuppressive drugs may be helpful in improving prognosis in some people.
What causes and what is the tx for dilated cardiomyopathy from alcohol
- Think it's because of the oxidative phosphorylation that occurs in mitochondria.
- Pt can be counseled to stop drinking and improve scenario.
When does peripartum CM occur?
presents w/HF symptoms between the last month of pregnancy and up to 6M post partum
Who is at risk for peripartum CM?
Those at higher risk: older mothers, AA, pt. w/multiple pregnancies.
Does ventricular function return to normal w/peripartum CM?
Maybe. Ventricular function returns to normal in about 50% of those women in the months following pregnancy but recurrence can happen w/subsequent pregnancies.
For DCM, the genetic variety is thought to be responsible for____% of what had previously been described as idiopathic.
- Various patterns of inheritance. (Autosomal dominant, autosomal recessive, x linked)
What is the bottom line for all of the etiologies for DCM?
problem w/contractile force generation and myocyte viability
What chambers are involved in DCM?
- Usually marked enlargement of all 4 chambers
- Sometimes limited to LV
- Less commonly limited to RV.
- Although the wall of the ventricle might be thickened, the chamber is dilated out of proportion to that. Under microscope the cells themselves have degenerated, myofibers have atrophied. Fibrosis that’s often fairly extensive.
Hallmark of DCM:
dilation of ventricles and decreased contractile function
In DCM, because the SV and CO are decreased because of contractility, there are a few compensatory mechanism activated
- 1. Frank Starling
- 2. Neural hormonal activation which initially means SNS gets activated→↑HR & ↑contractility. May be asymptomatic in early stages of ventricular dysfunction, but progressive disease, as heart muscle cells degenerate further, volume overload occurs and s/s of HF develop
- 3. Also ↓renal perfusion= RAAS, helps to buffer ↓CO.
- 4. ventricles enlarge
Ventricles enlarge in DCM to compensate but then what happens?
MV & TV pulled apart & can’t coapt properly during systole so we end up w/MR and TR→ cyclical regurgitation excessive vol/press. overload, get atrial dilation which causes AF. Regurgitation also means part of the SV is going back as opposed to forward, so decreased forward flow (CO). Then when regurgitation volume gets added to regular LV volume during diastole, there is even a greater volume load presented to already dilated LV.
What are the symptoms of DCM
Manifestations of ↓CO & ↓ forward flow (fatigue, syncope, exertional dyspnea) w/pulmonary congestion get (dyspnea, orthopnea, paroxysmal nocturnal dyspnea) systemic congestion from right side (Ascites and peripheral edema) Early on pt. may c/o being tired and recent weight gain or SOB on exertionFatigue Exertional dyspnea
What is the physical exam of DCM?
- Reflects decreased CO, peripheral vessels may vasoconstrict, extremities may feel cool to touch, expect BP to be low and HR to be high. Rales on auscultation. May be a murmur of MR. if the RV involved, associated changes in sys circulation and right cardiac function will also be seen.
What is the EKG of DCM look like?
- Atrial & ventricular enlargement
- Arrhythmias , BBB (Particularly if fibrous tissue in conduction system, LAE = AF, also Vtach.
- ST-T abnormalities
- Q waves (localized -Dense areas of myocardial
What does the CXR for DCM look like?
- Pulmonary vascular redistribution
What does the ECHO and Cath show in DCM?
- ECHO: 4- chamber enlargement, ↓ systolic function, MR or TR if leaflets don’t coapt properly
- Cath: diagnosis and see if any contribution of CAD (part of picture contributing to impaired LV function)
What is the treatment of DCM? (4 main things)
- Medical treatment of heart failure
- Prevention & treatment of arrhythmias
- Prevention of thromboembolic events
- Cardiac transplantation
In DCM, Arrhythmias are responsible for __% of deaths (Vtach and VF) important to check electrolytes.
40%; Studies show these antiarrhythmics don't prevent death from ventricular arrhythmias. But Amiodarone is most studied and believed to be safest for tx AF and other supra ventricular arrhythmias in this population
In DCM, an AICD is recommended for anyone w/chronic symptomatic cardiomyopathy and at least moderately reduced systolic function, meaning.....
an EF equal or less than 35% regardless whether ventricular arrhythmias have been detected
Ventricles may be dysynchronous, so using that cardiac synchronization therapy may be helpful
Why is there a risk of thromboembolic events in DCM?
- increased because of stasis of blood in the ventricles because of poor systolic function as well as stasis of blood in the atria because of chamber enlargement and likely AF.
- These patients may also have such poor circulatory flow (vasoconstriction) get venous stasis and may also contribute to risk of thromboembolism.
Only definitive indication for systemic anticoagulation in DCM is ????
- AF or prior thromboembolic event, or on ECHO if you see a thrombus in the heart.
- Strong indications, chronic oral anticoagulation for those w/LV EF <30%. No good prospective studies supporting this provided the pt. is in NSR.
For DCM, cardiac transplantation offers a better 5yr prognosis overall than standard TX. What are the 5 and 10 year survival rates?
- 5 yr= 74%
- 10yr = 55%
- ....but scarcity of donor hearts
True or false. In DCM, Up to 1/3 will experience spontaneous improvement following diagnosis of cardiomyopathy
What is the 5 yr survival rate for those with persistent DCM who don't get a transplant?
Prognosis is poor average 5yr survival is less than 50% if they have progressive DCM and don’t get a transplant
What is the etiology of HCM?
- Autosomal dominant genetic disorder with variable penetrance
- Genetic mutations determine: Age of onset of hypertrophy, Extent & pattern of remodeling, Risk of symptomatic heart failure or sudden death
What is the common abnormality found in young athletes who die suddenly in vigorous exertion 1:500 in general population
What is the pathology of HCM?
- Asymmetric hypertrophy of ventricular septum (usually)
- Myocardial fibers are disordered with fibrosis (Responsible for abnormal diastolic stiffness & Arrhythmias) rather than an orderly enlargement of myocardial cells that we see in AS or HTN
In HCM the hypertrophy can involve any part of the ventricles, what is most common?
Most common is asymmetric hypertrophy of ventricular septum (90% of cases)
In HCM, the main feature is marked LVH. There is decreased compliance and decreased diastolic relaxation and impaired filling. What else happens?
LVOTO (Left ventricular outflow tract obstruction)
In HCM, about 90% of pt. have this asymmetric septal hypertrophy and ___ of 90% of pt. will show this LVOTO and possible MR as well
Explain the LVOTO and MR that we see in HCM
- See abnormal motion of anterior leaflet of MV during systole. During systole the ejection of blood through AV is more rapid than usual, going through a narrowed opening because the septum is enlarged and moving over which narrows the opening.
- Because of that, there is a rapid jet of blood (Bernoulli's principle, decreased cross sectional area flow is fastest at point of greatest constriction) so speed is faster and pressure is decreased pressure at point of greatest constriction, pulling the anterior leaflet over. (like the shower curtain example)
What causes angina in HCM?
- Three reasons for angina: ↑muscle mass (↑
- O2 demand), Hypertrophy ventricular wall will narrow small branches of coronary arteries, & OTO (high systolic pressure will further increase O2 demand d/t wall stress)
During systolic obstruction, a pressure gradient will develop between the main body of the left ventricle and the outflow tract distal to the obstruction. This increase LVESP will increase wall stress, increase myocardial O2 consumption which causes angina
In HCM, the patient w/outflow obstruction the decreased compliance and outflow obstruction cause an ____LAP and pulmonary wedge pressure.
- MR that develops will further increase LAP and pulmonary wedge pressure beyond what would be d/t the hypertrophy and diastolic dysfunction alone and that can always increase LAP and lead to LAE and AF
TRUE or FALSE. Systolic pressure gradient that we see in obstructive HCM is static.
- FALSE. It's dynamic.
- Magnitude varies w/each systole and depends on the distance between the anterior mitral leaflet and the hypertrophied septum at any given time.
What will promote obstruction in HCM w/LVOTO and MR?
- Anything that decreases the size of the LV, the cavity of the LV, (↓preload, because if we were to decrease size of LV that will bring leaflet closer to septum and cause obstruction).
- In terms of contractility, if we increase contractility we’ll also promote obstruction. (DON’T WANT TO DO)
- ***Want to maintain or increase preload (intravascular volume) and decrease contractility.
What are the symptoms of HCM?
- Dyspnea (most common)
- Syncope (Syncope can appear d/t decreased venous return, may be orthostatic signs)
- Arrhythmias (contribute to syncope)
- The symptoms can vary widely from none to marked physical limitations. ↑ LAP & ↑
- pulmonary wedge pressure. Made worse by high systolic pressure in LV and the MR if present w/LVOTO. Angina is also a frequent symptoms may occur w/out CAD.
What is the average age of presentation of HCM?
What will you see upon physical exam of HCM?
- Could have a near normal exam!
- S 4
- Palpable presystolic impulse (felt over the apex from forceful LA contraction)
- Crescendo-decrescendo rough systolic murmur over left sternal border
- Holosystolic murmur of MR @ apex
Unfortunately the 1st sign of HCM may be VF resulting in sudden death, particularly in young adults during strenuous activity. What are the risk factors for this?
history of syncope, familial history of sudden death, certain high risk mutations, and also extreme hypertrophy of LV wall.
Murmur of LVOTO may be soft at rest but certain maneuvers you can do to differentiate from others (like AS), what can you do?
have the pt. valsalva or stand that will increase a murmur of HCM but decrease murmur of AS.
What can you expect to see on the EKG of a patient w/HCM?
- LVH & LAE
- Prominent Q waves in inferior & lateral leads (Lateral: I and avL. Inferior: II, III and aVF )
- Diffuse T wave inversions
- Arrhythmias (AF is particularly common. V. arrhythmias are ominous as they can herald VF and sudden death even in pt. who have been previously asymptomatic.
We can do an ECHO, cath, and genetic testing for our patient w/HCM. What will this show us?
- ECHO: measure degree and location of ventricular hypertrophy look for obstruction an movement of valve leaflets
- Cath: reserved for those who we don’t’ know what’s going on
- Genetic: looking for or excluding that etiology
What kinds of medications can we use to treat HCM?
- Beta blockers: **standard (↓HR &↓contractility so ↓ angina & dyspnea. ↓any LVOT gradient during exercise (↓contractility) ↑passive diastolic filling time because of ↓HR a & ↓
- frequency of PVCs.
- Calcium channel blockers:reduce ventricular stiffness and sometimes improve exercise capacity if pt. doesn’t respond to BB
- Anti-arrhythmics: (Amiodarone &/or Disopyramide). AF should be tx aggressively. Amiodarone is good choice for that
TRUE or FALSE. In spite of all those benefits of BB, not shown to prevent sudden cardiac death in HCM.
What do we want to avoid (medications) in HCM?
- MAYBE Diuretics but might be helpful if pulmonary congestion, don't want to decrease preload, want to maintain volume!
- Vasodilators should be avoided as well for this reason
- Digoxin: avoid d/t effect on contractility
Why is an ICD useful in HCM?
- Sudden death d/t VF or Vtach!
- Sudden death occurs w/exertion, so avoid sports as well
What surgery could a patient w/HCM have? Is there a less invasive option?
- Myomectomy, considered for pt. if symptoms don’t respond to other tx. Parts of hypertrophied septal muscle are excised in order to relieve that obstruction.
- Less invasive: Can also do a percutaneous septal ablation. Sm amount of ethanol injected into a septal coronary artery, branch of Lad, sm controlled MI decreases the thickness of the septum.
For HCM Incidence of sudden death____% per year in adults and ____% per year in kids
2-4% in adults and 4-6% in kids
Part of the anesthesia implications for HCM is to evaluate for the potential of
- Significant dynamic obstruction
- Malignant arrhythmias
- Myocardial ischemia
What is the management goal for anesthesia in a patient w/HCM?
- Goal = minimize LVOT obstruction
- Any drug or intervention that ↓s contractility or ↑s preload or afterload ↓ s LVOT obstruction
- Some degree of myocardial depression is desirable, achieved w/volatiles.
Pre-op, what would we do for the patient w/HCM?
- Careful patient & family history
- Listen for systolic murmur
- Need updated cardiac evaluation (including 12 lead EKG & ECHO)
- Continue beta blockers and calcium channel blockers
- Turn off ICD in immediate preop period & have external defibrillator immediately available
- Anxiolytic to decrease SNS stimulation
- IV fluid administration to minimize effects of positive pressure ventilation on venous return (PPV decreased preload and we want to increase preload)
What do we want to do on induction for HCM?
- Avoid sudden ↓ SVR, ↑ HR, or ↑ contractility
- Blunt response to laryngoscopy
How do we want to maintain anesthesia for the patient w/HCM?
- Small VT & ↑ RR to minimize effect of + pressure ventilation; avoid PEEP
- Advise surgeon to minimize intrabdominal pressure to less than 15 mmHg during laparoscopy
- Use NDMR with minimal effects on circulation (No pancuronium or atracurium)
- Volatile agent is good for mild cv depression
- Treat hypotension with phenylephrine (↑SVR but no ↑contractility)
- Maintain preload but avoid aggressive fluid administration
What do we want to do post-op for our patient w/HCM?
- Avoid SNS stimulation from pain, hypoxia, hypercarbia
- Maintain euvolemia
What are our HD goals for HCM?
- Preload: Full; one of the first treatments for hypotension is volume
- Afterload:Increased; treat hypotension aggressively with α adrenergic agonists
- Contractility: Prefer depression
- Rate: Normal range; Not too slow, not too fast; beta blockers decrease left ventricular outflow tract gradient and increase LVEDP
- Rhythm: Sinus rhythm is crucial; atrial pacing may be helpful
- MVO2: Not a problem
Which is more common restrictive CM or (DCM or HCM)?
DCM or HCM is more common than RCM
Give some examples of restrictive cardiomyopathy
- Noninfiltrative (Idiopathic & Scleroderma)
- Infiltrative (Amyloidosis & Sarcoidosis)
- Storage diseases (Hemochromatosis & Glycogen storage diseases)
- Endomyocardial disease (Endomyocardial fibrosis, Hypereosinophilic syndrome, Metastatic tumors, & Radiation therapy)
Describe restrictive cardiomyopathy
- Characterized by abnormally rigid but not necessarily thickened ventricles.
- Problem w/diastolic filling, but normal or near normal systolic function.
- Results from either fibrosis or some sort of scarring of myocardium.
- Could be infiltration of myocardium by amyloidosis or sarcoidosis
- Diastolic dysfunction is main abnormality but sometimes systolic can occur later is the disease.
- Infiltration in conduction system, can get conduction defects and arrhythmias as well
_____________is most common in non-tropical countries where these amyloid fibrils deposit in many tissues including the heart.
What is the pathophys of RCM?
- Decreased compliance of ventricles will result in upward shift of the passive ventricular filling curve abnormally high diastolic pressure.
- Increased pulmonary and venous pressures, decreased ventricular filling and CO
What are the symptoms and physical exam findings in RCM?
- Signs of L and R sided HF would be physical findings association w/restrictive CM.
- Fatigue, weakness, s/s of systemic and pulmonary congestion (hepatomegaly is systemic)
- Arrhythmias (AF are common, conduction blocks are common)
- What you see in physical exam depends on degree of congestion but al the signs we’ve talked about before
What are the diagnostic studies associated w/RCM?
- CXR (pulmonary congestion)
- EKG (non specific ST/T changes)
- Findings and HD profile will be similar to that of constrictive pericarditis but the latter is more TX situation. May be necessary to do CT or MRI to differentiate the two
What is the treatment for RCM?
- Very poor prognosis
- Treat underlying cause if possible (If cause is hemochromatosis. Phlebotomy and iron chelation therapy may be indicated)
- Salt restriction
- Cautious diuresis
- Maintain SR
- Possible anticoagulation
- Vasodilators might be helpful because systolic function is usually well preserved
RCM anesthesia implications
- Same as for patients with cardiac tamponade
- Life threatening hypotension can result form GA and + pressure ventilation in these patients (Decreased return from PPV from increased intrathoracic pressure)
- Maintain CO & BP
- Avoid ↓ contractility, ↓ SVR, ↓ HR
- Anesthesia causes vasodilation, direct myocardial depression
- Avoid bucking and coughing (↓ venous return)
Name the physiologic causes of shock
- Circulatory shock due to decreased CO (Cardiogenic shock & Hypovolemic shock)
- Circulatory shock with preserved CO (Hypermetabolic state & Abnormal tissue perfusion)
What is the "main problem" in shock
- Tissues don't get enough nutrients & O2, also waste products of cellular metabolism aren’t being removed (volatile and non-volatile acids).
- BP ↓ but occasionally almost normal arterial pressure because compensatory mechanism for circulation are working overtime.
- Can also be adequate tissue perfusion w/↓BP
What kind of shock do we see the most?
- For us the type of shock we’re most likely to see is hypovolemic (blood letting and we decrease tone).
- BP usually falls at same time as CO but not the same magnitude.
How does shock perpetuate itself?
- Once shock precedes to a particular stage (critical stage) shock will perpetuate itself and lead to more shock.
- Not perfusing all the tissues (the heart) makes the heart less able to pump and further decreases CO.
- So shock decrease perfusion and decreased perfusion causes more shock.
- So we’re always trying to stop the cycle in the early stages of hypovolemic shock.
STAGES of shock (based on severity)
- Non-progressive (compensated): The normal compensatory mechanisms are really effective in eventually causing full recovery w/out any intervention
- Progressive:All those compensatory mechanism are not sufficient
- Irreversible: W/out tx the shock will become worse and death will result. Got to point that all available tx is not enough to sustain life even thought at that point the pt. is still alive (technically)
The most common type of shock for us, hypovolemic, involves ↓ venous return, ↓
CO. The graph from Guyton, showed effect of blood loss on both BP and CO over a period of time. Describe this
- 10% of the blood volume w/almost no effect on either BP or CO but if loss continues both decrease.
- CO decreasing 1st. When the pt. loose 40-45% of blood volume we can see both CO and BP plummet to zero.
In hypovolemic shock it is important to remember that to control circulation, the baroreflex and various stretch receptor are important compensatory mechanism result in SNS stimulation. Why is this important
- SNS causes arteriolar constriction, that increases total peripheral resistance.
- Venoconstriction which ↑preload despite a total decrease in blood volume.
- ↑ HR also contributes to CO
- CO decline before BP is because of SNS causes arteriolar constriction which increases BP but not alter CO.
IF we didn’t have our SNS in hypovolemic shock, the loss of only ______% of blood volume in same 30min would lead to death. Compared w/_____% blood loss w/intact nervous system.
Upped the amount of volume we can loose before it becomes irreversible. The SNS double the amount of blood that can be lost w/out causing death.
On the graph for hypovolemic shock, there is a second plateau at about 50mmHg on arteriolar pressure curve. Why is this?
d/t activation of the CNS ischemic response that causes extreme SNS stimulation when the brain starts to suffer from lack of O2 or build up of CO2 (last ditch stand to try and keep BP from falling too low)
How do preserve coronary & cerebral perfusion in hypovolemic shock
There is autoregulation.Generally the flow of blood through heart and brain is maintained at essentially normal levels as long as BP doesn’t fall below 60-70mmHg even though the flow could be decreased in other tissues to as little as 25-30% of normal. This is because of vasoconstriction, the autoregulation works where we need it most in the heart and the brain.
What is non-progessive hemorrhagic shock?
- Compensated shock
- Not bad enough to cause its own deterioration. PT recovers because of multiple feedback mechanisms (baroreflex, cerebral ischemic response, reverse stress relaxation, RAAS, vasopressin, Epi/Norepi, & Fluid shifts)
What is the response rates of these compensatory mechanisms in non-progressive hemorrhagic shock?
- 30sec to a few minutes of hemorrhage: The SNS (baroreflex and CNS ischemic and secretion of Epi and norepi) become max effective activation within a few seconds, so 1st clue will be HR.
- 10min-1hr: angiotensin and vasopressin along w/reverse stress relaxation to respond completely, but important for raising filling pressures, (preload) and maintain BP.
- 1hr-2days: Fluid shifts but recovery occurs if shock not so severe that it enter progressive stage
What is the differential diagnosis of tachycardia intraop?
pain, light anesthesia, hypoxemia, hypercarbia, hypoglycemia, MH, thyroid storm, pheochromocytoma, etc.
What causes cardiac depression is progressive hemorrhagic shock?
- Low BP means decrease coronary blood flow, not enough O2 and nutrients, heart looses its ability to pump.
- Decreased CO creates positive feedback so shock becomes worse.
- Normally have built in reserve in that heart can pump 300-400% more blood than is required for adequate nutrition of the tissues but after a period of sustained shock there will be diminished pumping ability and heart will deteriorate.
- Diminished pumping capacity and deterioration of heart is most important factor in final lethal progression of shock
Describe vasomotor failure in progressive hemorrhagic shock
- vasomotor center in the medulla.
- Overtime becomes less active and eventually inactive. So during 1st 4-8min of circulatory arrest there is the most intense of all sympathetic discharge but the end of about 10-15min the vasomotor center is so depressed that no further sympathetic discharge could be detected.
- If the BP remains above 30mmHg (MAP) the vasomotor usually doesn't fail in early stages of shock.
What causes micro vessel blockage in progressive hemorrhagic shock?
- Guyton talks about sludge blood.
- In low flow situations, the tissue metabolism continues, end products is lactic acid (non volatile) and carbonic acid (volatile).
- So w/acid accumulation the pH goes down.
- So get acidosis along w/other end products of ischemic tissues will cause blood to coagulation and plug the microcirculation.
- This agglutination of blood even w/out complete occlusion that Guyton refers to as sludge blood
What causes an increase in capillary permeability in progressive hemorrhagic shock
- From lack of nutrients and O2, capillary walls loose integrity, increased capillary permeability and fluid will transudate into surrounding tissues.
- Loosing from intravascular space as well as surrounding tissues. Makes intravascular volume even worse.
- Doesn’t occur until late stages of prolonged shock. Goes back to anaerobic metabolism and decreased in ATP production, we need ATP for Na/K ATPase pump. Without oxygen, less ATP generation, then can’t be proper electrolyte gradients across the membranes
What causes toxin release in progressive hemorrhagic shock?
Always also been assumed process of shock release toxic substances (histamine, serotonin, & various tissue enzymes) which then also contribute to the progression of shock.
What causes the cardiac depression by endotoxin in progressive hemorrhagic shock?
- Endotoxin is one such toxic substance released from gram negative bacteria in intestine, released d/t decreased blood flow to GI tract.
- When that happens get increase in cellular metabolism even though nutrition is inadequate and ultimately results in depression on the heart.
- Particularly important in septic shock.
What causes cellular deterioration in hemorrhagic shock? ESPECIALLY where?!
- General cellular deterioration will occur throughout the body.
- Liver especially (high metabolic rate, needs O2/nutrients) not working effectively, build up of toxins.
- Cellular level we get decreased active transport Na and K, Na and Ca+ accumulate intracellularly. And K+ in extracellular fluid. So the cells will swell Na and Cl inside and K+ in extracellular so high it can become lethal.
- All the mitochondrial activity, metabolic activity in liver is dramatically reduced because no O2
- Enzymes contained in lysosomes in the cells, these get released so that will cause further cell breakdown.
- Depressed ability of the cell to metabolize glucose/other nutrients along w/actions of various hormones in late stages of shock including 100% of insulin.
- Deterioration of many organs but especially liver as well as lungs and myocardial depression.
Tissue necrosis is present in progressive hemorrhagic shock. Where does this occur?
- Parts of particular tissue more susceptible to shock than others.
- Some organs develop patchy areas of necrosis (found in liver, heart, kidneys and the lungs)
Why do we see acidosis in progressive hemorrhagic shock?
Lack of O2 and build of lactic acid. Because of decreased blood flow, CO2 not removed efficiently and that further leads to acidosis and perpetuates shock as well
Describe irreversible hemorrhagic shock
- Implies no TX that will be effective in turning situation around.
- Therapy may be effective in restoring BP and CO to normal or near normal but only for short period of time, but when you get to this stage it just progresses continued deterioration and eventually death
Shows that transfusion improves CO for a time but unfortunately the deterioration in myocardial cells among other will mean that the improved initial increase in CO can’t be maintained (That whole deterioration of the cells, acidosis, all those destructive enzymes breaking down cells) takes over and death will result no matter what the TX. Single most important factor in this result is the depletion of ATP (no O2 no nutrients no ATP)
Describe two ways there can be plasma loss in hypovolemic shock
- Intestinal obstruction: the intestines distended that causes a decrease in venous blood flow in walls of the intestine. That increases capillary hydrostatic pressure causing fluid to leak from capillaries into lumen of the intestine. The fluid that’s lost w/this has a high protein content, decrease in plasma protein as well as decrease in plasma volume (not blood) going in but high protein fluid. Loosing some of our oncotic pressure as well.
- Burns: because the integrity of the skin is lost. Significant fluid is also lost.
Differences in plasma loss vs hemorrhagic shock
Plasma loss: viscosity of blood increases significantly, this increase in viscosity will contribute to sluggish blood flow.
When fluid is lost from all tissue compartments it’s termed_________
- Other causes of decrease total body water: excessive diaphoresis, vomiting and diarrhea, excessive diuresis, inadequate fluid intake, and also adrenal cortical destruction (because if adrenal cortex is destroyed then aldosterone isn’t produced).
How is tissue trauma cause hypovolemic shock
Blood loss or 3rd spacing
3 causes of neurogenic shock
- Deep general anesthesia
- Spinal anesthesia
- Brain damage
How does deep GA cause neurogenic shock?
- Size of intravascular space not just the contents.
- Tank size changes w/volatiles, vasodilation increases size of tank
- Sudden loss of vasomotor tone throughout the body and massive vasodilation this is neurogenic shock.
- venodilation in particular causes a decrease in venous return or preload and a decrease in CO.
- So neurogenic can occur w/the deep general anesthesia (depression of vasomotor center, enough to cause vasomotor paralysis)
How does spinal anesthesia cause neurogenic shock?
- Sympathectomy of spinal anesthesia
- High spinal or total spinal, extends all the way up spinal cord sympathetic chain, don’t generally want (never want total spinal) but even w/relatively low spinal get some degree of sympathetic blockade.
How does brain damage cause neurogenic shock?
- vasomotor paralysis, pt. experience traumatic brain injury in basal regions of the brain may develop a neurogenic shock.
- Prolonged cerebral ischemia lasting 5-10min total inactivation of neurogenic neurons and neurogenic shock.
What causes anaphylactic shock?
- Histamine release from basophils & mast cells
- Increased in venous dilation decreased venous return, arteriolar dilation, decreased BP increased capillary permeability and fluid loss
What is septic shock
- Usually results from bacterial infection widely disseminated and present in the blood. Because it can result from any infection, it’s our role to be on top of abx.
- Usually contributed to some bacterial toxin stimulating cellular metabolism as well as hyperthermia.
- Sludging of blood can occur s/septic shock.
- DIC: using of clotting factors so hemorrhage may also occur.
Other than cardiogenic, what is the most frequently cause of shock related death in hospital.
What are some features of septic shock.
- High fever, often marked vasodilation particularly in infected tissues.
- High CO in about 50% of Pts. from, arterial vasodilation coupled w/high metabolic rate.
Treatment of shock
- Replacement therapy: PRBCs, Plasma, Dextran, Hetastarch
- Pharmacologic therapy: Sympathomimetics (Neurogenic shock & Anaphylactic shock) not useful if SNS already at max in hypovolemic
- Other strategies: Trendelenburg position, Oxygen, & Glucocorticoids (severe shock may ↑strength of heart in late stages of shock & stabilize lysosomes that contain destructive enzymes so they don’t’ get released into the cell. May also help in metabolism of glucose by severely damaged cell)
- IVF and phenylephrine to support BP