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Cardiogenic shock- importance

This is BIG trouble!
Cardiogenic Shock requires the highest level of care available in your hospital system, including nursing, CV technicians, Anesthesiologists, Cardiovascular Surgeons and Clinical Cardiologists.


Most cases of CS

Most cases are the result of Acute MI. Some with mechanical tissue disruption producing a VSD or Acute Severe Mitral Regurgitation.

Fewer cases are chronic CHF that decompensate and “spirals” down with hypotension decreasing CO thus decreasing BP, urine output, coma, death.


cardiogenic shock defn

Inadequate tissue perfusion due to cardiac dysfunction.
It is the combination of Hypotension and Pulmonary Edema.
Patient is wet and hypoperfused (cool)


CS secondary to AMI

CS complicates 6% of acute MI’s.
Most are STMI, but some are NSTMI, especially in people with prior MI. MI’s “add-up”


CS mortality

Mortality used to be 90%
Now it is lower 48% (2004)
This is because of faster treatment with IABP and direct PCI (stenting).


CS Predictors of Mortality:

Advancing age
Prior MI
Shock physical findings

Symptom onset to reperfusion time also determines benefit and lower mortality.
less than 2 hours 6% mortality rate.
Up to 12 hours.


CS Coronary anatomy

Most patients have severe and extensive CAD
Triple vessel disease
Left Main disease


CS echo predictors

lower EF and MR severity


CS meds

ASA, Heparin, IIb,IIIa, Inhibitors
Avoid BB
Drips: Dopamine, Dobutamine, Norepinephrine, Milrinone


things to keep an eye on in CS

Hemodynamic monitoring
IABP- the Adrian Kantrowitz MD story
LVAD-Left Ventricular Assist Device


treating CS

PCI is preferred over Fibrinolytics and has better outcomes.
I usually have the patient intubated on a Vent in the cath lab.
Often it is very helpful to have an Anesthesiologist in the cath lab


when does CS need to be treated by emergent surgery?

If the patient has Acute Severe MR or a VSD it needs to be treated by emergent surgery.


Shock from end stage CHF- treatment

This may be treated with an LVAD (Left Ventricular Assist Device), as a bridge to transplant or as a destination treatment



Atherothrombotic (Atherosclerosis) of the Lower Extremity Arteries

May be either progressive arterial narrowing or arterial-arterial embolization of atherothrombotic debris


pad symptoms due to?

an imbalance of supply (arterial) and demand (muscles), similar to angina


PAD Risk Factors-ACC Guidelines

1. Age >70
2. Age 50-69 with a history of smoking or DM
3. Leg symptoms of intermitant claudication, from Latin for “Limp”, or rest pain
4. Abnormal LE pulse exam
5. Known atherothrombosis of other sites


Some things we see with PAD

Advances with age, so with the ageing population it is increasing
Always ask about LE pain upon walking, in your H&P. May be Buttocks, hips, calf or foot.
Leriche Syndrome triad of intermitant claudication, absent or diminshed femoral pulses and erectile dysfunction


Blue Toes Syndrome

-due to peripheral embolization of atherthrombotic material from proximal atheroma, often from the aorta


PAD Clinical Presentations:

1. Asymptomatic 20-50%
2. Atypical Leg Pain 40-50%
3. Classic Claudication 10-35%
4. Threatened Limb 1-2%


The presence of PAD is a risk factors for

other vessels having atherothrombotic disease, including Carotid (stroke), Coronary (ACS, etc), Renal (CKI, Hypertension Renovascular)


Asymptomatic PAD

Diagnosed by screening:
PE with careful palpation of pulses to include Femoral, Popliteal, DP and PT (LE)
Brachial, radial, ulnar in the UE
Bruits, skin color and temperature, presence of skin ulcers and wounds


PAD Exam

should be supine after 15 minutes of rest, allowing the patient to “warm up” if it is cold outside
Use Doppler for more accurate assement when necessary


Critical PE component for PAD

ABI is critical.
The Ankle-Brachial Index is the Systolic BP in the arm (highest UE) compared to the Ankle SBP, ie 1.0 would be equal pressures in A/B systolic pressures
Correlation is general with ABI and symptoms:
Claudication: 0.4-0.9
Rest Pain: 0.2-0.4
Tissue Loss: 0.0-0.4

ABI less than 0.90 with no or mild/moderate symptoms has a high degree of sensitivity for PAD


Buerger Test

Patient supine, elevate foot (25 cm) drain venous blood, then make foot dependant, it should take less than 20 seconds for foot to refill, more time indicates severe PAD


ABI and exercise testing - PAD

Exercise testing will show a drop of the ABI by 0.2 in patients with significant PAD, who have normal ABIs at rest.
The exercise test will also demonstrate the time to claudication, how will this help your patient?


Gangrene and PAD

1. Dry-hard dry texture, distal toes and fingers, clear demarcation between viable and black necrotic tissue. This is common.

2. Wet-moist appearance, gross swelling, blistering. Less common and indicative of an emergeny.


Ulceration and non-healing wounds are signs of

severe rest ischemia. Always think PAD when assessing LE wounds so you don’t miss the diagnosis.


PAD and neuro exam

A Neurologic exam of the LE’s is essential to rule out Peripheral Neuropathy.

Remember “Fleas and Lice”, many of the patients with PAD have DM and PN.