cardio 10 Flashcards
Which type of shock will have increased mixed venous O2 saturation?
Septic shock because of increased cardiac output but low tissue oxygen utilization.
What is Mvo2 saturation?
Venous blood o2 saturation measured in a pulmonary artery by catheter. or
The tension represents the oxygen remaining in the venous bloodstream after the extraction of oxygen by the tissues.
What are normal SVCO2 and MSVo2 values?
SVCo2–60-80
MSVo2–65–75
Svo2 and Scv02 diference?
Svo2–Pulmonary artery
Scvo2–Superior venacava
What leads to a decrease in ScvO2 and Svo2 values?
1) Decrease CO
2) High tissue metabolic rate
3) All other causes factors lead to decrease arterial total oxygen content..
What factors will lead to an increase in Svo2?
1) High flow state (sepsis, hyperthyroidism, severe liver disease.
2) Increase o2 delivery(high Fio2, hyperbaric 02, and hyperoxia)
3) Low tissue O2 uptake(Anesthesia, hypothermia, and neuromuscular blockade, and severe tisue inflammation)
Why is Scv02 < S/Mvo2?
The high metabolism of the brain –Low SVC o2 saturation to that of IVC(low lower body metabolism especially kidney)—Low SVCO2 to that of MVO2
In which type of shock have high CVP?
Cardiogenic
Obstructive
In which type of shock have low CVP?
Hypovolemic Distrubitive (all type)
In which type of shock have High PCWP?
Cardiogenic Obstructive (Onley In case of pericardial effusion)
In which type of shock have Low PCWP?
Hypovolemic Obstructive(Exept in case of Pericardial temponad) Distributive all type
In which type of shock have a High cardiac index(LVO)?
Distributive (Septic or anaphylactic shock)
In which type of shock have a Low cardiac index(LVO)?
Hypovolemic
Cardiogenic
Obstructive
Distributive (In case of neurogenic one)
In which type of shock have a Low Svo2?
Hypolumic
Cardiogenic
Obstractive
Distributive(Nurogenic one)?
In which type of shock have a High Svo2?
Distributive(exept nurogenic one)
Cause of aortic stenosis?
3(three)
1-senile calcific aortic stenosis(in age >70)
2-Biscupid aortic valve (the most common cause under the age of 700.
3-Rheumatic fever.
What are the components of CHADSVAS?
CHF Hypertension Age>75 Diabetes STROKE/TIA/TE Vascular disease(MI, PAD, or aortic plaque) Age 65-75 Sex(female)
all score criteria have a value of 1 except?
Age >75 and Stroke/TIA/TE which have a value of 2.
What is the preferred treatment for value >=2
Non vitamin k dependent oral direct factor X inhibitors(NOAC)–like abixaban,rivaroxaban,dabigatran and endoxaban
Why NOAC preferred over warfarin?
Same or superior TE preventive effect
Low risk of ICH
Not require follow-Up
ECG future of Atrial Fib?
Absent P wave Or replaced by a chaotic fibrillary wave.
Irregular R-R interval
Narrow QRS complex
Origin of AFib wave?
Pulmonary vein
How pulmonary veins act as ectopy despite not have cardiac tissue?
Part of left atrial cardiac tissue extends to the pulmonary vein and acts as a spnicter.
Why this ectopic cardiac tissue is the common location?
They have different properties to that of surrounding cardiac tissue.
The therapeutic value of knowing these foci?
In AFib which not respond to medication we do catheter-based radiofrequency ablation–disrupt waves–disconnect the foci area electrical activity from the left atrial myocyte.
AVNRT ECG future?
Narrow QRS interval
Regular R-R interval
Absent /Retrograde P wave
P wave in front or after QRS
Pathophysiology?
Fast (found Superior and posterior to AV node) and slow(found inferior and posterior to AV node, anterior to coronary artery orifice) –form reentrant circuit at the right atrium. But unlike AVRT no pass ventricle by traversing the AV node.
Symptom?
The most common SVT Palpitation canon A waves Hypotension Lightheadedness Sudden onset and termination
Risk of chronic venous stasis?
Obesity
Advanced age
Previous DVT
Varicose vein
Pathophysiology?
low well tensile strength and venous hypertension–make valve more incompetent–back ward flow–plasma/protein and RBC leak through capillary–Dermatitis.
Clinical manifestation?
leg pain(Itchy and achy)
edema(pitting)
venous dilation(varicosities and telegectasis)
ulcer
woody induration and brown discoloration(due to hemosiderin accumulation)?
Ulcer(due to platelet, protein extravasation, and microvascular disease)common in medial malleolus.
Management?
Leg elevation
Stocking
exercise
Avoiding of prolonged standing
Diagnosis?
usualy clinical
Duplex u/s(not done routinley) specialy unilateral one to d/t from dvt
what we see on D U/S?
Venous HTN
Regurgitsnt flow
Necrobiosis lipoidica diabeticorum?
Found Inpatient with the diagnosis of DM
May precede DM(screen with HA1C)
clinical manifestation?
occur commonly in the pretibial area and maybe multifocal
brown dilated blood vessel with central epidermal atrophy.
Common S/E of CCB?
Peripheral edema
common in dihydropyridine one
pathophysiology?
precapillary arteriolar dilation—increase hydrostatic pressure
management?
ACE inhibitors or ARB(Dilate postcapillary venules)
what is the common location of edema that occurs secondary to ace inhibitor?
Lip, Tongue, Upper airway, and face
The complication of vasopressor treatment?
Decrease B/F to the periphery
- -Symetric extremity gangren
- -Renal Failure
- -Mesenteric ischemia
Does the most common disease occur in the next 5 years with patients having PAD and Have intermittent claudication?
MI and stroke(25%)
Death due to CVS event (15-30%)
mentioned as Coronary artery disease equivalent
Normal prognosis of PAD in 5 years?
70-80 %–remain the same
10-20%–progress to worsening of claudication?
1-2 %–complete ischemia–resting pain, nonhealing ulcer, gangrene–leg amputation
High ouput heart failure pathophisiology?
Decrease S.vascular resistance—High cardiac output–high venous return–increase preload– LV compensate early by an increased contraction and eccentric hypertrophy latley–LV decompensation lately–peripheral and pulmonary edema.
Factors that cause high output HF by what mechanism
Decrease S.vascular resistance
cause of decrease SVR.
- Increase the quality of pheripherial vesels
- Bypass of systemic arteriolar resistance
- Vasodilation due to unmet tissue metabolic demand
factors Increase the quality of pheripherial vesels?
Morbid obesity
Paget disease
factor cause bypass of systemic arteriolar resistance?
Congenital AV fistula
Acquired AV fistula–Trauma, Hemodialysis
Do factors cause vasodilation due to unmet tissue metabolic demand?
Anemia
Hyperthyroidism
Thiamin deficiency
Clinical manifestation?
Symptom of HF(both right and left) Hyperdynamic circulation(increase PP, brisk carotid puls
What factor increase mechanical complication occurs after MI?
Delay in-stent placment(>=24 Hr) start from symptom
What is mechanical complication occurs after MI and their day?
Ventricular failure(acute)
Papillary muscle rapture(3-5 day)
Ventricular septum rapture (3 days–5 week)
Fre wall rapture(5-7 day)
Ventricular aneurysm–up to several months
VSR symptom?
HF(R and L)
Harsh hollo-systolic murmur and thrill
cardiogenic shock
chest pain
The common cause of MSK pain?
costochondritis
clinical manifestation?
sharp,localize(CS and CC joint area) pain
aggravated bay movement, cough, and inspiration
localized tenderness and reproduce pain
pain occurs in rest to
Management?
Reassurance(self-limited, rarely progress to years)
Local or systemic NSAID
cause of MR in MI patient
Acutely–papillary muscle displacement due to LVM hypokinesis
Late(3-5 day)–papillary muscle rapture
Constrictive pericarditis causes?
Idiopathic/viral
surgery/radiation
Tuberculosis
Tumor/uremia
Clinical manifestation
right side HF symptom
pericardial knock
pulses paradoxus
kassmul sighn
CXR?
pericardial calcification
ECHO?
atrial enlargement
abnormal septal movment
pericardial thickening
ECG?
Non-specific
Afib sign
Low QRS voltage
jugular venous tracing?
rapid x and y decent
Laboratory?
hypoalbuminemia (due to intestinal lymphangiectasia due to increased CVP –protein-losing enteropathy)
Normal JVP?
<8 cm H2O
Normal serum albumin level?
3.4-5.4 mg/dl
management of constrictive pericarditis?
Diuretic–temporary relief
Pericardiotomy–definitive management for persistent symptoms
ISH definition?
systolic >140 and diastolic <90
a common cause of ISH?
Aging due to increasing stiffness in the aortic and arterial wall.
Differential for ISH?
Disease cause increase pulse pressure
How to d/t?
In disease cause increase PP there will be a sign of hyperdynamic circulation
management of ISH?
lifestyle modification
CCB and low dos thiazid
Loop diuretics S/E on HF patient.
Hypokalemia and Hypomagnesimia
This electrolyte imbalance also potentiate digoxin toxicity
Clinical manifestation of systemic amyloidosis?
Involve many systems
Renal?
Heavy proteinuria
pheripherial edema
cardiac?
restrictive cardiomyopathy
conduction abnormality
low voltage
CNS?
stroke
autonomic neuropathy
pheripherial neuropathy
GI?
hepatomegaly
malabsorption and dysmotility
Gi bleeding due to vascular fragility
Pulmonary?
pulmonary nodule
pleural effusion
tracheobronchial infilitration
MSK?
Tongue enlargement
Shoulder pad enlargement
hematology?
Anemia
Thrombocytopnia
skin?
Thickening of skin
subcutaneous nodule/plaque
ecchymosis
periorbital edema
